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"explanation": "Anticoagulation is indicated if her CHA<sub>2</sub>DS<sub>2</sub>-VASc score is 2 or more. She only has a score of 1 for being female",
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"explanation": "We can be fairly certain that this woman's onset of atrial fibrillation is less than 48 hours, and since she's presented to an acute medical unit, DC cardioversion would be the most appropriate management. Factors favouring rhythm control over rate control in this case include being symptomatic, the first presentation of atrial fibrillation, and her age. She may require anticoagulation prior to cardioversion.\n\nHad this patient presented to the GP, management in primary care could also be considered, depending on patient preferences and clinical judgement",
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"explanation": "Bisoprolol may be used to rate control atrial fibrillation (AF). However, as this is her first presentation of AF, she is young and symptomatic, and she has presented to the emergency department, rhythm control would be more favourable in the first instance.\n\nIn primary care, rate control may be initiated rather than cardioversion, depending on patient preference and clinical judgement",
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"explanation": "TOEs may sometimes be used to exclude a left atrial appendage thrombus before cardioversion if the onset of AF was more than 48 hours prior to the planned cardioversion, as an alternative to anticoagulation",
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"comment": "hello everyone - good luck for all your exams xoxo",
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"comment": "you too!! good luck :)",
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"comment": "Thank you!",
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"comment": "Would you not rate control and DC cardiovert as OP? She's 95bpm and no other evidence of haemodynamic compromise? Or is this because it's her first presentation you hit her with DCCV??",
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"comment": "If presenting with very recently started AF you cardiovert, if it is longer standing or there is doubt about onset then either rate control or delayed cardioversion with anticoagulation",
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"comment": "There is no evidence that she is symptomatic or haemodynamically unstable. She has presented <48 hours and so rhythm or rate control can be used. Does this question require re-writing?",
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"comment": "She IS symptomatic, she's come in to A&E with palpitations. Since the history is <48 hours, her risk of clots is low so she can be cardioverted straight away, as is preferred.",
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"comment": "in what world is she asymptomatic with palpitations? ",
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"explanation": "# Summary \r\n\r\nAtrial fibrillation (AF) is the most common arrhythmia characterised by irregular and uncoordinated atrial contraction at a rate of 300-600 beats per minute. Its prevalence increases with age, and it can be caused by various cardiac and non-cardiac factors. Symptoms of AF include palpitations, chest pain, shortness of breath, lightheadedness, and syncope. Diagnosis is confirmed by an ECG showing the absence of p waves and an irregularly irregular rhythm. Management depends on the acute or chronic nature of the AF and involves rate or rhythm control strategies. Anticoagulation is essential to mitigate the risk of stroke in chronic AF. Complications include heart failure, embolism, and bleeding. With appropriate management, AF has a favourable prognosis.\r\n\r\n# Definition \r\n\r\nAtrial fibrillation (AF) is characterised by irregular, uncoordinated atrial contraction usually at a rate of 300-600 beats per minute. Delay at the AVN means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response.\r\n\r\n# Epidemiology \r\n\r\nAF is the commonest sustained cardiac arrhythmia. The prevalence of AF roughly doubles with each advancing decade of age, from 0.5% at age 50 years to almost 9% at age 80 years.\r\n\r\n# Pathophysiology\r\n\r\nThe exact pathophysiology of AF is unclear, but factors that cause atrial dilatation through inflammation and fibrosis leads to disorganised electrical impulses (which originate near the pulmonary veins) that overwhelm the SAN. These disorganised electrical impulses are usually at a rate of 300-600 beats per minute and are intermittently conducted through the AVN leading to irregular activation of the ventricles. \r\n\r\n# Classification \r\n\r\n* Acute: lasts <48 hours\r\n* Paroxysmal: lasts <7 days and is intermittent\r\n* Persistent: lasts >7 days but is amenable to cardioversion\r\n* Permanent: lasts >7 days and is not amenable to cardioversion\r\n\r\nAtrial fibrillation can also be classified as to whether it is 'fast' or 'slow'. Fast AF refers to AF that is at a rate of =>100bpm. Slow AF refers to AF that is at a rate of <=60bpm. \r\n\r\n# Causes \r\n\r\nCardiac:\r\n\r\n* Ischaemic heart disease: most common cause in the UK. \r\n* Hypertension\r\n* Rheumatic heart disease (typically affecting the mitral valve): most common cause in less developed countries.\r\n* Peri-/myocarditis\r\n\r\nNon-cardiac:\r\n\r\n* Dehydration\r\n* Endocrine causes e.g. hyperthyroidism\r\n* Infective causes e.g. sepsis \r\n* Pulmonary causes e.g. pneumonia or pulmonary embolism\r\n* Environmental toxins e.g. alcohol abuse\r\n* Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia \r\n\r\n# Symptoms\r\n\r\n* Palpitations\r\n* Chest pain\r\n* Shortness of breath\r\n* Lightheadedness\r\n* Syncope\r\n\r\n# Signs\r\n\r\n* Irregularly irregular pulse rate with a variable volume pulse.\r\n* A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction).\r\n* An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles).\r\n* On auscultation there may be a variable intensity first heart sound.\r\n* Features suggestive of the underlying cause e.g. hyperthyroidism, alcohol excess, sepsis\r\n* Features suggestive of complications resulting from the AF e.g. heart failure.\r\n\r\n# Differential Diagnoses \r\n\r\nImportant differentials for atrial fibrillation include other common causes of narrow and broad complex tachycardias. Tachycardias may present with palpitations, shortness of breath, and dyspnoea. \r\n\r\n* **Atrial Flutter** \r\n\t* **Similarities**: atrial flutter may have a regular peripheral pulse or may be irregularly irregular if the flutter has variable block. Atrial fibrillation leads to an irregularly irregular peripheral pulse on palpation.\r\n\t* **Differences**: distinguishing between the two requires an ECG. Atrial fibrillation on ECG shows a fibrillating baseline with no visible p waves. Atrial flutter characteristically has a sawtooth baseline. \r\n\r\n* **Supraventricular Tachycardia**\r\n\t* **Similarities**: atrial flutter is a type of SVT, and other types including AVNRT and AVRT may present identically. \r\n\t* **Differences**: distinguishing between different types of SVT requires an ECG. \r\n\r\n* **Ventricular Tachycardia**\r\n\t* **Similarities**:both may present similarly. \r\n\t* **Differences**: the ECG patterns differ tremendously. \r\n\r\nFor palpitation histories, it is also important to consider whether the presentation is being driven by anxiety. However, it is important as a rule of thumb to rule out organic causes first. \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n**Definitive diagnosis: 12-lead ECG** shows absence of p waves with an irregularly irregular rhythmn. \r\n\r\n[lightgallery]\n\n- If a person has a suspected diagnosis of paroxysmal AF which is not detected on standard ECG, arrange ambulatory electrocardiography or cardiology referral, depending on the frequency and duration of symptoms and local referral pathways\r\n\r\n## Bloods \r\n\r\nRoutine bloods: to look for reversible causes including infection (raised WCC or CRP), hyperthyroidism (raised T3/T4) or alcohol use (raised MCV and GGT).\r\n\r\n## Imaging\r\n\r\nEchocardiogram: can be used to see if there is a cardiac cause of the AF e.g. left atrial dilatation secondary to mitral valve disease. \r\n\r\n# Management\n\nConsider emergency admission or Cardiology referral if a patient presents with:\n\n- New-onset AF within the past 48 hours and is haemodynamically unstable\n- Severe symptoms of AF due to rapid (bpm > 150 ) or very slow (bpm < 40) ventricular rate\n- Concomitant acute decompensated heart failure\n- Complications of AF, such as TIA/stroke\n- An acute, potentially reversible trigger such as pneumonia/sepsis or thyrotoxicosis\n\nIf they do not require acute management or emergency admission, they can be considered for anticoagulation and rate-control treatment in primary care.\r\n\r\n## Management of Acute or New-onset Atrial Fibrillation\r\n\r\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **synchronised DC cardioversion +/- amiodarone.**\r\n\r\n*If there are no adverse signs:* and the rhythm is irregular it is likely atrial fibrillation. \r\n\r\n* **If the patient is stable and onset of AF <48 hours**: \r\n\t* Rate or rhythmn control.\r\n\t* Rhythm control with DC cardioversion (+ sedation) or pharmacological anti-arrhythmics (fleicanide if no structural heart disease, amiodarone if history of structural heart disease). \r\n\t* If DC cardioversion is delayed then heparin will be required to anticoagulate the patient. \r\n\r\n* **If the patient is stable and onset of AF >48 hours/unclear time of onset**: \r\n\t* Rate control only. \r\n\t* Rate control with beta-blockers, diltiazem or digoxin. \r\n\t* Need to anticoagulate for 3/52 prior to attempting cardioversion due to the risk of throwing off a clot. You can also perform a TOE to exclude a mural thrombus. \r\n\r\nIf AF persists or reversible causes are not present then decisions should be made about rate control, rhythm control or electrical cardioversion.\r\n\r\n## Management of Chronic AF \r\n\r\nThe cornerstones of managing chronic AF are related to symptom control and mitigating stroke risk. \r\n\r\n## Symptom Management of Chronic AF \r\n\r\n### Rate vs. Rhythm Control \r\n\r\n#### Rate-Control\r\n\r\nThe aim of rate control is to reduce a patient's heart rate in order to reduce symptoms.\r\n \r\n* First line in most patients. See below for patients who should undergo rhythm control. \r\n* **1st line medications:** beta-blocker (bisoprolol) or rate-limiting calcium channel blocker (diltiazem). \r\n* **2nd line medications**: dual therapy (under specialist guidance) \r\n* Digoxin monotherapy may be considered in those with non-paroxysmal AF who are sedentary. \r\n \r\n#### Rhythm Control\r\n\r\nThe aim of rhythm control is to revert a patient back into sinus rhythm. \r\n \r\nRhythm control should be offered to patients who have: \r\n\r\n* AF secondary to a reversible cause\r\n* Heart failure thought to be caused by AF\r\n* New-onset AF\r\n* Or those for whom a rhythm control strategy would be more suitable based on clinical judgement. \r\n\r\nRhythm control can be achieved via two methods:\r\n\r\n* Electrical cardioversion\r\n* Pharmacological cardioversion: amiodarone, fleicanide or sotalol. \r\n\r\nThe moment of return to sinus rhythm poses the highest stroke risk. Therefore, rhythm control should only be attempted if the onset of AF <48 hours, a patient has undergone 3/52 of anticoagulation or has had a TOE to exclude a mural thrombus. \r\n\r\nNote that patients in chronic AF or those who have failed cardioversion before are unlikely to be successfully cardioverted so this would not be considered in most of these cases.\r\n\r\n#### Catheter Ablation \r\n\r\nA final option for rhythm control is catheter ablation of the arrhythmogenic focus between the pulmonary veins and left atrium. Even if teh foci is ablated, this does not reduce stroke risk and the patient must be anticoagulated. There is a high risk of recurrence (50% have recurrent AF). \r\n\r\n## Medications used for Rate Control \r\n\r\n### Beta-blockers\r\n\r\n* The most commonly used beta-blocker in AF is bisoprolol.\r\n* Commonly used medication for acute treatment and chronic management.\r\n* Technically it is contraindicated in COPD and asthma (in reality unless the conditions are considered _brittle_ it is not a problem). \r\n* Cannot be used in hypotension because it will drop blood pressure.\r\n* Note that sotalol CANNOT be used as a rate control agent because of its rhythm control action.\r\n\r\n### Non-dihydropyridine calcium channel blockers\r\n\r\n* Calcium channel blockers used in AF are diltiazem or verapamil.\r\n* They are not frequently used in hospital settings because they are negatively ionotropic and therefore they are contraindicated in heart failure.\r\n\r\n### Digoxin\r\n\r\n* Usual for patients who are hypotensive or who have co-existent heart failure.\r\n* Should be avoided in younger patients because it increases cardiac mortality.\r\n* Often used second-line in conjunction with beta-blockers if fast AF remains refractory.\r\n\r\n## Medications used for Rhythm Control\r\n\r\n* Flecainide\r\n * Can be either given regularly or as a \"pill in the pocket\" when symptoms come on.\r\n * Is preferred in _young patients_ who have _structurally normal hearts_ because it can induce fatal arrhythmias in those with structural heart disease.\r\n\r\n* Amiodarone\r\n * Extremely effective drug in controlling both rate and rhythm.\r\n * However it comes with a massive list of significant side-effects so should normally only be given to _older, sedentary patients_.\r\n\r\n* Sotalol\r\n * This is a beta blocker with additional K channel blocker action.\r\n * Used for those that don't meet the demographics for either flecainide or amiodarone.\r\n\r\n## Mitigating Stroke Risk in Chronic AF \r\n\r\nIn atrial fibrillation, the lack of organised atrial contraction can lead to blood stasis in the left atrium. Due to the left atrial appendage, blood clots easily here and if part of this clot embolises it can lead to a stroke. Therefore, if a patient has any history of atrial fibrillation or atrial flutter the need for anticoagulation must be considered. \r\n\r\nPatients need to be considered according to their stroke risk (CHADS2VASc score) and their bleeding risk (ORBIT score) to determine whether anticoagulation is appropriate. \r\n\r\n### CHADS2VASc Score\r\n\r\nPatients should be risk stratified using the CHADS2VASc score:\r\n\r\n* C: 1 point for congestive cardiac failure.\r\n* H: 1 point for hypertension.\r\n* A2: 2 points if the patient is aged 75 or over.\r\n* D: 1 point if the patient has diabetes mellitus.\r\n* S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA).\r\n* V: 1 point if the patient has known vascular disease.\r\n* A: 1 point if the patient is aged 65-74.\r\n* Sc: 1 point if the patient is female.\r\n\r\n#### Interpretation of the CHADS2VASc score\r\n\r\nThe minimum score is 0 (associated with 0% annual stroke risk) and maximum score is 9 (15% annual stroke risk).\r\nMales who score 1 or more or females who score 2 or more should be anticoagulated (as long as the risk of stroke outweighs the risk of bleeding). \r\n\r\n#### ORBIT Score\r\n\r\nRisks of anticoagulation also need to be considered. Historically the HASBLED score stratified bleeding risk:\r\n\r\n* H: Hypertension 1 point\r\n* A: Abnormal renal or liver function 2 points if both are present\r\n* S: Stroke (previous) 1 point\r\n* B: Major bleed (previous) 1 point\r\n* L: Labile INR 1 point\r\n* E: Elderly (>65) 1 point\r\n* D: Drugs/alcohol 1 point for drug or alcohol use (2 points if both are present)\r\n\r\nIn their 2021 AF guidelines NICE suggested the use of the ORBIT score which takes into account:\r\n\r\n* Sex\r\n* Haemoglobin (<13mg/Dl in males, <12mg<dL in females) 2 points\r\n* Age (>74) 1 point\r\n* Bleeding history 2 points\r\n* Renal function (eGFR <60) 1 point\r\n* Concomitant use of anti-platelets 1 point\r\n\r\n#### Interpretation of the HASBLED and ORBIT scores\r\n\r\nIn reality very little guidance exists about how to weigh up the stroke and bleeding risks when making a decision on anticoagulation. Choice of long term anticoagulation is generally a decision led by patient choice and clinical judgement.\r\n\r\n### Anticoagulation options in AF\r\n\r\n* **Direct oral anticoagulants (DOACs)**:\r\n * Considered first line for anticoagulation in AF. \r\n * Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran\r\n * **Do not** require monitoring\r\n * Generally associated with fewer bleeding risks compared to warfarin.\r\n * Most have approximately 12 hour half-lives therefore if a patient misses a dose they are not covered.\r\n\r\n* **Warfarin**:\r\n * Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially _prothrombotic_).\r\n * Requires regular INR monitoring.\r\n * INR can be affected by a whole host of drugs and foods.\r\n * Has 40 hour half-life therefore anticoagulant effect lasts days.\r\n * Is the only oral anticoagulant licenced for **valvular AF**.\r\n* **Low Molecular Weight Heparin (LMWH)**:\r\n * An example of a LMWH is enoxaparin.\r\n * A rare option in patients who cannot tolerate oral treatment.\r\n * Involves daily _treatment dose_ injections.\r\n\r\n# Complications\r\n\r\nMost complications are either from uncontrolled heart rate, embolism or from anticoagulation. They include:\r\n\r\n* Heart failure\r\n* Systemic emboli:\r\n * Ischaemic Stroke\r\n * Mesenteric ischaemia\r\n * Acute limb ischaemia\r\n* Bleeding:\r\n * GI\r\n * Intracranial\r\n \r\n# Prognosis \r\n\r\nIf patients are anticoagulated and are on either rhythm or rate control AF can remain a benign cardiac arrhythmia. \r\n\r\n# NICE Guidelines\r\n\n[Click here to see information on NICE CKS guidance for AF](https://cks.nice.org.uk/topics/atrial-fibrillation/)\r\n\r\n# References\r\n \r\n[Live Life in the Fast Lane AF ECG Summary](https://litfl.com/atrial-fibrillation-ecg-library/)",
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"question": "A 62-year-old woman presents to the Accident and Emergency department with a sudden onset of palpitations 6 hours earlier. In the department, her ECG shows atrial fibrillation at a rate of 95 beats per minute. She has a past medical history of asthma, and had an NHS Health Check the day before, where she was noted to be in sinus rhythm.\n\nWhich of the following is the most suitable next step in the management of this patient?",
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"explanation": "There is no indication of ST-elevation on this ECG. A STEMI will cause ST elevation acutely, but it is important to note that the ECG changes will evolve over time",
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"explanation": "Acute pericarditis is associated with global concave ST elevation and PR depression, which is not seen on this ECG",
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"explanation": "This ECG shows left ventricular hypertrophy (increased amplitude of the QRS complex, particularly noticeable in V1-V4) and non-specific T-wave inversion. In an otherwise young, healthy person, the most likely cause of left ventricular hypertrophy is HCM. This would also explain his symptoms of chest pain and shortness of breath on exertion. He should be referred for an urgent cardiology review for consideration of an implantable cardioverter-defibrillator (ICD)",
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"explanation": "Hyperkalaemia is classically associated with \"tall tented T waves\" on an ECG, which are not seen on this ECG",
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"explanation": "RBBB is associated with a QRS duration of >120ms and an RSR' pattern in V1-V3 (\"M-shaped\" as in \"WiLLiaM MaRRoW\"), which is not seen on this ECG",
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"comment": "can't see all of the ecg\n",
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"comment": "Doesnt seem like an LVH on ecg",
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"comment": "agreed - should be deep S waves in V1/V2 and tall R waves in V5/V6",
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"explanation": "# Summary\r\n\r\nHypertrophic cardiomyopathy (HCM) is an autosomal dominant condition characterised by left ventricular hypertrophy without an apparent cause. It is a common inherited cardiac condition and a significant cause of sudden cardiac death in young adults. HCM is attributed to mutations in genes encoding sarcomere proteins leading to chaotic and disorganized myocytes. HCM may be asymptomatic but can also lead to exertional syncope, dyspnoea, chest pain and heart failure. Definitive diagnosis is made via echocardiogram. Management involves lifestyle modifications, medication for symptom control, surgical or interventional procedures for severe cases, and consideration of implantable cardioverter-defibrillators in those at risk of sudden cardiac death. Prognosis varies, with an annual mortality rate of 1.1%, and a 20-year survival rate estimated at 81% after diagnosis.\r\n\r\n# Definition \r\n\r\nHypetrophic cardiomyopathy (HCM) is an autosomal dominant condition characterised by asymmetrical septal hypertrophy leading to left ventricular hypetrophy and diastolic dysfunction in the absence of an obvious cause (e.g. hypertension). \r\n\r\n# Epidemiology \r\n\r\nHCM is estimated to impact 1 in 500 people. It is the most common inherited cardiac condition. Inheritance of HCM is in an autosomal dominant fashion. However, 50% of cases result due to sporadic mutations. Most of the hypertrophy develops during childhood and adolescent, however, genetic variation means late-onset disease can occur.\r\n\r\n# Pathophysiology\r\n\r\nHCM is attributed to mutations in one or a number of genes that encode for sarcomere proteins. A common mutation is in the beta-myosin heavy chain gene leading to myocyte hypetrophy with chaotic and disorganised myocytes. \r\n\r\n# Symptoms\r\n\r\n* May be asymptomatic \r\n* Or can present with symptoms of left ventricular outflow obstruction, pulmonary congestion or heart failure: \r\n\t* Exertional syncope \r\n\t* Pre-syncope/syncope\r\n\t* Sudden cardiac death \r\n\t* Exertional dyspnoea \r\n\t* Fatigue\r\n\t* Chest pain: may be anginal (due to decreased blood flow through the coronary arteries) or atypical. \r\n\r\n# Signs\r\n\r\nPhysical examination can often be normal or non-specific, however typical findings may include:\r\n\r\n* \"Jerky\" pulse\r\n* Double apex beat\r\n* Harsh ejection systolic murmur\r\n* Apical thrill\r\n* A wave in JVP \r\n\r\n# Differential Diagnoses\r\n\r\n* Aortic Stenosis \r\n\t* Similarities: both may have an ejection systolic murmur and present similarly with chest pain, exertional syncope and dyspnoea. \r\n\t* Differences: can be difficult to delineate clinically, but demographics may be very different. Aortic stenosis tends to affect older patients, whilst HOCM is likely to be found in younger patients. \r\n\r\n* Hypertensive Disease \r\n\t* Similarities: chronic high blood pressure can lead to left ventricular hypertrophy. \r\n\t* Differences: echocardiogram reveals asymmetrical left ventricular hypertrophy in HOCM. Family history and patient demographics may also suggest HOCM over hypertensive disease. \r\n\r\n* Supravalvular Aortic Stenosis: \r\n\t* Similarities: both may have an ejection systolic murmur. \r\n\t* Differences: supravalvular aortic stenosis is a congenital cardiac condition whereas HOCM tends to develop over time. Supravalvular stenosis can be distinguished from HOCM on echocardiography due to the level of obstruction either above or below the aortic valve respectively. \r\n\r\n# Investigations\r\n\r\n**ECG** typically demonstrates: \r\n\r\n* Abnormal Q waves\r\n* Deep T wave inversion \r\n* LVH \r\n\r\n**Echocardiogram: definitive diagnosis** \r\n\r\n* HCM is reliably diagnosed on echocardiogram. \r\n* Findings of HOCM on echocardiogram can be remembered with the mnemonic 'MR SAM ASH'. \r\n\t* **M**itral **R**egurgitation\r\n\t* **S**ystolic **A**nterior **M**otion of the mitral valve leaflets \r\n\t* **A**symmetrical **S**eptal **H**ypertrophy. \r\n\r\n**Genetic testing:** there is a role for genetic testing in HCM in families where there are known cases of HCM. \r\n\r\n# Management\r\n\r\n## Conservative \r\n\r\nMany patients with HCM do not have any symptoms and have a normal life expectancy. They are often counselled on not undertaking particularly stressful exercise or competitive athletics. \r\n\r\n## Medical \r\n\r\nMedical treatment of HCM remains symptoms control. \r\n**1st line: beta-blockers** to reduce palpitations symptoms, ectopic beats and are anti-anginal. \r\n\r\nOther medications that can be used are: non-dihydropyridine calcium channel blockers (verapamil), anti-arrhythmics (amiodarone) and anticoagulation (for AF). \r\n\r\n## Surgical and Interventional\r\n\r\nManagement of the septal hypetrophy in those with severe left ventricular outflow tract obstruction (LVOTO) or symptoms that are refractory to medical management. \r\n\r\n* Surgical septal myectomy\r\n* Alcohol septal ablation\r\n\r\nFor those at significant risk of sudden cardiac death an ICD may be inserted to mitigate this risk. \r\n\r\n# Complications\r\n\r\nThe abnormal morphology of the left ventricle can cause severe consequences for heart function: \r\n\r\n* Left ventricular outflow tract obstruction (LVOTO)\r\n* Diastolic dysfunction: HFpEF\r\n* Ischaemia \r\n* Mitral regurgitation: MR SAM ASH on echocardiogram \r\n\r\n# Prognosis \r\n\r\nThe annual mortality rate for HCM is 1.1% of people per year and the HCM survival rate is estimated to be 81% at 20 years after diagnosis. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Non-Surgical Reduction of the Myocardium in HCM](<https://www.nice.org.uk/guidance/ipg40>)\r\n\r\n# References\r\n\r\n[Patient UK HCM Summary](<https://patient.info/doctor/hypertrophic-cardiomyopathy-pro>)\n\r\n[American Heart Association Article on HCM](<https://www.ahajournals.org/doi/full/10.1161/circresaha.116.309348>)",
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"question": "An 18 year old man attends to his GP with chest pain and shortness of breath on exertion. He has no significant past medical history. An ECG is performed:\n\n[lightgallery]\n\nWhich of the following is the most likely to account for the ECG findings?",
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"explanation": "Unstable angina does not produce ST elevation on an ECG. Much like NSTEMI, unstable angina can produce ECG changes such as ST-segment depression and T wave flattening or inversion. Unstable angina can be differentiated from NSTEMIs as unstable angina does not cause a rise in cardiac enzymes 8-12 after the onset of symptoms",
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"explanation": "An NSTEMI, by definition, does not produce ST elevation on an ECG. ECG changes in an NSTEMI include ST-segment depression and T wave flattening or inversion, and can be differentiated from unstable angina by raised cardiac enzymes 8-12 after the onset of symptoms",
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"explanation": "GORD will not produce ECG changes, however, does manifest as burning chest pain",
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"explanation": "The ECG demonstrates ST elevation (>0.1mV) in the inferior leads (II, III and aVF) as well as reciprocal depression in the anterior leads. Central crushing chest pain is the classical symptom associated with a STEMI",
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"explanation": "# Summary\r\n\r\nAcute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.\r\n\r\n# Definition \r\n\r\nAcute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). \r\n\r\n# Epidemiology \r\n\r\nIn the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. \r\n\r\n# Pathophysiology\r\n\r\nCoronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). \r\n\r\n# Risk Factors\r\n\r\nCoronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. \r\n\r\n* Non-modifiable:\r\n * Age\r\n * Male sex\r\n * Family history\r\n * Ethnicity (particularly South Asians)\r\n* Modifiable:\r\n * Smoking\r\n * Hypertension\r\n * Hyperlipidaemia\r\n * Hypercholesterolaemia\r\n * Obesity\r\n * Diabetes\r\n * Stress\r\n * High fat diets\r\n * Physical inactivity\r\n\r\n# Classification \r\n\r\nAcute coronary syndrome can be split up into three distinct diagnoses: \r\n\r\n1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. \r\n2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. \r\n3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. \r\n\r\n*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*\r\n\r\nIt is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.\r\n\r\n*Type 2 Myocardial Infarction* \r\n\r\nIt is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. \r\n\r\n# Symptoms and Signs\r\n\r\n* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:\r\n * Site - Central/left sided\r\n * Onset - Sudden\r\n * Character - Crushing ('like someone is sitting on your chest')\r\n * Radiation - Left arm, neck and jaw\r\n * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope\r\n * Timing - Constant\r\n * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN\r\n * Severity - Often extremely severe\r\n* Atypical presentations may include:\r\n * Epigastric pain\r\n * No pain (more common in elderly and **patients with diabetes**):\r\n * Acute breathlessness\r\n * Palpitations\r\n * Acute confusion\r\n * Diabetic hyperglycaemic crises\r\n * Syncope\r\n\r\n# Differential Diagnoses\r\n\r\nIt is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:\r\n\r\n* Cardiac\r\n * Myocarditis\r\n * Pericarditis\r\n * Cardiomyopathy\r\n * Valvular disease\r\n * Cardiac trauma\r\n* Pulmonary\r\n * PE\r\n * Pneumonia\r\n * Pneumothorax\r\n* Vascular\r\n * Aortic dissection\r\n* GI\r\n * Oesophageal spasm\r\n * Oesophagitis\r\n * Peptic ulcer\r\n * Pancreatitis\r\n * Cholecystitis\r\n* MSK\r\n * Rib fracture\r\n * Costochondritis\r\n * Muscle injury\r\n * Herpes zoster\r\n\r\n# Diagnosis of ACS \r\n\r\nDiagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.\r\n\r\n* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.\r\n* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**\r\n* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).\r\n\r\n## Diagnosis of STEMI\r\n\r\n* ST segment elevation **>2mm** in adjacent chest leads\r\n* ST segment elevation **>1mm** in adjacent limb leads\r\n* New left bundle branch block (LBBB) with chest pain or suspicion of MI\r\n\r\n## Diagnosis of NSTEMI\r\n\r\nDiagnosis of NSTEMI requires two of the following:\r\n\r\n* Cardiac chest pain\r\n* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. \r\n* Raised troponin (with no other reasonable explanation)\r\n\r\n# Investigations\r\n\r\n## Bedside \r\n\r\n* ECG \r\n\t* Looking for ST-elevation, LBBB or other ST abnormalities\r\n\t* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.\r\n\t* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.\r\n\r\n## Bloods \r\n\r\n* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. \r\n* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. \r\n* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. \r\n* FBC and CRP - rule out infectious causes of chest pain\r\n* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*\r\n\r\n## Imaging \r\n\r\n* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). \r\n\r\n# ECG Interpretation - Cardiac Territories and Affected Vessels\r\n\r\nThe importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different \"views\". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.\r\n\r\n| Location of ST elevation | Area of myocardium | Coronary artery |\r\n| -------------------------- | ------------------ | -------------------- |\r\n| II, III, aVF | Inferior | RCA |\r\n| V1-2 | Septal | Proximal LAD |\r\n| V3-4 | Anterior | LAD |\r\n| V5-6 | Apex | Distal LAD/ LCx/ RCA |\r\n| I, aVL | Lateral | Lcx |\r\n| V7-V9 (ST depression V1-3) | Posterolateral | RCA/ LCx |\r\n\r\n\r\nRCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex\r\n\r\n[lightgallery]\r\n\r\n[lightgallery2]\r\n\r\n[lightgallery3]\r\n\r\n[lightgallery4]\r\n\r\n\r\nNSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.\r\n\r\n# Troponin Interpretation\r\n\r\nTroponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.\r\n\r\nDifferent hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:\r\n\r\n* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.\r\n* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.\r\n * If repeat troponin is raised on the repeat they are having an MI.\r\n * If repeat troponin is stable or falling then they are unlikely to be having an MI.\r\n* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)\r\n\r\n## Non-ACS causes of a raised troponin\r\n\r\nAlthough troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:\r\n\r\n* Myocardial infarction\r\n* Pericarditis\r\n* Myocarditis\r\n* Arrythmias\r\n* Defibrillation\r\n* Acute heart failure\r\n* Pulmonary embolus\r\n* Type A aortic dissection\r\n* Chronic kidney disease\r\n* Prolonged strenuous exercise\r\n* Sepsis\r\n\r\nIt is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.\r\n\r\n# Management\r\n\r\nAcute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. \r\n\r\n# Management of STEMI\r\n\r\n[lightgallery5]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg**\r\n - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)\r\n - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Primary percutaneous coronary intervention (PPCI) for those who:\r\n - Present **within 12 hours of onset of pain** AND\r\n - Are **<2 hours** since <u>first medical contact</u>\r\n\r\nRemember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.\r\n\r\n# Management of NSTEMI/Unstable Angina\r\n\r\n[lightgallery6]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg** and fondaparinux\r\n * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram\r\n6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.\r\n\r\nNote that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.\r\n\r\n# Post-MI management\r\n\r\n[lightgallery7]\r\n\r\n* ALL patients post-MI patients should be started on the following 5 drugs:\r\n 1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)\r\n 2. **Beta blocker (normally bisoprolol)**\r\n 3. **ACE-inhibitor (normally ramipril)**\r\n 4. **High dose statin (e.g. Atorvastatin 80mg ON)**\r\n* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.\r\n* All patients should be referred to **cardiac rehabilitation**.\r\n* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. \r\n\r\n# Complications\r\n\r\n* Ventricular arrhythmia\r\n* Recurrent ischaemia/infarction/angina\r\n* Acute mitral regurgitation\r\n* Congestive heart failure\r\n* 2nd, 3rd degree heart block\r\n* Cardiogenic shock\r\n* Cardiac tamponade\r\n* Ventricular septal defects\r\n* Left ventricular thrombus/aneurysm\r\n* Left/right ventricular free wall rupture\r\n* Dressler's Syndrome\r\n* Acute pericarditis\r\n\r\n## Ventricular Arrhythmias\r\n\r\n* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.\r\n* Most post-MI ventricular arrhythmias are short lived and self-resolve.\r\n* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.\r\n\r\n## Recurrent Ischaemia/Infarction/Angina\r\n\r\n* Occasionally inserted stents can thrombose requiring reintervention.\r\n* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.\r\n* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.\r\n\r\n## Congestive Heart Failure\r\n\r\n* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.\r\n* It should be treated as any other acute heart failure.\r\n* Ventricular function may improve over months as the heart muscle recovers.\r\n\r\n## Heart Block\r\n\r\n* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).\r\n* These may be treated with:\r\n * Simple observation (as many will revert back to sinus rhythm)\r\n * Transcutaneous/venous pacing (if symptomatic)\r\n * Permanent pacing (if failing to resolve)\r\n\r\n## Left Ventricular Thrombus/Aneurysm\r\n\r\n* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.\r\n* It may be silent, cause arrhythmias or embolic events.\r\n* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.\r\n* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.\r\n* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.\r\n\r\n## Left/Right Ventricular Free Wall Rupture\r\n\r\n* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.\r\n* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.\r\n* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.\r\n\r\n## Acute Mitral Regurgitation\r\n\r\n* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. \r\n* This presents with:\r\n * Pansystolic murmur heard best at the apex\r\n * Severe and sudden heart failure\r\n* It is diagnosed on echocardiogram and may require surgical correction.\r\n\r\n## Ventricular Septal Defect\r\n\r\n* Interventricular septal rupture is a short-term complications of myocardial infarction.\r\n* Rupture caused by an anterior infarct is generally apical and simple.\r\n* Rupture caused by an inferior infarct is generally basal and more complex.\r\n* Without reperfusion, septal rupture typically occurs within the first week after the infarction.\r\n* Features of septal rupture include:\r\n * Shortness of breath\r\n * Chest pain\r\n * Heart failure\r\n * Hypotension\r\n * Harsh, loud pan-systolic murmur along the left sternal border.\r\n * Palpable parasternal thrill.\r\n* Diagnosis is with echocardiogram.\r\n* Patients are managed with emergency cardiac surgery.\r\n\r\n## Dressler's syndrome\r\n\r\n* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.\r\n* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.\r\n* Symptoms usually resolve after several days.\r\n* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.\r\n* Management: **high dose aspirin**\r\n\r\n# Prognosis \r\n\r\nDue to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)\r\n\n[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)\r\n\r\n# References\r\n\r\n[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)",
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"question": "A 52-year-old Polish man is brought to the accident and emergency department by ambulance. He speaks no English, but he points to his chest to suggest that he is in pain. Blood tests have not yet returned. His ECG is as follows:\n\n[lightgallery]\n\nWhich of the following is the most likely cause for this man's presentation?",
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"explanation": "Flecainide can be used to treat VT, but is not as effective as amiodarone",
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"comment": "The question does not clarify whether the VT is mono- or polymorphic. Although IV mag sulph isn't an answer, it does make the question more confusing",
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"comment": "don't introduce what ifs. If the VT was polymorphic they would have to say so. ",
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"comment": "She has acute exacerbation of heart failure does this not mean DC cardioversion?",
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"comment": "however she is haemodynamically stable\n",
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"comment": "no because heat failure is a long standing problem that is not caused by the arrhythmia ",
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"comment": "How do we know this is Broad Complex? ",
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"explanation": "# Summary \n\nVentricular Tachycardia (VT) is a regular broad complex tachycardia that originates from the ventricles of the heart. The patient may have a pulse or not - if VT is pulseless it is one of the shockable cardiac arrest rhythms. Emergency management involves identification of VT on an ECG or heart monitor, then treating patients with a pulse and no adverse features with IV amiodarone. Patients who do not respond to this or have adverse features should be treated with synchronised DC cardioversion. Patients in cardiac arrest with VT should be treated as per the Advanced Life Support (ALS) algorithm with cardiopulmonary resuscitation (CPR), adrenaline and amiodarone as well as unsynchronised shocks. \n\n# Definition\n \nVentricular Tachycardia (VT) is a type of broad complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of more than 120ms. Other types of broad complex tachycardias include Torsades de Pointes (which is a type of ventricular tachycardia described as polymorphic, where there are multiple ventricular foci) and Supraventricular Tachycardia with aberrant conduction.\n \n[lightgallery]\n \n\n# Aetiology\n \nFactors that increase the risk of VT include:\n \n- Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia\n- Structural heart disease including previous myocardial infarction and cardiomyopathies\n- Drugs that cause QT prolongation e.g. clarithromycin, erythromycin (for Torsades de Pointes) \n- Inherited channelopathies e.g. Romano-Ward syndrome (for Torsades de Pointes)\n\n# Management\n \n**Pulseless VT:**\n\nPulseless VT is one of the four cardiac arrest rhythms, as so is managed as per Advanced Life Support guidelines:\n\n- CPR will be in progress\n- 120-360 J unsynchronised shock should be administered as early as possible, then every 2 minutes\n- IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock\n- Adrenaline should be administered every 3-5 minutes thereafter\n- A further dose of amiodarone 150 mg IV should be given after 5 shocks\n\n**Pulsed VT with adverse features:**\n\nIf a patient has a pulse, management is determined by whether they have any of the following adverse features:\n\n - Heart failure\n - Myocardial ischaemia (chest pain)\n - Shock\n - Syncope\n\nIf one or more of these are present, attempt to cardiovert the patient using synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia.\n\nIf this is not effective, an amiodarone infusion would be the next step under expert guidance (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours).\n\n**Pulsed VT with no adverse features:**\n\nFirst line treatment is amiodarone 300mg IV over 10-60 minutes.\n\nIf this is ineffective then attempt to cardiovert using synchronised DC shocks (up to 3 attempts) with sedation or anaesthesia.\n\n**Torsades de Pointes:**\n\nThis is a special situation which is managed differently to monomorphic VT - Torsades de Pointes often self-terminates but the risk is that it deteriorates into ventricular fibrillation (causing cardiac arrest).\n\nIV Magnesium is the mainstay of treatment, along with treatment of any underlying cause identified (e.g. correcting electrolyte imbalance, stopping QT-prolonging medications).\n\n# References\n \n[Resuscitation Council UK - Adult advanced life support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n\n[Resuscitation Council UK - Adult Tachycardia Algorithm](https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf)\n\n[Patient UK - Torsades de Pointes](https://patient.info/doctor/torsades-de-pointes)",
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"question": "A medical emergency call is put out for a 70-year-old female patient on a medical ward. Ventricular tachycardia (VT) is present on her ECG. She is haemodynamically stable. On examination, she is well perfused, has a GCS of 15, and has pitting oedema to her knees bilaterally.\n\nShe was admitted to hospital three days prior for an exacerbation of heart failure and was being treated with intravenous furosemide.\n\nWhich of the following treatments is most appropriate to manage VT in this patient?",
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"explanation": "This is the management for hyperkalaemia. There are no signs of hyperkalaemia on this ECG",
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"comment": "how do you know this is 2:1 heart block and not U waves?",
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"comment": "Two p waves : One QRS complex\nThe reason its not a U wave is because you can tell there is a QRS complex missing between both p waves in the middle of the rhythm strip ",
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"explanation": "# Summary\r\n\r\nHeart block refers to an obstruction in the electrical conduction system of the heart. This obstruction can occur at various points in the conduction system, including the sinoatrial node, atrioventricular node, Bundle of His, or bundle branches. Atrioventricular heart block specifically affects the conduction between the atria and ventricles. The severity of heart block can range from first degree, which is generally benign, to second degree (Mobitz Type I and II), to complete (third degree) heart block, which requires immediate management with a permanent pacemaker due to the risk of asystole. The underlying causes and management strategies differ for each type of heart block.\r\n\r\n# Definition \r\n\r\nHeart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves. \r\n\r\nSinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail. \r\n\r\nPatients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death. \r\n\r\n# First Degree Heart Block\r\n\r\n## Definition\r\n\r\nThis is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.\r\n\r\n[lightgallery]\r\n\r\n## Causes\r\n\r\n* High vagal tone: e.g. athletes\r\n* Acute inferior MI\r\n* Electrolyte abnormalities: e.g. hyperkalaemia\r\n* Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors\r\n\r\n## Management\r\n\r\nFirst degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.\r\n\r\n# Second Degree Heart Block \r\n\r\nSecond degree heart block is split into Mobitz Type I and Mobitz Type II heart block. \r\n\r\n# Mobitz Type I\r\n\r\n## Definition\r\n\r\nWenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.\r\n\r\n[lightgallery1]\r\n\r\n## Causes\r\n\r\n* MI (mainly inferior)\r\n* Drugs such as beta/calcium channel blockers, digoxin\r\n* Professional athletes due to high vagal tone\r\n* Myocarditis\r\n* Cardiac surgery\r\n\r\n## Management\r\n\r\nIt is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.\r\n\r\n# Mobitz Type II\r\n\r\n## Definition\r\n\r\nMobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The _PR interval is constant_ (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.\r\n\r\nIn most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.\r\n\r\n[lightgallery2]\r\n\r\n## Causes\r\n\r\n* Infarction: particularly anterior MI which damages the bundle branches\r\n* Surgery: mitral valve repair or septal ablation\r\n* Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis\r\n* Fibrosis: Lenegre's disease\r\n* Infiltration: sarcoidosis, haemochromatosis, amyloidosis\r\n* Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone\r\n\r\n## Management\r\n\r\nDefinitive management is with a permanent pacemaker as these <u>_patients are at risk of complete heart block_</u> and at risk of becoming haemodynamically unstable.\r\n\r\n# Complete (Third degree) Heart Block\r\n\r\n## Definition\r\n\r\nComplete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.\r\n\r\nECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest. \r\n\r\n[lightgallery3]\r\n\r\n## Causes\r\n\r\n* Myocardial infarction: especially inferior\r\n* Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine\r\n* Idiopathic fibrosis\r\n\r\n## Management\r\n\r\nManagement of complete (third degree) heart block is via the acute bradycardia guideline (see below). Permanent pacemaker insertion is eventually required due to the risk of sudden death.\n\nAcute management:\n\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **500 micrograms atropine IV**\r\n * Atropine blocks the vagal nerve which increases firing rate of the SAN. \r\n* **2nd line** = if the first dose of atropine is not working can consider giving additional doses of atropine 500mcg up to 3mg until response. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs but a risk of asystole, or a satisfactory response to 500mcg atropine:*\r\n\r\n* Risk of asystole: recent asystole, mobitz type II block, complete heart block + broad QRS, ventricular pauses >3s. \r\n* **1st line** = administer **500 micrograms atropine IV**. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs and there is no risk of asystole*\r\n\r\n* Observe\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Pacing](<https://www.nice.org.uk/guidance/ta88/chapter/2-clinical-need-and-practice>) \r\n\r\n# References\r\n\r\n[Life in the Fast Lane Heart Block ECG Summary](https://litfl.com/heart-block-and-conduction-abnormalities/)\r\n\r\n[Resuscitation Council Adult Bradycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2020-05/G2015_Adult_bradycardia.pdf>)",
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"question": "A 75-year-old man is brought to the emergency department by ambulance with a collapse. He reportedly lost consciousness with no pre-syncopal symptoms, was unconscious for approximately 20 seconds, and regained consciousness quickly. He reports this has happened twice in the last few weeks. Part of the rhythm strip from his ECG performed by the ambulance service may be seen below.\n\n[lightgallery]\n\nWhich of the following is the most suitable treatment for this patient?",
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"explanation": "# Summary\r\n\r\nHeart failure (HF) is a clinical syndrome characterised by the heart's inability to pump enough blood to meet the body's needs. It is a common condition primarily affecting the elderly population. HF can be classified based on various factors, such as the type of dysfunction (systolic or diastolic), the onset (acute or chronic), and the severity of symptoms (NYHA classification). The clinical features of HF differ depending on whether it primarily affects the left or right ventricle, but broadly include fatigue, shortness of breath, and peripheral oedema. Diagnosis involves evaluating symptoms, NT-pro-BNP levels, and echocardiography. Management includes lifestyle modifications, medical therapy, and, in some severe cases, cardiac resynchronisation therapy. The prognosis for HF varies, but approximately 50% of those diagnosed are alive at 5 years.\r\n\r\n# Definition \r\n\r\nHeart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.\r\n\r\n# Epidemiology \r\n\r\n* HF is common: the prevalence in the UK is estimated at 1-2%.\r\n\r\n* HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population.\r\n\r\n* In Europe and North America the most common causes are coronary artery disease, hypertension, and valvular disease.\r\n\r\n* Although Chagas disease is a rare cause in Europe and North America, it is a significant cause of heart failure in Central/South America.\r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology for HF is diverse and depends on the aetiology of the HF. \r\n\r\n# Classification \r\n\r\nHF can be classified in different ways. It can be classified as being low output vs. high output HF, predominantly systolic or diastolic dysfunction, whether the process has been acute or chronic, or by the severity of symptoms (and consideration for predominantly left or right ventricle features). \r\n\r\n## Low-output HF vs. High-output HF \r\n\r\nLow-output HF is much more common than high-output HF. Low-output HF occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body's needs. Conversely, high-output HF refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet. \r\n\r\nThe common causes of low-output HF will be further discussed below. Common causes of high-output HF include: \r\n\r\n* Anaemia\r\n* Arteriovenous malformation\r\n* Paget's disease\r\n* Pregnancy\r\n* Thyrotoxicosis\r\n* Thiamine deficiency (wet Beri-Beri)\r\n\r\nThese can be remembered with the AAPPTT mnemonic. \r\n\r\n## Systolic vs. Diastolic HF\r\n\r\nSystolic dysfunction refers to an impairment of ventricular contraction. The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction). Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis). \r\n\r\nIn comparison, diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction). Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypertrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis. \r\n\r\n## Acute vs. Chronic HF \r\n\r\nHF can also be classified according to the time of onset. Acute HF occurs with new-onset HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF. In comparison, chronic HF progresses more slowly and may take many years to develop. \r\n\r\n## Severity of Symptoms\r\n\r\n**New York Heart Association (NYHA) Classification of HF**\r\n\r\nThe NYHA Classification system is used to classify HF through the severity of symptoms. It runs from Class I (no limitation) to Class IV (discomfort at rest). \r\n\r\n* Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea.\r\n* Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea.\r\n* Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).\r\n* Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.\r\n\r\n# Symptoms and Signs\r\n\r\nThe clinical features of HF can be considered according to the ventricle most impacted. However, a common presenting complaint for all types of heart failure is **fatigue**. \r\n\r\n\r\n## Clinical features of left heart failure (LHF)\r\n\r\nLHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up in the LHS of the heart and there is backpressure to the lungs) and systemic hypoperfusion.\r\n\r\n### Symptoms \r\n\r\n* Shortness of breath on exertion\r\n* Orthopnoea\r\n* Paroxysmal nocturnal dyspnoea\r\n* Nocturnal cough (± pink frothy sputum)\r\n* **Fatigue**\r\n\r\n### Signs \r\n\r\n* Tachypnoea\r\n* Bibasal fine crackles on auscultation of the lungs\r\n* Cyanosis\r\n* Prolonged capillary refill time \r\n* Hypotension\r\n* Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation. \r\n\r\n## Clinical features of right heart failure \r\n\r\nRight heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).\r\n\r\n### Symptoms \r\n\r\n* Ankle swelling \r\n* Weight gain \r\n* Abdominal swelling and discomfort \r\n* Anorexia and nausea \r\n\r\n### Signs\r\n\r\n* Raised JVP\r\n* Pitting peripheral oedema (ankle to thighs to sacrum)\r\n* Tender smooth hepatomegaly\r\n* Ascites\r\n* Transudative pleural effusions (typically bilaterally)\r\n\r\n*NB. Sometimes left-sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases, signs and symptoms of both left and right-sided heart failure may be present. This is congestive cardiac failure.* \r\n\r\n# Differential Diagnoses\r\n\r\n* **Chronic Obstructive Pulmonary Disease (COPD)** \r\n\t* **Similarities**: both may present with dyspnoea (and significant respiratory distress) and fatigue. \r\n\t* **Differences**: in heart failure, the shortness of breath is typically worse on lying flat (orthopnoea) and may be accompanied by paroxysmal nocturnal dyspnoea and peripheral oedema. Shortness of breath in COPD tends to be worse with exertion and is likely accompanied by other symptoms including chronic productive cough, wheeze and a significant smoking history. \r\n\r\n* **Acute Respiratory Distress Syndrome** \r\n\t* **Similarities**: both may present with shortness of breath, tachypnoea and respiratory distress. Both lead to the accumulation of fluid in the lungs and impaired gaseous exchange leading to hypoxaemia. \r\n\t* **Differences**: the underlying pathology between the two is different. Heart failure is a result of raised pressures in pulmonary capillaries, whereas ARDS is usually due to increased pressures in pulmonary capillaries secondary to a large insult (e.g. pneumonia, aspiration, or trauma). They can be distinguished by taking pulmonary capillary wedge pressures. \r\n\r\n* **Renal Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload. \r\n\t* **Differences**: other signs and symptoms will allow distinction between HF and renal failure. In the latter, you may find uraemic symptoms(nausea, anorexia, uraemic flap) and potentially signs of renal replacement therapy. \r\n\r\n* **Liver Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload especially ascites. \r\n\t* **Differences**: liver failure patients will present with other signs and symptoms including jaundice, hepatic encephalopathy and chronic liver disease signs (gynaecomastia, spider naevi, and excoriations). \r\n\r\n\r\n# Investigations\r\n\r\nIf a stable patient is presenting to the GP with suspected chronic heart failure, investigations should be carried out as per NICE guidelines. \r\n\r\n**1st line = NT-pro-BNP level**\r\n\r\nNT-pro-BNP is released by the ventricles in response to myocardial stretch. It has a high negative predictive value.\r\n\r\nInterpret NT-pro-BNP results as follows: \r\n\r\n* >2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks. \r\n* 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks. \r\n* If <400ng/L: diagnosis of heart failure is less likely. \r\n\r\n**Arrange a 12-lead ECG in all patients** \r\n\r\nECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias). \r\n\r\n**Transthoracic echocardiogram (TTE)**\r\n\r\nAn echocardiogram will confirm the presence and degree of ventricular dysfunction.\r\n\r\n* Ventricular dysfunction is normally measured by the ejection fraction (EF). \r\n * EF <40% = HF with reduced ejection fraction (HFrEF, systolic dysfunction). \r\n * EF >40% but with raised BNP = HF with preserved ejection fraction (HFpEF, diastolic dysfunction).\r\n * EF 50-70% with normal BNP = normal. \r\n\r\n**Other Investigations:** \r\n\r\n* **Bloods**: U&E (renal function for medication and hyponatraemia), LFTS (deranged LFTs suggest hepatic congestion), TFTs (hyperthyroidism and high-output HF), glucose and lipid profile (modifiable CV risk factors)\r\n\r\n* **CXR**: CXR findings in heart HF can be remembered by the ABCDEF mnemonic:\r\n * A: **Alveolar** oedema (with 'batwing' perihilar shadowing)\r\n * B: **Kerley B** lines (caused by interstitial oedema)\r\n * C: **Cardiomegaly** (cardiothoracic ratio >0.5)\r\n * D: upper lobe blood **diversion**\r\n * E: **Pleural effusions** (typically bilateral transudates)\r\n * F: **Fluid in the horizontal fissure**\r\n\r\n[lightgallery]\r\n\r\n[lightgallery1] \r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\n* Weight loss if BMI >30. \r\n* Smoking cessation \r\n* Salt and fluid restriction - improves mortality\r\n* Supervised exercise-based group rehabilitation programme for people with heart failure. \r\n\r\nOffer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure. \r\n\r\n## Medical management\r\n\r\n**Symptom management**: \r\n\r\n* For fluid overload, prescribe loop diuretics (e.g. furosemide or bumetanide). These do not affect overall mortality from heart failure. \r\n\r\n\r\n**Management which improves mortality**:\r\n \r\n1st line = ACE-I and beta-blocker \r\n\r\n* Consider ARB if intolerant to ACE-I. \r\n* Consider hydralazine if intolerant to ACE-I/ARB. \r\n\r\nIf symptoms persist and NYHA Class 3 or 4 consider adding:\r\n\r\n* Aldosterone antagonists = spironolactone or eplerenone. \r\n* Hydralazine and a nitrate for Afro-Caribbean patients. \r\n* Ivabradine if in sinus rhythm and impaired EF. \r\n* Digoxin = useful in those with AF. This <u>worsens</u> mortality but improves morbidity.\r\n\r\nNICE also advices seeking specialist guidance for prescribing **SGLT2 inhibitors** (dapagliflozin or empagliflozin). These should be given in symptomatic chronic heart failure with preserved or reduced ejection fraction, or as an add-on for patients already optimised with ACE-i/ARB/sacubitril-valsartan (i.e. combination), beta-blockers and aldosterone antagonists.\r\n\r\n**BASH Mnemonic**\r\n\r\n* BASH medications demonstrate a mortality benefit in patients with HFrEF = Beta-blockers, ACE-inhibitors/ARB, Spironolactone and Hydralazine. \r\n* There are no medications that improve mortality in diastolic heart failure. \r\n\r\n[lightgallery2]\r\n\r\n# Surgical/Interventional management \r\n\r\n* Cardiac resynchronisation therapy\r\n* Implantable cardiac defibrillators (ICDs) are indicated if the following criteria are fulfilled: \r\n * QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III\r\n * QRS interval 120-149ms without LBBB, NYHA class I-III\r\n * QRS interval 120-149ms with LBBB, NYHA class I\r\n\r\n## Adverse effects of heart failure medications\r\n\r\nThe common side-effects for different heart failure medications are listed below\r\n\r\n* **Beta blockers**: Bradycardia, hypotension, fatigue, dizziness\r\n* **ACE inhibitors**: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema\r\n* **Spironolactone**: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido\r\n* **Furosemide**: Hypotension, hyponatraemia/kalaemia,\r\n* **Hydralazine/nitrates**: Headache, palpitations, flushing\r\n* **Digoxin**: Dizziness, blurred vision, GI disturbances\n* **SGLT-2 inhibitors:** Thrush, UTIs, DKA in patients with pre-existing diabetes\r\n\r\n# Prognosis \r\n\r\nIt is estimated that >50% of people diagnosed with HF will survive after 5 years. Approximately 35% will be alive in 10 years. \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines on Acute Heart Failure](https://www.nice.org.uk/guidance/cg187/chapter/1-Recommendations)\n\n[NICE Guidelines on Chronic Heart Failure](https://cks.nice.org.uk/topics/heart-failure-chronic)\r\n\r\n# References \r\n\r\n[2022 Stat Pearls Summary of Congestive Heart Failure](https://www.ncbi.nlm.nih.gov/books/NBK430873)",
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"question": "An 80 year old female is admitted to hospital with heart failure. Her ECG demonstrates sinus rhythm with wide QRS complexes of approximately 190ms. Her blood pressure is 130/85 mmHg, her heart rate is 78 bpm.\n\nWhich of the following is indicated in this patient?",
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"explanation": "She is haemodynamically stable and apyrexial and therefore intravenous antibiotics are not indicated at this point",
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"explanation": "# Summary\n \n\nMastitis is an inflammation of the breast, often associated with lactation in postpartum women, referred to as puerperal mastitis. Key signs and symptoms include localised pain, tenderness, redness and heat in the breast, along with systemic symptoms such as fever, rigours, myalgia, fatigue, nausea and headache. Diagnosis is primarily clinical. Ultrasound may be used if a breast abscess is suspected. Management strategies focus on reassurance about continued breastfeeding, advice on milk removal, analgesia, antibiotics, and in severe cases, surgical intervention.\n \n\n# Definition\n \n\nMastitis is the inflammation of the breast tissue, which can be with or without an infection. When associated with lactation in postpartum women, the condition is specified as puerperal mastitis. Alternatively, mastitis can be seen in women who are not breastfeeding.\n \n\n# Epidemiology\n \n\nNon-lactational mastitis is significantly less common than lactational mastitis, and its most common in women with immunodeficiency and diabetes. \n \n\n# Aetiology\n \nMastitis unrelated to pregnancy and breastfeeding is typically due to obstruction of the ducts from cellular debris. This can result in a local inflammatory response in non-infectious mastitis. \n\nIn infectious mastitis, bacteria from the skin can then enter the ducts, causing inflammation and may progress to peri-areolar abscesses. The most common causative pathogen is Staphylococcus aureus. \n\nRisk factors for non-lactational mastitis include:\n\n- Cigarette smoking\n- Nipple rings \n- Diabetes mellitus\n- Immunocompromise \n \n\n# Signs and Symptoms\n \n\nMastitis diagnosis is primarily clinical, based on characteristic local and systemic symptoms.\n \n\n - Localised symptoms: Painful, tender, red, and hot breast.\n - Systemic symptoms: Fever, rigours, myalgia, fatigue, nausea, and headache.\n - Additional information: The condition is usually unilateral and tends to present within the first week postpartum.\n \n\nIn some cases, mastitis may develop into a breast abscess, manifesting as a fluctuant, tender mass with overlying erythema.\n \n\n# Differential Diagnosis\n \n\nThe differential diagnosis for mastitis should include other conditions that also cause breast pain and inflammation:\n \n\n - **Breast abscess**: Fluctuant mass, tenderness, overlying erythema, systemic signs of infection.\n - **Inflammatory breast cancer**: Swelling, skin changes resembling orange peel, nipple inversion, axillary lymphadenopathy.\n - **Breast engorgement**: Typically bilateral and associated with milk stasis, painful, and tense breasts.\n \n\n# Investigations\n \n\nWhile the diagnosis of mastitis is primarily clinical, further investigations may be necessary in certain circumstances.\n \n\n - Ultrasound: Utilised to identify a potential abscess, appearing as a collection of pus.\n - Additional information: Early referral to secondary care is vital if an abscess is suspected.\n \n\n# Management\n \n\nManaging mastitis involves multiple strategies:\n \n\n - Provide analgesia to manage symptoms (i.e. paracetamol, ibuprofen)\n\t - Warm and cold compresses may also help.\n - Antibiotics may be considered if acute pain, severe symptoms or symptoms lasting more than 12-24 hours, fever or positive cultures \n\t - Flucloxacillin or clindamycin for those with penicillin allergy\n\t - Treatment is indicated for 10-14 days.\n - In cases where the condition does not improve, consider intravenous antibiotics (i.e. vancomycin) or ultrasound to evaluate for the presence of a breast abscess.\n - Patients may also benefit from antifungal therapy (i.e. nystatin) for concomitant nipple candidiasis \n\n \n# Complications\n \nComplications of mastitis include:\n \n - Breast abscess\n - Recurrence:\n\t - More common if treatment is delayed or too short in duration \n \n\n# NICE Guidelines\n \n[NICE CKS on mastitis and breast abscess](https://cks.nice.org.uk/topics/mastitis-breast-abscess/)\n\n# References\n\n[BMJ Best Practice Mastitis and Breast Abscess](https://bestpractice.bmj.com/topics/en-gb/1084)\n\n[Patient Info Benign Breast Diseas](https://bestpractice.bmj.com/topics/en-gb/1084) \n\n[NHS Mastitis](https://www.nhs.uk/conditions/mastitis/)",
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"question": "A 33-year-old woman presents to the out of hours general practitioner with a tender, fluctuant mass in her left breast, with associated erythema of the overlying skin. She is currently breast feeding. A breast abscess is confirmed on ultrasound and percutaneous drainage is performed uneventfully.\n\nHer observations are as follows:\n\nPulse 80 beats per minute\n\nRespiratory rate 17 breaths per minute\n\nBlood pressure 115/75mmHg\n\nTemperature 37.2°\n\nShe looks otherwise well, and is alert and orientated. Her renal function and liver function is within normal limits and she has an allergy to penicillin\n\nWhich of the following is the most appropriate antibiotic therapy?",
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"explanation": "Trastuzumab (Herceptin) is only useful in HER2 positive breast cancers",
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"explanation": "This is a hormone therapy (LHRH agonist) used in the treatment of prostate cancer",
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"comment": "Unlikely but are we outright assuming she's post-menopause?",
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"comment": "At 70? That's not much of an assumption mate",
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"comment": "Bruh... she's 70!!",
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"comment": "70 is the new 30",
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"explanation": "# Summary\n\n\nBreast carcinoma is the most prevalent form of cancer among women and the second leading cause of cancer death in the UK. It manifests in various histological subtypes including ductal, lobular, medullary, and phyllodes tumours, each displaying distinct characteristics. Certain genetic mutations, especially BRCA1 and BRCA2, can increase the risk for breast carcinoma. Notable signs and symptoms include unexplained breast mass, nipple discharge, retraction, or skin changes suggestive of breast cancer. Key investigations comprise a triple assessment—clinical examination, radiological examination, and biopsy. Treatment strategies encompass surgical management (wide local excision or mastectomy), radiotherapy, chemotherapy, biological therapy, and hormonal therapy. Risk factors for breast cancer include increased hormone exposure, susceptibility gene mutations, advancing age, and lifestyle factors like obesity, physical inactivity, and alcohol and tobacco use.\n\n\n# Definition\n\n\nBreast carcinoma refers to a malignant tumour originating from the cells of the breast tissue. It exhibits different subtypes each with unique cellular properties and clinical implications. The carcinomas can be invasive, indicating they have broken through the basement membrane of the tissue of origin and have the potential to metastasize, or non-invasive (in situ), suggesting they are confined to the initial location.\n\n\n# Epidemiology\n\n\nBreast carcinoma is the most common type of cancer in women and accounts for approximately 15% of new cancer cases, representing 50,000 new cases annually. It is the second most common cause of cancer death in the UK.\n\n\n# Aetiology\n\nMost breast cancers are either ductal (arising from the epithelial lining of the ducts) or lobular (originating from epithelial cells in the terminal ducts of the lobules).\n\n\nRisk factors for breast carcinoma include:\n\n\n- Being female\n- 99% of breast cancer cases occur in women\n- Increased hormone exposure\n- Early menarche or late menopause\n- Nulliparity or late first pregnancy\n- Oral contraceptives or Hormonal Replacement Therapy\n- Susceptibility gene mutations\n- Most commonly BRCA mutations (BRCA1/BRCA2)\n- Advancing age\n- Caucasian ethnicity\n- Obesity and lack of physical activity\n- Alcohol and tobacco use\n- History of breast cancer\n- Previous radiotherapy treatment\n\n\n# Classification\n\n\nBreast cancer is not a single disease, but a collection of several subtypes, each with its unique characteristics, prognosis, and treatment options.It can be classified based on its origin cell type such as:\n\n\n- **Invasive ductal carcinoma (IDC)**: This is the most common type, accounting for about 80% of all breast cancers. It starts in a milk duct, breaks through the wall of the duct, and invades the fatty tissue of the breast.\n- **Invasive lobular carcinoma (ILC)**: This type begins in the milk-producing glands (lobules) and can spread to other parts of the body.\n- **Ductal carcinoma in situ (DCIS)**: This is a non-invasive or pre-invasive cancer where the cells are confined to the ducts in the breast and have not spread into the surrounding breast tissue.\n- **Lobular carcinoma in situ (LCIS)**: This is not a cancer but an area of abnormal cell growth that increases a person's risk of developing invasive breast cancer later.\n- **Paget's disease of breast**: Infiltrating carcinoma of nipple epithelium.\n\n\nIt can also be classified based on the hormone receptors present on the surface of the breast cancer:\n\n- **Inflammatory breast cancer (IBC)**: This is a rare but aggressive type of breast cancer that causes the lymph vessels in the skin of the breast to become blocked.\n\n- **Triple-negative breast cancer (TNBC)**: This type lacks estrogen receptors, progesterone receptors, and does not have an excess of the HER2 protein on the cancer cell surfaces. It tends to be more aggressive and has fewer targeted treatments available.\n\n- **HER2-positive breast cancer**: This is a cancer that tests positive for a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. It tends to be more aggressive than other types of breast cancer, but it may respond well to targeted therapies that can block HER2.\n\n\n# Signs and Symptoms\n\n\nCommon clinical manifestations of breast carcinoma include:\n\n\n- Unexplained breast mass in patients aged 30 and above, with or without pain\n- In those aged 50 and older, nipple discharge, retraction/inversion, or other concerning symptoms\n- This can also include eczema-type changes surrounding the nipple as seen in Paget's disease of the breast\n- Skin changes suggestive of breast cancer\n- This includes skin retraction, peau d'orange appearance or ulceration of the skin above an underlying mass.\n- Unexplained axillary mass in those aged 30 and above\n\n\nApproximately 25% of cases are found in routine breast cancer screening (mammography).\n\n\n# Differential Diagnosis\n\n\nWhile an unexplained breast mass is a key indicator of breast carcinoma, it can also represent various other conditions, each characterized by distinct signs and symptoms:\n\n\n- **Fibroadenoma**: Typically presents as a solitary, painless, and well-circumscribed breast lump in young women\n- **Breast Cyst**: Characterized by a round or oval, well-defined, and movable mass. It may be painful and size may vary with the menstrual cycle.\n- **Mastitis**: Typically presents in breastfeeding women, characterized by a painful, warm, red breast often accompanied by systemic symptoms like fever.\n- **Lipoma**: Presents as a soft, mobile, and painless lump.\n\n\n# Breast Cancer Screening in the UK\n\n\nIn the United Kingdom, the NHS Breast Screening Programme provides free breast screening services for all women registered with a GP. The programme invites women between the ages of 50 and 70 for breast screening every three years, with the first invitation to screening usually sent to women before they turn 53.\n\n\nThis screening process involves a mammogram, which is an X-ray of the breasts that can help detect breast cancers early, often before they can be felt. The aim of breast cancer screening is to find cancer at an early stage when treatment is most effective.\n\n\nIn 2018, the age range for screening was extended as part of a trial, and some women were invited for screening from the age of 47 up to the age of 73. Women over 70 can still self-refer for screening every three years.\n\n\n# Investigations\n\nCriteria for 2-week wait:\n\n- Age 30 or more with unexplained breast lump (with or without pain)\n- Age 50 or more with nipple discharge, retraction or other changes\n- Consider a 2-week wait if a patient is 30 or over with skin changes suggestive of breast cancer or an unexplained lump in the axilla\n\nNB: a non-urgent referral should be considered for patients under the age of 30 with an unexplained breast lump.\n\n### Triple Assessment\n\nTriple assessment is used to investigate suspected breast carcinoma:\n\n\n1. Clinical examination: of the breast and surrounding lymph nodes\n2. Radiological examination:\n\t- Ultrasound is used for women under the age of 40 or those with higher breast density.\n\t- A mammogram is commonly used for women over 40 years.\n\t- If there are concerns of metastatic disease, a CT or PET scan may be done.\n3. Biopsy: often a core needle biopsy or fine needle aspirate (FNA)\n\t- Fine needle aspiration (FNA): Often combined with mammography, however, has a high rate of false negatives.\n\t- Core needle biopsy: method of choice, can be combined with imaging to aid accuracy.\n\t- DCIS biopsy will show cellular atypia and hyperchromatic nuclei involving the ducts, but not passing the basement membrane\n\t- In invasive breast cancer, these abnormal cells will pass the basement membrane\n\t- In lobular carcinoma, the abnormal cells will be found within the lobular acini\n\n### Further Investigations\n\nFollowing the triple assessment, further investigations will include:\n\n- Biopsies to determine\n- Oestrogen and progesterone receptor status\n- Epidermal growth factor receptor status\n- Routine blood tests (i.e. LFTs)\n- CXR\n- MRI is not routinely used. It is used for women with:\n- Discrepancy between the extent of disease between clinical examination and imaging\n- Dense breast tissue limiting mammography\n- Invasive lobular carcinoma to evaluate tumour size when planning breast-conserving surgery\n- BRCA1/2 testing is done for women < 50 years with triple-negative breast cancer regardless of family history\n\n\n### Staging\n\nStaging involves the TNM system considering the size of the tumour (T), the spread to the lymph nodes (N), and the presence of metastases (M). For locally invasive breast cancer, this can include:\n\n- Axilla ultrasound with needle sampling if abnormal lymph nodes are identified\n\nIf the cancer is deemed to be advanced, staging investigations should include:\n\n- CT, MRI or bone scintigraphy to determine the presence and extent of visceral and bony metastasis\n- PET CT is only used to diagnose metastasis\n\n\n# Management\n\n\nThe management strategy for breast carcinoma can vary based on several factors including the subtype of carcinoma, stage, hormonal receptor status, and the patient's overall health and preferences.\n\n\n- Surgical management: Wide local excision (WLE) or mastectomy, with sentinel node biopsies for invasive cancers and possible axillary node clearance for positive nodes. Breast reconstruction can be done concurrently or later.\n- Radiotherapy: Adjuvant radiotherapy is commonly offered following WLE to reduce recurrence. It may also be given to patients with higher-stage cancers post-mastectomy.\n\n**Chemotherapy:**\n\n- Suggested for hormone receptor-negative and HER2 over-expressing patients. Neoadjuvant chemotherapy may be given to downstage tumours before surgery. This commonly includes an anthracycline (i.e. doxorubicin) and a taxane (i.e. paclitaxel)\n- Biological Therapy:\n\t- Trastuzumab (Herceptin) should be given to HER2-positive patients with tumour size T1c and above in combination with surgery, chemotherapy and radiotherapy. Patients should have regular cardiac function assessments.\n\t- Abermaciclib (selective inhibitor of cyclin-dependent kinases 4 and 6) for HER2-negative, hormone receptor-positive breast cancer\n\t- Pembrolizumab for triple-negative breast cancer\n\t- Olaparib (PSTP inhibitor) for BRCA positive, HER2 negative high-risk early breast cancer\n- **Hormonal Therapy** for oestrogen-positive breast cancer:\n\t- Anastrozole (aromatase inhibitor) for postmenopausal women\n\t- Tamoxifen (oestrogen receptor antagonist) for premenopausal patients\n\t- Bisphosphonates: May be used for reducing occurrence in node-positive cancers.\n\t- Zoledronic acid has been shown to improve disease-free survival in postmenopausal women with node-positive invasive breast cancer.\n\t- Bisphosphonates are also advised for treatment-induced menopause in women treated with aromatase inhibitors\n\n\n# Complications\n\n### Complications of Breast Carcinoma\n\n- Fatigue\n- Bone metastases\n- Brain metastases\n- Psychological difficulties: Anxiety, depression and damage to the individual's self-esteem.\n- Recurrence:\n\t- Local: recurrence in the same breast as the original tumour\n\t- Regional: recurrence in the axillary or sub-clavicular lymph nodes draining the breast cancer\n\t- Distant: recurrence once already metastasized to other parts of the body (i.e. liver, lungs, brain, bone)\n\n\n### Side Effects of Medication Used to Treat Breast Cancer\n\n\nTreatment for breast cancer often involves medication, including chemotherapy, hormone therapy, and targeted drug therapy. Each of these can have different side effects.\n\n\n**Chemotherapy** drugs are powerful medications that aim to destroy rapidly dividing cells, such as cancer cells. However, they can also affect healthy cells, leading to a range of side effects, including fatigue, hair loss, easy bruising and bleeding, infection, anaemia, nausea and vomiting, appetite changes, peripheral neuropathy, and problems with concentration or memory.\n\nChemotherapy agents can have specific side effects such as:\n\n- Doxorubicin is associated with cardiac toxicity (e.g. cardiac arrhythmias, myopericarditis)\n- Paclitaxel is associated with lung fibrosis.\n\n\n**Hormone therapy** drugs, such as tamoxifen and aromatase inhibitors, are used to treat hormone receptor-positive breast cancers. Common side effects include hot flushes, vaginal dryness or discharge, menstrual changes, fatigue, mood changes, and osteoporosis. In rare cases, tamoxifen can increase the risk of serious conditions like endometrial cancer and blood clots.\n\n\n**Targeted drug therapies** such as trastuzumab (Herceptin), pertuzumab (Perjeta), and ado-trastuzumab emtansine (Kadcyla), are designed to interfere with specific proteins or processes that contribute to cancer growth.\n\nSide effects include:\n\n- Infections\n- Bruising and easy bleeding\n- Anaemia\n- Cardiac (i.e. arrhythmias)\n- Insomnia\n- GI side effects (i.e. diarrhoea, vomiting, constipation, appetite loss, weight loss)\n- Runny nose\n- Conjunctivitis\n- Hair loss\n- Nail changes\n- Hand foot syndrome: the palms and plantar surfaces become sore, peel, crack and blister.\n- Hepatotoxicity\n\n\n\n### Surgical Complications\n\nKey surgical complications include:\n\n- Venous thromboembolism\n- Lymphoedema\n- Pain\n\n\n### Breast Cancer in Pregnancy\n\nBreast cancer is the most common malignancy to occur during pregnancy. Radiotherapy and chemotherapy are most commonly delayed until completion of pregnancy, but surgical intervention can be considered.\n\n# Prognosis\n\nThe prognosis for individuals with breast cancer has vastly improved, almost doubling over the past 50 years. The ten-year survival for breast cancer in England is 75.9%\n\nA poorer prognosis is associated with:\n\n- Advancing age\n- Being male\n- Stage III or IV\n- Tumour size\n- Tumour grade\n- Hormone receptor-negative tumours (oestrogen or progesterone receptor-negative)\n- HER 2 positive tumours\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Early and Locally Advanced Breast Cancer](https://www.nice.org.uk/guidance/ng101)\n\n[NICE Guidelines on Advanced Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n# References\n\n[Patient Info Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n[BMJ Best Practice Breast Cancer](https://bestpractice.bmj.com/topics/en-gb/718?q=Metastatic%20breast%20cancer&c=suggested)\n\n[NHS Breast Cancer in Women](https://www.nhs.uk/conditions/breast-cancer-in-women/)\n\n[Cancer Research UK Breast Cancer](https://www.cancerresearchuk.org/about-cancer/breast-cancer/survival)",
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"explanation": "Hyperkalaemia is defined as serum potassium concentration >5.5mmol/L, and can be further categorised as mild (5.5-5.9 mmol/l), moderate (6.0-6.4 mmol/l) or severe (≥ 6.5 mmol/l).\n\nModerate or severe hyperkalaemia, or any hyperkalaemia with ECG changes should be treated with insulin/dextrose or insulin/glucose infusion, particularly if the patient is systemically unwell (e.g. with an AKI). Insulin promotes potassium to shift into cells and the dextrose is to counteract the hypoglycaemic effects of insulin.\n\nAccording to the UK Kidney Association Guidelines, Calcium Gluconate should only be given if (1) there is severe hyperkalaemia >6.5 mmol/l irregardless of ECG changes or (2) there is mild to moderate (5.5-6.5 mmol/l) hyperkalaemia in the presences of ECG changes.\n\n",
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"explanation": "# Summary\n\nHyperkalaemia is a potentially life-threatening electrolyte abnormality, defined as a serum potassium concentration greater than 5.5mmol/L. A potassium of 6.0-6.5 mmol/L is classed as moderate hyperkalaemia, and > 6.5 mmol/L is classed as severe. Causes include acute or chronic renal impairment, medications such as ACE inhibitors, adrenal insufficiency and rhabdomyolysis. Pseudohyperkalaemia is also common and occurs when there is haemolysis of the blood collected that causes potassium to leak from cells. Key investigations include an ECG, a blood gas to confirm hyperkalaemia is true, and U&Es for renal function. Management depends on the severity of hyperkalaemia and may include calcium gluconate or calcium carbonate to stabilise the myocardium and insulin-dextrose infusion to drive potassium into the cells, as well as treating the cause of hyperkalaemia. Potassium binders such as sodium zirconium cyclosilicate (Lokelma) may also be used. The main complication is cardiac conduction abnormalities, with possible findings including tall tented T waves, flattened P waves, bradyarrhythmias and QRS widening with bizarre morphology. \n\n# Definition\n\nHyperkalaemia is a common electrolyte abnormality that is defined as an abnormally high serum potassium. The normal range is 3.5-5.0 mmol/L, with a level of > 5.5 mmol/L generally described as hyperkalaemia. It is seen in around 1-10% of hospital inpatients and is often asymptomatic.\n\n# Aetiology\n\n- Impaired excretion of potassium\n - Acute kidney injury\n - Chronic kidney disease\n - Medications (ACE inhibitors, potassium sparing diuretics, NSAIDs, heparin, trimethoprim, ciclosporin)\n - Type 4 renal tubular acidosis\n - Hypoadrenalism (e.g. Addison's disease)\n- Increased potassium intake\n - Oral intake (especially if combined with impaired excretion)\n - Excessive IV potassium\n- Increased cellular release \n - Metabolic acidosis\n - Hyperglycaemia\n - Rhabdomyolysis\n - Tumour lysis syndrome\n - Packed red blood cell transfusion\n - Digoxin toxicity\n - Beta blockers\n - Severe burns\n - Hyperkalaemic periodic paralysis\n\n# Classification\n\nThe European Resuscitation Guidelines stratify severity of hyperkalaemia as follows:\n\n||Serum potassium (mmol/L)|\n|--------------------------|------------------------------------|\n|**Mild**|5.5–5.9|\n|**Moderate**|6.0–6.4|\n|**Severe**|≥6.5|\n\n# Signs and Symptoms\n\nHyperkalaemia is often asymptomatic and only detected on blood tests - there may be symptoms or signs of the underlying cause however (e.g. dark urine in rhabdomyolysis)\n\n**Symptoms include:**\n\n- Palpitations\n- Fatigue\n- Chest pain\n- Shortness of breath\n- Paralysis\n\n**Signs include:**\n\n- Arrhythmias (e.g. bradycardia)\n- Reduced muscle power +/- flaccid paralysis\n- Hyporeflexia\n\n# Differential Diagnosis\n\n**Pseudohyperkalaemia** is common and refers to an artifactual increase in potassium in the sample tested - causes of this include:\n\n- Prolonged tourniquet time\n- Difficult venepuncture\n- Excessive fist clenching\n- Delayed specimen processing\n- Contamination with potassium EDTA anticoagulant in FBC bottles\n- Thrombocytosis\n- Leukocytosis\n\n# Investigations\n\n- **Blood gas** to confirm hyperkalaemia rapidly and check acid-base status and lactate\n- **ECG** to look for cardiac conduction abnormalities associated with hyperkalaemia. ECG changes include tall-tented T waves, PR prolongation, p wave flattening and QRS broadening.\n- **U&Es** to confirm hyperkalaemia, check sodium (may be an associated hyponatraemia e.g. in adrenal insufficiency) and renal function\n\n# Management \n\n**Conservative management:**\n\n- Stop any potassium-containing fluids\n- Address any underlying causes e.g. stop any contributing medications where possible, manage constipation\n- Consider advising the patient on a low potassium diet (e.g. in patients with chronic kidney disease) - dietician referral may be helpful\n- Patients with ECG changes may require cardiac monitoring\n- Mild-moderate cases of hyperkalaemia without ECG changes may be managed by addressing the underlying cause alone\n\n**Medical management:**\n\n- Patients with ECG changes or severe hyperkalaemia require treatment\n- Give 10 ml of IV 10% calcium carbonate or 30ml of IV 10% calcium gluconate immediately\n- This does not reduce serum potassium but acts to stabilise the myocardium and reduce the risk of arrhythmias\n- Further doses may be given if required\n- Give an insulin and glucose infusion (e.g. 10 units of Actrapid in 50 ml of 50% glucose over 15-30 minutes\n- This reduces serum potassium by shifting potassium into cells, however does not eliminate potassium from the body\n- Nebulised salbutamol may be given in addition which has the same effect\n- Potassium binders may be considered to eliminate potassium via the gut, especially in patients with chronic or refractory hyperkalaemia\n- Newer agents such as sodium zirconium cyclosilicate (Lokelma) are better tolerated than older resins (e.g. sodium polystyrene sulfonate)\n- Furosemide may also be useful to increase urinary potassium excretion especially in patients with fluid overload\n- Consider sodium bicarbonate for patients with acidosis and hyperkalaemia\n- Medical treatment may be required to correct the cause of hyperkalaemia (e.g. IV fluids for a pre-renal AKI or rhabdomyolysis)\n\n**Interventional management:**\n\n- Refractory hyperkalaemia despite medical therapy is an indication for emergency dialysis\n\n# Complications\n\nThe main complication of hyperkalaemia is cardiac conduction abnormalities and arrhythmias which in the most severe cases may cause cardiac arrest - changes in order of increasing severity are:\n\n1. Tall tented T-waves\n2. Flattened P-waves\n3. Prolonged PR interval\n4. Widened QRS complexes\n5. Idioventricular rhythms (bradycardia of ventricular origin)\n6. Sine wave pattern (pre-terminal rhythm)\n7. Ventricular fibrillation/asystole\n\n# References\n\n[BNF Treatment Summary - Hyperkalaemia](https://bnf.nice.org.uk/treatment-summaries/hyperkalaemia/)\n\n[The Renal Association - Treatment of Acute Hyperkalaemia in Adults](https://www.ukkidney.org/sites/default/files/RENAL%20ASSOCIATION%20HYPERKALAEMIA%20GUIDELINE%20-%20JULY%202022%20V2_0.pdf)\n\n[Patient UK - Hyperkalaemia in adults](https://patient.info/doctor/hyperkalaemia-in-adults)\n\n[Whittington Hospital Hyperkalaemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6250)\n\n[Life in the Fast Lane - Hyperkalaemia](https://litfl.com/hyperkalaemia-ecg-library/)",
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"question": "An inpatient being treated for an acute kidney injury (AKI) has their potassium level returned at 6.2 mmol/L (normal range 3.5-5.3 mmol/L). The day before it had been 5.9 mmol/L. There are no hyperkalaemic changes on the ECG.\n\n\nThey are being managed with intravenous (IV) 0.9% NaCl at 100ml/hr. They feel well and have no symptoms to report.\n\n\nWhat is the best next step for this patient?",
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"explanation": "Trimethoprim inhibits tubular creatinine secretion, leading to an increase in serum creatinine independent of the true glomerular filtration rate (GFR). This leads to a falsely low eGFR as creatinine concentration is used in the calculation of GFR",
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"explanation": "Nitrofurantoin is not a nephrotoxic itself and will not cause an increase in serum creatinine, however, it is contraindicated in those with renal impairment due to reduced renal elimination of the antibiotic in these patients",
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"name": "Atorvastatin",
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"explanation": "Ramipril is an ACE inhibitor which is a nephrotoxic. It may cause an increase in serum creatinine but this is because of a **true** decrease in glomerular filtration rate",
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"name": "Ramipril",
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"comment": "Fun fact trimethoprim has a chemical structure very close to the potassium sparing diuretic amiloride and is also well known to cause a rise in potassium in addition to falsely elevated creatinine (esp when used with ACEi etc)",
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"comment": "So just to confirm she has new onset AKI that is causing her confusion/delirium (explained by the high creatine) and the low eGFR (that is usually indicative of CKD which she has no history of) is caused by the trimethoprim?",
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"comment": "could someone please explain the \"true rise\" bit for ramipril? I dont get it ",
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"comment": "By reducing angiotensin II levels, ramipril dilates the efferent arteriole. This lowers the pressure within the glomerulus, which can reduce the glomerular filtration rate (GFR). As a result, waste products like creatinine may not be filtered out as efficiently, leading to an increase in blood creatinine levels.",
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"explanation": "# Pathophysiology\n\nTrimethoprim can lead to a transient rise in creatinine levels by reducing the creatinine excretion of the kidneys. \n\nThis does NOT reflect the actual GFR and therefore this phenomenon is not reflective of an Acute kidney injury but rather the calculated eGFR due to a transient rise in Creatinine.",
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"question": "A 60-year-old lady presents to the emergency department with confusion. She has the following blood tests:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|136 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Urea|6 mmol/L|2.5 - 7.8|\n|Creatinine|300 µmol/L|60 - 120|\n|eGFR|15 mL/min/1.73m<sup>2</sup>|> 60|\n\n\nHer previous blood tests from 2 months ago suggest that her baseline creatinine is approximately 70umol/L.\n\n\nThere is no information on the computer system about her medications but you find the following medications in her bag: trimethoprim, nitrofurantoin, bisoprolol, ramipril, and atorvastatin.\n\n\nWhich of the following medications would lead to a falsely low estimated glomerular filtration rate (eGFR)?",
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"explanation": "Patients with SIADH are usually euvolaemic or hypervolaemic. Clinical dehydration suggests other causes for hyponatraemia such as secondary to diuretics or acute kidney injury",
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"explanation": "In SIADH there are high levels of antidiuretic hormone (ADH) in the blood. This leads to increased retention of water, but not sodium. There is therefore low levels of salt in the blood and therefore low plasma osmolality. Urine produced is more concentrated (as less water is excreted) and has more sodium, leading to a high urine osmolality and high urine sodium level. Urine osmolality greater than plasma osmolality can only be induced by inappropriately high levels of ADH in the bloodstream",
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"explanation": "Hypothyroidism is one of the potential causes for SIADH and so TFTs should be checked when investigating for SIADH. However, whether TFTs are normal or abnormal has no bearing on the diagnosis of SIADH",
"id": "31806",
"label": "d",
"name": "Normal thyroid function tests (TFTs)",
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"explanation": "In SIADH, due to increased water retention secondary to the high levels of ADH, concentrated urine with high sodium levels is produced (high urine osmolality). As excessive sodium is being excreted and water is excessively retained, plasma sodium is low and plasma osmolality is high. Therefore, by definition, urine osmolality will be greater than plasma osmolality",
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"name": "Plasma osmolality greater than urine osmolality",
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"comment": "how is this diagnostic if urine osmolarity is higher than plasma in healthy patients? ",
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"comment": "SIADH is inappropriate activation of V2 (aquaporin) receptor so more water is reabsorbed back into the capillaries lowering urine water volume. Lower urine water volume means that theres more solutes in the urine so the osmolality would be higher. Osmolality is the measure of how many substances are dissolved in 1kg of water.",
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"explanation": "# Summary\n\nSyndrome of Inappropriate ADH secretion (SIADH) refers to excessive antidiuretic hormone (ADH) release, causing water to be retained resulting in a euvolemic hyponatraemia. There are a wide range of causes including medications, malignancy, central nervous system (CNS) disorders and infections. Patients may be asymptomatic and detected through an incidental finding of a low serum sodium, or may present with features of severe hyponatraemia (e.g. confusion, seizures) and/or the underlying cause of SIADH. Key investigations include U&Es for sodium, cortisol and thyroid function to rule out other causes of hyponatraemia and urinary sodium and osmolality (which will be greater than 30 mmol/L and 100 mOsm/kg respectively). First-line management is with fluid restriction to 500-1000 ml/day, as well as treating the underlying cause (e.g. stopping causative medications). Severe cases may require hypertonic saline, and resistant cases may be treated with tolvaptan (an vasopressin V2-receptor antagonist).\n\n# Definition\n\nSyndrome of Inappropriate ADH secretion (SIADH) is an important cause of hyponatraemia that occurs when there is inappropriate release of antidiuretic hormone (ADH) outside of normal homeostatic mechanisms, which leads to reduced urine output. The increase in total body water effectively dilutes serum sodium, leading to hyponatraemia. \n\nNormally, ADH (also referred to as vasopressin) is produced in the hypothalamus and released from the posterior pituitary when serum osmolality is high. It acts to normalise osmolality by acting on the distal convoluted tubules and collecting ducts of the kidney to stimulate increased water reabsorption. \n\nSIADH may involve excessive release of ADH from the pituitary gland or production of ADH by an abnormal non-pituitary source (e.g. a tumour).\n\n# Aetiology\n\nSIADH has a wide range of causes - these are some examples:\n\n- Pulmonary causes:\n\t- Pneumonia\n\t- Chronic Obstructive Pulmonary Disease (COPD)\n\t- Tuberculosis (TB)\n- Central Nervous System (CNS) disorders:\n\t- Meningitis\n\t- Stroke\n\t- Subarachnoid haemorrhage\n\t- Traumatic brain injury\n\t- Psychosis\n- Malignancies:\n\t- Small cell lung cancer\n\t- Pancreatic cancer\n\t- Lymphoma\n\t- Mesothelioma\n\t- Thymoma\n\t- Nasopharyngeal cancer\n- Medications:\n\t- Carbamazepine\n\t- Selective Serotonin Reuptake Inhibitors (SSRIs)\n\t- Opiates\n\t- Anti-psychotics\n\t- Cyclophosphamide\n- Other: \n\t- HIV\n\t- Surgery\n\t- Acute intermittent porphyria\n\t- Idiopathic\n\n# Signs and Symptoms\n\nSIADH presents with a euvolaemic hyponatraemia, and so patients may be asymptomatic or present with features of the underlying cause (e.g. pneumonia).\n\nSigns and symptoms of hyponatraemia are more likely to develop in severe cases and where sodium has fallen rapidly:\n\n- Lethargy\n- Anorexia\n- Headache\n- Nausea and vomiting\n- Muscle cramps\n- Drowsiness\n- Confusion\n- Seizures\n\n# Differential Diagnosis\n\nSee the Hyponatraemia chapter for a full list of differentials - other causes of a euvolaemic hyponatraemia include:\n\n- **Beer potomania** is a cause of hyponatraemia in the context of alcohol excess combined with low solute intake due to a poor diet\n- **Primary polydipsia** occurs when people drink excessive amounts of water, leading to polyuria with dilute urine (as opposed to the smaller volume of concentrated urine seen in SIADH)\n- **Hypothyroidism** may cause hyponatraemia in severe cases; patients will usually have other symptoms such as fatigue, cold intolerance and constipation\n- **Adrenal insufficiency** causes hyponatraemia with hyperkalaemia; other features include hypotension, abdominal pain and weakness\n- **Exercise-induced hyponatraemia** occurs during or in the 24 hours following prolonged exercise (e.g. running a marathon), usually due to excess intake of hypotonic fluids\n- **Hypotonic intravenous fluids** such as 5% dextrose or 0.45% saline may lead to iatrogenic hyponatraemia\n\n# Investigations\n\n**Bedside:**\n\n- **Venous blood gas** to confirm hyponatraemia - if there is a significant discrepancy between the sodium on the gas and the U&Es, suspect pseudohyponatremia (see Hyponatraemia chapter for details) \n- **Urine osmolality** will be high (> 100 mOsm/kg)\n- **Urine sodium** will be high (> 30 mmol/L)\n- NB urine osmolality and sodium cannot be interpreted in patients taking diuretics and so these need to be stopped prior to investigations\n\n**Blood tests:**\n\n- **U&Es** to confirm hyponatraemia; urea will also likely be low due to dilution\n- **Serum osmolality** will be low (< 280 mOsm/kg)\n- **Thyroid function tests** to exclude hypothyroidism as a cause of hyponatraemia\n- **9am serum cortisol** to exclude adrenal insufficiency as a cause of hyponatraemia\n\n**Imaging:**\n\n- **Chest X-ray** if there is no obvious cause of SIADH as an initial screen for malignancy and pulmonary disease (e.g. tuberculosis, pneumonia)\n- **CT chest, abdomen and pelvis** and **MRI head** may be considered to exclude occult malignancy if there is no identified cause\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. stopping causative medications where possible)\n- Patients with suspected SIADH in primary care should be referred to endocrinology to confirm the diagnosis and advise on treatment\n- Closely monitor sodium levels and ensure these are corrected no faster than 8-10 mmol/L per 24 hours \n- Fluid restriction is the first-line management in most cases, usually to 500-1000 ml/day \n\n**Medical:**\n\n- Severe hyponatraemia should be treated with hypertonic saline, usually in the intensive care setting\n- In some cases (e.g. SIADH resistant to fluid restriction), tolvaptan may be considered - this is a vasopressin V2-receptor antagonist\n\n# Complications\n\n- **Cerebral oedema** may complicate severe and/or acute hyponatraemia and may be life-threatening - patients develop raised intracranial pressure with symptoms of vomiting, headache, seizures and coma\n- **Central pontine myelinolysis** is a complication of rapid correction of hyponatraemia - patients may present with confusion, ataxia, spastic quadriparesis and pseudobulbar palsy with dysphagia and dysarthria\n- Chronic hyponatraemia, especially in the elderly, increases the risk of **falls** as well as **cognitive impairment**\n\n# NICE Guidelines\n\n[NICE CKS - Hyponatraemia](https://cks.nice.org.uk/topics/hyponatraemia/)\n\n# References\n\n[Life in the Fast Lane - Hyponatraemia](https://litfl.com/hyponatraemia/)\n\n[Life in the Fast Lane - SIADH](https://litfl.com/siadh-syndrome-of-inappropriate-adh-secretion/)\n\n[Whittington Hospital Hyponatraemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6089)",
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"explanation": "# Summary\n\nStevens-Johnson syndrome (SJS) is a serious, immune-complex-mediated hypersensitivity disorder often triggered by medication or, less commonly, viral, bacterial, or fungal infections. Clinically, it's characterized by symptoms resembling an upper respiratory tract infection, followed by erythematous macules and mucosal ulceration, affecting less than 10% of the body surface. Diagnosis is usually clinical, supplemented by skin biopsy. Management is largely supportive, with a focus on skin and eye care.\n\n# Definition\n\nStevens-Johnson syndrome (SJS) is an immune-complex-mediated hypersensitivity disorder. It ranges from mild to severe forms, part of a spectrum that includes toxic epidermal necrolysis (TEN) at its most severe end.\n\n# Epidemiology\n\nSJS is a rare disorder, with an incidence estimated between 2.6 to 6.1 cases per million people annually. It affects both genders and all age groups, although some studies suggest a slightly higher incidence in females and middle-aged adults.\n\n# Pathophysiology\n\nThe predominant cause of SJS is adverse drug reactions, most commonly from sulfonamides, beta-lactams (penicillins and cephalosporins), antiepileptics, allopurinol, and NSAIDs. Infectious agents, particularly viral pathogens like herpes simplex virus, Epstein-Barr virus, HIV, influenza, and hepatitis, can also trigger SJS. Bacterial and fungal infections are much less common causes.\n\n# Signs and Symptoms\n\n- SJS often presents within a week of medication intake, initially resembling an upper respiratory tract infection with symptoms such as cough, cold, fever, and sore throat.\n- Erythematous macules, later becoming target-shaped, appear after a few days.\n- Flaccid blisters develop and the Nikolsky sign is positive.\n- SJS affects less than 10% of the body surface, in contrast to TEN, which involves more than 30% of the skin.\n- Mucosal ulceration is seen in at least two of the following: conjunctiva, mouth, urethra, pharynx, or gastrointestinal tract. \n\nSJS has a 10% mortality rate, primarily due to dehydration, infection, or disseminated intravascular coagulation. In comparison, TEN has a 30% mortality rate.\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis of SJS includes:\n\n- Erythema Multiforme: Characterized by target lesions, typically on the hands and feet, and less severe mucosal involvement.\n- Drug Rash with Eosinophilia and Systemic Symptoms (DRESS): Presents with fever, rash, and internal organ involvement, often with a delay of 2-6 weeks after drug exposure.\n- Acute Generalized Exanthematous Pustulosis (AGEP): Noted for the rapid development of numerous small non-follicular sterile pustules on a background of edematous erythema.\n\n# Investigations\n\nThe diagnosis of SJS is primarily clinical but can be supported by a skin biopsy, which can reveal necrotic keratinocytes and a sparse lymphocytic infiltrate.\n\n# Management\n\nManagement of SJS is largely supportive, focusing on skin care and prevention of ocular complications through timely ophthalmology referrals. Patients may require hospitalization for fluid and electrolyte management, pain control, and potential treatment of secondary infections.\n\n# References\n\n[Click here for more information on Stevens-Johnson syndrome](https://patient.info/doctor/stevens-johnson-syndrome)",
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"question": "A 40-year-old man presents to the accident and emergency department with a painful rash which has established quickly over the last few hours. He is pyrexial and reports general arthralgia. He was started on a course of amoxicillin for sinusitis the preceding day. He has no significant past medical or dermatological history.\n\nHis rash can be seen below.\n\n[lightgallery]\n\nWhich of the following is the most likely diagnosis in this patient?",
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"explanation": "### Summary\n\nBullous Pemphigoid and Pemphigus Vulgaris are both autoimmune blistering disorders with different blister locations and antigens involved. The clinical features, investigations, and treatments are similar, with steroids forming the mainstay of treatment. \n\n### Bullous Pemphigoid\n\n#### Definition\n\nOne of the autoimmune blistering disorders characterised by tense subepidermal blisters\n\n#### Pathophysiology\n\n- Autoantibodies targeting the hemidesmosomes that bind the basal keratinocytes of the epidermis to the basement membrane. The antigens are the BP180 and BP230 components of hemidesmosomes\n- This causes the development of tense, sub-epidermal blisters that are not readily deroofed\n- On immunoflouresence, this produces a linear pattern of immunoflouresence along the basement membrane\n- Autoantibodies may also be identified in the circulation\n- May sometimes represent a paraneoplastic process, so a careful history and examination is important\n- Other associations include drugs (PD-1 inhibitors in melanoma, ACEi and penicillamine), psoriasis treatment (phototherapy), injury to skin, neurological disease, and genetics\n\n#### Clinical Features\n\n- Usually affects older people\n- Prodrome of itch, irritation, erythematous, eczematous, urticarial skin changes, followed by tense subepidermal blisters\n- Nikolsky's sign is negative\n- The mucous membrane's are spared, except for the cicatrial variant (characterised by marked scarring and predilection for the mucous membranes) \n\n[lightgallery]\n\n#### Investigations\n\n- Biopsy for immunoflouresence from lesion edge\n- Anti BP180/BP230 antibodies circulating\n\n#### Treatment\n\n- Topical potent steroids at onset of symptoms e.g. itch\n- Doxycycline for anti-inflammatory effect\n- Systemic steroids (0.5-1mg/kg of prednisolone), continued until no further lesions for one year. Then tapered very gradually over many, many months\n- Steroid sparing agents include azathioprine and mycophenolate if relapse during steroid withdrawal\n- The cicatrial variant is particularly difficult to treat \n\n### Pemphigus Vulgaris\n\n#### Definition\n\nOne of the autoimmune blistering skin conditions characterised by flaccid intra-epidermal blisters.\n\n#### Pathophysiology\n\n- IgG autoantibodies are targeted against desmosomes, structures that link keratinocytes to other keratinocytes within the epidermis\n- The specific antigens are desmoglein 1 and desmoglein 3\n- This leads to the development of blisters within the epidermis, which are flaccid and often deroofed\n- Immunoflouresence shows a fish-net/chicken-wire pattern of staining within the epidermis\n- Drug triggers have been noted (such as ACEi and penicillamine), and it may be associated with an underlying malignancy as a paraneoplastic phenomenon\n\n#### Clinical Features\n\n- Flaccid, thin walled blisters leading to erosions across the body \n- Mucous membranes may be involved\n- Nikolsky's sign is positive\n- Patients can be quite unwell with pemphigus vulgaris and mortality is high without treatment\n\n[lightgallery1]\n\n#### Investigations\n\n- Biopsy for immunoflouresence from the edge of the lesion\n- Detection of autoantibodies against desmoglein 1 and desmoglein 3 using indirect immunofluorescence (IIF) or enzyme-linked immunosorbent assay (ELISA)\n\n#### Treatment\n\n- Treatment is very similar to Bullous Pemphigoid, with oral predniosolone\n- Risk of secondary bacterial infections is high and these often need treating with antibiotics \n\n### Memory Aid\n\nPemphigu**s** = **s**uperficial blisters, pemphigoi**d** = **d**eep blisters\n\nHere's a table comparing the two conditions:\n\n| | Bullous pemphigoid | Pemphigus vulgaris |\n| ------------- |:-------------:| :-----:|\n| Pathophysiology | IgG antibodies against hemidesmosomal proteins, primarily BP180 and BP230 | IgG antibodies against desmoglein 1 and desmoglein 3|\n| Clinical features | Tense, subepidermal blisters, rarely mucous membrane involvement | Painful, fragile blisters and erosions, mucous membrane involvement (oral membranes almost always)|\n| Investigation findings | Direct immunofluorescence (DIF) demonstrates linear IgG and complement along the basement membrane zone; Indirect immunofluorescence (IIF) or ELISA detects circulating antibodies against BP180 and BP230 | DIF demonstrates intercellular IgG deposits in the epidermis; IIF or ELISA identifies antibodies against desmoglein 1 and desmoglein 3 |\nTreatment | High-potency topical corticosteroids for local disease, oral corticosteroids for extensive involvement; immunosuppressive medications (AZT, MMF) for severe or refractory cases | High-dose systemic corticosteroids to induce remission, topical steroids for mucous membranes; adjunctive immunosuppressive agents (AZT, MMF, rituximab) to reduce corticosteroid dependence|\n\n\n\n### References\n[Bullous pemphigoid - DermNet NZ](https://dermnetnz.org/topics/bullous-pemphigoid)\n\n[Pemphigus vulgaris - DermNet NZ](https://dermnetnz.org/topics/pemphigus-vulgaris)\n",
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"explanation": "# Summary\n\nAcne vulgaris is a common chronic disorder of the pilo-sebaceous unit, resulting in blockage of the follicle, formation of comedones and inflammation. Key signs and symptoms include open/closed comedones, inflammatory papules and pustules, and in severe cases, nodules and cysts. The disorder predominantly affects the face, neck, chest, and back, and has a significant psychological impact due to altered physical appearance. Acne is primarily diagnosed clinically, with further investigations necessary only in uncertain cases or prior to commencing certain treatments like isotretinoin. Treatment is guided by severity and may involve topical or systemic therapy based on the NICE guidelines. Potential complications include post-inflammatory hyperpigmentation, hypopigmentation, erythema, psycho/social/sexual dysfunction, and scarring.\n\n\n# Definition\n\n- A a chronic disorder of the skin affecting the pilo-sebaceous unit, in which there is blockage of the follicle leading to comedones and inflammation. \n- Vulgaris translates as \"common\", which is true as this condition affects over 80% of adolescents.\n\n# Epidemiology\n\n* It is one of the most common dermatological conditions globally, affecting individuals of all ethnicities and ages.\n* Prevalence is highest in adolescents and young adults, with up to 80% of individuals experiencing some degree of acne during their lifetime.\n* While most common in adolescents, adult-onset acne can occur, affecting people well into their 30s and beyond.\n* Acne affects both males and females, but the prevalence and severity may vary between genders.\n* The psychological impact of acne can be significant, affecting self-esteem and overall quality of life.\n\n# Risk Factors\n\nSeveral factors contribute to the development and exacerbation of acne, including:\n\n* Hormonal changes (e.g. during puberty, menstrual cycle, polycystic ovary syndrome)\n* Increased sebum (oil) production\n* Blockage of hair follicles and sebaceous glands by keratin and sebum\n* Bacterial colonization (Propionibacterium acnes)\n* Family history of acne\n* Certain medications (e.g. corticosteroids, hormonal treatments)\n\n# Pathophysiology\n\n- In normal skin, skin cells in the stratum corneum of the epidermis (corneocytes) desquamate successfully without blocking pilo-sebaceous units.\n- In acne, the corneocytes are excessively cohesive. They do not detach successfully.\n- Because of this, the keratin rich corneocytes accumulate and block off hair follicles causing follicular hyperkeratinisation.\n- Sebum is trapped in the hair follicle since it cannot be drained away. Androgens may also contribute to this causing sebaceous gland hyperplasia and increased sebum production. \n- This combination of sebum and keratin forms micro-comedones - the earliest feature of acne vulgaris. This is only visible under a microscope.\n- Gradually, the follicle becomes more distended with keratin and sebum, and the micro-comedone enlarges to become a comedone. \n- Initially, these are closed comedones, referred to as whiteheads. The contents are not exposed to the skin surface or oxygen, and therefore appear as fleshy/white papules. \n- Eventually, closed comedones become open comedones. As their contents become exposed to oxygen, they oxidise which causes black discolouration. Open comedones are therefore referred to as blackheads.\n- Comedones are then colonised with a gram positive bacillus called Propionibacterium (Cutibacterium) acnes. This is a commensal organism (part of the normal skin flora) but leads to an inflammatory response in the right conditions of the comedone, in a predisposed patient. \n- The comedone is subsequently transformed into an inflammatory papule, which is now associated with erythema. A papule is a solid, raised lesion less than 0.5cm in diameter. \n- As things progress and more neutrophils accumulate, the inflammatory papule becomes a pustule; this is a lesion less than 0.5cm in diameter that contains pus. \n- Eventually, the inflammatory papule or pustule becomes so distended that it ruptures into the dermis, triggering a marked and deep seated inflammatory response. \n- This leads to the formation of nodules/cysts, which are painful and red. A nodule is a solid lesion larger than 0.5cm, and cysts are walled off fluid containing structures. \n\n[lightgallery]\n\n# Classification\n\n- Non-inflammatory: blackheads and whiteheads.\n- Inflammatory: inflammatory papules, pustules, and nodules (cysts.)\n- Mild acne: predominantly non-inflammatory lesions. \n- Moderate acne: predominantly inflammatory papules and pustules. \n- Severe acne: nodules (cysts), scarring, acne fulminans, and acne conglobata. \n\n# Clinical Features\n\n- Open/closed Comedones, inflammatory papules and pustules, nodules, and cysts may be present.\n- The face is most often affected. The neck, chest and back may also be affected.\n- Psychological dysfunction due to changes physical appearance\n- Scarring: associated with inflammatory acne. Hypertrophic and keloid scars are more common in darker skin tones. \n\t- Atrophic: flat or indented, such as ice-pick, box-car, or rolling scars.\n\t- Hypertrophic: raised scars.\n\t- Keloid: raised scars that extend beyond the initial boundaries of the injury. \n- Post-inflammatory hyperpigmentation and hypopigmentation: associated with inflammatory acne. \n- Post inflammatory erythema: associated with inflammatory acne.\n- Acne fulminans: an uncommon but severe, serious acne presentation. \n\t- Inflammatory nodules/cysts that are painful, ulcerating, and haemorrhagic appear, with associated systemic upset (raised white cell count, joint pain, fever, fatigue.) \n\t- These patients should be reviewed urgently within 24 hours. It usually affects teenage male patients.\n- Acne conglobata: another uncommon presentation of severe nodular/cystic acne with interconnecting sinus tracts and extensive scaring. \n\n[lightgallery1]\n\n[lightgallery2]\n\n# Investigations\n\n- Acne is a clinical diagnosis and investigations are not usually needed. \n- Swabs may be indicated if the diagnosis is uncertain (e.g. if ruling out infectious pustules.)\n- Investigations will be required prior to commencing isotretinoin if indicated.\n- In some particular presentations where an endocrine cause is suspected, there may be endocrinological investigations (hyperandrogenic states such as PCOS or androgen secreting tumours.)\n\n# Treatment\n\nManagement of acne is multifaceted including education, topical/oral treatments and lifestyle modifications. \n\n- Each treatment combination is given as a 12 week course. \n- Combination therapies help reduce antimicrobial resistance. \n- Antibiotics are used predominantly since they have anti-inflammatory effects, rather than for their antimicrobial effects.\n- **Mild-moderate acne** is treated with any 2 of the following in combination:\n\t- Topical benzoyl peroxide.\n\t- Topical antibiotics (clindamycin)\n\t- Topical retinoids (tretinoin/adapalene)\n- **Moderate-severe acne** is treated with a 12-week coures of the following first line options:\n\t- Topical retinoids (tretinoin/adapelene) + topical benzoyl peroxide.\n\t- Topical retinoids + topical antibiotics (clindamycin)\n\t- Topical benzoyl peroxide + topical retinoid (tretinoin/adapelene) + oral antibiotic (lymecycline/doxycycline.) \n\t- Topical azelaic acid + oral antibiotic (lymecycline/doxycycline) \n\t- Second line oral antibiotics: trimethoprim and erythromycin e.g. in pregnant/breast-feeding women where tetracyclines are contra-indicated. \n\t- Combined oral contraceptives (COCPs) (if not contraindicated) in combination with topical agents can be considered as an alternative to systemic antibiotics in women\n\nNB: topical retinoids and oral tetracyclines are contraindicated during pregnancy and when planning a pregnancy, and so women of childbearing potential will need to use effective contraception, or choose an alternative treatment to these options.\n\t\n- As per NICE guidelines, referral to specialist Dermatology is indicated in the case of:\n\t- Acne fulminans.\n\t- Mild-moderate acne not responding to two 12 week courses of treatment as above.\n\t- Moderate-severe acne not responding to one 12 week course of treatment as above, including an oral antibiotic.\n\t- Psychological distress/mental health disorder contributed to by acne.\n\t- Acne with persistent pigmentary changes.\n\t- Acne with scarring.\n- Other available agents:\n\t- Co-cyprindiol: anti-androgenic contraceptive agent - may be trialled in primary care on female patients, but usually second line COCP due to increased risk of venous thromboembolism, and can only be given for 3 months. \n\t- Spironolactone: anti-androgenic - not often used. Not for male patients. \n\t- **Isotretinoin (oral retinoid):** the usual next step if the standard treatment fails and is prescribed by a dermatologist. \n\t\t* Notable adverse effects: dry skin/mouth/eyes/lips (most common), teratogenecity, photosensitivity, low mood, nose bleeds, hair thinning, raised triglycerides, intracranial hypertension \n\t\t* Isotretinoin is a well established teratogen that results in miscarriages and severe birth defects. As a result, the manufacturer recommends that all female patients taking isotretinoin are also using two forms of contraception from one month before until one month after use. For this reason a pregnancy test should also be done before initiating treatment\n\t\t* There is a controversial association between isotretinoin and depression/suicide. Recent research has shown that concerns about links between isotretinoin and depression or suicide are not established. This has now been included into the NICE guidelines. However it is still important to screen for depression/suicidal ideation before prescribing and during treatment.\n\t\n\t\n# Complications\n\n- Post-inflammatory erythema\n- Post-inflammatory hyper- and hypo- pigmentation\n- Psycho/social/sexual dysfunction \n- Scars (atrophic, hypertrophic, keloid)\n\t- Keloid scars: over-proliferating scar tissue/collagen extending beyond the boundaries of the lesion. Takes 3-4 weeks typically to develop after injury. They can cause itch and pain. It is fleshy, smooth, firm, and does not regress with time. The original injury may be minor, for example piercing or insect bite. Treatment is usually with intralesional steroids (triamcinolone). Cryotherapy and laser may also be used. Surgical resection is unlikely to be successful due to further scarring. Risk factors include:\n\t\t- Darker skin/Chinese/Hispanic origin \n\t\t- Less than 30 years of age\n\t\t- Previous keloid scarring \n\t- These are distinct from hypetrophic scars, which are thick and raised but remain within the injured boundary and tend to improve over time. \n\n# NICE Guidelines\n\n[NICE CKS for Acne Vulgaris](https://cks.nice.org.uk/topics/acne-vulgaris/)",
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"explanation": "# Summary\n\nA vestibular schwannoma is a benign subarachnoid tumour that predominantly affects the VIII cranial nerve. Key signs and symptoms include unilateral hearing loss, progressive ipsilateral tinnitus, and in severe cases, signs of raised intracranial pressure due to mass effect. Key investigations primarily involve an MRI scan, especially in patients presenting with unilateral tinnitus and sensorineural deafness. The definitive management strategy is surgical intervention for tumours over 40mm, while those under 40mm are monitored with 6-monthly annual surveillance scans via MRI.\n\n# Definition\n\nA vestibular schwannoma is defined as a benign subarachnoid tumour that exerts local pressure effects on the VIII cranial nerve.\n\n# Epidemiology\n\nIn the UK, vestibular schwannomas, also known as acoustic neuromas, are relatively rare and are estimated to occur in about 1 in 100,000 people annually, most commonly presenting in adults between the ages of 40 and 60.\n\n# Aetiology\n\nVestibular schwannomas, are benign tumors that develop from the Schwann cells of the vestibulocochlear nerve, with the majority being sporadic cases, though a small percentage are associated with a genetic disorder called neurofibromatosis type II.\n\n# Signs and Symptoms\n\n- The most common symptoms reported are asymmetric or unilateral hearing loss and progressive ipsilateral tinnitus.\n- Larger tumours may cause a mass effect leading to signs of raised intracranial pressure and can result in focal neurology including compression of the fifth, seventh, and eighth cranial nerves.\n- Additional symptoms include: dizziness, headaches, and disequilibrium.\n\n# Differential Diagnosis\n\n\n* **Meniere's Disease:** Characterized by recurrent episodes of vertigo, hearing loss, and tinnitus. While both conditions may cause vertigo, Meniere's disease has a different clinical presentation and is not a tumor.\n* **Labyrinthitis:** An inflammation of the inner ear, often caused by viral or bacterial infections, resulting in symptoms similar to vestibular neuromas.\n* **Benign Paroxysmal Positional Vertigo (BPPV):** A common cause of recurrent vertigo, often triggered by head movements. BPPV is not associated with tumors but with dislodged otoliths in the inner ear.\n* **Migraine-Associated Vertigo:** Individuals with migraines may experience vestibular symptoms, which can sometimes be mistaken for vestibular neuromas.\n* **Other Intracranial Lesions:** While less common, intracranial lesions, such as brainstem or cerebellar tumors, can present with similar vestibular symptoms.\n* **Posterior Circulation Stroke:** Vertigo can be a symptom of a stroke, especially when associated with other neurological deficits.\n* **Autoimmune Inner Ear Disease:** An immune-mediated condition affecting the inner ear, causing hearing loss and vestibular symptoms.\n* **Otosclerosis:** An abnormal bone growth in the middle ear that can lead to hearing loss and sometimes imbalance.\n* **Superior Semicircular Canal Dehiscence (SSCD):** A rare condition where there is a hole in the bone covering the superior semicircular canal, leading to vertigo triggered by loud sounds or pressure changes.\n\n\n\n# Investigations\n\nIn patients presenting with unilateral tinnitus and sensorineural deafness, an MRI scan should be performed to exclude the evidence of malignancy.\n\n[lightgallery]\n\n# Management\n\nThe definitive management of vestibular schwannoma is surgery, specifically for tumours over 40mm in size. For tumours under 40mm in size, 6-monthly annual surveillance scans via MRI are recommended.\n\n# References\n\n[Click here for NICE CKS on hearing loss in adults](https://cks.nice.org.uk/topics/hearing-loss-in-adults/)\n\n[Click here for NICE CKS on tinnitus](https://cks.nice.org.uk/topics/tinnitus/)",
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"question": "A 30 year old man is referred to the outpatient ENT clinic with gradual onset bilateral sensorineural hearing loss and tinnitus.\n\nOn examination, he has absent corneal reflexes bilaterally.\n\nAn MRI cerebellopontine angle confirms bilateral vestibular schwannomas.\n\nWhat is the most likely underlying diagnosis?",
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"comment": "Difference between Epley manoeuvre and \"Brandt-Daroff exercises\" ?",
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"comment": "\"There are alternative manoeuvres that can be used to treat BPPV, such as an Epley manoeuvre. Your specialist may perform an Epley manoeuvre with you in clinic and then recommend Brandt-Daroff exercises for you to use at home as these are easier to perform unsupervised.\"\n\nFrom a patient leaflet about the two... had never heard of it either! ",
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"explanation": "# Summary\n\nBenign Paroxysmal Positional Vertigo (BPPV) is a condition characterised by sudden episodes of vertigo, typically following head movement. It is the most common cause of vertigo, particularly in the elderly due to calcium deposition within the semicircular canals. The key signs and symptoms include sudden attacks of rotational vertigo lasting for 30 seconds to 1 minute, triggered by changing head positions. There are no associated auditory symptoms. Diagnosis is made using the Dix-Hallpike manoeuvre, and management primarily involves the Epley manoeuvre. \n\n# Definition\n\nBenign Paroxysmal Positional Vertigo (BPPV) is a medical condition characterised by sudden, episodic attacks of vertigo induced by changes in head position. This condition is due to detachment of otoliths in the inner ear, which results in hair cell stimulation and subsequent vertigo symptoms.\n\n# Epidemiology\n\nBPPV is the leading cause of vertigo and is especially prevalent within the elderly population. This increased prevalence is largely attributed to the accumulation of calcium deposits, known as cholelithiasis, within the semicircular canals of the inner ear.\n\n# Aetiology\n\nBPPV arises due to a detachment of otoliths from the utricle of the inner ear. These detached particles can migrate into the semicircular canals, where they stimulate hair cells and lead to symptoms of vertigo.\n\n# Signs and Symptoms\n\nKey clinical features of BPPV include:\n\n- Vertigo attacks provoked by specific head movements, such as turning the head to one side while in bed or looking upwards\n- Episodes of rotational vertigo lasting between 30 seconds to 1 minute\n- Absence of auditory symptoms\n- Recurrent episodes, often resolving naturally over weeks to months\n\n# Differential Diagnosis\n\nDifferential diagnoses for BPPV include other conditions that can cause vertigo such as Meniere's disease, vestibular neuritis, and labyrinthitis. Key signs and symptoms for these conditions include:\n\n- Meniere's disease: episodic vertigo, tinnitus, hearing loss, and a sensation of fullness in the ear\n- Vestibular neuritis: sudden onset of severe vertigo, nausea, and imbalance lasting for several days\n- Labyrinthitis: vertigo, hearing loss, and tinnitus\n\n# Investigations\n\nThe primary diagnostic test for BPPV is the Dix-Hallpike manoeuvre. This test involves a series of specific head movements that provoke the characteristic vertigo and nystagmus associated with BPPV.\n\n[Click here for more information](https://www.thebsa.org.uk/wp-content/uploads/2014/04/HM.pdf)\n\n# Management\n\nThe mainstay of BPPV management is the Epley manoeuvre. This therapeutic manoeuvre aims to move the detached otoliths out of the semicircular canal and back to the utricle where they originate.\n\n[Click here for more information](https://www.racgp.org.au/download/Documents/AFP/2013/January/February/201301handi.pdf)\n\n# References\n\n[Click here for NICE CKS on benign paroxysmal positional vertigo](https://cks.nice.org.uk/topics/benign-paroxysmal-positional-vertigo/)",
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"question": "An 88 year old woman presents to her GP with recurrent episodes of dizziness and vertigo which she says is often brought on when rolling over in bed. The GP performs the Dix-Hallpike manoeuvre which is positive. She is keen for something to manage her symptoms.\n\nWhat is the next best step in managing this patient's dizziness?",
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"comment": "im sorry but no. you would pack and send to A+E for cauterising",
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"comment": "they're already in A&E",
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"comment": "im sorry but no, cautery goes ahead of nasal packing if an obvious bleeding site is seen and you are in the ED ",
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"comment": "You're not Dr brighton yet xx",
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"explanation": "# Summary\n \nEpistaxis refers to nosebleeds, which are a common condition ranging significantly in severity. Many are mild and self-limiting with simple first-aid, however larger bleeds may be life-threatening and require rapid intervention and resuscitation. Contributing factors include trauma (e.g. nose-picking), inflammation, drug use (e.g. cocaine), recent surgery, tumours and bleeding diatheses. Management of epistaxis involves a stepwise approach starting with direct pressure on the cartilaginous part of the nose, cautery, nasal packing, followed by interventions such as arterial embolisation or ligation if bleeding is refractory to other treatments. \n \n# Definition\n \nEpistaxis refers to bleeding from the nose - this usually originates from the anterior nasal septum (Little's area and Kiesselbach's plexus specifically) but around 10% of cases are posterior, originating from branches of the sphenopalatine artery. \n \n# Aetiology\n \nMost cases of epistaxis are mild and self-limiting, with no specific underlying cause identified. Factors that may contribute to epistaxis include:\n\n- Trauma (e.g. nose-picking, blunt trauma, septal perforations and foreign bodies in the nose)\n- Oxygen via nasal cannulae (causes drying and irritation of the nasal mucosa)\n- Recent ENT or maxillofacial surgery\n- Tumours, either malignant (e.g. squamous cell carcinomas) or benign (e.g. angiofibromas)\n- Inflammation (e.g. rhinosinusitis, nasal polyps)\n- Alcohol excess\n- Illicit drug use e.g. snorting cocaine \n- Medications such as nasal steroids\n- Vasculitides (e.g. granulomatosis with polyangiitis)\n- Bleeding diatheses (e.g. thrombocytopenia, Von Willebrand disease, haemophilia, antiplatelet or anticoagulant medications)\n- Environmental factors e.g. inhaled irritants, temperature and humidity\n\n# Signs and symptoms\n\nThe major symptom is nasal bleeding - other signs and symptoms may include:\n\n- Bleeding down the throat (which may present as haemoptysis or haematemesis) - may signify posterior epistaxis\n- Bleeding from both nostrils is another sign of possible posterior epistaxis\n- Signs and symptoms of haemodynamic instability if blood loss is significant (e.g. tachycardia, pallor, syncope)\n- Signs and symptoms of an underlying cause (e.g. nasal obstruction and rhinorrhoea may indicate a tumour or nasal polyps)\n\n# Investigations\n\nIn most cases of nosebleeds, no investigations are required.\n\nIf bleeding is significant, a **venous blood gas** and **FBC** should be done to look for anaemia and thrombocytopenia, a **clotting screen** looking for coagulopathy and a **group and save** or **crossmatch** if blood transfusion is required.\n\nInvestigations may also be required if an underlying serious cause is suspected, e.g. imaging or flexible nasendoscopy for a suspected tumour, or specific blood tests for bleeding disorders such as Von Willebrand disease.\n\n# Management\n\n- The first step in management is **direct compression**.\n- The patient should sit forward (minimising bleeding into the nasopharynx), breathing through their mouth, and pinch the cartilaginous part of the nose for 10-15 minutes. \n- Sucking ice cubes, cold drinks or placing an ice pack on the back of the neck can help to reduce bleeding.\n- This is sufficient to resolve the majority of anterior epistaxis.\n- A **topic antiseptic** (e.g. Naseptin or mupirocin) may be prescribed to reduce crusting and rebleeding.\n- If direct compression does not resolve the epistaxis and a bleeding point can be visualised, **cautery** may be performed. \n- This involves applying a local anaesthetic spray with a vasoconstrictor (e.g. lidocaine with phenylephrine) to temporarily halt bleeding, then apply silver nitrate (chemical cautery) or electrocautery to the area. \n- Only one side of the septum should be cauterised to avoid perforation.\n- If a bleeding point cannot be visualised or bleeding continues despite cautery, **nasal packing** may be used. \n- The most common devices used are nasal tampons (e.g. Merocel) or inflatable packs (e.g. Rapid-Rhino). \n- Both nostrils can be packed to increase pressure on the area of bleeding.\n- In cases of posterior epistaxis, **posterior packing** may be required which may involve insertion of a Foley catheter with the balloon inflated to compress the bleeding area.\n- Packing should be left in place for 24-48 hours to ensure bleeding has stopped.\n- If bleeding continues despite packing, a **surgical approach** may be required (e.g examination under anaesthesia with ligation of bleeding vessels) or interventional radiology may perform an **embolisation**.\n- **Tranexamic acid** should be given to all patients with severe bleeding.\n- Antiplatelets and anticoagulants should usually be held - may need speciality input (e.g. cardiology) in difficult cases such as patients with metallic heart valves.\n- Anticoagulation may need to be reversed with haematology input if needed.\n- Patients who are haemodynamically unstable may need resuscitation and blood transfusion.\n\n# Complications\n\n- Anaemia\n- Recurrent epistaxis\n- Hypovolaemia\n- Aspiration of blood and airway compromise\n- Nasal cautery may cause septal perforation\n- Nasal packing may lead to sinusitis, septal haematoma or pressure necrosis\n\n# NICE Guidelines\n\n[NICE CKS - Epistaxis](https://cks.nice.org.uk/topics/epistaxis-nosebleeds/)\n\n# References\n\n[ENT UK - Epistaxis Guideline](https://www.entuk.org/_userfiles/pages/files/guidelines/global%20ent%20guidelines/nosebleeds.pdf)\n \n[Life in the Fast Lane - Epistaxis](https://litfl.com/a-case-of-epistaxis/)\n\n[Patient UK - Epistaxis](https://patient.info/doctor/nosebleed-epistaxis-pro)",
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"question": "A 24 year old male presents to the Emergency Department with epistaxis which started 1 hour prior to being seen. The nurse practitioner has already applied nasal pressure for 15 minutes. On examination using a nasal speculum, there is an obvious bleeding site in the anterior aspect of the septum. The patient is haemodynamically stable.\n\nWhat is the next best step in management of this patient's epistaxis?",
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"comment": "Well TIL. Good question",
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"comment": "Evidence is moving away from glucagon being used in BB overdose btw - so you'd be more correct saying bicarb...",
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"explanation": "# Summary\r\n\r\nBradycardia is defined as a heart rate <60bpm. It may be physiological or pathological. Bradycardic patients may present with fatigue, lightheadedness and/or syncope. Diagnosis of a bradycardia is made on ECG. It a patient has an acute bradycardia and adverse features then this is a medical emergency requiring immediate treatment. Emergency management is according to the Resus Council Algorithm and may involve atropine administration and transcutaneous/transvenous pacing. Longer-term management involves the insertion of a permanent pacemaker. \r\n\r\n# Definition \r\n\r\nBradycardia is defined as a heart rate <60bpm. If a patient has an acute bradycardia and adverse features (shock, syncope, heart failure or evidence of myocardial ischaemia) then this is a medical emergency requiring immediate treatment. \r\n\r\n# Epidemiology \r\n\r\nThe most common cause of pathological bradycardia is sick sinus syndrome and is estimated to have an incidence of 1 in 600 peopel over the age of 65. It affects both sexes equally. \r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology of bradycardias depends on the cause. The most common cause of bradycardia is sick sinus syndrome and this is due to the dysfunction of pacmemaker cells within the sinoatrial node (physiological pacemaker) as a person gets older. \r\n\r\n# Classification\r\n\r\nBradycardia can be classified according to cause: \r\n\r\n* Physiological: common in younger populations, athletes and during sleep. \r\n\r\n* Cardiac: \r\n * Sick sinus syndrome: disorder of the sinoatrial node. \r\n * Heart block: disorder of the atrioventricular node. \r\n * Post-myocardial infarction: post-inferior myocardial infarction. The right coronary artery supplies the SAN (pacemaker of the heart). \r\n * Aortic valve disease: the right coronary artery origin is disrupted just above the aortic valve. \r\n\r\n* Non-cardiac: \r\n * Vasovagal \r\n * Endocrinological: hypothyroidism. \r\n * Hypothermia \r\n * Electrolyte abnormalities\r\n * Cushing's triad of raised ICP: bradycardia, irregular breathing and hypertension. \r\n * Medications: beta-blockers, calcium channel blockers, digoxin etc. \r\n\r\n# Symptoms and signs\r\n\r\n## Symptoms\r\n\r\n* Lightheadedness \r\n* Syncope\r\n* Fatigue \r\n* Shortness of breath\r\n\r\n## Signs \r\n\r\n* Nil signs apart from bradycardia \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n* **ECG**: help indicate underlying cause for the bradyarrhythmia. E.g. sick sinus syndrome with severe bradycardia and long pauses vs. heart block with prolonged PR interval. \r\n\r\n## Bloods \r\n\r\n* If considering a non-cardiac cause of the bradyarrhythmia (e.g. heart block).\r\n\r\n## Imaging \r\n\r\n* TTE: if considering causes such as post-MI (looking for regional wall motion abnormalities) or aortic valve disease. \r\n\r\n# Management\r\n\r\n## Initial management\r\n\r\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **500 micrograms atropine IV**\r\n * Atropine blocks the vagal nerve which increases firing rate of the SAN. \r\n* **2nd line** = if the first dose of atropine is not working can consider giving additional doses of atropine 500mcg up to 3mg until response. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs but a risk of asystole, or a satisfactory response to 500mcg atropine:*\r\n\r\n* Risk of asystole: recent asystole, mobitz type II block, complete heart block + broad QRS, ventricular pauses >3s. \r\n* **1st line** = administer **500 micrograms atropine IV**. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs and there is no risk of asystole*\r\n\r\n* Observe\r\n\r\n## Further management \r\n\r\nTranscutaneous pacing may be used as an interim measure whilst awaiting expert help for transvenous pacing/permanent pacemaker insertion. \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines for Symptomatic Bradycardias](https://www.nice.org.uk/guidance/ta88/ifp/chapter/what-is-symptomatic-bradycardia)\r\n\r\n# References\r\n\r\n[Click here to see the algorithm on the Resus Council website on management of bradycardia](https://www.resus.org.uk/library/2015-resuscitation-guidelines/peri-arrest-arrhythmias)",
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"question": "A 75 year old is brought to the emergency department by his son who believes he has taken an intentional overdose of his bisoprolol. On arrival to the department he has a reduced GCS, a blood pressure of 88/58 mmHg, and a heart rate of 40 beats per minute. He is initially given atropine, but his heart rate only increases to 50 beats per minute and he remains hypotensive.\n\nWhich of the following is the next best step in the management of this patient's bisoprolol overdose?",
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"explanation": "High flow oxygen is not indicated at this stage. He has normal saturations on room air and, in addition to this, it is not unreasonable to suspect that this patient might be oxygen sensitive given his background of COPD",
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"comment": "With the new guidelines, even if there are high-risk characteristics such as existing lung disease would we not now just observe with regular x-ray and follow-up?\n",
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"comment": "in secondary pneumothorax, if pt is breathless or it's >2cm (of which this pt has both) you go with chest drain\nfor secondary, i think you only admit and observe if they'er asymptomatic and it's <1cm",
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"explanation": "# Summary\n \nA pneumothorax is characterised by the abnormal presence of air in the pleural cavity, which may be spontaneous or traumatic in origin. Key signs and symptoms include sudden-onset shortness of breath, pleuritic chest pain, reduced chest expansion and reduced or absent breath sounds on the affected side. Chest X-ray is the key diagnostic investigation (although in cases of tension pneumothorax the diagnosis should be clinical). Management decisions depend on the size of the pneumothorax, the patient's clinical condition and their wishes. Options include conservative management, needle aspiration, chest drain insertion or an ambulatory device. In cases of tension pneumothorax needle decompression is the initial emergency management.\n \n# Definition\n \nA pneumothorax refers to a collection of air in the pleural cavity which may cause collapse of the underlying lung parenchyma. \n\n# Classification\n\n- They may be **spontaneous** or **traumatic** (including iatrogenic causes).\n\n- Spontaneous pneumothoraces can be further divided into **primary** pneumothoraces (in patients without an underlying lung disease) and **secondary** (in patients with underlying lung diseases such as COPD or asthma).\n\n- Patients aged over 50 years old with a significant smoking history who present with a spontaneous pneumothorax are generally considered to have a secondary pneumothorax. \n\n- A **tension pneumothorax** occurs when the defect in the pleura that has led to the pneumothorax creates a one-way valve effect whereby air can enter the pneumothorax but not leave it.\n - This causes the pneumothorax to progressively expand, putting pressure on the heart and great vessels and causing **mediastinal shift**\n - This is a medical emergency that rapidly leads to cardiac arrest if untreated\n \n\n# Signs and Symptoms\n \nThere may be no signs or symptoms (small pneumothoraces may be detected incidentally on imaging) however in an emergency presentation these may include:\n\n- Sudden onset shortness of breath\n- Pleuritic chest pain\n- Dry cough\n- Tachypnoea and increased work of breathing\n\nThe following signs will be found on the affected side of the chest:\n\n- Unilateral reduced expansion\n- Unilateral hyper-resonance to percussion\n- Reduced or absent breath sounds\n- Reduced vocal resonance or tactile vocal fremitus\n \nPatients with a tension pneumothorax may also have:\n\n- Tracheal deviation to the contralateral side\n- Tachycardia\n- Hypotension\n- Distended neck veins\n\n# Investigations\n \nPatients with a suspected tension pneumothorax should be diagnosed and treated with needle decompression based on the clinical picture, with no delay for investigations.\n\nFor other patients, an **erect PA chest X-ray** is diagnostic. \n\n [lightgallery]\n \n\n [lightgallery1]\n \n**CT chest** should be used in high-risk patients where it is not clear from the chest X-ray whether it is safe to place a chest drain.\n\n**Arterial blood gases** are not usually indicated however they may be of use in certain situations e.g. titrating oxygen in a patient with COPD and low saturations.\n\n# Management \n\n**Tension Pneumothoraces:** \n\n- If a tension pneumothorax is suspected, emergency management is to decompress this by inserting a large-bore cannula into the second intercostal space on the affected side, mid-clavicular line, or fifth intercostal space, mid-axillary line if a traumatic cause is suspected, as per ATLS guidelines.\n\n\n- If this fails, open thoracostomy should be done immediately\n- After initial emergency decompression, a chest drain should be inserted\n\nFor **primary or secondary spontaneous pneumothoraces**, management is guided by the 2023 BTS Guidelines as summarised below:\n\n [lightgallery2]\n \n- **Conservative management** involves no intervention for the pneumothorax, and patients are monitored to ensure they do not deteriorate and any symptoms resolve\n- **Ambulatory devices** (e.g. pleural vents) are one-way valves which allow air to leave the pneumothorax but not re-enter it\n - They can be inserted in a simple procedure under local anaesthetic\n - Patients can then be followed up as outpatients\n- Symptomatic patients with larger pneumothoraces (usually 2cm or larger on CXR - CT may be used if unclear) or those with high-risk features (significant hypoxia, bilateral pneumothoraces, underlying lung disease, 50 or older with a significant smoking history, haemopneumothorax) require a **chest drain** and admission for monitoring\n- In symptomatic patients without high-risk features but with pneumothoraces large enough for treatment (2cm or larger), management depends on their priorities\n - Conservative management allows avoidance of any procedure\n - Both needle aspiration and ambulatory devices offer more rapid symptomatic relief (ambulatory device insertion may not be available in all hospitals) \n\n\n**Follow up:**\n\n- All patients should be reviewed in an outpatient clinic 2–4 weeks after presenting with a pneumothorax (with repeat chest imaging)\n- Patients should be advised on smoking cessation if relevant\n - Advise patients not to fly until 7 days after chest imaging has confirmed resolution of the pneumothorax\n - Advise patients they should not take part in underwater diving for life (except in rare cases where they have been treated with bilateral open surgical pleurectomy)\n \n# References\n \n[British Thoracic Society Guidelines](https://thorax.bmj.com/content/thoraxjnl/78/11/1143.full.pdf)\n\n[Royal College of Emergency Medicine - Spontaneous Pneumothorax](https://www.rcemlearning.co.uk/reference/spontaneous-pneumothorax/)\n\n[Radiopaedia - Tension Pneumothorax](https://radiopaedia.org/articles/tension-pneumothorax)\n\n[Pleural Vent Ambulatory Devices](https://www.nth.nhs.uk/resources/pleural-vent-ambulatory-device/)",
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"question": "A 55 year old presents to the emergency department with sudden onset of breathlessness. He is known to have chronic obstructive pulmonary disease (COPD) and has smoked 20 cigarettes per day for approximately 40 years. His chest x-ray shows a pneumothorax of approximately 3cm in size.\n\nHis observations are all normal and his saturations are 96% on air.\n\nWhat is the next step in this patient's management?",
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"explanation": "PEA is a non-shockable rhythm and therefore shocks are not indicated",
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"name": "Give 1 shock, immediately resume CPR and reassess rhythm in 2 minutes",
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"comment": "you would give Adrenaline as soon as possible- question is wrong",
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"comment": "That's not an option. Also, high quality BLS always takes priority over ALS",
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"comment": "However, it is the next step according to advanced life support guidelines as per question.",
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"comment": "Not true. After checking the rhythm, if it is non shockable, the next step is resume cpr. Giving adrenaline comes after cpr has been restarted and in practice would be done by another person to prevent interruption. Question is right.",
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"explanation": "# Summary\n\nAdvanced Life Support (ALS) describes an algorithmic approach to the management of a cardiac arrest by those trained in delivering it. It involves early recognition, taking steps to secure the airway and initiate high quality chest compressions and obtaining intravenous or intraosseous access promptly. Cardiac monitoring should be applied to identify if the rhythm is shockable or non-shockable, which determines what treatment is given. Shockable rhythms require defibrillation, with adrenaline and amiodarone given later on; non-shockable rhythms are treated with adrenaline. \n\n# Definition\n\nAdvanced Life Support is a guideline-based approach to treating patients who have had a cardiac arrest to improve the chances of successful resuscitation and survival. \n\n# Epidemiology\n\nCardiac arrests can be categorised into those that occur out of hospital and those that occur in hospitals. Most out of hospital cardiac arrests occur at home (72%) and 8 out of 10 are due to a cardiac cause. In 7 out of 10 cases resuscitation is attempted, however only 9% of these patients survive to hospital discharge.\n\nIn hospital cardiac arrests tend to occur in older patients (average age 70), with return of spontaneous circulation (ROSC) achieved in 53% of patients. However, only 24% of patients survive to hospital discharge. \n\n# Aetiology\n\nCauses of cardiac arrest can be remembered using the 4Hs and 4Ts mnemonic:\n\n- Hypoxia\n- Hypovolaemia\n- Hypo/hyperkalaemia (and other electrolyte abnormalities)\n- Hypo/hyperthermia\n- Thromboembolism (pulmonary embolism or coronary artery thrombosis)\n- Tamponade\n- Tension pneumothorax\n- Toxins \n\n# Classification\n\nCardiac arrests are managed differently depending on whether the rhythm is **shockable** or **non-shockable**.\n\n**Shockable** rhythms are:\n\n- **Pulseless Ventricular Tachycardia (pVT)** - regular broad complex tachycardia\n- **Ventricular Fibrillation (VF)** - chaotic irregular deflections of varying amplitude\n\n**Non-shockable** rhythms are:\n\n- **Pulseless Electrical Activity (PEA)** - electrical activity that should produce a pulse, but doesn't due to absent or insufficient cardiac output \n- **Asystole** - no detectable electrical activity \n\n# Management\n\n## Management for all cardiac arrests\n\n- **Rapid recognition** of cardiac arrest (ineffective breathing or absent central pulse) is key \n- The first responder should start **cardiopulmonary resuscitation (CPR)** immediately and **call for help**, for example by asking for a cardiac arrest call (2222) to be put out\n- Every two minutes CPR should be stopped for a **rhythm check**\n- Secure the **airway**\n - Oropharyngeal or nasopharyngeal airways may be used initially with a bag valve mask for ventilation\n - Either a supraglottic airway (laryngeal mask airway or i-gel) or an endotracheal tube should be inserted\n - Tracheal intubation should only be attempted by those with a high success rate\n - Confirm the position of the endotracheal tube with waveform capnography (measuring end-tidal carbon dioxide)\n- Give **high-flow oxygen**\n- Gain IV access - if not possible the intraosseous (IO) route can be used\n- Consider reversible causes (as above) and treat as appropriate\n - IV or IO fluids if secondary to hypovolaemia\n - Thrombolysis if secondary to pulmonary embolism\n - Point of care ultrasound (POCUS) may be used to investigate for cardiac tamponade and pneumothorax\n \n## Management of shockable rhythms\n\n- **Defibrillation** should be delivered as early as possible\n - Remove oxygen (ventilator circuits can remain attached)\n - Ensure no one is touching the patient before the shock is delivered\n - No specific energy is specified in guidelines; anything from 120 to 360 joules is suitable\n- Immediately resume CPR after the shock is delivered for two minutes\n- After 3 shocks, give 300mg amiodarone and 1mg adrenaline IV or IO\n- Give repeat doses of adrenaline every 3-5 minutes (i.e. every other cycle)\n- After 5 shocks, give a further dose of amiodarone 150mg\n\n## Management of non-shockable rhythms \n\n- Give adrenaline 1mg IV or IO as soon as possible\n- Give repeat doses of adrenaline every 3-5 minutes (as per shockable rhythms)\n- Defibrillation and amiodarone are not used unless the rhythm changes to a shockable one\n\n# NICE Guidelines\n\n[NICE CKS - Advanced Life Support](https://cks.nice.org.uk/topics/cardiac-arrest-out-of-hospital-care/management/advanced-life-support-adult/)\n\n# References\n\n[Resuscitation Council UK - Adult Advanced Life Support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n \n[Resuscitation Council UK - Epidemiology of Cardiac Arrest](https://www.resus.org.uk/library/2021-resuscitation-guidelines/epidemiology-cardiac-arrest-guidelines)\n\n[BNF Treatment Summaries - Cardiopulmonary Resuscitation](https://bnf.nice.org.uk/treatment-summaries/cardiopulmonary-resuscitation/)",
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"explanation": "This is the management for hyperkalaemia. This patient has a normal potassium level and likely has hyperosmolar hyperglycaemic state (HHS). There is evidence to suggest that patients with HHS actually tend to have worse outcomes if they are treated with the diabetic ketoacidosis (DKA) protocol such as with an insulin infusion",
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"explanation": "This is incorrect. This patient has hyperosmolar hyperglycaemic state (HHS) which should be treated with fluids. There is evidence to suggest that patients with HHS actually tend to have worse outcomes if they are treated with the diabetic ketoacidosis (DKA) protocol such as with an insulin infusion",
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"explanation": "# Summary \n \nHyperosmolar Hyperglycaemic State (HHS) is a life-threatening complication of type 2 diabetes, where patients become severely hyperglycaemic and fluid deplete over several days. It tends to present with polyuria and polydipsia, confusion and nausea, and is often triggered by intercurrent infection. Key investigations include blood glucose, ketones and a blood gas to check pH (patients with HHS should not be acidotic or have significant ketonaemia - presence of these may suggest an overlapping syndrome with diabetic ketoacidosis). Bloods including U&Es should be done and serum osmolality calculated or measured. The mainstay of treatment is fluid resuscitation to normalise osmolality and blood glucose. Foot care and venous thromboembolism prophylaxis are also important to prevent complications.\n \n# Definition\n \nHyperosmolar Hyperglycaemic State (HHS) is a complication of type 2 diabetes that is usually seen in older patients with known diabetes (although it may represent a first presentation).\n\nThe key features of HHS are:\n\n- Blood glucose ≥ 30 mmol/L\n- Serum osmolality ≥ 320 mOsm/kg\n- Significant hypovolaemia \n- Blood ketones ≤ 3 mmol/L\n- pH ≥ 7.3 and bicarbonate ≥15.0 mmol/L\n\nPatients who otherwise meet the criteria for HHS but are acidotic or have high blood ketones may have a mixed picture of HHS and diabetic ketoacidosis (DKA) - these patients require an insulin infusion alongside fluid resuscitation in order to suppress ketosis. \n\n# Aetiology\n\nFactors that may precipitate HHS include:\n\n- Infection (commonly chest or urinary tract)\n- Recent trauma or surgery\n- Other acute events e.g. stroke or myocardial infarction\n- Medications e.g. steroids\n\n# Signs and symptoms\n \nSymptoms often develop over the course of several days to short weeks, including:\n \n - Polyuria\n - Polydipsia\n - Nausea\n - Lethargy\n - Weakness\n - Confusion\n - Drowsiness\n - Loss of consciousness\n \nSigns:\n\n- Tachycardia\n- Hypotension\n- Altered mental state\n- Sunken eyes\n- Dry mucous membranes\n\n# Investigations\n \n**Bedside tests:**\n\n- Capillary blood glucose - if 30 or higher indicates HHS\n- Venous blood gas - to check acid-base status\n- Capillary blood ketones - if > 3 suspect HHS/DKA overlap\n- ECG - to look for precipitating events or complications e.g. ischaemic changes\n- Urine dip and MSU - looking for urinary tract infection, will show glycosuria\n\n**Blood tests:**\n\n- Serum osmolality **(can calculate as (2xNa+) + glucose + urea)**\n- Serum glucose\n- U&Es - looking for AKI and electrolyte imbalances\n- FBC and CRP - inflammatory markers may be raised in intercurrent infection\n- LFTs - may be deranged in some triggering infections e.g. ascending cholangitis\n- Bone profile - looking for other causes of confusion e.g. hypercalcaemia\n- Blood cultures - if infection suspected\n\n**Imaging:**\n\n- Chest X-ray - as part of septic screen \n- Other imaging based on suspected triggers - e.g. CT head for suspected stroke, liver ultrasound if suspected biliary infection\n\n# Management\n \n- The key to emergency management of HHS is prompt initiation of fluid resuscitation\n - Start with 1L of 0.9% saline over 1 hour\n - Close monitoring is needed especially in elderly patients or those at risk of heart failure\n - Catheterisation may be required for close monitoring of fluid balance\n- An insulin infusion is **not** required initially unless there is a mixed picture of HHS and DKA\n- Potassium replacement:\n\t- if <3.5 or >6, senior review/ICU input required\n\t- 5.5-5.9 - nil potassium needed\n\t- 3.5-5.5 - add 40mmol/L to next bag of fluids\n- Patients should be assessed for an underlying cause of HHS (e.g. sepsis, stroke) and appropriate management instigated\n- Assess foot health and instigate foot care (offload heels, daily checks)\n- Intensive monitoring is required with hourly bloods to check glucose, ketones, U&Es and calculate serum osmolality for the first 6 hours\n - The target is for osmolality to fall by 3-8 mOsm/kg/hr\n - If this is not achieved with 0.9% saline and fluid balance is adequate, fluids may be switched to 0.45% saline\n - If glucose plateaus and fluid balance is adequate, consider starting an insulin infusion at 0.05 units/kg/hour\n- Ensure venous thromboembolism prophylaxis is prescribed (patients are high risk due to immobility and dehydration)\n- Refer to the inpatient diabetes team for assessment prior to discharge\n\n# Complications\n\n* Hypovolemic shock\n* Cerebral oedema\n* Thromboembolic events\n* Acute kidney injury\n* Cardiac arrhythmias\n* Respiratory failure\n* Long-term neurological sequelae\n\n# NICE Guidelines\n\n[NICE CKS - Type 2 Diabetes](https://cks.nice.org.uk/topics/diabetes-type-2/)\n\n# References\n \n[Association of British Clinical Diabetologists - Management of\nHyperosmolar Hyperglycaemic State in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_06_The_Management_of_Hyperosmolar_Hyperglycaemic_State_HHS_%20in_Adults_FINAL_0.pdf)\n\n[ABCD - HHS algorithm](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_06_HHS_care_pathway_in_adults_2022.pdf)",
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"question": "A known type 2 diabetic presents to the emergency department with generalised fatigue and vomiting. They have a reduced level of consciousness and are clinically dehydrated.\n\n\nThey are currently prescribed metformin 500mg once daily for their type 2 diabetes.\n\n\nTheir biochemical results may be seen below:\n\n||||\n|---------------------------|:-------:|------------------------------|\n|Non-fasting Glucose|35 mmol/L|< 6.1|\n|Sodium|144 mmol/L|135 - 145|\n|Potassium|4.5 mmol/L|3.5 - 5.3|\n\n - Serum osmolarity: raised\n - Ketones: normal\n\n\nWhat is the next best step in the management of this patient?",
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"explanation": "Oral bicarbonate is not advisable as raising the pH of the gastrointestinal lumen can lead to remaining salicylate tablets in the gastrointestinal tract to dissolve and increase absorption of salicylates",
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"explanation": "# Summary\n \nAspirin overdose (which is the most common type of salicylate poisoning) may occur accidentally or intentionally as a means of self-harm. Symptoms include nausea and vomiting, epigastric pain, tinnitus, lethargy and confusion. Signs include fever, diaphoresis, seizures and coma. Acid-base balance is complex, with respiratory alkalosis occurring secondary to hyperventilation as well as a metabolic acidosis secondary to the aspirin itself. Investigations include salicylate levels, a VBG to look at acid-base status and bloods for electrolyte levels. Management includes activated charcoal for recent ingestion, intravenous fluids with electrolyte replacement, and sodium bicarbonate which acts to enhance urinary excretion of salicylates. Haemodialysis may be required in severe cases where there are complications such as renal failure, severe metabolic acidosis or seizures.\n \n\n# Definition\n \nAspirin overdose occurs when an excessive amount of aspirin is ingested, either accidentally or intentionally. There is a spectrum of clinical manifestations, ranging from mild toxicity to severe and life-threatening complications.\n\n# Signs and symptoms\n\nSymptoms include:\n\n- Nausea and vomiting\n- Tinnitus\n- Epigastric pain \n- Confusion\n- Dizziness\n\nSigns include:\n\n- Hyperventilation\n- Tachycardia and a bounding pulse\n- Diaphoresis\n- Fevers\n- Pulmonary oedema\n- Seizures\n- Coma\n\n# Investigations\n \n**Bedside tests:**\n\n- **Venous blood gas** classically shows respiratory alkalosis initially due to hyperventilation, before progressing to a metabolic acidosis\n- **Capillary blood glucose** screening for hypo or hyperglycaemia causing altered mental state; aspirin overdose can cause hypoglycaemia\n- **ECG** - aspirin overdose can cause QRS widening, AV block or ventricular arrhythmias\n- **Urinary pH** may be measured to guide urinary alkalinisation \n\n**Blood tests:**\n\n- **Salicylate levels** at repeated intervals (e.g. 2 hourly) until levels stop rising (as absorption of aspirin may be slow), helps to assess severity of poisoning and guide need for haemodialysis if very high\n- **U&Es** to monitor electrolytes (hypokalaemia may occur) and for renal failure\n- **Paracetamol levels** to screen for a mixed overdose\n \n# Management\n \n- Give activated charcoal if aspirin ingestion occurred less than 1 hour ago\n- IV fluid resuscitation if volume-deplete\n- Correct hypokalaemia if present before giving bicarbonate\n- IV sodium bicarbonate is given to alkalinise the urine which enhances excretion of salicylates (can cause hypokalaemia so need to monitor potassium as well as urinary pH)\n- Manage complications e.g. cooling measures for hyperthermia, benzodiazepines for seizures\n- Haemodialysis may be required for severe poisoning, for example:\n - Salicylate levels > 700mg/kg\n - Severe metabolic acidosis \n - Seizures or coma\n- Once stabilised, psychological assessment for patients presenting with an intentional overdose\n\n# NICE Guidelines\n\n[NICE CKS - Poisoning or Overdose](https://cks.nice.org.uk/topics/poisoning-or-overdose/)\n\n# References\n \n[BNF - Emergency Treatment of Poisoning](https://bnf.nice.org.uk/treatment-summary/poisoning-emergency-treatment.html)",
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"question": "A 21 year old female presents to the emergency department. She claims she has taken an overdose of aspirin 90 minutes ago. She has a GCS of 15 and her blood tests reveal a salicylate concentration of 550 mg/L (normal therapeutic range 15-30 mg/dL).\n\n\nWhich of the following is the best management for this patient?",
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"explanation": "Vitamin K may be used to reverse warfarin ovedose",
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"explanation": "This is a tertiary option after IV sodium bicarbonate and IV benzodiazepine",
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"explanation": "This, or IV lorazepam, is a second line option after IV sodium bicarbonate",
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"explanation": "Sodium bicarbonate is indicated in patients with a tricyclic antidepressant (TCA) overdose who have an arrhythmia. This should be bolused, and once narrowing of the QRS is shown, this should be switched to an infusion",
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"explanation": "# Summary\n\nTricyclic antidepressants (TCAs) e.g. amitriptyline, are primarily noradrenaline and serotonin reuptake inhibitors, which may be fatal in overdose. Key signs and symptoms include drowsiness, confusion, arrhythmias, seizures, vomiting, headache, dry mouth and dilated pupils. Investigations include a blood gas looking for acidosis, bloods for electrolyte disturbances (hypokalaemia may occur) and an ECG to check for arrhythmias. Management is supportive; activated charcoal can be given to patients presenting within an hour of the overdose and sodium bicarbonate is used to treat arrhythmias and acidosis. \n \n# Definition\n \nTricyclic antidepressants (TCAs) are a class of drugs that act as noradrenaline and serotonin reuptake inhibitors. Examples include amitriptyline, dosulepin and nortriptyline.\n\nThey are now less commonly prescribed than other antidepressant classes, but are often used for other indications such as neuropathic pain or migraine prophylaxis. \n\nTCA overdose can cause severe toxicity due to blockade of sodium channels and antimuscarinic effects. Neurological and cardiovascular toxicities predominate, although anticholinergic symptoms are wide-ranging.\n\n# Aetiology\n\nThe majority of cases of TCA overdose are intentional as a means of self-harm or a suicide attempt. Accidental ingestion may also occur, particularly in children.\n\nTCAs have a narrow therapeutic index and a dose of 10-20 mg/kg represents a potentially fatal overdose.\n \n# Signs and Symptoms\n \nSymptoms include:\n\n- Palpitations\n- Drowsiness\n- Dry mouth\n- Hot, dry skin\n- Confusion\n- Hallucinations\n- Headache\n- Nausea and vomiting\n\nSigns include:\n\n - Reduced level of consciousness\n - Seizures\n - Mydriasis\n - Urinary retention\n - Ileus\n - Hypotension\n - Tachycardia\n \n\n# Differential Diagnosis\n\n- **Sodium channel blocker overdose** e.g. antiarrhythmics such as flecainide or quinine; cause similar ECG findings with arrhythmias and QRS widening as well as seizures and coma\n- **Anticholinergic overdose** other medications such as carbamazepine, antipsychotics and antihistamines as well as plants (e.g. deadly nightshade) have similar manifestations in overdose with cardiovascular and neurological effects\n- **Alcohol intoxication** can cause overlapping symptoms of nausea and vomiting, drowsiness and reduced levels of consciousness but not the anticholinergic effects\n\n# Investigations\n\n**Bedside tests:**\n\n- **ECG** typically shows a widened QRS and prolonged QTc, may progress to life-threatening arrhythmias (QRS > 100ms is predictive of seizures; >160ms of ventricular arrhythmias)\n- **Venous blood gas** looking for acidosis (usually mixed respiratory and metabolic)\n- **Bladder scan** if urinary retention is suspected to confirm need for a catheter\n- **Capillary blood glucose** to rule out hypoglycaemia as a cause of symptoms\n\n**Blood tests:**\n\n- **Full blood count** as a baseline\n- **U&Es** looking for hypokalaemia that increases the risk of arrhythmias, and renal impairment that increases the risk of toxicity\n- **Bone profile and magnesium** looking for other electrolyte abnormalities that may contribute to arrhythmias\n- **LFTs** especially if concurrent paracetamol overdose is suspected\n- **Paracetamol and salicylate levels** to screen for other concurrent overdoses\n \n[lightgallery]\n \n# Management\n \n- A to E approach; ensure airway is secured if reduced level of consciousness or seizures\n- **Cardiac monitoring** if significant overdose or ECG changes\n- Give **activated charcoal** if within 1 hour of overdose (via an NG tube if needed)\n- Resuscitate with **IV fluids** +/- vasopressors if hypotensive\n- Give **IV sodium bicarbonate** if acidotic, QRS prolongation or arrhythmias \n- **Benzodiazepines** may be required for agitation or seizures\n- **Intensive care admission** may be required in significant overdose - hyperventilation can be used in intubated patients to treat acidosis\n- **Catheterise** if in urinary retention\n- **Psychiatry input** once recovered for patients who have taken an intentional overdose\n\n# NICE Guidelines\n\n[NICE CKS - Antidepressant toxicity in overdose](https://cks.nice.org.uk/topics/depression/prescribing-information/antidepressant-toxicity-in-overdose/)\n\n# References\n \n[Life in the Fast Lane - Tricyclic Overdose](https://litfl.com/tricyclic-overdose-sodium-channel-blocker-toxicity/)\n\n[Emergency Medical Minute - Tricyclic Overdose](https://emergencymedicalminute.org/tca-overdose/)",
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"question": "A patient self presents after taking an overdose of their amitriptyline approximately two and a half hours ago. An ECG shows a ventricular arrhythmia.\n\nWhich of the following is indicated in this patient?",
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"explanation": "HHS leads to a significantly elevated glucose and not such a significant acidosis",
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"explanation": "This is likely euglycaemic DKA. Although this is a rare phenomenon, one of the most known causes is SGLT2 inhibitors. These are typical symptoms associated with DKA, and her blood tests are all typical of DKA, with the exception of the normal glucose. Therefore, this is euglycaemic DKA. She should be treated with the local DKA protocol",
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"explanation": "Gastroenteritis is unlikely to cause polyuria and acidosis such as this",
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"explanation": "Pyelonephritis is associated with dysuria and urinary frequency, not polyuria. It may cause nausea and vomiting. It would not normally cause an acidosis such as this",
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"explanation": "This is unlikely if her abdomen is soft and non-tender. Metabolic acidosis may occur in patients with peritonitis secondary to a perforated appendix, but they would almost certainly have a tender and rigid abdomen if this was the case",
"id": "31876",
"label": "d",
"name": "Appendicitis",
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"__typename": "QuestionComment",
"comment": "Hiiiiiigh yield fam",
"createdAt": 1648805682,
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"comment": "such a great question but. like so many things it tests. impressed I am. ",
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"comment": "wouldnt you expect hyperglycaemia in this case?",
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"comment": "SGLT2 inhibitors (-flozin) can cause euglycaemic DKA where they are in diabetic ketoacidosis but with normal range serum glucose",
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"comment": "SGLT2 inhibitors (-flozin) are known to cause ketoacidosis that is euglycaemic, so the serum glucose is normal",
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"comment": "why would you get DKA though with T2DM? Thought it was typically T1DM that you get DKA?",
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"comment": "DKA and euglycemic DKA are not the same bloody thing",
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"comment": "feel like it would have been easier if they put euglycaemic DKA as an answer option yea",
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"explanation": "# Summary\n \nDiabetic ketoacidosis (DKA) is a life-threatening medical emergency characterised by hyperglycemia, acidosis and ketosis. DKA may be triggered by infection, dehydration or fasting, or may be the initial presentation of Type 1 diabetes. Symptoms include a 'fruity' breath odour, vomiting, dehydration, abdominal pain and altered mental state. Key investigations include blood glucose and ketones, urea and electrolytes and a venous blood gas to check pH. Management involves IV fluids and a fixed rate insulin infusion, with close monitoring both clinically and biochemically. Important complications that should be monitored for include cerebral oedema, hypoglycaemia and hypokalaemia. \n\n# Definition\n \nDiabetic ketoacidosis (DKA) is a medical emergency characterised by the triad of:\n \n - Hyperglycemia (blood glucose >11 mmol/L)\n - Ketosis (blood ketones >3 mmol/L or urinary ketones ++ or higher)\n - Acidosis (pH <7.3 or bicarbonate <15 mmol/L)\n - Note: patients on SGLT-2 inhibitors may present with euglycemic DKA (where glucose is normal)\n \n\n# Epidemiology\n \nDKA is most common in individuals with Type 1 diabetes (T1DM) but around a third of cases occur in patients with Type 2 diabetes. The incidence of DKA is highest in young people aged 18-24. \n\nDKA is the leading cause of death in people aged under 58 years old with T1DM, with cerebral oedema the most common cause of mortality. However, mortality in the UK is still <1%.\n \n\n# Aetiology \n\n- DKA occurs due to insulin deficiency (absolute or relative) leading to hyperglycaemia\n- Ketones, including acetone, 3-beta-hydroxybutyrate, and acetoacetate, are produced from ketogenesis, whereby fatty acids are metabolised as an alternative energy source\n- These ketones are responsible for the acidosis seen\n- Hyperglycaemia causes an osmotic diuresis that contributes to severe dehydration as well as electrolyte imbalance\n- Vomiting and decreased fluid intake secondary to altered mental state also exacerbate dehydration\n\n**10-20% of presentations of DKA represent a first presentation of Type 1 Diabetes**\n\n**Common triggers for DKA include:**\n\n- Infections\n- Dehydration and fasting\n- Missing doses of insulin\n- Medications e.g. steroid treatment or diuretics\n- Surgery\n- Stroke or myocardial infarction\n- Alcohol excess or illicit drug use\n- Pancreatitis\n\n# Classification\n\nPatients with at least one of the following may be classified as having **severe DKA**, which should prompt consideration of referral for higher dependency care:\n\n- Blood ketones > 6mmol/L\n- Bicarbonate < 5mmol/L\n- Blood pH < 7\n- Anion gap above 16\n- Hypokalaemia on admission\n- GCS less than 12\n- Oxygen saturations < 92% in air\n- Systolic BP < 90mmHg\n- Brady or tachycardia (heart rate < 60 or > 100bpm)\n\n\n# Signs and Symptoms\n \n**Symptoms:**\n\n- Nausea and vomiting\n- Abdominal pain\n- Polyuria\n- Polydipsia\n- Weakness\n\n**Signs:**\n\n- Dry mucous membranes\n- Hypotension\n- Tachycardia\n- Altered mental state (drowsiness, confusion, coma)\n- Kussmaul's breathing (deep, sighing breathing to compensate for metabolic acidosis by blowing off carbon dioxide)\n- Fruit-like smelling breath (due to ketosis)\n\n# Investigations\n \n**Bedside tests:**\n \n - Capillary blood glucose\n - Blood or urinary ketones\n - Urine dip +/- MSU (looking for evidence of a urinary tract infection which may precipitate DKA)\n - ECG (for ischaemic changes which may precipitate DKA, or changes secondary to electrolyte imbalance e.g. hypokalaemia)\n\n**Blood tests:**\n\n- Venous blood gas (for acid-base balance)\n- Urea and electrolytes (for electrolyte imbalance and AKI)\n- Full blood count and CRP (for infection markers) \n- Blood cultures (if infection is suspected)\n- HbA1c (to assess diabetic control over recent months)\n\n**Imaging:**\n\n- Consider chest X-ray as part of septic screen (if signs of infection as a trigger for DKA)\n\n# Management\n\n**Initial management:** \n\n- Initial **A to E assessment**\n - Drowsy patients may require airway protection and an **NG tube** to prevent aspiration\n - Ensure adequate IV access\n - If hypotensive give up to 1L in **fluid boluses** then seek urgent senior input if not resolved\n - Consider urinary catheterisation and monitor fluid balance\n- **IV fluid replacement with normal saline**\n - A regimen of large volumes of IV fluid replacement given relatively quickly initially then over longer durations should be followed\n - Slower infusion rates should be considered in young adults, the elderly, those with heart or kidney failure or other serious comorbidities\n - An example in a healthy adult would be 1L over 1 hour, then 2x 1L over 2 hours, then 2x 1L over 4 hours, then 1L over 6 hours\n - **Potassium replacement** should be added after the first bag, depending on serum potassium levels, bearing in mind potassium can be infused at a maximum of 10mmol/h:\n\n| Potassium level (mmol/L) | Potassium replacement mmol/L of next infusion | \n| :---------------: | :----------------: \n| > 5.5 | Nil | \n| 3.5 - 5.5 | 40 mmol/L | \n| < 3.5 | senior review – additional potassium required | \n \n \n- After IV fluids have started, a **fixed rate insulin infusion** should be set up \n- This is provided as an infusion of 50 units of Actrapid in 50ml of 0.9% NaCl, at a rate of 0.1 units/kg/hour\n- Continue long-acting insulin if the patient is already on this \n- Investigation and management of any underlying triggers (e.g. septic screen and start antibiotics if evidence of infection)\n- Ensure **VTE prophylaxis** with low molecular weight heparin is prescribed as patients are at high risk of developing clots due to dehydration\n\n**Ongoing emergency management:**\n\n- Patients should be closely monitored with hourly blood glucose and ketones\n - The aim is for ketones to fall by > 0.5mmol/L/hour\n - Blood glucose should fall by 3 mmol/L/hour\n - If these targets are not met, the rate of insulin infusion should be continued\n- Once blood glucose is below 14, a **10% glucose infusion** should be started alongside ongoing saline and insulin\n- Regular venous blood gases should also be done to monitor potassium, bicarbonate and pH\n- DKA is considered resolved once ketones are less than 0.6 mmol/L and pH is over 7.3 \n - If at this point they are able to eat and drink, a subcutaneous regimen of insulin should be started (usually with the input of a specialist diabetes team)\n - The insulin infusion should be stopped half an hour after the first dose of subcutaneous short acting insulin has been given \n\n# References\n \n[ABCD Guidelines: The Management of Diabetic\nKetoacidosis in Adults](https://abcd.care/sites/default/files/site_uploads/JBDS_Guidelines_Current/JBDS_02_DKA_Guideline_with_QR_code_March_2023.pdf)\n\n[RCEM - Diabetic Ketoacidosis](https://www.rcemlearning.co.uk/reference/diabetic-ketoacidosis/#1635853037528-05d8fa0f-621f)\n\n[Patient UK - Diabetic ketoacidosis](https://patient.info/doctor/diabetic-ketoacidosis#presentation)",
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"question": "A 30-year-old female presents to the Emergency Department with a one-week history of polyuria, reduced appetite, nausea and vomiting. On examination, her abdomen is soft and non-tender. She has the following blood tests:\n\n||||\n|---------------------------|:-------:|------------------------------|\n|Non-fasting Glucose|5.8 mmol/L|< 6.1|\n|Bicarbonate|17.5 mmol/L|22 - 29|\n|pH|7.26|7.35 - 7.45|\n|Anion gap|20 mEq/L|6 - 12|\n\n\nShe has a background of type 2 diabetes, for which she takes dapagliflozin and metformin.\n\n\nWhich of the following is the most likely diagnosis in this patient?",
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"explanation": "Advanced osteoarthritis can, in fact, produce a higher than normal T-score on DEXA scan due to osteophytes and disc narrowing, making the bone appear denser than it is. This patient has a low T-score",
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"comment": "Wouldn't osteopenia have deranged blood test?",
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"comment": "is this not a fragility fractur e= instant osteoporosis",
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"explanation": "# Summary \r\n\r\nOsteoporosis is a chronic condition characterised by low bone density and increased propensity to sustain fragility fractures. It is diagnosed with a dual-energy X-ray absorptiometry (DEXA) scan if a patient's T-score is less than -2.5. It is very common in older patients, especially post-menopausal women, with other risk factors including long-term corticosteroid use, low body weight and immobility. Other key investigations include checking calcium and vitamin D levels as these may require supplementation if low. Treatment is with bone-sparing treatment, with bisphosphonates being the first-line option in the majority of patients. Lifestyle changes such as smoking cessation, taking regular exercise and maintaining a healthy diet are important. Falls risk assessment is also key to reducing the risk of fragility fractures, especially in older patients. \r\n\r\n# Definition\r\n\r\nOsteoporosis refers to a state of low bone density with structural deterioration of bones. This causes bones to weaken, increasing the risk of fragility fractures (defined as a fracture sustained due to a fall from standing or without any trauma). \r\n\r\nPatients are defined as having osteoporosis if their bone mineral density (BMD) is at least 2.5 standard deviations below the mean peak mass of young healthy adults. This is measured with a dual-energy X-ray absorptiometry (DEXA) scan which gives BMD for the lumbar vertebrae and the femur. \r\n\r\n# Epidemiology\r\n\r\n- In the UK, around 2 million people are estimated to have osteoporosis\r\n- Post-menopausal women are particularly at risk due to accelerated bone loss secondary to decreased oestrogen production\r\n- Prevalence also increases significantly with age\r\n- Almost 50% of 80 year old women have osteoporosis\r\n- White ethnicity is also a risk factor\r\n- There are approximately 300,000 fragility fractures per year in the UK, with osteoporosis often being undiagnosed at the time of presentation\r\n\r\n# Aetiology\r\n\r\nRisk of fragility fractures increases as bone density declined, however there are many other factors that increase fracture risk:\r\n\r\n| Risk factors reducing bone density | Risk factors that do not reduce bone density |\r\n|----------|----------|\r\n| Low body weight | Older age |\r\n| Menopause | Inflammatory arthritis (e.g. rheumatoid arthritis) |\r\n| Immobility | Prolonged use of oral corticosteroids |\r\n| Chronic disease e.g. chronic kidney disease, chronic obstructive pulmonary disease, chronic liver disease | Smoking |\r\n| Malabsorption e.g. coeliac disease, inflammatory bowel disease, pancreatic insufficiency | Alcohol excess |\r\n| Endocrine disease e.g. hyperparathyroidism, hyperthyroidism | History of fragility fracture |\r\n| Certain medications (proton pump inhibitors, selective serotonin reuptake inhibitors, carbamazepine) - mixed evidence | Parental hip fracture |\r\n\r\n# Signs and Symptoms\r\n\r\nOsteoporosis itself is asymptomatic and so is usually diagnosed either with screening of people at high risk (e.g. those on long-term corticosteroids) or when someone presents with a fragility fracture.\r\n\r\nThe most common fragility fractures seen are:\r\n\r\n- Vertebral body\r\n- Neck of femur (hip)\r\n- Distal radius\r\n- Proximal humerus\r\n- Pelvis\r\n\r\nSome osteoporotic fractures (e.g. vertebral fractures) may also be asymptomatic acutely. Loss of height and kyphosis may occur due to multiple vertebral fractures, with severe kyphosis leading to reduced mobility and function.\r\n\r\nOther common symptoms of fragility fractures include acute severe pain, difficulty weight-bearing (e.g. for a hip fracture) and mobilising. \r\n\r\nSigns include deformities, such as a shortened and externally rotated leg due to a hip fracture or a \"dinner fork\" deformity in a Colles' wrist fracture.\r\n\r\nThe area around the fracture may be bruised, swollen and tender to touch. \r\n\r\n# Differential Diagnosis\r\n\r\n- **Bone metastases** may lead to pathological fractures, either in patients with known malignancies or as a first presentation of cancer (especially lung, prostate, breast, kidney and thyroid)\r\n- **Osteomalacia** usually occurs secondary to severe vitamin D deficiency and increases fracture risk due to bone weakening; other symptoms include bone pain, muscle pain and proximal weakness with a waddling gait\r\n- **Multiple myeloma** also is associated with pathological fractures, as well as hypercalcaemia, renal impairment, anaemia and bone pain\r\n- **Paget's disease** increases the risk of fracture due to abnormal bone remodelling, leading to features of bone pain and bowing of the long bones\r\n- **Osteogenesis imperfecta** is a genetic condition that commonly presents in childhood with fragility fractures, bowing of the long bones, short stature and blue sclera\r\n- **Avascular necrosis** may mimic a spontaneous fracture with severe pain after no or minimal trauma, commonly affecting the femoral head\r\n\r\n# Investigations\r\n\r\n- The diagnostic investigation for osteoporosis is a **dual-energy X-ray absorptiometry scan (DEXA)**\r\n- This measures **bone mineral density (BMD)**\r\n- A T-score of -2.5 or less is considered diagnostic of osteoporosis\r\n- If the T-score is between -1 and -2.5 this is referred to as osteopenia\r\n- Z-score is also reported (this compares bone density to a age, sex and ethnicity matched population rather than healthy young adults) - below -2 is low for their age\r\n- The following patients should be offered a DEXA scan as the initial step in assessment\r\n- Aged over 50 presenting with a fragility fracture\r\n- Aged under 40 with a major risk factor for fragility fracture (e.g. long-term steroids) \r\n- Those about to start treatment that will rapidly decrease bone density (e.g. hormone deprivation in breast cancer) - consider\r\n- All other patients with risk factors should have their fracture risk assessed as the initial step\r\n- **QFracture** and **FRAX** are the two online assessment tools used\r\n- These both predict a patient's 10-year risk of hip and major osteoporotic fractures\r\n- QFracture is interpreted based on whether the risk score is greater or less than 10%\r\n- FRAX plots fracture risk versus age on a graph that stratifies people into low/intermediate/high risk\r\n- With QFracture, those at approximately 10% risk or more at 10 years should have a DEXA scan \r\n- With FRAX, patients at intermediate or high risk of fracture should have a DEXA\r\n- In women over the age of 75 with a history of fragility fractures, a clinical diagnosis of osteoporosis may be appropriate (if a DEXA is unfeasible)\r\n\r\nOther investigations required in all patients include:\r\n\r\n- **Vitamin D** to check for deficiency; this is needed prior to starting bisphosphonate treatment\r\n- **Bone profile** to check serum calcium as this may also require supplementation\r\n- **X-rays** or other imaging modalities (e.g. CT or MRI) may be required to diagnose and assess fragility fractures\r\n\r\nIf an underlying cause is suspected, the following investigations may be appropriate:\r\n\r\n- **Full blood count** which may show anaemia in malabsorption or malignancy, and leukocytosis in malignancy or inflammatory disease\r\n- **Liver function tests** for chronic liver disease\r\n- **U&Es** for chronic kidney disease\r\n- **ESR** or **CRP** which may be raised in inflammatory disease or malignancy\r\n- **Thyroid function tests** if hyperthyroidism is suspected\r\n- **Testosterone** and **sex hormone-binding globulin** if hypogonadism is suspected in men\r\n- **Anti-TTG antibodies** for coeliac disease if there is evidence of malabsorption\r\n\r\n# Management\r\n\r\n**Conservative management:**\r\n\r\n- Identification and treatment of any underlying condition contributing to osteoporosis\r\n- Optimisation of risk factors e.g. smoking cessation, alcohol reduction\r\n- Advise patients to take regular weight-bearing exercise to improve muscle strength, including walking, strength training and balance and flexibility training\r\n- Advise patients to eat a balanced diet and assess their calcium intake\r\n- Assess falls risk and consider measures to reduce this, including referral to multidisciplinary falls teams \r\n- Referral to specialist services for patients with very high fracture risk (e.g. T score less than -3.5, multiple vertebral fractures)\r\n\r\n**Medical management:**\r\n\r\n- Prescribing vitamin D supplementation for patients not exposed to adequate sunlight\r\n- Prescribing calcium supplements to patients with an inadequate dietary calcium intake\r\n- For patients at high risk of fragility fracture, prescribe bone-sparing treatment\r\n- Treatment should be started promptly after a fragility fracture to reduce the risk of another fracture\r\n- Oral bisphosphonates are the first-line treatment in the majority of patients \r\n- Options include alendronate and risedronate, which can be given either daily or weekly\r\n\t- These must be taken on an empty stomach, at least 30 minutes before food or other medications\r\n\t- Tablets need to be swallowed whole with a glass of water whilst the patient is upright; they should stay upright for at least 30 minutes after this\r\n\t- Common side effects include nausea, dyspepsia, gastritis, abdominal pain and musculoskeletal pains\r\n\t- Rarer side effects include oesophagitis or ulceration, stricturing or erosions, osteonecrosis of the jaw or external auditory canal and atypical stress fractures\r\n\t- To minimise risk of osteonecrosis of the jaw, patients with poor dentition or malignancy should have a dental check-up (and any work required performed) before starting bisphosphonates\r\n\t- They should also continue to have routine dental checks and maintain good oral hygiene during treatment \r\n\t- Contraindications include severe chronic kidney disease, hypocalcaemia or vitamin D deficiency, and oesophageal abnormalities such as stricture or achalasia \r\n\t- Patients with recent peptic ulceration, upper gastrointestinal bleeding or surgery, dysphagia, gastritis or duodenitis should be prescribed bisphosphonates with caution\r\n- If oral bisphosphonates are not tolerated or unsuitable, options for bone-sparing treatment include:\r\n\t- Parenteral bisphosphonates (e.g. zoledronate)\r\n\t- Denosumab\r\n\t- Raloxifene hydrochloride\r\n\t- Strontium ranelate\r\n\t- Hormone replacement therapy should be considered for younger women experiencing menopausal symptoms as this will also reduce their fragility fracture risk\r\n\t- Teriparatide and romosozumab are other bone-sparing treatments that may be recommended first-line in women with severe osteoporosis - these are then followed by bisphosphonate treatment\r\n\r\n**Surgical management:**\r\n\r\n- Fragility fractures may require surgical fixation or joint replacement (e.g. hip arthroplasty for a fractured neck of femur)\r\n\r\n# Complications\r\n\r\n- Hip fractures are high-consequence injuries and lead to permanent disability in 50% and death in 20% of patients \r\n- Vertebral fractures may lead to disabling and painful kyphosis which may in turn cause difficulty breathing and gastrointestinal problems such as dyspepsia\r\n- Wrist fractures can significantly affect independence and functional ability\r\n- Many patients experience a \"fracture cascade\" where further fractures occur in the years following the initial one\r\n- Pain from fractures can lead to poor sleep, low mood and reduced quality of life\r\n- Complications of treatment may be significant (e.g. osteonecrosis of the jaw or oesophageal ulceration with bisphosphonates)\r\n\r\n# Prognosis\r\n\r\n- There is no cure for osteoporosis\r\n- In general however, prognosis is good with effective treatment\r\n- Bisphosphonate treatment should be reviewed after 3-5 years\r\n- If patients remain at high risk of fracture it may be continued for up to 7-10 years\r\n- Patients with previous hip or vertebral fractures, those aged 70 or older or those who sustain another fragility fracture whilst on bone protection often require longer durations of treatment\r\n- Repeat DEXA may be appropriate to aid decision making\r\n- If bone protection is stopped, fracture risk should be reassessed 18 months to 3 years later\r\n\r\n# NICE Guidelines\r\n\r\n[NICE CKS: Osteoporosis - prevention of fragility fractures](https://cks.nice.org.uk/topics/osteoporosis-prevention-of-fragility-fractures/)\r\n\r\n[NICE - Osteoporosis: assessing the risk of fragility fracture](https://www.nice.org.uk/guidance/cg146)\r\n\r\n# References\r\n\r\n[National Osteoporosis Guideline Group - Prevention and Treatment of Osteoporosis](https://www.nogg.org.uk/full-guideline)\r\n\r\n[BNF Treatment Summary - Osteoporosis](https://bnf.nice.org.uk/treatment-summaries/osteoporosis/)\r\n\r\n[Radiopaedia - Dual-energy x-ray absorptiometry](https://radiopaedia.org/articles/dual-energy-x-ray-absorptiometry-1?lang=gb)\r\n\r\n[WHO - Fragility fractures](https://www.who.int/news-room/fact-sheets/detail/fragility-fractures)\r\n\r\n[International Longevity Centre UK report on Osteoporosis](https://ilcuk.org.uk/wp-content/uploads/2018/10/OsteoporosisUK.pdf)\r\n\r\n\r\n",
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"question": "A 70-year-old female presents with acute back pain, and an x-ray spine reveals a fracture of the 4th lumbar vertebra.\n\n\nShe has the following blood tests:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Alkaline Phosphatase (ALP)|110 IU/L|25 - 115|\n|Vitamin D|45 nmol/L|>50|\n|Calcium|2.4 mmol/L|2.2 - 2.6|\n|Phosphate|1.0 mmol/L|0.8 - 1.5|\n\n\nA DEXA scan is later performed, which produces a T-score of -2.3.\n\n\nWhat is the most likely diagnosis in this patient?",
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"explanation": "The histology above displays Kimmelstiel-Wilson nodules which are the spherical, eosinophilic, sclerotic nodules characteristic of nodular diabetic glomerulosclerosis",
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"explanation": "# Summary\n\nNephrotic syndrome refers to the clinical triad of proteinuria, hypoalbuminemia and peripheral oedema. It occurs due to increased permeability of the glomerular basement membrane, which occurs either due to a variety of both primary (idiopathic) or secondary diseases. Renal biopsy is the key investigation to differentiate between causes and should be considered in all adults. Other investigations include a urine dip and protein:creatinine ratio, LFTs for albumin and investigations for an underlying cause such as myeloma or diabetes. First-line management is usually with steroids; other immunosuppressants may need to be added. Management options for oedema include lifestyle changes (low salt diet, fluid restriction) and/or diuretics.\n\n# Definition\n\nNephrotic syndrome occurs when there is excessive loss of protein in the urine, leading to hypoalbuminemia and peripheral oedema. Other resulting features include hyperlipidaemia, abnormal coagulation and immunodeficiency. \n\n# Aetiology\n\nThe common underlying pathology leading to nephrotic syndrome is damage to the glomerular basement membrane leading to excessive leakage of protein into the urine.\n\nThere are a wide variety of conditions that may lead to nephrotic syndrome which may be classified as either primary (idiopathic) or secondary (due to another underlying disease) - these include:\n\n- **Minimal change disease** causes the majority of cases of nephrotic syndrome in young children\n- It is usually idiopathic but may rarely be associated with lymphoma or NSAID use\n- Glomeruli are normal under light microscopy\n- Electron microscopy shows diffuse effacement of the podocyte food processes\n- Steroid responsiveness is characteristic\n- **Focal segmental glomerulosclerosis** may be primary or secondary to conditions including HIV, extensive nephron loss or drugs (e.g. heroin)\n- Biopsy shows sclerosis of segments of the glomerular tuft, only affecting some glomeruli\n- **Membranous nephropathy** is the leading cause of nephrotic syndrome in older people\n- Biopsy shows thickening of the glomerular basement membrane without cellular proliferation\n- A classic \"spike and dome\" appearance is described where subepithelial immune deposits are interspersed with new basement membrane growth\n- Most cases are primary; usually associated with PLA2R antibodies\n- Others may be secondary to malignancy, infections, autoimmune disease or drugs\n- **Membranoproliferative glomerulonephritis** is also referred to as membranoproliferative glomerulonephritis\n- It can present with nephrotic or nephritic syndrome\n- It may be idiopathic or secondary to infections such as hepatitis C or systemic lupus erythematosus\n- **Diabetic nephropathy** may affect patients with longstanding type 1 or 2 diabetes\n- It tends to be a progression from microalbuminuria, especially if untreated\n- Patients are at risk of end-stage renal disease\n- Biopsy shows thickening of the glomerular basement membrane, mesangial expansion and Kimmelstiel-Wilson nodules\n- **Amyloidosis**, especially AA amyloid due to chronic inflammation\n- AL amyloid (due to light chain deposition) and hereditary amyloidosis can also cause nephropathy\n- On biopsy, amyloid deposits stain with Congo red and display apple green birefringence under polarized light\n- **Multiple myeloma** can present with a variety of renal manifestations, with proteinuria and renal insufficiency the most common\n- Nephrotic syndrome occurs in a minority of cases and may be due to a number of underlying mechanisms\n- **Lupus nephritis** i.e. renal involvement due to systemic lupus erythematosus\n- Class V (membranous lupus nephritis) is the most likely to cause nephrotic syndrome\n- This is characterised histologically by subepithelial immune complex deposition\n- **Medications** are a rarer cause of nephrotic syndrome, including:\n- Bisphosphonates\n- NSAIDs\n- D-penicillamine\n- Probenecid\n- Tolbutamide\n\n# Classification\n\nThe diagnosis of nephrotic syndrome requires the presence of all of:\n\n- Proteinuria > 3.5 grams/24 hours\n- Serum albumin < 30 grams/litre\n- Peripheral oedema\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n- Frothy urine due to proteinuria\n- Swelling of the face and body\n- Weight gain due to fluid retention\n- Fatigue\n- Lethargy\n- Anorexia\n\n**Signs include:**\n\n- Oedema - typically peripheral and periorbital\n- Muehrcke's lines refers to paired white transverse lines across the nails that may occur secondary to hypoalbuminemia\n- Signs of hyperlipidaemia such as xanthelasma (yellow plaques over the eyelids)\n- Signs of pleural effusion e.g. dull bases to percussion with decreased air entry\n\nPatients may also present with signs and symptoms of complications e.g. infection, thrombosis.\n\n# Differential Diagnosis\n\n- **Heart failure** is a common cause of peripheral oedema; typically however patients cannot lie flat due to breathlessness and so facial oedema is unusual; proteinuria is not a feature\n- **Cirrhosis** is commonly complicated by fluid accumulation, usually in the form of ascites; although ascites may occur in nephrotic syndrome it is less common than fluid accumulation in the peripheries and face; proteinuria is not a feature\n- **Chronic kidney disease** may present with fluid retention, especially in patients with end-stage renal disease - it may coexist with nephrotic syndrome however renal function is often preserved\n- **Medications** may cause peripheral oedema including calcium channel blockers, NSAIDs and corticosteroids\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** looking for proteinuria; glycosuria may be present in diabetes but haematuria is not usually seen\n- **Urine protein:creatinine ratio** should be over 2 or **24 hour urine collection** should show proteinuria >3.5g/day\n\n**Blood tests:**\n\n- **LFTs** to confirm hypoalbuminemia\n- **U&Es** for renal function (significant impairment is unusual)\n- **FBC** may show anaemia in persistent nephrotic syndrome\n- **Vitamin D** may be low as this is lost in urine\n- **Bone profile** may show hypocalcemia secondary to decreased calcium absorption due to vitamin D deficiency\n- **Coagulation screen** is usually normal although there is a hypercoagulable state wiht increased risk of thromboembolism\n- **HbA1c** or **fasting glucose** for diabetes\n- **Lipid profile** often shows dyslipidemia\n- **CRP** and **ESR** may be raised due to an underlying inflammatory, malignant or infectious process\n- **Myeloma screen** i.e. immunoglobulins and serum protein electrophoresis if myeloma is suspected\n- **Autoimmune screen** e.g. for suspected systemic lupus erythematosus (antinuclear antibody, complement levels etc.)\n- **Infection screen** i.e. hepatitis B and C serology, HIV testing\n\n**Imaging tests:**\n\n- **Chest X-ray** if there are clinical signs of pleural effusion\n- **US KUB** (kidneys, ureters and bladder) if there is renal impairment to assess for obstruction and any structural abnormalities of the kidneys\n- Imaging may be required to diagnose complications, such as a **CT pulmonary angiogram** for suspected pulmonary embolism or **doppler ultrasound** of the limbs for suspected deep vein thrombosis\n\n**Special tests:**\n\n- **Renal biopsy** is the key investigation to diagnose the cause of nephrotic syndrome - this is important both for prognosis and to guide management \n- Biopsy is usually indicated in adults, however in children there are specific indications e.g. if not responsive to steroids\n\n# Management\n\n**Conservative:**\n\n- Restrict salt intake to <2g/day\n- Fluid restriction to <1.5L/day \n- Weight should be monitored, with a target of 1-2 kg weight loss per day until the patient reaches their predicted \"dry weight\" (i.e. weight when not oedematous)\n- Dietary changes (e.g. avoiding a high protein diet, limiting fat intake) may be advised and dietician input may be indicated\n- Mechanical thromboprophylaxis (TEDS) to reduce risk of venous thromboembolism\n\n**Medical:**\n\n- **Corticosteroids** are usually first-line for management of nephrotic syndrome - these should be weaned after remission is achieved\n- Other immunosuppressive drugs (e.g. ciclosporin, cyclophosphamide, mycophenolate mofetil or rituximab) may be added as steroid sparing agents or for severe or refractory cases\n- Diuretics are used to treat significant peripheral oedema, usually furosemide but potassium sparing and thiazide diuretics may be added as adjuncts\n- Risk of thromboembolism should be assessed and prophylactic anticoagulation considered\n- Antihypertensives may be required to maintain a normal blood pressure; ACE inhibitors and angiotensin II receptor blockers may also help to reduce proteinuria\n- Ensure patients are up to date with vaccinations (however live vaccines should not be given to patients who are immunocompromised)\n- In some cases hyperlipidaemia may require treatment with statins \n- Patients taking steroids may require co-administration of proton pump inhibitors for gastric protection and consideration of bone protection\n\n**Surgical:**\n\n- If nephrotic syndrome results in end-stage renal failure, renal replacement therapy may be required either with dialysis or renal transplantation\n\n# Complications\n\n- **Increased risk of infection** as immunoglobulins are lost in urine\n- **Venous thromboembolism** due to urinary loss of anti-thrombotic proteins such as antithrombin III\n- **Hyperlipidaemia** due to increased hepatic production of lipoproteins to compensate for hypoalbuminemia - this may also present with lipiduria (which may cause urine to appear milky) \n- **Acute kidney injury** may occur due to excessive diuresis or renal vein thrombosis\n- **Chronic kidney disease** may occur secondary to the underlying cause of nephrotic syndrome (e.g. diabetes, amyloidosis)\n- **Medication side-effects** especially with chronic steroid use (e.g. osteoporosis, psychiatric effects)\n- **Hypothyroidism** due to urinary losses of T4 and T3 with their binding proteins\n- **Vitamin D deficiency** as this is also lost in urine\n- **Anaemia** may result from persistent nephrotic syndrome as iron bound to transferrin and erythropoietin are lost in urine\n\n# Prognosis\n\nPrognosis varies between subtypes, for example minimal change disease rarely progresses to end-stage renal failure (1% of cases), whereas 50% of patients with FSGS will do over 5-10 years.\n\nMortality has been greatly reduced with the use of steroids and immunosuppression.\n\nRelapses are common and may require repeated courses of steroids or escalation to other immunosuppressive medications.\n\n# References\n\n[KDIGO Guidelines on Glomerular Diseases](https://kdigo.org/guidelines/gd/)\n\n[Patient UK - Nephrotic syndrome](https://patient.info/doctor/nephrotic-syndrome-pro)\n\n[Radiopaedia - Nephrotic syndrome](https://radiopaedia.org/articles/nephrotic-syndrome?lang=gb)",
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"explanation": "This is a GLP-1 analogue. It is recommended that patients who are hyperglycaemic after commencing enteral feeding should be started on insulin",
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"explanation": "# Summary\n\nSecondary causes of type 2 diabetes mellitus (T2DM) encompass a variety of conditions and factors that can induce or exacerbate hyperglycemia. These range from pancreatic and endocrine disorders to specific medications and glycogen storage diseases. It's important to consider these in patients with new-onset diabetes that presents atypically or doesn't respond to typical management.\n\n# Definition\n\nSecondary diabetes refers to forms of the disease where there is a clear causative factor aside from the typical insulin resistance or pancreatic β-cell failure associated with T2DM.\n\n# Epidemiology\n\nThe prevalence of secondary diabetes varies based on the causative condition. While some causes such as pancreatic cancer are relatively common, others, like glycogen storage disorders, are quite rare.\n\n# Aetiology\n\nSecondary causes of T2DM include:\n\n**Pancreatic Causes**\n\n- Cystic fibrosis: An autosomal recessive disorder leading to mucus accumulation in various organs including the pancreas, resulting in fibrosis and loss of exocrine and endocrine function.\n- Chronic pancreatitis: Long-standing inflammation of the pancreas can result in damage to islet cells, leading to diabetes.\n- Haemochromatosis: Iron overload can lead to deposition in various organs including the pancreas, leading to diabetes.\n- Cancer: Pancreatic neoplasms can destroy the islet cells, leading to diabetes.\n\n**Endocrine Causes**\n\n- Cushing's syndrome/disease: Elevated cortisol levels increase insulin resistance.\n- Acromegaly: Excess growth hormone leads to insulin resistance.\n- Pheochromocytoma: These rare adrenal tumors can induce diabetes through chronic catecholamine-induced glucose intolerance.\n- Thyrotoxicosis: Thyroid hormone excess can enhance hepatic gluconeogenesis and glycogenolysis and impair insulin secretion.\n\n**Drug Causes**\n\n- Steroids: Chronic use can lead to glucose intolerance and diabetes due to increased insulin resistance.\n- Atypical neuroleptics: These medications can lead to weight gain and increased insulin resistance.\n- Thiazides: These diuretics may impair glucose tolerance, possibly by reducing insulin secretion.\n- Beta-blockers: They can impair glycemic control through inhibition of insulin secretion and promoting insulin resistance.\n\n**Glycogen Storage Disorders**\n\n- Glycogen Storage Disease Type 1 (von Gierke's disease): The inability to perform gluconeogenesis can lead to hypoglycemia and secondary hyperglycemia.\n- Glycogen Storage Disease Type 2 (Pompe disease): It affects the heart and skeletal muscles more than it causes diabetes, but can present with variable symptoms.\n\n# Management\n\nManagement primarily involves addressing the underlying condition responsible for secondary diabetes. In cases where this is difficult/not possible, for example, pancreatic cancer, patients may require insulin therapy to manage hyperglycemia.\n\n\n\n# NICE Guidelines\n\n[NICE CKS on type 2 diabetes](https://cks.nice.org.uk/topics/diabetes-type-2/)",
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"comment": "Because they're in A&E do they not have to admitted under a 5(2) first? And then psych can come see them and put in place a section 2 for treatment? Thanks in advance:)",
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"comment": "sec 5(2) and 5(4) are is not valid for A and E",
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"comment": "Section 5 applies to patient's in the ward rather than ED",
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"comment": "In A and E surely they should be initially placed under a Section 4, then converted to a section 2?",
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"comment": "This is what I was thinking as well. During my Psych placement, the psychiatrist told me it can sometimes take 5 days to get a section 2!",
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"comment": "Section 2 can't be applied in an emergency department",
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"comment": "In some hospitals the ED counts as a public place so think it can?",
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"comment": "section 3 would be a better answer as she's already got a diagnosis and been assessed",
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"comment": "I'm pretty sure an explanation to a previous (similar) question said section 2 is specifically for 'assessment' and section 3 is specifically for 'treatment'",
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"comment": "yeah but you can still give treatment under section 2",
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"comment": "Section 2 is assessment/investigation, she already has a formal diagnosis so should be a section 4 then section 3 when appropriate",
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"explanation": "# Summary\n\nAnorexia nervosa is a severe psychiatric disorder characterized by extreme dietary restriction, an intense fear of gaining weight, and a distorted body image. This complex condition predominantly affects young individuals, particularly females, and poses significant health risks, including malnutrition, electrolyte imbalances, and potential life-threatening complications. It has the highest mortality rate of all psychiatric disorders.\n\n# Definition\n\nAnorexia nervosa is a serious mental health disorder characterized by self-imposed starvation and a relentless pursuit of extreme thinness. Individuals with anorexia nervosa have a distorted body image, viewing themselves as overweight even when they are dangerously underweight. There are two main subtypes:\n\n- **Restrictive Subtype:** Characterized by minimal food intake and excessive exercise.\n- **Bulimic Subtype:** Involves episodic binge eating followed by behaviors like laxative use or induced vomiting.\n\nIt is diagnosed based on specific criteria outlined in both the International Classification of Diseases, 11th Edition (ICD-11) and the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5):\n\n**ICD-11 Criteria:**\n\nTo meet the ICD-11 criteria for anorexia nervosa, individuals must exhibit the following:\n\n1. **Significantly Low Body Weight:** The individual's body weight is significantly below the normal or expected weight for their age and height.\n\n2. **Fear of Gaining Weight:** There is an intense fear of gaining weight, or becoming fat, even when underweight.\n\n3. **Distorted Body Image:** The individual has a distorted self-perception, with an overemphasis on their weight and shape.\n\n4. **Restrictive Eating:** There is persistent restrictive eating, often leading to malnutrition.\n\n**DSM-5 Criteria:**\n\nThe DSM-5 criteria for anorexia nervosa include the following:\n\n1. **Restriction of Energy Intake:** The individual persistently limits their food intake, leading to low body weight relative to their age, sex, developmental trajectory, and physical health.\n\n2. **Intense Fear of Gaining Weight:** A preoccupation with body weight or shape, as well as the fear of gaining weight, is a core feature.\n\n3. **Body Image Disturbance:** A distorted body image, where the individual perceives themselves as overweight despite being underweight, is present.\n\nThe specific criteria may vary between ICD-11 and DSM-5, but the essential elements of severe dietary restriction, weight and shape preoccupation, and distorted body image are central to the diagnosis. Note that BMI and amenorrhoea are no longer specifically mentioned in DSM-5 anymore.\n\n# Epidemiology\n\nAnorexia nervosa primarily affects adolescents and young adults, with a higher prevalence among females. However, it can occur in individuals of any age or gender. The condition is more common in industrialized countries and often co-occurs with other psychiatric disorders, such as depression and anxiety.\nThe incidence of anorexia nervosa is 6/100,000, with the highest incidence occurring between age 13-17. \n\n# Pathophysiology\n\n- Anorexia nervosa is not due to a single causative factor, with complex biopsychosocial factors at play:\n\t- Biological factors include the presence of family history and genetic influence\n\t- Psychological: Presence of comorbid mental health disorders, such as anxiety, depression, obsessive-compulsive disorders or obsessive/perfectionist personalities\n\t- Social: Maternal encouragement of weight loss or at risk professions such as models, dancers or sportspeople\n\n# Clinical features\n\n- History:\n\t- Preoccupation with food and calories\n\t- Starvation via restricting intake, purging (through induced emesis, diuretic or laxative abuse) or excessive exercise\n\t- Poor insight \n\t- Overvalued, intrusive obsession with weight, shape and fear of becoming fat\n\t- Weight/calorie goals in mind regardless of their impact on physical health \n- Examination:\n\t- BMI <17.5 kg/m<sup>2</sup> (contrast with bulimia nervosa, where there may be many similar features, but the BMI is normal‚ a key distinguishing feature)\n\t- Hypotension\n\t- Bradycardia\n\t- Enlarged salivary glands\n\t- Lanugo hair (fine hair covering the skin)\n\t- Amenorrhoea (hypogonadotropic hypogonadism)\n\t- Additional features in the 'bulimic' subtype may include hypokalaemic hypochloraemic metabolic alkalosis, pitted teeth, parotid swelling, and scarring of the dorsum of the hand (Russell’s sign).\n\n# Investigations\n\n- Blood results:\n\t- Deranged electrolytes - typically low calcium, magnesium, phosphate and potassium \n\t- Low sex hormone levels (FSH, LH, oestrogen and testosterone)\n\t- Leukopenia\n\t- Raised growth hormone and cortisol levels (stress hormones)\n\t- Hypercholesterolaemia\n\t- Metabolic alkalosis, either due to vomiting or use of diuretics \n\n# Management \n\nManagement approaches are multi-faceted and tailored to the patient's specific needs. In adults, interventions may include:\n\n- **Cognitive Behavioral Therapy for Eating Disorders (CBT-ED):** Focusing on changing thoughts and behaviors related to eating and body image.\n- **MANTRA (Maudsley Model of Anorexia Nervosa Treatment for Adults):** Targeting the core beliefs behind anorexia.\n- **Specialist Supportive Clinical Management (SSCM):** Providing a supportive framework for treatment.\n\nFor individuals under 18, AN-focused family therapy is often the first-line approach, with CBT-ED as a second-line option.\n\n- **Medical**\n\t- Selective serotonin release inhibitors (SSRIs) may be used‚ these have not been shown to be effective at treating the anorexia nervosa directly, but may be effective for comorbid mental health issues, commonly depression and anxiety\n- **Mental Health Act**\n\t- In some cases where the patient's life is considered at immediate risk, admission under the Mental Health Act with structured feeding (and in some cases nasogastric tube feeding) is warranted\n\t- Under the Mental Health Act, feeding is a treatment for anorexia nervosa and, as such, treatment can occur without patient consent under this framework\n\n**Inpatient Admission:**\n\nIndications for specialist inpatient programs may include severe or rapid weight loss, significant suicide risk, or inability to perform the SUSS test (sit-up, squat, and stand). Admission is also indicated if proximal muscle weakness suggests weak respiratory muscles.\n\nIf patients are very unwell the **MARSIPAN checklist** should be used to guide management.\n\n# Complications \n\n- Refeeding syndrome:\n\t- A potentially fatal disorder that occurs when nutritional intake is resumed too rapidly after a period of low caloric intake\n\t- symptoms may include oedema, confusion and tachycardia\n\t- \tRapidly increasing insulin levels lead to shifts of potassium, magnesium and phosphate from extracellular to intracellular spaces‚ these need to be replenished\n\t- Preventative measures include: \n\t - The provision of high-dose vitamins (eg. Pabrinex<sup></sup>) before feeding commences\n\t - Monitoring with daily bloods and replenishing electrolytes early \n\t - Building caloric intake gradually with the help of a dietitian‚ NICE recommends that refeeding is started at no more than 50% of calorie requirement in 'patients who have eaten little or nothing for more than 5 days'\n- Cardiac arrhythmias: \n\t- These patients are at higher risk of arrhythmias and an ECG should be performed periodically, especially if they are complaining of cardiac symptoms (eg. palpitations, fainting episodes or dizzy/light-headed spells)\n\t- Bradycardia and prolonged QTc are often seen\n- Osteoporosis‚ a long-term complication\n\n# Prognosis\n\n- Positive prognostic indicators include:\n\t- The presence of normal social‚ emotional milestones‚ this is important to form bonds with therapists during CBT\n- Negative prognostic indicators include:\n\t- Presentation after the age of 20 years‚ difficult to reverse fixed beliefs\n\t- BMI <16 kg/m<sup>2</sup>\n\t- Marked anxiety when eating in front of others, which indicates issues with socialisation \n\t- Binging/vomiting responds less well to CBT than starvation\n\n# NICE Guidelines \n\n[NICE Guidelines: Eating Disorders](https://www.nice.org.uk/guidance/ng69)",
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"question": "A 19-year-old female with a background of anorexia nervosa is brought to the emergency department by her mother, who is concerned about her physical health. Her mother reports that she hasn't eaten anything in 5 days. On examination, she appears cachectic, has a heart rate of 55 beats per minute, and a blood pressure of 85/50mmHg. The patient refuses to be admitted to hospital.\n\nThe multi-disciplinary team are all in agreement that this patient should be admitted for artificial feeding. Under which section of the Mental Health Act should this be done?",
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"explanation": "This is one of the few circumstances in which a doctor can break patient confidentiality. In this circumstance, the wider risk to the public is deemed more important than the patient's right to confidentiality and, if the patient refuses to inform the DVLA themselves, the clinician is obliged to notify the DVLA",
"id": "31899",
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"name": "Only inform the DVLA if the patient gives you his permission",
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"explanation": "This would be breaking patient confidentiality. The clinician should inform the DVLA but should not speak to a next of kin against the patient's wishes",
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"name": "Ring his next kin and insist they inform the DVLA on his behalf",
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"explanation": "If the clinician has concerns that the patient has not informed the DVLA that they shouldn't be driving, then they should inform the DVLA as soon as reasonably possible. By delaying this for a week, they would be putting the wider public at risk",
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"label": "e",
"name": "Arrange a follow-up appointment for one week and ensure then that he has informed the DVLA",
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"explanation": "This is correct. This is one of the few circumstances where the clinician is obliged to break confidentiality and inform the DVLA if the patient refuses to, as the risk to the general public is more important than the patient's right to confidentiality. It is best practice to inform the patient that you will notify the DVLA before you do so",
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"name": "Inform the patient that you will have to inform the DVLA if he does not",
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"explanation": "There is no legal requirement to inform the police if patients are driving against advice",
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"explanation": "# Overview\n\nPatients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality.\n\nHowever, this right to confidentiality is not absolute. There are a number of situations in which the law obliges doctors to breach confidentiality, i.e. there is a legal duty to breach confidentiality. There are also some situations where a doctor has a legal defence to breach confidentiality.\n\n# Legal Duties to Breach Confidentiality\n\n1. If ordered to by a court or judge\n2. To satisfy statutory requirements\n\n _e.g. to inform the local authority about notifiable diseases under the Public Health Act 1984_\n\n _e.g. under the Road Traffic Act, must provide identifying information to the police on request_\n\n _e.g. under the Terrorism Act 2000, must report any suspicions of terrorism_",
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"question": "A 45-year-old male attends his GP. He is currently being investigated for a seizure that he had five days ago. He works as a lorry driver. He has been informed that he should notify the DVLA and stop driving. However, at his GP practice, he discloses that he has continued to drive and refuses to inform the DVLA.\n\nWhich of the following is the next best step?",
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"explanation": "This is not necessary as there has been a clear formal discussion with the patient whilst she had capacity where she made her wishes clear.",
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"name": "Discuss with the hospital legal department",
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"explanation": "The next of kin has no role in decision making about resuscitation. It is good practice to discuss resuscitation decisions with the next of kin; however, it is ultimately the patient and/or medical practitioner who decides, depending on the circumstances",
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"label": "b",
"name": "Consider DNACPR based on wishes of next of kin",
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"explanation": "This patient should not be for resuscitation as there is a previously documented discussion where she has refused. It can be re-discussed if she regains capacity and can hold this conversation.",
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"name": "Leave for resuscitation until she is awake enough to have a formal discussion",
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"explanation": "As this patient clearly stated that they would not like to be resuscitated whilst she had capacity, a DNACPR form should be instigated. It it important to take into consideration the patient's prior wishes when considering DNACPR forms. ",
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"label": "a",
"name": "Complete DNACPR form",
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"explanation": "This patient should not be for resuscitation as ultimately patients have a right to refuse resuscitation as long as they have capacity. When this patient discussed resuscitation, she did have capacity.",
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"name": "Document that this patient is for resuscitation",
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"comment": "Is the documented discussion enough to retrospectively fill out a DNACPR form? ",
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"comment": "i thought that in-hospital DNACPR forms were only valid for that hospital admission and had to be reassessed and rewritten on each admission? If she'd changed her mind etc. wouldn't it be better to ask loved ones until she's able to communicate herself?",
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"comment": "Agreed, each DNACPR form can either be written for that specific hospital admission or with no-end date. NHS website says \"It's recommended that a DNACPR is reviewed each time your situation changes – for example, when you leave hospital.\"",
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"explanation": "# Overview\n\nA Do Not Attempt CPR (DNACPR) decision can also be known as Do Not Attempt Resuscitation (DNAR)\n\nA DNACPR decision provides information to healthcare professionals present on the best action to take if an individual suffers a cardiac arrest. A DNACPR is recorded, normally on a CPR Decision form, but is not in itself legally binding. This means that a doctor can overrule an existing DNACPR if they believe the circumstances do mean CPR would be in the patient's best interests.\n\nA DNACPR can be made if cardiac or respiratory arrest is an expected part of the dying process, and either CPR will not be successful, or if CPR may be successful but the clinical outcomes (e.g. trauma and prognosis) mean it is not clinically appropriate. A patient with capacity may also refuse CPR.\n\n# Best Interests \n\nDoctors can ultimately make the decision to put a DNACPR in place if it is in the patient's _best interests_, even if the patient themselves or their family disagrees. However, following a legal case in 2014, doctors must engage the patient and those close to them on the decision to make a DNACPR, and inform them if the decision to make a DNACPR order has occurred.\n\n# R (Tracey) v Cambridge University Hospitals NHS Foundation Trust, 2014 \n\nJanet Tracey died in Addenbrooke's Hospital in March 2011. She had been diagnosed with terminal lung cancer and had subsequently been involved in a car crash, in which she sustained a spinal injury. She required ventilation in the Intensive Care Unit (ICU), and after attempts to remove her from the ventilator were unsuccessful, a DNACPR notice was placed in her medical notes. Neither Janet Tracey nor her family were consulted about or informed of this decision.\n\nThe legal case concluded in favour of Tracey, finding that her Human Rights had been breached. The case acknowledged that the decision to put a DNACPR in place is ultimately a medical decision, and patients cannot demand treatment. But, the case did result in changes to DNACPR guidance:\n\nFirstly, the decision to not tell a patient about a DNACPR notice can no longer be based on the fact that telling them would cause “distress”. Only if discussing a DNACPR order would cause the patient “physical or psychological harm”, can doctors justify not discussing it. In other circumstances, doctors are legally obliged to discuss a DNACPR order that has been made.\n\nSecondly, it used to be the case that doctors were not obliged to discuss a DNACPR decision if the clinical decision has been made that CPR would be futile. This case amended this, making it a legal obligation for doctors to inform the patient that a DNACPR decision has been made, regardless of whether or not CPR could ever be successful (i.e. futility of CPR is justification for doctors making a best interests decision to make a DNACPR order - even if the patient wants CPR, but doctors are still legally obliged to inform the patient that a DNACPR order has been made).\n\nA DNACPR decision relates only to CPR, and is not a refusal of any other treatment.",
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"question": "A 90-year-old is admitted to hospital from a care home with a two day history of dysuria, urinary incontinence and increased confusion. She is pyrexial and extremely drowsy and is unable to hold a conversation. She has a background of congestive heart failure, hypertension, dementia and recurrent urinary tract infection. On her electronic patient record, there is a discussion documented from an admission with a fall three months ago where she states that she would not like to be resuscitated in the event of a cardiac arrest. It was documented by the team at the time that she had capacity. \n\nWhich of the following is the next best step?",
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"answer": false,
"explanation": "Consent is required for intimate examinations such as a rectal examination",
"id": "31912",
"label": "e",
"name": "No consent required",
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"explanation": "Verbal consent should be documented in the notes",
"id": "31909",
"label": "b",
"name": "Verbal consent, no need to document this in the notes",
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"__typename": "QuestionChoice",
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"explanation": "Consent in writing is not required for a rectal examination; verbal consent will suffice. Consent should be obtained before the examination",
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"name": "Consent in writing after rectal examination",
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"explanation": "Consent in writing is not required for a rectal examination; verbal consent will suffice. A formal consent form with the patient's signature is required for surgical procedures",
"id": "31910",
"label": "c",
"name": "Consent in writing before the rectal examination",
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"explanation": "Verbal consent is required for an intimate examination, and this should be documented formally",
"id": "31908",
"label": "a",
"name": "Verbal consent and document this in the notes",
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"comment": "fairs to the 2% who decided they dont need consent x",
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"explanation": "# Consent \n\nConsent must be obtained from a patient before undertaking a treatment or procedure. If it is not, then this could constitute the offence of **battery** (\"touching in a harmful or offensive manner without consent or lawful justification\") - even if there was no hostile intent or harm caused.\n\n# Conditions for valid consent\n\nUnder the **Mental Capacity Act**, there are a number of conditions that have to be met for valid consent to be obtained from a patient:\n\n1. The patient must have **capacity**. For this, the individual must be able to: understand information, retain information, weigh the information and reach a conclusion, and communicate the decision they have reached.\n\n2. The consent must be **freely given** (i.e. uncoerced) and the patient must be **suitably informed** (i.e. have been given a suitable level of detail of the procedure, and expected outcomes and risks).\n\n# Assumed Capacity \n\nFor an adult, capacity is assumed unless there is reason to doubt; for example the patient has learning difficulties which impacts on their ability to understand and process new information.\n\n# How Is Consent Taken?\n\nValid consent can be received in writing, verbally or tacitly (where it is implied or indicated). A signed consent form does not - by itself - equal 'consent', it is purely _related evidence_.\n\n# Who Can Obtain Consent?\n\nThe person who should obtain the consent from a patient should be the professional undertaking the procedure, or someone familiar with it, who is able to explain all the necessary information and answer any questions the patient may have.",
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"explanation": "# Summary\n\nCrohn's disease (CD) is a chronic, relapsing inflammatory bowel disease (IBD) characterized by transmural granulomatous inflammation. Key signs and symptoms include gastrointestinal and systemic symptoms, such as crampy abdominal pain, diarrhoea, weight loss, and fever. The disease is diagnosed primarily through blood tests and endoscopy with imaging. Management strategies include monotherapy with glucocorticoids, azathioprine, mercaptopurine, and biological agents for severe cases. Surgical management is rarely curative and should be maximally conservative.\n\n# Definition\n\nCrohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD). It is characterised by transmural granulomatous inflammation which can affect any part of the gastrointestinal tract ('from mouth to anus', most commonly the terminal ileum, leading to fistula formation or stricturing.\n\n# Aetiology\n\nThe exact cause is unknown, but it is thought to be an inappropriate reaction to gut flora in a susceptible person. Important risk factors include:\n\n- Family history - 10-25% of patients have a first-degree relative who also suffers from Crohn's disease\n- **Smoking** - x3 increased risk\n- Diets high in refined carbohydrates and fats have been implicated\n\n# Epidemiology\n\nIn Europe the incidence of Crohn's disease is 5.6 per 100, 000 at ages 15-64. The disease is more common in northern climates and developed countries. In the last 60 years the incidence of Crohn's disease has increased in Europe and North America, and is now approximately equal to that of ulcerative colitis.\n\nCrohn's disease has a bimodal age of onset: the most common age of onset is between 15 and 40 years old, but there is a smaller secondary peak between 60-80 years.\n\nCrohn's disease is more common in Caucasian people than in Asian and black people. Ashkenazi Jews have a 2-4 fold higher risk of Crohn's disease.\n\n\n# Signs and Symptoms\n\nSymptoms: \n\n- Gastrointestinal symptoms (crampy abdominal pain and non-bloody diarrhoea)\n- Up to 50% have perianal disease\n- Systemic symptoms (weight loss and fever)\n\nSigns: \n\n- General appearance: cachectic and pale (secondary to anaemia), clubbing.\n- Abdominal examination: aphthous ulcers in the mouth, right lower quadrant tenderness and a right iliac fossa mass.\n- PR examination to check for perianal skin tags, fistulae, or perianal abscess.\n\n[lightgallery] \n\n**Extra-gastrointestinal manifestations include:**\n\nDermatological manifestations:\n\n- Erythema nodosum (painful erythematous nodules/plaques on the shins)\n- Pyoderma gangrenosum (a well-defined ulcer with a purple overhanging edge)\n\n[lightgallery1] [lightgallery2]\n\nOcular manifestations:\n\n- Anterior uveitis (painful red eye with blurred vision and photophobia)\n- Episcleritis (painless red eye).\n\nMusculoskeletal manifestation:\n\n- Enteropathic arthropathy (symmetrical, non-deforming)\n- Axial spondyloarthropathy (sacro-iliitis), \n\nHepatobiliary manifestations:\n\n- Gallstones (these are more common in Crohn's disease than in ulcerative colitis) - reduced bile acid reabsorption and increased calcium loss predisposes to gallstones\n\nHaematological and renal manifestations:\n\n- AA amyloidosis (secondary to chronic inflammation) and renal stones (more common in Crohn's disease than in ulcerative colitis)\n\n# Investigations \n\n- Bedside:\n\t- Stool culture is necessary to exclude infection (MC&S and ovas/cysts/parasite).\n\t- **Faecal calprotectin** (an antigen produced by neutrophils) will be raised (this helps distinguish inflammatory bowel disease from irritable bowel syndrome).\n\n- Blood tests:\n - Raised white cell count\n - Raised ESR/CRP\n - Thrombocytosis\n - Anaemia (secondary to chronic inflammation)\n - Low albumin (secondary to malabsorption)\n - Haematinics and iron studies including (B12, folate) due to terminal ileum involvement\n\n\n- Imaging:\n\t- Endoscopy with imaging is required for diagnosis. Small bowel video capsule endoscopy can be used for proximal disease\n\t- MRI can be used for suspected small bowel disease.\n\t- Upper GI series may show the 'string sign of Kantour'. This is used to describe the string-like appearance of contrast-filled narrowed terminal ileum, and is suggestive of Crohn's disease.\n\t- Colonoscopy with biopsy will reveal:\n\t\t- Intermittent inflammation **('skip lesions')**\n\t\t- Cobblestone mucosa (due to ulceration and mural oedema)\n\t\t- Rose-thorn ulcers (due to transmural inflammation), ± fistulae or abscesses.\n\t\t- Non-caseating granulomas\n\n# Management\n\n- As a general management point, it is paramount to advise patients with Crohn's who are smokers to **stop smoking** as this is known to strongly impact disease activity\n\n## Inducing remission\n\n- The first step of treatment is inducing remission in patients having a flare\n- Patients should be offered monotherapy with glucocorticoids (oral prednisolone, or IV hydrocortisone if first presentation is severe flare necessitating admission).\n- There is an increasing role for biologics for acute management of severe flares\n\n## Maintaining remission\n\n- Azathioprine or mercaptopurine may be added on to induce remission if there are 2 or more exacerbations in a 12-month period or the glucocorticoid cannot be tapered.\n\n - It is important to assess for thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine. If there is underactivity, this greatly increases the risk of profound bone marrow suppression if the above medications are given\n\n- Methotrexate may be considered in patients who are intolerant/have a contraindication to azathioprine or mercaptopurine or who do not respond to azathioprine or mercaptopurine monotherapy.\n- Biological agents (such as infliximab or adalimumab) are recommended in patients with severe Crohn's disease who fail to respond to the above.\n\t- These patients should have a CXR before treatment initiation due to the risk of re-activation of latent TB\n\n\n## Surgical management\n\nSurgical management is rarely curative in Crohn's disease (unlike in ulcerative colitis) because disease can occur anywhere along the GI tract, however 50-80% of Crohn’s patients end up requiring surgery at some point.\n\nSurgical options will depend on the part of the GI tract that is affected, and is indicated in those who have failed medical therapy or in those with severe stricturing or fistulating disease:\n\r\n-\tControl fistulae \r\n-\tResection of strictures\r\n-\tRest/defunctioning of the bowel\r\n\n\n### Management of peri-anal fistulae\n\n- Drainage seton is the management of choice for high (trans-sphincteric) fistulae. A seton is a thread passed through the fistula tract, forming a ring between the internal and external openings. It is used in the management of high trans-sphincteric fistulae, to prevent division of the anal sphincter muscles and incontinence. Closure of the fistula occurs by the formation of granulation tissue.\n- Fistulotomy is the management of choice for low (submucosal) fistulae. Fistulotomy involves dissecting the superficial tissue and opening the fistula tract. This is not a treatment option for high fistulae due to the risk of incontinence.\n- 'Sphincter saving' methods include fibrin glue and fistula plug - these are still under investigation and have not yet been approved in mainstream management.\n\n### Management of peri-anal abscess\n\n- The patient should be started on intravenous antibiotics e.g. ceftriaxone + metronidazole.\n- Patients typically require examination under anaesthetic and incision and drainage. An incision is made in the affected region, the pus is broken up, the infected tissue material is excised, and anti-septic soaked packs are inserted. Healing occurs by secondary intention.\n\n# Complications\n\n- **Fistulas:**\n - Formation of abnormal connections between different parts of the digestive tract or between the digestive tract and other organs.\n - Commonly involves the small intestine and other structures like the bladder or skin.\n\n- **Strictures:**\n - Narrowing or tightening of the intestinal walls.\n - Can lead to bowel obstruction and difficulties with the passage of stool.\n\n- **Abscesses:**\n - Collection of pus within the abdomen, often near areas of inflammation.\n - Presents with localized pain, swelling, and may require drainage.\n\n- **Malabsorption:**\n - Impaired absorption of nutrients due to inflammation and damage to the intestinal lining.\n - Can lead to nutritional deficiencies and weight loss.\n\n- **Perforation:**\n - Formation of a hole or tear in the intestinal wall.\n - Can result in peritonitis, a serious and potentially life-threatening condition.\n\n- **Nutritional Deficiencies:**\n - Chronic inflammation can affect nutrient absorption.\n - Common deficiencies include vitamin B12, vitamin D, and iron.\n\n- **Increased Risk of Colon Cancer:**\n - Prolonged inflammation may elevate the risk of developing colorectal cancer, particularly in long-standing disease involving the colon.\n\n- **Osteoporosis:**\n - Reduced bone density due to chronic inflammation and corticosteroid use.\n - Increases the risk of fractures.\n\n- **Intestinal Obstruction andToxic Megacolon:**\n - Severe inflammation can lead to the dilation of the colon.\n - Presents as abdominal distension, fever, and can be a medical emergency.\n\n\n# Comparison with Ulcerative Colitis\n\nPlease see below a summary table comparing Crohn's disease and Ulcerative colitis:\n\n| Characteristic | Crohn's Disease | Ulcerative Colitis |\n|------------------------------------|---------------------------------------|-------------------------------------|\n| **Location** | Any part of the digestive tract, from the mouth to the anus (most commonly affects the terminal ileum and colon) | Limited to the colon and rectum |\n| **Inflammation Pattern** | Patchy, skip lesions | Continuous, involves the entire colon|\n| **Depth of Inflammation** | Full thickness (transmural) | Limited to the inner lining (mucosa and submucosa)|\n| **Symptoms** | Abdominal pain, non-bloody diarrhoea, weight loss | Bloody diarrhoea, abdominal cramps |\n| **Complications** | Fistulas, strictures, abscesses | Toxic megacolon, colon cancer risk |\n| **Extraintestinal Manifestations** | Joint pain, skin problems, eye inflammation | Joint pain, skin problems, eye inflammation |\n| **Endoscopy Findings** | Cobblestone appearance, deep ulcers | Continuous colonic inflammation, ulcers |\n| **Diagnostic Imaging** | Transmural inflammation visible on imaging (e.g, MRI) | Limited to the colonic mucosa and submucosa, visible on colonoscopy |\n| **Treatment Approach** | Individualised, may involve medications (e.g. steroids, immunosuppressants) and surgery | Medications (e.g. aminosalicylates, steroids, immunosuppressants), surgery (in severe cases) |\n| **Prognosis** | Variable, chronic condition with periods of remission and exacerbation | Variable, can be chronic with periods of remission, may require surgery in some cases |\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on Crohn's disease](https://cks.nice.org.uk/topics/crohns-disease/)\n\n",
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"explanation": "# Summary\n\nAutoimmune hepatitis is a condition typically seen in young and middle-aged women, characterised by inflammation of the liver caused by an autoimmune response. Key signs and symptoms include jaundice, fatigue, hepatomegaly, and abdominal pain. Key investigations include liver function tests which often show a hepatic pattern of disease and hypergammaglobulinemia. The main types of autoimmune hepatitis are Type I, II, and III, identified by different antibody profiles. Management strategies often depend on the severity of symptoms and disease, and typically include steroid induction therapy followed by maintenance therapy with azathioprine.\n\n# Definition\n\nAutoimmune hepatitis is a chronic, inflammatory disease of the liver that occurs when the body's immune system attacks liver cells leading to inflammation and damage. It is classified into three main types based on the presence of specific antibodies.\n\n# Epidemiology\n\nAutoimmune hepatitis is most frequently observed in young and middle-aged women. There is a notable association with other autoimmune disorders, including: pernicious anaemia, ulcerative colitis, Hashimoto’s/Grave’s, autoimmune haemolytic anaemia, primary sclerosing cholangitis.\n\n# Aetiology\n\nAutoimmune hepatitis occurs due to an abnormal autoimmune reaction against hepatocyte surface antigen, with HLA-B8 and DR3 most frequently implicated. Specifically, there are 3 different types of autoimmune hepatitis:\n\nType 1) ANA positive, with anti-smooth muscle antibodies\n\nType 2) anti-liver/kidney mitochondrial type 1 antibodies (LKM1) – can be remembered as ‘Little Kids’ – children predominantly get Type 2\n\nType 3) Antibodies directed against soluble liver-kidney Antigen \n\n# Signs and Symptoms\n\n- Can present as an acute hepatitis - fever, jaundice, malaise, abdominal pain urticarial rash, polyarthritis, pulmonary infilitration, glomerulonephritis\n- It can also present as chronic liver disease - ascites, jaundice, leuconychia, spider naevi \n\nOther signs and symptoms include:\n\n- Fatigue\n- Anorexia\n- Hepatomegaly\n- Splenomegaly\n\n\n# Differential Diagnosis\n\nThe main differentials for autoimmune hepatitis are other causes of:\n\n- Acute hepatitis e.g. viral A/E/B, drugs (paracetamol poisoning), ischaemia\n- Chronic liver disease e.g. alcohol, NAFLD, hepatitis B and C\n\n\n# Investigations\n\n- Bloods: Abnormal liver function tests often indicate autoimmune hepatitis, showing a hepatic pattern of disease, such as raised ALT and bilirubin with normal or mildly raised ALP. \n- Additionally, patients may present with an IgG predominant hypergammaglobulinemia. \n- The presence of specific antibodies helps to differentiate between the three types of autoimmune hepatitis:\n\t- Type I: Characterised by raised levels of anti-smooth muscle antibodies (80%) and possibly positive antinuclear antibodies (10%).\n\t- Type II: Less common and often more severe, typically positive for anti liver/kidney microsomal antibodies type 1.\n\t- Type III: Also less common, often positive for anti-soluble liver antigen.\n\n# Management\n\n* Management of autoimmune hepatitis is largely dependent on the severity of symptoms and the severity of disease, as determined by blood results and liver biopsy. \n* Initial treatment of acute episodes involves steroid (prednisolone) induction therapy, followed by maintenance therapy with azathioprine, which is effective in most cases. \n* For patients who do not respond to standard treatment, second-line treatment with other immunosuppressants can be considered.\n* In patients presenting with chronic liver disease with decompensated cirrhosis or those who have failed to respond to immunosuppression, liver transplantation is the only management option.\n\n# References\n\n[British Society of Gastroenterology - Management of AIH](https://www.bsg.org.uk/clinical-resource/bsg-guidelines-for-the-management-of-autoimmune-hepatitis/)",
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"question": "A 20-year-old female presents to the emergency department with fever and jaundice. Their LFTs are deranged, and their liver viral screen is negative. Autoimmune hepatitis (AIH) is suspected.\n\nThe presence of which of the following antibodies is classically associated with Type I AIH?",
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"explanation": "Ascitic glucose is typically normal in SBP and low in secondary bacterial peritonitis. However, a normal glucose would not **confirm** a diagnosis of SBP",
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"explanation": "An ascitic pH of <7.0 suggests bacterial infection but will not confirm a diagnosis",
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"explanation": "This is correct. Neutrophils will be raised in bacterial peritonitis due to the localised inflammatory response. Positive ascitic fluid bacterial cultures will also confirm. E.coli is the most common bacteria grown",
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"explanation": "Ascitic amylase is typically raised in pancreatic ascites and is usually normal in SBP",
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"explanation": "This is associated with malignancy or haemorrhagic pancreatitis. In SBP, the ascitic fluid may appear cloudy, but there should not be any visible blood",
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"explanation": "# Summary\n\nAscites is the accumulation of fluid within the peritoneal cavity, commonly seen in patients with cirrhosis. Key signs and symptoms include abdominal distension, discomfort, and dyspnea. The primary investigation is an ascitic tap to analyse the fluid's content, and the Serum Ascites Albumin Gradient (SAAG) helps determine the cause. Management strategies target the underlying cause, dietary restrictions, and diuretic therapy. Refractory cases may require regular therapeutic paracentesis.\n\n# Definition\n\nAscites is defined as the abnormal accumulation of fluid within the peritoneal cavity. This condition is typically associated with liver disease, particularly cirrhosis, but can also occur due to other medical conditions affecting the heart, kidneys, or peritoneum.\n\n# Epidemiology\n\nAscites is a common complication of cirrhosis and represents a key landmark in the natural history of chronic liver disease. The prevalence and incidence of ascites depend significantly on the severity and duration of liver disease.\n\n# Aetiology\n\nThe mechanism of ascites formation is complex and not fully understood. It is thought to involve portal hypertension causing increased hydrostatic pressure, leading to the transudation of fluid into the peritoneal cavity.\n\nCauses include liver disorders (cirrhosis, acute liver failure, liver metastases), cardiac causes (right heart failure) and others such as Budd-Chiari, Portal vein thrombosis etc. (see below).\n\nOther types of ascites can form due to reduced oncotic pressure (nephrotic syndrome, Kwashiorkor), or due to malignancy (peritoneal carcinomatosis, or peritoneal metastasis), or infection (increased permeability – TB), and other causes of 3rd spacing (acute pancreatitis).\n\n# Signs and Symptoms\n\n\n- Abdominal distension\n- Abdominal discomfort or pain\n- Dyspnea\n- Reduced mobility\n- Anorexia and early satiety due to pressure on the stomach\n- Tense abdomen\n- Shifting dullness\n- Stigmata of the underlying cause (see below)\n\n# Differential Diagnosis\n\nThe differential diagnosis for ascites includes conditions like:\n\n- Cirrhosis: jaundice, spider angioma, palmar erythema, hepatic encephalopathy\n- Heart failure: dyspnea, orthopnoea, lower extremity oedema\n- Budd Chiari syndrome: abdominal pain, liver enlargement, jaundice\n- Constrictive pericarditis: dyspnea, peripheral oedema, raised jugular venous pressure\n- Hepatic failure: jaundice, coagulopathy, mental status changes\n- Peritoneal cancer: abdominal pain, weight loss, changes in bowel habits\n- Tuberculosis: fever, night sweats, weight loss, cough\n- Pancreatitis: severe abdominal pain, nausea, vomiting\n- Nephrotic syndrome: proteinuria, hypoalbuminaemia, edema\n\n# Investigations\n\n- The primary investigation for ascites is an ascitic tap, which can provide valuable information about the content of the ascitic fluid. This is usually done under USS guidance to avoid e.g. perforating bowel.\n- The SAAG can help to determine the cause of ascites. It is calculated by subtracting the albumin concentration of the ascitic fluid from the serum albumin concentration.\n- Bloods (to help determine the underlying cause) - FBC, U+E, LFTs, CRP\n- Imaging - CT abdomen, CXR (looking for signs of right-sided heart failure)\n\n[lightgallery]\n\n\n\n# Serum ascites albumin gradient (SAAG)calculation\n\nThe **serum ascites albumin gradient** (SAAG) can help to determine the cause of ascites.\n\nCalculation: serum albumin concentration – ascites albumin concentration\n\n## Causes of a high SAAG (>11g/L)\n\n- Cirrhosis\n- Heart failure\n- Budd Chiari syndrome\n- Constrictive pericarditis\n- Hepatic failure\n\nA high SAAG (>11g/L) suggests that the cause of the ascites is due to raised portal pressure. Raised hydrostatic pressure forces water into the peritoneal cavity whilst albumin remains within the vessels, thus resulting in a higher difference in the albumin concentration between the serum and ascitic fluid.\n\n## Causes of a low SAAG (<11g/L)\n\n- Cancer of the peritoneum, metastatic disease\n- Tuberculosis, peritonitis and other infections\n- Pancreatitis\n- Hypoalbuminaemia - nephrotic syndrome, Kwashiokor\n\n# Management\n\nThe management of ascites primarily involves:\n\n- Addressing the underlying cause\n- High SAAG - implementing a salt-restricted diet and fluid restriction\n- Administering **spironolactone** is first line. Providing adjunctive diuretic therapy such as furosemide if spironolactone is insufficient.\n- Conducting regular therapeutic paracentesis for patients with ascites refractory to medical management, whereby the fluid is drained from the abdomen over a few hours. These patients require replacement with human albumin solution (HAS) in order to avoid the ascites re-accumulating.\n- If the ascitic tap shows neutrophils >250mm<sup>3</sup>, this is diagnostic of **spontaneous bacterial peritonitis**, a serious complication of ascites. This is treated with intravenous piperacillin-tazobactam.\n\t- Prophylactic antibiotics – 1st line = ciprofloxacin (indication if cirrhotic with ascites and ascites protein <15g/L, until ascites has resolved OR previous SBP OR hepato-renal syndrome OR child pugh C)\n- For refractory ascites in portal hypertension, a TIPS (transjugular intrahepatic portosystemic) shunt procedure can be considered.\n\n# References\n\n[British Society of Gastroenterology - Management of Ascites in Cirrhosis](https://www.bsg.org.uk/clinical-resource/guidelines-on-the-management-of-ascites-in-cirrhosis/)\n",
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"question": "A 50-year-old female with known non-alcoholic fatty liver disease (NAFLD) and associated ascites presents to the emergency department unwell. She is pyrexial and has generalised abdominal pain. Paracentesis is performed.\n\nWhich of the following results from the ascitic fluid would confirm a diagnosis of spontaneous bacterial peritonitis (SBP)?",
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"explanation": "According to the modified KCC, hepatic encephalopathy grade III or IV and serum creatinine concentration >300umol/L and prothrombin time >100 seconds meets the criteria for possible liver transplantation",
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"explanation": "According to the modified KCC, an arterial lactate of >3.5mmol/L on admission or >3.0mmol/L 24 hours after paracetamol ingestion or after fluid resuscitation meets the criteria for possible liver transplantation",
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"explanation": "According to the modified KCC, hepatic encephalopathy grade III or IV and serum creatinine concentration >300umol/L and prothrombin time >100 seconds meets the criteria for possible liver transplantation",
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"explanation": "According to the modified KCC, hepatic encephalopathy grade III or IV and serum creatinine concentration >300umol/L and prothrombin time >100 seconds meets the criteria for possible liver transplantation",
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"comment": "Isn't it arterial pH <7.3 if 24h after ingestion ",
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"comment": "hw can i rmeber this\nTo remember the modified King's College Criteria (KCC) for liver transplantation, you can use a mnemonic or a story. Here's a mnemonic that might help:\n\n\"PHLaSH\":\n\nP: pH < 7.3\n\nH: Hepatic encephalopathy (Grade III or IV)\n\nL: Lactate > 3.5 mmol/L (early) or > 3.0 mmol/L (after resuscitation)\n\nS: Serum creatinine > 300 µmol/L\n\nH: Prothrombin Time (PT) > 100 seconds",
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"explanation": "# Summary\n \nParacetamol overdose accounts for 44% of all adult self-poisoning cases in the UK and results in approximately 150,000 hospital admissions annually. Some patients may be asymptomatic, or present with nausea, vomiting, abdominal pain, jaundice or altered mental state. Investigations should include baseline bloods including a clotting and a blood gas, as well as a paracetamol level. Management depends on the dose taken, timing of ingestion and the patient's clinical condition, with N-acetylcysteine being the mainstay of treatment. The decision to treat is often guided by a nomogram although in certain situations N-acetylcysteine should be started immediately.\n \n# Definition \n \nParacetamol overdose refers to when a potentially toxic dose of paracetamol is taken, either accidentally or in the context of a self-harm or suicide attempt. \n \n# Epidemiology \n \nParacetamol is the most common agent ingested in the context of intentional self-harm in the UK. Paracetamol overdose accounts for 44% of all adult self-poisoning cases in the UK, with approximately 150,000 people admitted to hospital each year due to poisoning.\n \n\n# Aetiology\n \n- The pathophysiology of paracetamol toxicity involves the build-up of its toxic metabolite NAPQI (N-acetyl-p-benzoquinone-imine). \n- Normally, NAPQI is inactivated by glutathione in the blood, but in a paracetamol overdose, glutathione stores are rapidly depleted. \n- NAPQI therefore accumulates, unmetabolised, and binds to cellular proteins, causing cell death.\n- This causes both severe hepatotoxicity and nephrotoxicity that can lead to liver and kidney failure. \n\n# Classification\n \n - **Acute overdose** - excessive paracetamol taken in less than 1 hour, usually in the context of self-harm\n - **Staggered overdose** - excessive paracetamol ingested over longer than 1 hour, usually in the context of self harm\n - **Therapeutic excess** - excessive paracetamol taken with the intent to treat pain or fever and without self-harm intent, ingested at a dose greater than 75mg/kg/24 hours.\n\n\n# Signs and Symptoms\n \n- These depend on how long has passed since the overdose was taken\n- In the first 24 hours patients may be asymptomatic or have nausea and vomiting\n- After this, up to around 72 hours, right upper quadrant pain and hypotension may develop\n- From 72 to 96 hours patients may develop liver and renal failure with resulting metabolic acidosis, encephalopathy and coagulopathy, with symptoms of:\n - Confusion\n - Drowsiness\n - Reduced urine output\n - Loin pain\n - Jaundice\n - Bleeding diathesis\n\n# Differential Diagnosis \n\n - **Acute gastroenteritis:** has similar symptoms of nausea, vomiting and abdominal pain; may have diarrhoea and history of unwell contacts\n - **Renal colic:** may also present with haematuria, nausea and vomiting; pain more likely to be \"loin to groin\" rather than right upper quadrant\n - **Decompensation of chronic liver disease:** can present with jaundice, abdominal pain and encephalopathy\n - **Sepsis:** can lead to a lactic acidosis and acute kidney injury; patients are often febrile and may have localising signs or symptoms of infection\n \n# Investigations\n \nBlood tests for paracetamol levels should be taken at least 4 hours after ingestion, as this is when plasma paracetamol concentration peaks so an earlier blood test may underestimate levels\n\nOther important blood tests include:\n \n - Full Blood Count (FBC)\n - Urea and Electrolytes\n - Clotting Screen\n - Liver Function Tests\n - Venous Blood Gas (may show metabolic acidosis)\n - Blood glucose (could also do a bedside capillary blood glucose)\n - Salicylate levels (to look for a mixed overdose with aspirin)\n\n# Management\n \n**Conservative:**\n\n- Weigh patient (important for determining dose of paracetamol taken per kg and to calculate N-acetylcysteine dosing)\n- Consider if any other substances may have been taken with paracetamol\n- If overdose was intentional, refer to liaison psychiatry for a mental health assessment\n - Consider if 1:1 observations are required for high-risk patients\n - Assess risk to self and ongoing suicidal ideation\n - Discharge planning and assess need for ongoing psychiatric input\n- Treat any other self-harm\n\n**Medical:**\n\nDecisions on medical treatment are guided by a nomogram which plots paracetamol levels against time from ingestion. \n\nThe management of paracetamol overdose is dependent on the timing of ingestion, the dose taken, and the patient's clinical condition:\n \n - **Ingestion less than 1 hour ago + dose >150mg/kg**: Administer activated charcoal\n - **Ingestion 1-4 hours ago**: Wait until 4 hours to take a level and treat with N-acetylcysteine (NAC) based on level\n - **Ingestion within 4-8 hours + dose >150mg/kg**: Start NAC immediately if there is going to be a delay of ≥8 hours in obtaining the paracetamol level, otherwise wait for level and treat if level high (above the treatment line on the nomogram)\n - **Ingestion within 8-24 hours + dose >150mg/kg**: Start NAC immediately\n - **Ingestion >24 hours ago**: Start NAC immediately if the patient has jaundice, right upper quadrant tenderness, elevated ALT, INR >1.3 or if the paracetamol concentration is detectable\n - **Staggered overdose**: Start NAC immediately\n \nNAC is given as an IV medication - it acts by increasing glutathione levels thereby preventing toxicity. \n\nThere are two ways to give NAC:\n\n- Standard regimen of 3 consecutive infusions totalling 21 hours in duration \n- The newer SNAP protocol (now recommended by Royal College of Emergency Medicine as standard) where the same dose of NAC is given over 12 hours in two infusions\n- If after either of these are completed, bloods show deranged LFTs, clotting or renal function NAC infusions should be continued and the patient discussed with local liver transplant services\n- Anaphylactoid reactions are a common side effect of NAC, characterised by urticaria, angioedema, nausea and vomiting, tachycardia and bronchospasm but rarely shock\n- These are managed by suspending treatment and giving chlorphenamine and salbutamol nebulisers before restarting (possibly at a slower rate)\n \n**Surgical:**\n\nPatients who develop acute liver failure may require an urgent liver transplant as a life-saving measure - the following groups of patients should be transferred to a liver transplant centre:\n\n- INR > 3 at 48 hours or > 4.5 at any time\n- Oliguric or creatinine > 200\n- pH < 7.3 despite fluid resuscitation\n- Hypotension (systolic blood pressure < 80mmHg)\n- Severe thrombocytopenia\n- Encephalopathy\n \nThe King's College Criteria is used to predict mortality from paracetamol overdose and to identify those patients who would potentially benefit from liver transplantation. It advises consideration of liver transplantation if:\n \n- Blood pH < 7.3\n \n\nOr **all** of:\n \n- Serum creatinine > 300 µmol/L\n- INR > 6.5 (Prothrombin time > 100s)\n- Grade III or IV hepatic encephalopathy\n\n# NICE Guidelines\n\n[NICE CKS - Poisoning or overdose](https://cks.nice.org.uk/topics/poisoning-or-overdose/)\n\n# References\n\n[BNF - Poisoning](https://bnf.nice.org.uk/treatment-summary/poisoning-emergency-treatment.html)\n\n[MHRA - Treating paracetamol overdose with intravenous acetylcysteine](https://www.gov.uk/drug-safety-update/treating-paracetamol-overdose-with-intravenous-acetylcysteine-new-guidance)\n\n[RCEM - SNAP Protocol Position Statement](https://rcem.ac.uk/wp-content/uploads/2021/11/Use_of_SNAP_for_Treatment_of_Paracetamol_Toxicity_Nov_2021.pdf)\n\n[Life in the Fast Lane - liver transplanation for paracetamol toxicity](https://litfl.com/liver-transplantation-for-paracetamol-toxicity/)",
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"learningPoint": "An arterial pH of less than 7.3 indicates a candidate for liver transplantation in paracetamol overdose according to modified King's College Criteria.",
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"question": "A 25-year-old female presents to the emergency department with a paracetamol overdose. She has hepatic encephalopathy grade II.\n\n\nShe has the following blood tests:\n\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.2|7.35 - 7.45|\n|Creatinine|200 µmol/L|60 - 120|\n|Prothrombin Time (PT)|80 seconds|10 - 12|\n|Lactate|3.1 mmol/L|0.6 - 1.4|\n\n\nWhich of the following means that she is a candidate for liver transplantation according to the modified King's College Criteria (KCC)?",
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"explanation": "There is no indication that this patient would not, at present, be able to manage at home. Indications for referral to hospital would include stridor, clinical suspicion of acute epiglottitis, dehydration, or signs of any complications. He does not appear to be systemically unwell from his observations. Immunosuppression is another indication to urgently refer to hospital, which we have no reason to think that this patient is",
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"explanation": "Antibiotic are indicated in this patient as he has a FeverPAIN score of 5 or a Centor score of 3",
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"explanation": "Doxycycline is not indicated for use in tonsillitis. Doxycycline is most commonly used in respiratory tract infections particularly in those who are penicillin allergic or intolerant",
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"name": "Prescribe doxycycline 200mg for 1 dose, then maintenance 100mg OD for 5 days total",
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"explanation": "Amoxicillin is not indicated for use in tonsillitis. Common indications for amoxicillin include respiratory tract and urinary tract infections",
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"explanation": "NICE recommend using either the FeverPAIN criteria or Centor criteria to identify which patients are more likely to benefit from antibiotics. This patient has a FeverPAIN score of 5 (for fever, purulence, attended rapidly, inflamed tonsils, and no cough or coryza) and a Centor score of 3 (tonsillar exudate, history of ever and s=absence of cough). Both of these mean that the patient should receive antibiotics. The first line for a patient not allergic or intolerant to penicillin is phenoxymethylpenicillin. In patients who are penicillin allergic or intolerant, alternative antibiotic choices include clarithromycin or erythromycin",
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"comment": "doesnt centor criteria need fever of >38.5?",
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"comment": ">38 I believe",
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"comment": "Swear the prescription is for 10 days and not 5 which is what threw me off",
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"explanation": "# Summary\n \nTonsillitis is an acute inflammation of the tonsils, often with a purulent exudate in bacterial cases. The most common cause of tonsillitis are viruses, however, the most common bacterium causing tonsillitis is Streptococcus pyogenes (group A streptococcus). The CENTOR criteria can be used to determine the likelihood of a bacterial infection, and management of bacterial tonsillitis often involves antibiotic treatment. Key signs and symptoms can include tonsillar exudate, tender anterior cervical lymphadenopathy, fever over 38 degrees Celsius, and absence of a cough. \n \n# Definition\n \n\nTonsillitis is a form of pharyngitis characterised by acute inflammation of the tonsils, often with a purulent exudate present in bacterial tonsillitis.\n \n\n# Epidemiology\n \n\nIn the UK, tonsillitis is a common condition that predominantly affects children and adolescents, with an estimated 7.4% of GP consultations for children under 15 years involving a sore throat or tonsillitis as the primary reason for the visit.\n \n\n# Aetiology\n \n\nThe most common causative organism of tonsillitis is Streptococcus pyogenes (group A streptococcus). Epstein-Barr virus (EBV) is another common cause.\n \nRisk factors for tonsillitis include:\n \n - Age 5-15 years\n - Immunodeficiency \n - Family history of tonsillitis \n - Close contact with an infected individual \n \n\n# Signs and Symptoms \n \n - Sore throat \n - The child may also complain of referred pain in the ears or a headache \n - Changes to the sound of the child's voice or cry \n - Purulent and inflamed tonsils\n - Lymphadenopathy \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for tonsillitis include the following:\n \n\n - **Bacterial Tonsillitis**: Main signs and symptoms include cervical lymphadenopathy, tonsillar exudate, and fever.\n - **Viral Tonsillitis**: Symptoms are often milder, and accompanied by coryzal symptoms (i.e. cough, rhinorrhoea). \n - **Infectious Mononucleosis**: Also known as glandular fever, this is more common in teenagers. This presents with enlarged tonsils, fatigue and occasionally with splenomegaly. \n - **Hand, foot and mouth disease**: This is caused by the Coxsackie virus, and will feature blisters on the tonsils and roof of the child's mouth. Blisters may also be found on the feet and hands.\n \n\n# Investigations\n \n\nThe CENTOR criteria can be used to indicate the likelihood of a sore throat being due to a bacterial infection. The criteria are as follows:\n \n\n 1. Tonsillar exudate\n 2. Tender anterior cervical lymphadenopathy\n 3. Fever over 38 degrees Celsius\n 4. Absence of a cough\n \n\n [lightgallery]\n \n\nEach of the CENTOR criteria scores 1 point, with a maximum score of 4. A score of 0, 1 or 2 is thought to be associated with a 3 to 17% likelihood of isolating Streptococcus. A score of 3 or 4 is thought to be associated with a 32 to 56% likelihood of isolating Streptococcus.\n\nAlternatively, the FeverPAIN score can be used. The criteria for this include:\n\n- **Fever**\n- **P**us on tonsils\n- **A**ttended within 3 days of symptom onset\n- **I**nflamed tonsils\n- **N**o cough or coryza \n\nDiagnosis is usually clinical, however, in some cases, further investigations may include:\n\n- Throat swab for microscopy and culture\n- Monospot (heterophile antibody) test for glandular fever \n \n\n# Management\n \n\nBacterial tonsillitis with a CENTOR criteria score of 3/4, FeverPAIN score of 4 or 5, or evidence of systemic upset/immunosuppression warrants prescribing antibiotics:\n \n\n- 1st line: Penicillin V PO QDS for 5-10 days\n - Dose is dependent on age, see BNFc for dosing \n- Alternative in penicillin allergy: Clarithromycin/Erythromycin PO BD for 5 days\n - Dose is dependent on age, see BNFc for dosing \n\nFor patients with a CENTOR score of 0-2 or FeverPAIN score of 0 or 1:\n\n- Advise that antibiotics are not needed as they do not tend to alter how long symptoms last and may cause side effects such as diarrhoea and nausea.\n- Conservative management including paracetamol for analgesia and ensuring adequate fluid intake. \n\nIf the child is systemically very unwell or has severe complications, consider referring the child to the hospital. \n\n# Complications\n\n- Quinsy (peritonsillar abscess)\n- Acute otitis media \n- If tonsillitis is due to Group A beta haemolytic step:\n - Rheumatic fever\n - Syndenham's chorea \n - Glomerulonephritis \n - Scarlet fever \n\n# Prognosis \n\nTonsillitis is usually self-resolving within 3-4 days. Some children will have recurrent tonsillitis, and this recurrence may be reduced by smoking cessation for the parents or through tonsillectomy. \n\nTonsillectomy may be indicated for severe recurrent tonsillitis (more than 7 episodes/year for one year, more than 5 episodes/year for two years and more than 3 episodes per year for 3 years). This may be done via diathermy or coblation. \n\n\n# NICE Guidelines\n\n[NICE Guidelines Sore Throat (acute)](https://www.nice.org.uk/guidance/ng84) \n\n[NICE Flowsheet on Antimicrobial Prescribing](https://www.nice.org.uk/guidance/ng84/resources/sore-throat-acute-in-adults-antimicrobial-prescribing-visual-summary-pdf-11315864557) \n \n\n# References\n \n[NHS Information on Tonsillitis](https://www.nhs.uk/conditions/tonsillitis/)\n\n[Patient Info Tonsillitis](https://patient.info/doctor/tonsillitis-pro) \n\n[Great Ormond Street Hospital Tonsillectomy](https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and-treatments/your-child-having-his-or-her-tonsils-andor-adenoids-removed/)",
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"question": "A 25 year old man presents to his general practice with a sore throat which started 2 days ago. He also reports feeling feverish and unwell and denies a cough or coryza. He is still able to eat and drink. He has no allergies and does not take any regular medications.\n\nHis observations are as follows:\n\n- Heart rate: 70 beats per minute\n- Blood pressure: 115/80mmHg\n- Respiratory rate: 14 breaths per minute\n- Saturations: 99% on room air\n- Temperature: 38.1 degrees Celsius\n\nOn examination, his tonsils are inflamed and purulent. He does not have any tender cervical lymphadenopathy.\n\nWhat is the next best step in the management of this patient?",
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"explanation": "There is no indication for antibiotics at present at they are producing the same amount of sputum and it has not changed colour. NICE guidelines advise other indications for considering antibiotics in exacerbations of COPD include risk of complications",
"id": "31944",
"label": "b",
"name": "Prescribe prednisolone 30mg OD for 5 days and doxycycline for 5 days",
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"explanation": "Steroids are indicated for this patient as they are having increased breathlessness on exertion and increased cough. This is likely an exacerbation of his COPD",
"id": "31947",
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"name": "Reassure that there is no indication for antibiotics or steroids at present",
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"explanation": "This patient is systemically well and there is no indication from the question stem that this patient currently requires a hospital admission. NICE guidelines suggest consideration of emergency admission in the following cases: severe breathlessness, inability to cope at home, rapid onset of symptoms, cyanosis, acute confusion, saturations of less than 90% on pulse oximetry, changes on chest x-ray, or already receiving long term oxygen therapy",
"id": "31945",
"label": "c",
"name": "Refer urgently to hospital",
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"explanation": "NICE guidelines recommend only considering chest x-rays in those with an exacerbation of COPD if the person has recurrent chest infections or to exclude other conditions",
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"label": "d",
"name": "Chest x-ray",
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"explanation": "This is correct. This patient is likely having a non-infective exacerbation of their COPD. No antibiotics are indicated at present as they are not producing more sputum than normal and it hasn't changed colour. They should be counselled on the effects of prolonged steroid therapy",
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"label": "a",
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"comment": "given the COPD Hx, what from the details we were given would rule out a spontaneous pneumothorax as a differential (ik there's no ans options, just curious)",
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"comment": "Worsening cough is not a feature of pneumothorax. The breathlessness would not be gradually increasing, it would be sudden onset. The examination would not reveal global wheeze but instead hyperresonance on percussion & reduce air entry over the pneumothorax area. ",
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"comment": "this is wrong, anyone who comes into the hospital with resp symptoms gets a chest x ray to rule out other pathologies",
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"comment": "He presented to his GP, would the GP refer for an outpatient xray or prescribe pred?",
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"explanation": "# Summary\n\nChronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).\n\n# Definition\n\nChronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). \n\n# Epidemiology\n\nIn the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. \n\nAround 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.\n\n# Risk Factors\n\n- Tobacco smoking and passive smoke exposure\n- Marijuana smoking \n- Occupational exposure to dusts and fumes\n- Household air pollution from wood or coal burning\n- Alpha-1 antitrypsin deficiency\n\nPrognosis is variable, with the following factors associated with higher morbidity and mortality:\n\n- Poor exercise tolerance\n- Smoking\n- Low body mass index\n- Multi-morbidity and frailty\n- Exacerbations requiring admission to hospital or frequent exacerbations\n- Severe obstruction on spirometry (as measured by a lower FEV1)\n- Chronic hypoxia\n- Cor pulmonale\n\n# Pathophysiology\n\nChronic Bronchitis:\n\n- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.\nCilia are not able to remove the excess mucus and so it obstructs the small airways.\nOngoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.\n\nEmphysema:\n\n- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. \n- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.\n- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.\n\n# Classification\n\nThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. \n\n| GOLD Grade | Severity | Post-Bronchodilator FEV₁ (% Predicted) |\n|------------|--------------------------|----------------------------------------|\n| 1 | Mild | ≥ 80% |\n| 2 | Moderate | 50-79% |\n| 3 | Severe | 30-49% |\n| 4 | Very Severe | < 30% |\n\n\nThe two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:\n\n| Grade | Description |\n|-------|----------------------------------------------------------------------------------------------------|\n| 0 | I only get breathless with strenuous exercise. |\n| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |\n| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |\n| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |\n| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |\n\n# Signs and symptoms\n\n- Shortness of breath that worsens with exertion\n- Reduced exercise tolerance\n- Chronic productive cough\n- Recurrent lower respiratory tract infections\n- Wheeze\n- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present\n\nExamination may be normal, though signs may include:\n\n- Wheeze or crackles on auscultation\n- Accessory muscle usage\n- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)\n- Cyanosis \n- Hyperinflation of the chest\n- Cachexia\n- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)\n\n# Investigations\n\n- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.\n\n- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history\n- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:\n\t- Right axis deviation\n\t- Prominent P waves in inferior leads\n\t- Inverted P waves in high lateral leads (I, aVL)\n\t- Low voltage QRS\n\t- Delayed R/S transition in leads V1-V6\n\t- P pulmonale\n\t- Right ventricular strain pattern\n\t- RBBB\n\t- Multifocal atrial tachycardia\n\n- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.\n\n[lightgallery1]\n\n- **Sputum culture** - during exacerbations to target antibiotic therapy\n\n# Differential diagnosis\n\n- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.\n- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.\n- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.\n- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.\n- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.\n- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.\n\n# Management of Chronic COPD\n\n**Conservative:**\n\n- Patient education, ensure all patients have a personalised self-management plan\n- Smoking cessation support\n- Nutritional support and dietician referral if malnourished\n- Annual influenza and one-off pneumococcal vaccination\n- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)\n- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques\n\n**Medical:**\n\n\n- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler\n- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). \n- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).\n\nPatients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).\n\nManagement of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:\n\n**Group A**\n \n- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**:\n - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.\n - If symptoms are not controlled, consider switching to a long-acting bronchodilator: \n - **LAMA** or **LABA**, depending on individual tolerance and symptom profile. \n\n**Group B**\n \n- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**: \n - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy. \n - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**. \n\n**Group E**\n \n- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden. \n- **Management**: \n - First-line therapy is **LAMA** for exacerbation prevention. \n - If exacerbations persist, escalate to: \n\t - **Dual therapy (LABA + LAMA)**. \n\t - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**. \n - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**. \n\n\n\n| **Group** | **Phenotype** | **Initial Therapy** | **Escalation Therapy** | \n|-------------|--------------------------------|------------------------------|------------------------------------| \n| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed | LAMA or LABA | \n| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA | LABA + LAMA | \n| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation\t | LAMA | LABA + LAMA or LABA + LAMA + ICS | \n\n\nOther medical treatments that may be considered include:\n\n- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.\n- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.\n- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.\n- Long-term oxygen therapy (LTOT) - see below for more details\n\n\n**Surgical:**\n\n- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. \n- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung. \n\n### Long term oxygen therapy (LTOT)\n\n**The following patients should be referred for assessment for LTOT:**\n\n- Oxygen saturations <92% in air or cyanosis\n- FEV1 <30% predicted (consider referring if <49%)\n- Polycythaemia\n- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)\n\nThis assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. \n\nPatients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):\n\n- PaO2 below 7.3kPa\n- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension\n\n# Complications\n\n## Acute exacerbations\n\n- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. \n- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. \n- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).\n\n- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. \n- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. \n- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.\n\n## Polycythaemia\n\n- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). \n- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. \n\n\n## Cor Pulmonale\n\nCor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.\n\nThe pathophysiology is as follows:\n\n- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.\n- This increases vascular resistance in the lungs.\n- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.\n- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).\n\nPeripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.\n\n## Pneumothorax\n\n- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. \n- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).\n\n## Depression and anxiety\n- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. \n- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. \n- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)\n\n[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)\n\n# References\n\n[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)\n\n[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)\n\n[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)\n\n[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)",
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"question": "A 65 year old man with a past medical history of chronic obstructive pulmonary disease (COPD) presents to his general practice with a worsening cough and increased breathlessness on exertion over the last week. He is currently producing the same amount of sputum as normal, which remains transparent. He says he is currently coping at home.\n\nHis observations are as follows:\n\n- Heart rate: 80 beats per minute\n- Respiratory rate: 15 breaths per minute\n- Saturations: 95% on room air\n- Blood pressure: 140/100mmHg\n- Temperature: 37.1 degrees Celsius\n\nOn examination, there is mild expiratory wheeze globally but no added crepitations. He does not appear confused.\n\nWhat is the next best step in the management of this patient?",
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"explanation": "This is correct. All women aged 25 to 49 are invited for \"routine recall\" if a cervical sample is negative for high-risk HPV",
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"explanation": "Colposcopy is only indicated if the cytology of the cells is abnormal, or there are two consecutive inadequate samples. In the current \"HPV first\" system in the NHS screening programme, the sample is only tested for cytology if it is positive for high risk strains of HPV. As this patient's sample was negative, it was not tested for cytology",
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"explanation": "All women aged 25 to 49 are invited for routine cervical screening every 3 years. Between the ages of 50 and 64 this becomes every 5 years",
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"comment": "This has very recently been changed to 5 years instead of 3 (with quite a bit of controversy)",
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"comment": "its been changed in wales and scotland!",
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"comment": "For England and Northern Ireland – you get an invite every 3 years if you are aged 25 to 49. After that, you get an invite every 5 years until the age of 64.\n\nFor Wales and Scotland – you get an invite every 5 years if you are aged 25 to 64.\n",
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"comment": "Yes I agree, feel this needs to state which country the patient is in as this is varies across the UK \n",
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"comment": "Yeah as per previous comments, in Scotland this is 5 years",
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"explanation": "# Summary\n \n \nCervical cancer is the 3rd most common cancer worldwide and the 4th largest cause of cancer death. It is primarily caused by persistent human papillomavirus (HPV) infection and is commonly squamous cell carcinoma. The key clinical features include vaginal discharge, bleeding, discomfort, and changes in urinary or bowel habits. Investigations involve an urgent colposcopy and CT scans for staging. Management strategies depend on the stage of cancer and the patient's fertility desires, ranging from conisation and radical trachelectomy for early-stage cancers to radiotherapy and chemotherapy for more advanced cases.\n \n \n# Definition\n \n \nCervical cancer is a type of cancer that occurs in the cells of the cervix (the lower part of the uterus that connects to the vagina). The majority of cervical cancers are squamous cell carcinomas. \n \n \n# Epidemiology\n \n \nCervical cancer is the 4th most common cancer in women worldwide. In the UK, it is the 14th most common cancer amongst women.\nOver 90% of cervical cancer deaths and similarly higher prevalence is seen in low- and middle-income countries (LMICs), highlighting inequity in access to HPV-prevention (vaccination), cervical cancer screening and treatment options between LMICs and high-income countries. \n \n \n# Aetiology\n \nCervical cancer is strongly associated with persistent human papilloma virus (HPV) infection. The majority of cases are squamous cell carcinoma.\n \nRisk factors for cervical cancer include: \n \n - HPV 16 and 18 infection (accounts for 70% of cases)\n - Multiple sexual partners\n - Smoking\n - Immunosuppression (e.g. HIV or organ transplants)\n \n \n# Signs and symptoms\n \n \nMost cases of cervical cancer are picked up asymptomatically at cervical screening. Other clinical features include:\n \n - Vaginal discharge\n - Bleeding (e.g. postcoital or with micturition or defaecation)\n - Vaginal discomfort\n - Urinary or bowel habit change\n - Suprapubic pain\n - Abnormal white/red patches on the cervix.\n - Pelvic bulkiness on PV examination\n - Mass felt on PR examination\n \n \n# Differential diagnosis\n \n \nThe differential diagnosis for cervical cancer includes other causes of abnormal vaginal bleeding or discharge such as vaginitis, cervicitis, endometrial cancer, and cervical polyps. Key signs and symptoms of these differentials include:\n \n \n1. **Vaginitis:** itching, burning, pain, and abnormal discharge\n2. **Cervicitis:** abnormal discharge, pelvic pain, and postcoital bleeding\n3. **Endometrial cancer:** abnormal vaginal bleeding, pelvic pain, and unintentional weight loss\n4. **Cervical polyps:** abnormal vaginal bleeding, discharge, and pain during intercourse\n \n \n# Investigations\n\n**Bedside:**\n\n* Speculum examination (with sample for cytology and HPV testing) \n\n**Bloods:**\n\n* FBC (anaemia)\n* LFTs (liver involvement)\n* U&Es (renal involvement) \n\n**Imaging:**\n\n* CT chest/abdomen/pelvis (for staging)\n\n**Invasive:** \n\n* Colposcopy (urgent) and cervical biopsy \n \n\n# Management\n \n \nThe treatment for cervical cancer depends on the stage of the cancer, and also whether the woman wants to retain fertility.\n \n \n - For very small cancers in stage IA treatment options include conisation with free margins if aiming to spare fertility. Conisation is done using a scalpel (cold-knife conisation), laser, or electrosurgical loop, and is usually performed as an outpatient.\n - Radical trachelectomy can be done for slightly more advanced, yet still early-stage cancers when the aim is to spare fertility. This involves removal of the cervix, the upper vagina and pelvic lymph nodes.\n - Where maintaining fertility is not an aim a laparoscopic hysterectomy and lymphadenectomy is offered for women for early-stage cancer.\n - For invasive, infiltrating and early metastatic cancer a radical (Wertheim's) hysterectomy can be performed which involves removal of the uterus, primary tumour, pelvic lymph nodes, and sometimes the upper third of the vagina and uterovesical and uterosacral ligaments.\n - If the cancer has spread outside the cervix and uterus, then surgical management is often unlikely to be curative. These cancers are treated with radiotherapy and/or chemotherapy.\n \n# Complications \n\n* Surgical complications: bladder dysfunction, leg oedema (due to lymphadenectomy), preterm birth \n* Radiation complications: vaginal stenosis, vaginal atrophy, bladder dysfunction, urethral strictures\n\n# Prognosis \n\nCervical cancer is preventable through screening. Mortality has decreased significantly as a result of improved treatment and screening programmes. Overall 5-year survival is 67%. However, this varies based on stage of disease at diagnosis:\n\n* Stage I: >90%\n* Stage II-III: 50-70%\n* Stage IV: <20%\n\n# Cervical Screening\n \n \n - For all women and people with a cervix between the age of 25-64 years. \n - Cervical sample is taken and tested for high-risk HPV viruses. \n - From 24 to 49 women are called every three years, and afterwards every five years.\n- The idea behind the screening process is to identify dyskaryotic cells which are pre-cancerous allowing management before invasive cancer can develop.\n \n \n## Outcomes in screening\n \n \nOutcomes from screening can be as follows:\n \n \n - Anybody with a negative HPV test is returned to routine recall.\n - Anybody with a positive HPV test has cytological testing. \n - Patients who are HPV positive but have negative cytology results should have a repeat HPV test in 12 months and again at 24 months if still positive. If they remain positive at 24 months they should be referred to colposcopy.\n - In some cases the sample may be inadequate, in which case the smear should be repeated. If it still not adequate for the next two samples, then the woman should be referred for colposcopy.\n \n \n# HPV Vaccination\n \n \n - Girls and boys aged 12 to 13 years are offered the HPV vaccine as part of the NHS vaccination programme\n - The vaccine helps protect against cancers caused by HPV, including cervical cancer, some mouth and throat cancers and some cancers of the anal and genital areas. It also helps protect against genital warts\n - Gardasil is the vaccination used and protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52 and 58\n \n# NICE Guidelines\n \n [Click here for NICE CKS on Cervical cancer](https://cks.nice.org.uk/topics/cervical-cancer-hpv/)\n \n \n [Click here for NICE CKS on Cervical cancer screening](https://cks.nice.org.uk/topics/cervical-screening/)\n \n \n# References\n \n[Cancer UK](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/cervical-cancer) \n[NHS Page](https://www.nhs.uk/conditions/cervical-cancer/)",
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"question": "A 25 year old female presents to her general practice for her first routine cervical screening. She has no gynaecological symptoms.\n\nOn speculum examination, her cervix appears normal.\n\nThe sample returns as negative for human papillomavirus (HPV).\n\nWhat is the next best step?",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 20 year old female presents to her general practice to discuss contraception options. She has had the same regular partner for the last 2 years. Her periods are normally regular. Her past medical history includes migraine with aura. She does not smoke and drinks on average 3 units of alcohol per week.\n\nA sexually transmitted disease screen returns negative, as does a urine beta-HCG.\n\nWhich of the following contraception options is contraindicated in this patient?",
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"explanation": "According to NICE guidelines, specialist assessment on the same day is only indicated if the patient has a blood pressure of more than 180/120mmHg and either signs of retinal haemorrhage of papilloedema or life threatening symptoms such as a new onset confusion, chest pain, signs of heart failure or acute kidney injury",
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"explanation": "An ACE inhibitor (eg. ramipril) can be switched to a angiotensin II receptor blocker (eg. candesartan) if the ACE inhibitor is causing adverse effects such as a cough. This does not appear to be the case in this patient",
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"comment": "I thought 2 consecutive BP readings were needed showing HTN? 3 months is definitely more appropriate than slamming meds",
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"comment": "I thought ARBs where better for diabetics than ACEi?",
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"comment": "No ACE is for type 2 diabetics. Remember ACEi is renal protective",
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"comment": "Surely you would take it more than once? How do you know it’s not white coat syndrome?",
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"comment": "honestly thought they were hinting at White Coat Syndrome too :(\n\nBP readings from Mon-Weds seem fine but is 155/100 when examined *in the practice* ",
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"comment": "100 diastolic pressure in practice and at home is not fine, it classes as 2nd stage hypertension which is what the question is hinting at hope that helps.",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"question": "A 65 year old man presents to his general practice for a routine blood pressure check. He does not appear confused and he denies chest pain or cough.\n\nHe has a blood pressure monitor at home and presents a piece of paper with his recordings on it:\n\n- Monday AM: 132/95mmHg\n- Monday PM: 136/92mmHg\n- Tuesday AM: 142/105mmHg\n- Tuesday PM: 135/95mmHg\n- Wednesday AM: 143/105mmHg\n- Wednesday PM: 139/101mmHg\n\nThe patient currently takes the following medications:\n\n- Ramipril 10mg OD\n- Amlodipine 10mg OD\n- Metformin 500mg BD\n\nA fundoscopy examination is normal. At the practice, his blood pressure is 155/100mmHg.\n\nWhat is the next best step in the management of this patient?",
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"explanation": "Although this patient has COPD, there is no requirement for spirometry testing prior to initiation of Donepazil",
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"comment": "Before starting the patient on an alzheimers medication, shouldnt a CT scan be done to rule out organic causes? I see why we should do an ECG before commencing the medication, but there is no formal diagnosis of dementia so surely the correct answer is CT?",
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"comment": "My guess is because the neuro exam was entirely normal and the Hx/symptoms are very much in line with Alzheimer's so no need for a CT? But I agree think a CT would be appropriate",
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"comment": "no focal neurology therefore: no",
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"explanation": "# Summary\n\nAlzheimer's disease, the most common form of dementia, is a progressive neurodegenerative disorder that leads to cognitive decline, memory impairment, and a range of behavioural and psychological symptoms. Its impact extends beyond the individual, affecting families and healthcare systems worldwide. This comprehensive guide explores the key aspects of Alzheimer's disease, from its definition and pathophysiology to clinical features, diagnostic considerations, management approaches, and prognosis. Adherence to NICE guidelines ensures evidence-based care for patients with this challenging condition.\n\n# Definition\n\nAlzheimer's disease is a chronic, neurodegenerative disorder characterized by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain. This leads to the deterioration of cognitive function, memory loss, and various behavioural and psychological symptoms.\n\n\n# Epidemiology\n\nAlzheimer's disease is a global health concern, with an increasing prevalence as the population ages. It is estimated that millions of individuals worldwide are affected, with higher incidence rates in older age groups. Women are more commonly affected than men, and several genetic and environmental factors influence disease risk.\n\n\n# Pathophysiology\n\n\nAlzheimer's disease is a complex and progressive neurodegenerative disorder characterized by distinct pathophysiological hallmarks. These hallmarks are responsible for the gradual decline in cognitive function and the characteristic clinical features observed in affected individuals.\n\n1. **Amyloid Plaques:** The accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature. These abnormal protein deposits are believed to disrupt neuronal communication, trigger inflammation, and ultimately lead to cell death.\n\n2. **Tau Tangles:** Inside nerve cells, abnormal tau protein accumulates, forming neurofibrillary tangles. These tangles interfere with the transport of essential nutrients within neurons, contributing to their dysfunction and eventual demise.\n\n3. **Neuronal Loss and Brain Atrophy:** As the disease progresses, significant neuronal loss occurs, particularly in brain regions responsible for memory and cognitive function, such as the hippocampus and the cerebral cortex. This loss is associated with brain atrophy, visible on imaging studies.\n\n4. **Neurotransmitter Imbalance:** Alzheimer's disease disrupts the balance of neurotransmitters, particularly acetylcholine, which plays a crucial role in memory and learning. Reduced acetylcholine levels further contribute to cognitive decline.\n\n5. **Inflammatory Response:** Chronic neuroinflammation, characterized by the activation of microglia and astrocytes, is a prominent feature in Alzheimer's disease. Inflammation may exacerbate neuronal damage and contribute to the progression of the disease.\n\n# Risk Factors\n\nSeveral factors influence an individual's risk of developing Alzheimer's disease. These include:\n\n- **Age:** Advanced age is the most significant risk factor, with the incidence of Alzheimer's disease increasing exponentially after the age of 65.\n\n- **Genetic Predisposition:** Mutations in specific genes, such as the apolipoprotein E (APOE) gene, increase the risk of developing Alzheimer's disease. Additionally, individuals with Down's syndrome are at a higher risk due to a triplication of chromosome 21, which carries the amyloid precursor protein (APP) gene.\n\n- **Family History:** Having a first-degree relative with Alzheimer's disease can increase one's susceptibility.\n\n- **Cardiovascular Risk Factors:** Conditions like hypertension, diabetes, obesity, and hypercholesterolemia have been associated with an elevated risk of Alzheimer's disease.\n\n- **Lifestyle Factors:** Physical inactivity, smoking, and a diet high in saturated fats may contribute to increased risk.\n\n- **Traumatic Brain Injury:** A history of head injuries, particularly repeated concussions, has been linked to a higher risk of developing Alzheimer's disease.\n\n- **Low Educational Attainment:** Lower levels of education may be associated with an increased risk.\n\nUnderstanding these risk factors and their relationship to the disease's pathophysiology is crucial for early identification, prevention, and management of Alzheimer's disease.\n\n# Clinical Features\n\nAlzheimer's disease is characterized by a constellation of cognitive and behavioural symptoms, which may include:\n\n* **Memory Impairment:** Early in the disease, individuals often experience difficulties in recalling recent events and conversations.\n* **Language Impairment:** This may manifest as difficulty finding words, struggling to express oneself, and, in later stages, aphasia.\n* **Executive Dysfunction:** Impaired ability to plan, organize, and carry out tasks, leading to difficulties in activities of daily living.\n* **Behavioural Changes:** Individuals may exhibit agitation, aggression, or apathy, sometimes accompanied by mood swings and irritability.\n* **Psychological Symptoms:** Hallucinations, delusions, and paranoia can occur, particularly in later stages of the disease.\n* **Disorientation:** Affected individuals may become disoriented in familiar surroundings, unable to recognize places or people.\n* **Loss of Motor Skills:** In advanced stages, motor skills decline, leading to difficulties with mobility and self-care.\n\n# Differential Diagnosis\n\n\n1. **Vascular Dementia:** Cognitive impairment in vascular dementia often presents suddenly and is associated with a history of cerebrovascular events.\n\n2. **Lewy Body Dementia:** Visual hallucinations and fluctuating cognitive impairment are more common in Lewy body dementia.\n\n3. **Frontotemporal Dementia:** This condition typically presents with profound behavioural and personality changes, often affecting social conduct.\n\n4. **Mild Cognitive Impairment (MCI):** MCI is a transitional state between normal cognitive aging and dementia. Unlike Alzheimer's, MCI may not significantly impact daily functioning.\n\n5. **Normal Age-Related Cognitive Decline:** Age-related cognitive changes are common but do not interfere significantly with daily activities.\n\n# Investigations\n\nDiagnosing Alzheimer's disease may involve a series of assessments, including:\n\n- **History** - including a functional history, which may be informed using a structured instrument such as the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) or the Functional Activities Questionnaire (FAQ). A collateral history may be necessary, and a risk assessment should also be taken.\n- Assess cognitive decline using an approved scoring tool such as MMSE, MOCA, 10-point Cognitive Screener (10-CS), 6-item Cognitive Impairment Test (6-CIT), 6-item Screener, Memory Impairment Screen (MIS), Mini-Cog, Test Your Memory (TYM) \n- **Examination** - physical examination including a full neurological examination looking for abnormaliities in coordination, gait, sensation and motor signs.\n- **Blood tests** - to rule out reversible causes, this is known as a confusion screen and is often done in primary care. It includes FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV. If there is an acute onset of symptoms delirium should be considered as this is a different pathway.\n- Once reversible causes are ruled out and a diagnosis of dementia is still suspected, refer to a specialist dementia diagnostic service (such as a memory clinic or community old age psychiatry service. Here, a full functional assessment is carried out and the patient will be referred for **neuroimaging**, such as CT or MRI.\n\t- **Brain Imaging:** Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans can reveal brain atrophy and the presence of amyloid plaques.\n\t- **Cerebrospinal Fluid Analysis:** May be used to detect specific biomarkers associated with Alzheimer's disease.\n\n# Management\n\n- **Non-Pharmacological Approaches:** Psychological interventions, cognitive stimulation therapy, and occupational therapy can help manage behavioural and psychological symptoms.\n\n- **Support for Caregivers:** Education and support for family members and caregivers are vital to help them navigate the challenges of providing care.\n\n- **Patient-Centered Care:** Tailoring interventions to the individual's needs and preferences, while ensuring their safety and well-being.\n- **Pharmacological Intervention:** Medications, such as cholinesterase inhibitors (e.g. donepezil) and N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. memantine), may be prescribed to manage cognitive symptoms.\n\t- Pharmacological treatments may have modest benefits, and include the cholinesterase inhibitors rivastigamine, galantamine, and donpezil in mild-moderate dementia, and the NMDA inhibitor memantine in severe dementia (as classified using the MMSE score: severe: <10; moderate: 10-20; mild: 21-26/30. \n\t- If there is evidence of behavioral and psychological symptoms of dementia (BPSD), low-dose risperidone may be started\n\n\n# NICE Guidelines\n\n[NICE CKS - Dementia](https://cks.nice.org.uk/topics/dementia/)\n\n# References\n\n[NHS UK - Alzheimer's Disease](https://www.nhs.uk/conditions/alzheimers-disease/)\n\n[Alzheimer's Association](https://www.alz.org/alzheimers-dementia/what-is-alzheimers)\n\n\n\n\n\n",
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"question": "A 85 year old man is seen at the neurology clinic with his daughter. The daughter reports that he has been increasingly forgetful, has a shortened attention span compared to his usual self and has become very clumsy. She says that this has been a gradual decline over several months. The patient denies any changes in mood or any suicidal ideation.\n\nHis only significant past medical history is chronic obstructive pulmonary disease (COPD) for which he takes salbutamol PRN. He has no significant psychiatric history.\n\nOn examination, he has normal tone of his upper and lower limbs, a normal gait, and normal power throughout.\n\nThe neurologist decides to start him on Donepazil. Which investigation should be performed prior to commencing this medication?",
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"explanation": "This patient appears to be having a flare of his ulcerative colitis, a barium enema would not be an appropriate investigation, and in fact may increase risk of bowel perforation",
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"explanation": "A plain abdominal x-ray should first be conducted in this patient to investigate for toxic megacolon. The symptoms that he presents with are consistent with this",
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"explanation": "A CT abdomen/pelvis may be indicated later in his admission to look or any complications such as abscesses, but would first require an abdominal x-ray",
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"explanation": "# Summary\n\nThe acute abdomen, a common presentation in clinical practice, refers to the sudden onset of severe abdominal pain. It is often a medical and/or surgical emergency, requiring prompt evaluation and intervention. Causes of an acute abdomen can be divided into surgical and medical causes, and while investigations and management of these are specific to the underlying cause, there are broad principles which should always be followed. This section explores the diverse aetiologies and clinical manifestations of acute abdominal conditions, emphasising the importance of timely diagnosis and management. \n\n# Epidemiology\n\nWhile prevalence varies geographically, acute abdomen accounts for a substantial proportion of emergency department admissions worldwide. A broad spectrum of age groups is affected, with appendicitis being more common in younger individuals, while conditions like diverticulitis and cholecystitis are prevalent in older populations. Additionally, comorbidities and lifestyle factors, including smoking and diet, may contribute to the incidence of acute abdominal conditions. \n\n# Differential Diagnosis\n\n## Surgical Acute Abdomen\n\nHere's a summary table with surgical differential diagnoses for each of the specified types of abdominal pain. It's important to note this is a guide and not all of these pathologies can only present with one type of pain, and there can be overlap with atypical presentations.\n\n\n| Type of Abdominal Pain | Surgical Differential Diagnoses |\n|-----------------------------|-----------------------------------------------------------------------|\n| **Central Abdominal Pain** | - Mesenteric ischemia <br /> - Acute pancreatitis (complicated) <br /> - Aortic dissection <br /> - Appendicitis <br /> - Intestinal obstruction <br /> - Perforated viscus <br /> - Abdominal wall hernia (strangulated) <br /> - Ruptured AAA |\n| **Epigastric Pain** | - Acute pancreatitis (complicated) <br /> - Perforated peptic ulcer <br /> - Cholecystitis (with gallbladder perforation) <br /> - Gastro-oesophageal perforation <br /> - Aortic dissection <br /> - Abdominal aortic aneurysm (AAA) <br /> - Gastric or duodenal ulcer (complicated) |\n| **Left Upper Quadrant Pain** | - Gastrointestinal perforation <br /> - Left-sided diverticulitis <br /> - Left renal pathology (e.g. abscess) <br /> - Perforated gastric or duodenal ulcer <br /> - Abdominal aortic aneurysm (AAA) <br /> - Spleen-related conditions (e.g. splenic infarction, rupture, abscess) <br /> - Gastric or duodenal ulcers (complicated) |\n| **Left Iliac Fossa Pain** | - Diverticulitis (complicated) <br /> - Gynecological emergencies (e.g. ovarian torsion, ovarian cyst rupture, ectopic pregnancy) <br /> - Left ureteral stone (with obstruction) <br /> - Ulcerative colitis <br /> - Perforated sigmoid diverticulitis <br /> - Ischaemic colitis (left-sided) <br /> - Left renal pathology (e.g. abscess) <br /> - Ileocecal tuberculosis (rare) <br /> - Sigmoid volvulus <br /> - Left-sided appendicitis (rare) |\n| **Right Upper Quadrant Pain** | - Acute cholecystitis <br /> - Biliary colic <br /> - Ascending cholangitis <br /> - Perforated peptic ulcer (anterior) <br /> - Liver pathology (e.g. hepatic abscess) <br /> - Right renal pathology (e.g. abscess) <br /> - Right-sided diaphragmatic hernia (e.g. Morgagni hernia) <br /> - Subphrenic abscess <br /> - Appendicitis (retrocecal) |\n| **Right Iliac Fossa Pain** | - Appendicitis <br /> - Caecal diverticulitis (rarely) <br /> - Right-sided gynecological emergencies (e.g. ovarian torsion, ovarian cyst rupture, ectopic pregnancy) <br /> - Right ureteral stone (with obstruction) <br /> - Ileocecal tuberculosis (rarely) <br /> - Right renal pathology (e.g. infarction, abscess) <br /> - Gastrointestinal perforation (e.g. perforated appendicitis) <br /> - Crohn's disease (terminal ileitis) |\n| **Suprapubic Pain** | - Acute appendicitis (atypical presentation) <br /> - Diverticulitis (with involvement of sigmoid) <br /> - Bladder pathology (e.g. bladder rupture) <br /> - Right ureteral stone (with lower migration) <br /> - Urethral pathology (e.g. urethral diverticulum) <br /> - Colonic pathology (e.g. ischaemic colitis) <br /> - Testicular torsion <br /> - Inguinal hernia (rare) <br /> - Pubic osteomyelitis (rare) |\n\n## Medical Acute Abdomen\n\nUnless otherwise specified, these causes can often present with very generalised abdominal pain which is often poorly localised.\n\n- Myocardial infarction (especially inferior MI which can present with epigastric pain)\n- Pericarditis\n- Pulmonary embolism\n- Gastroenteritis\n- Pneumonia (left/right lower lobes)\n- Mesenteric adenitis\n- Vasculitis (such as Henoch-Schonlein purpura)\n- Diabetic ketoacidosis\n- Addison's disease\n- Hypercalcaemia\n- Acute intermittent porphyria\n- Abdominal migraine\n- Irritable bowel syndrome\n- UTI and urinary retention (often suprapubic pain)\n- Sickle cell crisis\n\n# Investigations\n\n### Bedside\n- Blood glucose and ketones \n- Urine (urine dip, cultures and **pregnancy test in all females of childbearing age**\n- Stool (culture, faecal calprotectin), FIT testing in primary care (less urgent in acute setting)\n- ECG (looking for ischaemic changes)\n\n### Blood tests\n- VBG (raised lactate may indicate ischaemia, metabolic disturbances can be indicative of several medical causes such as DKA, addison's disease and hypercalcaemia)\n- FBC (anaemia may indicate haemorrhage, underlying malignancy; raised infection markers), CRP, U+E, LFTs, coagulation profile and group and save (especially if surgical intervention is likely), amylase/lipase, beta-HCG, troponin/d-dimer **(if indicated)**, blood cultures\n- Less urgent blood tests include tumour markers (CEA, CA 19-9)\n\n### Imaging\n- AXR +/- erect CXR (to assess for pneumoperitoneum and perforation)\n- USS of abdomen/renal tract/pelvis/testes\n- CT abdomen pelvis/urinary tract, CT angiogram (if ischaemia/AAA rupture suspected)\n- MRI may be indicated if e.g. looking for abscesses\n- MRCP (gallstones)\n- Endoscopy - OGD/colonoscopy/flexible sigmoidoscopy which may also be therapeutic\n\n# Management\n\nThough specific management strategies will depend on the underyling cause (see separate sections on each differential diagnosis), here are broad principles which will be applicable to the majority of the above differentials:\n\n- Conservative management - IV fluids +/- NG tube insertion ('drip and suck'), analgesia, anti-emetics, anti-spasmodics (such as hyoscine butylbromide), nutritional support (e.g. pabrinex)\n- Medical management - oral/IV antibiotics if suspected infectious cause, PPI (e.g. omeprazole)\n- Surgical management - may include but not limited to: endoscopy, ERCP, laparoscopic intervention.\n\n\n# NICE Guidelines\n\nNICE CKS Summaries:\n\n- [Acute pancreatitis](https://cks.nice.org.uk/topics/pancreatitis-acute/)\n- [Diverticular disease](https://cks.nice.org.uk/topics/diverticular-disease/)\n- [Appendicitis](https://cks.nice.org.uk/topics/appendicitis/)\n- [Ectopic pregnancy](https://cks.nice.org.uk/topics/ectopic-pregnancy/)\n- [Cholecystitis](https://cks.nice.org.uk/topics/cholecystitis-acute/)\n- [Gallstones](https://cks.nice.org.uk/topics/gallstones/)\n- [Crohn's disease](https://cks.nice.org.uk/topics/crohns-disease/)\n- [Ulcerative colitis](https://cks.nice.org.uk/topics/ulcerative-colitis/)\n\n",
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"question": "A 30 year old man with a past medical history of ulcerative colitis presents to the accident and emergency department. They report that they have been passing approximately six blood-stained stools per day. He denies nausea or vomiting at present.\n\nTheir observations are as follows:\n\n- Respiratory rate: 18 breaths per minute\n- Saturations: 99% on air\n- Heart rate: 105 beats per minute\n- Blood pressure: 110/85mmHg\n- Temperature: 38.2 degrees Celsius\n\nOn examination, their abdomen is mildly distended with mild generalised tenderness. Bowel sounds are present.\n\nWhich of the following investigations should be first conducted in this patient?",
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"explanation": "This is a sensible differential in a trauma patient with haemodynamic instability, although it would not explain the petechial rash and is unlikely to cause such significant respiratory compromise and neurological disturbance",
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"explanation": "This would not explain his respiratory compromise or petechial rash. Although a subarachnoid haemorrhage is the most common type of brain haemorrhage secondary to trauma in the acute phase",
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"explanation": "Although this may explain his respiratory compromise, it would not explain the petechial rash. It is unlikely to cause acute confusion and drowsiness in someone so young, and the normal temperature is also going against this diagnosis. Pneumonia would also typically cause unilateral crackles on auscultation",
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"explanation": "Fat embolism classically presents with the triad of respiratory compromise, neurological disturbance and a petechial rash. It typically occurs 24-72 hours after a long bone injury or surgical procedure",
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"comment": "Can someone explain the crackles?",
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"comment": "would it give you hypotension though",
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"explanation": "# Summary\n\nFat embolism refers to a medical condition characterized by the entry of fat fragments into the systemic circulation, subsequently lodging in the small vessels of the lungs or other tissues. This typically occurs due to fractures, especially long bone fractures. Clinical manifestations vary depending on the site of embolism, with breathlessness being a common symptom in pulmonary fat embolism. Investigations may include radiographic imaging and serum markers. The mainstay of management is supportive care, focused on oxygenation and symptomatic relief.\n\n# Definition\n\nFat embolism is a clinical syndrome resulting from the dissemination and subsequent lodgment of fat droplets or fat globules in the small vessels of the systemic and/or pulmonary circulation. This event typically follows trauma, particularly fractures of long bones or pelvic bones, but it can also occur after non-traumatic events such as orthopedic surgery or severe burns.\n\n# Epidemiology\n\nThe incidence of fat embolism varies and is largely dependent on the context. It is estimated to occur in 1-3% of all long bone fractures, but the incidence can be as high as 10-30% in patients with polytrauma or after major orthopedic surgeries. Fat embolism syndrome, a severe manifestation of fat embolism characterized by multisystem involvement, is estimated to occur in approximately 10% of all cases of fat embolism.\n\n# Aetiology\n\nThe aetiology of fat embolism generally involves:\n\n- Trauma, particularly long bone and pelvic fractures\n- Non-traumatic events such as orthopedic surgeries (hip or knee arthroplasty)\n- Severe burns\n- Liposuction\n- Prolonged corticosteroid therapy\n\n# Signs and Symptoms\n\nThe signs and symptoms of fat embolism are largely determined by the site of embolization:\n\n- Pulmonary: Breathlessness, hypoxia, tachycardia, tachypnea, and fever\n- Neurologic: Altered mental status, seizures, focal deficits, or coma\n- Dermatologic: Petechial rash predominantly on the upper body\n\n# Differential Diagnosis\n\nDifferential diagnosis for fat embolism includes conditions that present similarly such as:\n\n- Pulmonary embolism: Presents with sudden onset shortness of breath, chest pain, and hemoptysis.\n- Acute respiratory distress syndrome (ARDS): Presents with severe shortness of breath, rapid breathing, and bluish skin coloration (cyanosis).\n- Pneumonia: Presents with cough (often productive), fever, shortness of breath, and chest discomfort.\n- Sepsis: Presents with fever, increased heart rate, increased respiratory rate, and confusion.\n\n# Investigations\n\nThe diagnosis of fat embolism is typically clinical, supported by relevant investigations:\n\n- Imaging studies: Chest X-ray may reveal diffuse bilateral infiltrates; CT of the chest may show fat within the vessels.\n- Laboratory tests: Serum markers such as fat macroglobulinemia, increased serum lipase, and increased serum LDH.\n- Bronchoalveolar lavage: To identify fat droplets in macrophages.\n\n# Management\n\nManagement of fat embolism is primarily supportive and includes:\n\n- Oxygen therapy: To relieve hypoxia and dyspnea.\n- Fluid resuscitation: To maintain hydration and support circulatory function.\n- Pharmacological therapy: Prophylactic low-molecular-weight heparin may be considered to prevent thromboembolic events.\n- Fracture stabilization: Early immobilization of fractures can reduce the incidence of fat embolism.\n\n# References\n\n- [Ortho Bullets: Fat Embolism Syndrome](https://www.orthobullets.com/basic-science/9055/fat-embolism-syndrome)",
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"question": "A 40 year old man is admitted to hospital following a road traffic accident. He has a pelvic x-ray which shows a stable pelvic fracture which is managed conservatively.\n\nApproximately 48 hours later, he becomes acutely confused, drowsy and breathless.\n\nHis observations are as follows:\n\n- Respiratory rate: 25 breaths per minute\n- Saturations: 90% on room air\n- Heart rate: 90 beats per minute\n- Blood pressure: 95/65mmHg\n- Temperature: 36.5 degrees Celsius\n\nOn examination, auscultation of his chest reveals bibasal coarse crackles. There is also a petechial rash on the anterior aspect of his chest.\n\nWhat is the most likely diagnosis?",
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"explanation": "This may rarely present with bowel perforation, but is not as common a cause for bowel perforation as diverticulosis. Advanced colon cancer may more likely present with bowel obstruction or PR bleeding",
"id": "31985",
"label": "c",
"name": "Colon cancer",
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"answer": false,
"explanation": "This may rarely present with bowel perforation, but is not as common a cause for bowel perforation as diverticulosis",
"id": "31987",
"label": "e",
"name": "Appendicitis",
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"answer": false,
"explanation": "This would cause perforation of the duodenum or stomach rather than bowel perforation",
"id": "31984",
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"explanation": "Diverticular disease is the most common underlying pathology found in cases of bowel perforation in elderly patients. Diverticulosis refers to the asymptomatic presence of diverticula in the large bowel",
"id": "31983",
"label": "a",
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"explanation": "It is unlikely that a man of this age would present with ulcerative colitis for the first time. It may also rarely cause bowel perforation but is not as a common a cause as diverticulosis",
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"comment": "duodenum not bowel? ",
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"explanation": "# Summary\n\nDiverticular disease is a clinical condition characterized by the presence of diverticula, or outpouchings of the mucosa and submucosa, typically affecting the sigmoid colon. Key signs and symptoms include constipation, left lower quadrant abdominal pain, and potentially rectal bleeding. Key investigations include physical examination, abdominal imaging, and blood tests. In cases of inflammation of the diverticula, known as diverticulitis, the primary management strategy includes oral antibiotics, and in more severe cases, hospital admission and intravenous antibiotics. Surgical intervention may be required for complications such as perforation, abscess formation, and fistulas.\n\n\n# Definition\n\n**Diverticular disease** is a term used to describe conditions related to the presence of diverticula, which are small, bulging pouches that can form in the lining of the digestive system, most commonly in the lower part of the colon (sigmoid colon).\n\n**Diverticulosis** refers to the simple presence of diverticula. In many cases, diverticulosis is asymptomatic, and individuals may not even be aware that they have these diverticula as they are typically discovered incidentally during tests for other conditions.\n\n**Diverticulitis**, a subset of diverticular disease, occurs when these diverticula become inflamed or infected. This condition is typically characterized by severe abdominal pain, fever, and nausea. Diverticulitis often requires treatment, which can include antibiotics, pain relievers, and, in severe cases, surgery.\n\n# Epidemiology\n\nDiverticular disease is most common in individuals over the age of 50 and those who consume a Western (low fibre) diet.\n\n# Aetiology\n\nThe primary risk factor for diverticular disease is age, with the condition being more prevalent in individuals over the age of 50. Other risk factors include consuming a low-fibre Western diet, obesity, lack of exercise, and certain medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates.\n\n# Signs and Symptoms\n\nDiverticular disease typically presents with:\n\n- Constipation\n- Left lower quadrant abdominal pain\n- Possible rectal bleeding\n\nPhysical examination may be normal or may demonstrate tenderness in the left lower quadrant on digital rectal examination.\n\nIn cases of diverticulitis, the condition presents acutely with:\n\n- Left lower quadrant abdominal pain\n- Fever\n- Nausea/vomiting\n- Pyrexia and left lower quadrant tenderness/guarding on physical examination\n- Diffuse abdominal tenderness suggestive of perforation or generalised peritonitis.\n\n# Differential Diagnosis\n\nThe differential diagnosis for diverticular disease includes:\n\n- Irritable bowel syndrome: Characterised by chronic abdominal pain, bloating, and alterations in bowel habits without an identifiable cause.\n- Colonic carcinoma: Presents with a change in bowel habits, rectal bleeding, abdominal pain, and unexplained weight loss.\n- Inflammatory bowel disease: Marked by abdominal pain, diarrhoea, bloody stools, weight loss, and fatigue.\n- Gynaecological disorders (in women): May present with abdominal or pelvic pain, menstrual irregularities, and various urinary symptoms.\n- Urological disorders: These may involve symptoms such as frequency, urgency, dysuria, and lower abdominal pain.\n\n# Investigations\n\nDiverticular disease can be confirmed through a variety of tests, such as:\n\n- Abdominal imaging (CT scan or ultrasound)\n- Blood tests demonstrating inflammation (leukocytosis)\n- Colonoscopy/endoscopy\n\n# Management\n\nManagement of diverticular disease depends on the severity and symptoms presented:\n\n- Asymptomatic diverticulosis: No treatment is required if diverticula are seen incidentally on imaging or endoscopy.\n- Symptomatic diverticular disease: Patients should be advised to increase dietary fibre intake and hydration. If there is evidence of diverticulitis (leukocytosis, fever), patients are initially managed with oral antibiotics (e.g. 7 days co-amoxiclav). Analgesia may also be required, prescribed in a step-wise fashion, starting with oral paracetamol. A low residue diet is also advised.\n- Management of diverticulitis: Patients unresponsive to antibiotics, or presenting with an abscess, perforation, stricture, or obstruction may require surgical intervention. A localised abscess may be drained under CT/ultrasound guidance, with surgery considered if this fails.\n- Recurrent severe episodes of diverticulitis may necessitate consideration for elective colectomy.\n- For acute rectal bleeding: Haemodynamic stabilisation of the patient should be followed by endoscopic haemostasis. Surgery is an option if bleeding continues despite endoscopy.\n\n# Complications\n\nDiverticular disease can lead to both short and long-term complications:\n\nShort-term complications include:\n\n- Abscess formation: Initially managed with bowel rest, broad-spectrum antibiotics ± CT-guided percutaneous drainage. Surgical management is considered if medical management fails.\n- Perforation: A surgical emergency suspected in cases of generalised peritonitis. Free air on the abdominal x-ray and high clinical suspicion necessitate urgent exploratory laparotomy.\n\nLong-term complications include:\n\n- Fistula formation: Most commonly colovesical fistulas, presenting with pneumaturia, faecaluria, and recurrent UTIs. Diagnosed with cystoscopy or cystography and require surgical repair. Colovaginal, coloenteric, colouterine, and colourethral fistulas may also occur.\n- Fibrosis: Secondary to inflammation, resulting in strictures and large bowel obstruction.",
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"question": "A 80 year old man presents to the accident and emergency department with sudden onset abdominal pain and feeling generally unwell for the last 2 hours. He has no significant past medical history.\n\nAn erect chest x-ray shows free air under the diaphragm, and a CT abdomen/pelvis confirms a bowel perforation.\n\nWhat is the most likely underlying pathology in this patient?",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no link with hepatitis B and oesophageal candidiasis or dysphagia",
"id": "31996",
"label": "d",
"name": "Hepatitis B antigen",
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"votes": 199
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would investigate systemic lupus erythematosus (SLE), which is a cause of dysphagia, but the endoscopy image above clearly shows oesophageal candidiasis, which would not be explained by SLE",
"id": "31995",
"label": "c",
"name": "Anti-nuclear antibodies (ANA)",
"picture": null,
"votes": 1106
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "The endoscopy image above shows a severe case of oesophageal candidiasis. The most common cause of this includes HIV and topical steroid treatment such as steroid inhalers",
"id": "31993",
"label": "a",
"name": "HIV testing",
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"votes": 5047
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would investigate systemic lupus erythematosus (SLE), which is a cause of dysphagia, but the endoscopy image above clearly shows oesophageal candidiasis, which would not be explained by SLE",
"id": "31997",
"label": "e",
"name": "Anti-dsDNA",
"picture": null,
"votes": 594
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would investigate for myasthenia gravis which may be a cause of dysphagia. However, the endoscopy image above shows oesophageal candidiasis",
"id": "31994",
"label": "b",
"name": "Antibodies against acetylcholine receptor (AChR)",
"picture": null,
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"comment": "My thought process: Esophageal dysmotility -> CREST syndrome -> Sclerosis -> Autoimmune -> ANA",
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"comment": "This is undergrad med bro ",
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"createdAt": 1711467455,
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"comment": "For a second i thought this was IBD lmaoo",
"createdAt": 1685120406,
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"explanation": "# Summary\n \n\nCertain diseases are considered clinical indicator diseases for adult HIV infection. Patients that present with these diseases are considered at risk of underlying HIV infection, and are thus routinely tested for HIV infection. Similarly, certain conditions can be complicated by HIV infection, for example pregnancy and TB, so HIV testing is commonplace in these situations. \n \n\n# Who should be offered a HIV test?\n \nAs per NICE & BASHH guidelines, the following groups of patients should be offered a HIV test:\n\n|Classification |Examples |\n|---|---|\n|Increased risk of exposure to HIV |Men who have sex with men; injected drug users; sex workers; people from a country with high seroprevalence; children of HIV-positive mothers; sexual partners of those with HIV |\n|Healthcare services |Sexual health; addiction & substance misuse; antenatal; termination of pregnancy; hepatitis, tuberculosis, lymphoma; chemotherapy & immunosuppression; areas with high HIV seroprevalence |\n| AIDS-defining conditions | Kaposi's sarcoma; Cryptosporidiosis diarrhoea; severe candidiasis; non-Hodgkin lymphoma; cervical cancer; cytomegalovirus; cerebral toxoplasmosis; progressive multifocal leukencephalopathy; pneumocystis pneumonia; mycobacterial diseases |\n|HIV indicator conditions |Oral hairy leukoplakia; exanthema; herpes zoster; seborrhoeic dermatitis; mononucleosis-like illness; anal & cervical dysplasias; viral hepatitis; sexually transmitted infections; pneumonias & invasive pneumococcal disease; chronic/unexplained lymphadenopathy, diarrhoea, renal impairment, neurological symptoms, weight loss |\n \nNB: Repeat tests may be indicated, taking into account the window period. The window period is the time between becoming infected and antibodies appearing - HIV antibodies usually appear 4-6 weeks after infection but can take up to 12 weeks.\n\n\n# NICE guidelines\n \n\n [Click here to see the NICE guidelines on HIV testing](https://cks.nice.org.uk/topics/hiv-infection-aids/diagnosis/asymptomatic-hiv-infection/)\n \n# References\n \n\n [Click here for the BIVA/BASHH guidelines on HIV testing ](https://www.bashhguidelines.org/current-guidelines/hiv/hiv-testing-guidelines-with-bhivabia-2020)",
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"learningPoint": "Oesophageal candidiasis often suggests underlying immunosuppression, such as HIV infection, and individuals presenting with this condition should be tested for HIV.",
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"question": "A 25 year old woman presents with pain in her throat on swallowing. She has no significant past medical history.\n\nShe has an endoscopy which shows the following:\n\n[lightgallery]\n\nWhich of the following blood tests is best to do next in this patient?",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no indication for an ultrasound of the kidneys at present",
"id": "32000",
"label": "c",
"name": "Ultrasound of kidneys",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is only indicated if there is protein in the urine, which there is not",
"id": "32002",
"label": "e",
"name": "Send urine for PCR",
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"__typename": "QuestionChoice",
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"explanation": "There is no need to send this urine for culture if it is negative for nitrites and leukocytes, it is unlikely to be due to an infection",
"id": "32001",
"label": "d",
"name": "Urine culture",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct. This is a simple test to investigate the next most common cause of dysuria in a young female patient",
"id": "31998",
"label": "a",
"name": "Sexually transmitted disease (STD) screen",
"picture": null,
"votes": 5841
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Simpler investigations should first be carried out before referral for consideration of cystoscopy",
"id": "31999",
"label": "b",
"name": "Refer for cystoscopy",
"picture": null,
"votes": 269
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"explanation": "# Candidiasis \n\n\nThe most common cause of Candidiasis is Candida Albicans. This is the causative organism in 85-90% of cases. Candida infection is associated with pregnancy, antibiotic use and immunosuppression. The method of transmission is generally non-sexual.\n\n\n- Symptoms in women include: itching, white curdy discharge, sour milk odour, dysuria, superficial dyspareunia\n\n\n- Examination in women: redness, fissuring, swelling, intertrigo, thick white discharge\n\n\n- Symptoms in men: soreness, pruritis, redness\n\n\n- Examination in men: dry, dull, red glazed plaques and papules\n\n\n# Bacterial Vaginosis \n\n\nBacterial Vaginosis is a bacterial overgrowth, leading to vaginal discharge with an associated fishy odour. This is associated with UPSI and menstruation\n\n\nIn order to diagnose Bacterial Vaginosis, the Amstel criteria are used. Three out of four features are needed to confer a diagnosis:\n\n\n- Vaginal pH >4.5\n- Homogenous grey discharge\n- Whiff test - 10% potassium hydroxide produces fishy odour\n- Clue cells present on wet mount\n\n\nThe treatment of choice is Metronidazole or Clindamycin. The treatment used in pregnancy is Metronidazole.\n\n\n# Trichomoniasis \n\n\nTrichomonas infection is caused by Trichomonas Vaginalis, a flagellated protozoan. Transmission is usually sexual, with an incubation period of around 7 days.\n\n\n- Symptoms in women: can be asymptomatic, but classically profuse, frothy, yellow vaginal discharge. There can also be vulval irritation and dyspareunia present.\n\n\n- Symptoms in men: can cause non gonococcal urethritis, can be asymptomatic\n\n\n- On examination:commonly normal, strawberry cervix is a rare sign\n\n\n- Diagnosis: Direct microscopy and culture\n\n\n- Treatment: Metronidazole (PO state or BD for 7 days), follow up in one week, screen sexual contacts.\n\n\n# Chlamydia \n\n\nChlamydia trachomatis is an obligate intracellular bacterium, responsible for the infection of 1/10 women in the UK. Incubation is less than 4 weeks for men\n\n\n- Asymptomatic infections are common. The most common symptoms in men are urethral discharge and dysuria, with the main symptoms in women being dysuria, inter menstrual bleeding and vaginal discharge. Neonates can be affected with pneumonia and conjunctivitis.\n\n\n- Diagnosis is made by collecting endocervical swab and analysing using the NAAT test, the current investigation of choice. In males, urine and urethral swabs can be collected and analysed in a similar manner.\n\n\n- Treatment is either by using Doxycycline BD for 7 days or Azithromycin 1g single dose. There is no need for a test of cure.\n\n\n# Gonorrhoea \n\n\nNeisseria Gonorrhoeae is a gram-negative diplococcus.\n\n\n- Symptoms in men: asymptomatic, discharge, dysuria, tender inguinal nodes.\n\n\n- Symptoms in women: discharge, dysuria, abnormal bleeding.\n\n\n- Examination may show discharge from the os, Skene's gland or Bartholin's gland.\n\n\n- There can be extra-genital complications,including pharyngitis, rectal pain and discharge and disseminated infection.\n\n\n- Diagnosis is made by microscopy and successful culture.\n\n\n- The current guidance on treatment recommends treatment with both Ceftriaxone and Azithromycin to cover possible Chlamydia co-infection. A test of cure is recommended.",
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"explanation": "Postmenopausal bleeding raises a high suspicion for endometrial cancer. An urgent transvaginal ultrasound is the most useful first-line test to determine endometrial thickness and assess for any uterine abnormality (e.g. fibroids). The ultrasound result would determine the need for further investigation such as endometrial biopsy, blood tests, hysteroscopy or further pelvic imaging",
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"explanation": "# Summary\n \n \nPostmenopausal bleeding is an important symptom that requires thorough investigation due to the potential for serious underlying pathology, such as endometrial cancer. The primary investigations include referral to gynaecology, transvaginal ultrasound, and biopsy of the endometrium. Management strategies will be determined based on the underlying cause of the bleeding. \n \n \n# Definition\n \nPostmenopausal bleeding is any vaginal bleeding that occurs after a patient has not experienced periods for 12 months or more, and who are not receiving hormone therapy. If a woman is receiving hormone replacement therapy (HRT), bleeding is considered postmenopausal if it occurs more than 6 months after menstruation has stopped.\n \n \n# Aetiology\n \nThe most common causes of postmenopausal bleeding include:\n\n* Endometrial atrophy\n* Vaginal atrophy\n* Endometrial polyps\n* Uterine fibroids\n* Endometrial cancer. \n\nOther less common causes include cervical cancer, ovarian tumours and certain medications, such as hormone replacement therapy (HRT) and anticoagulants.\n \n \n# Signs and symptoms\n \n \nFurther symptoms to postmenopausal bleeding will depend on the underlying cause, but may include pelvic pain, weight loss, and systemic symptoms of malignancy.\n \n \n# Differential Diagnosis\n \n \n - **Endometrial cancer:** Often the only symptom is postmenopausal bleeding.\n - **Vaginal atrophy:** Can also cause pruritus, dyspareunia, and vaginal discharge.\n - **Cyclical combined HRT:** Causes regular vaginal bleeding. With continuous HRT, it is common to experience breakthrough bleeding in the first 6 months.\n - **Bleeding disorders:** May be suggested if there is frequent bleeding elsewhere (e.g. recurrent epistaxis) or a family history of a bleeding disorder.\n \n \n# Investigations\n \nAll cases of postmenopausal bleeding should be referral to gynaecology under the 2-week wait pathway. \n\nThe gynaecologist will likely consider the following investigations: \n\n**Bedside:**\n\n- Bimanual and speculum examination\n\n**No blood tests** are required for diagnosis in the first instance, though if underlying bleeding/clotting disorders are suspected a clotting screen would be indicated. \n\n**Imaging:**\n\n - Transvaginal ultrasound to look for abnormal thickening of the endometrium\n - CT CAP: performed following diagnosis of endometrial cancer, for FIGO staging \n\n**Special tests:**\n\n - Biopsy of the endometrium, obtained via hysteroscopy or pipelle\n\n**2 Week Wait Criteria**\n\n- All cases of postmenopausal bleeding in women aged 55 or older should be referred to gynaecology under a 2-week wait. \n\n- In women aged under 55, a 2-week wait referral should also be considered.\n\n- For those not referred in the immediate instance who have a TV USS performed, refer under 2-week wait if endometrial thickness is >4mm, or if otherwise high clinical suspicion of endometrial cancer remains. \n\n \n# Management\n \n \nThe management of postmenopausal bleeding is guided by the underlying cause. This may include hormonal therapy for conditions such as endometrial atrophy, surgical interventions for polyps or cancers, or supportive care for symptoms related to vaginal atrophy. In all cases, ongoing monitoring is essential to ensure that treatment is effective and to detect any changes in the patient's condition.\n\n\n# NICE Guidelines\n\n[Click here for NICE guidelines on Gynaecological Cancers](https://cks.nice.org.uk/topics/gynaecological-cancers-recognition-referral/)\n\n# References\n\n[Patient Info: Postmenopausal bleeding](https://patient.info/doctor/postmenopausal-bleeding)",
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"question": "A 65 year old woman comes into A&E with a 2 week history of bloody spotting on her underwear. She is surprised to find this as she went through menopause 15 years ago. She has been married to her husband of 25 years and has no children. Past medical history includes type 2 diabetes and obesity.\n\nWhat is the next best investigation?",
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"explanation": "Methotrexate is utilised for medical management of ectopic pregnancy under specific circumstances where the patient is haemodynamically stable. This patient is unstable and would therefore not be suitable for medical management",
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"explanation": "Ectopic pregnancy may result in hypovolaemia secondary to blood loss. A blood transfusion may be considered if there is a large volume of blood loss with a significant drop in haemoglobin. Bloods should be sent off for group and save, and 2-4 units crossmatched. However, in the acute setting, the patient should be resuscitated with IV fluids first",
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"comment": "surely give blood in preference to crystalloids (replace like for like) - your explanation says could transfuse if there is significant blood loss which this patient (SBP of 75) obviously has! I get in reality fluids more available but best theoretical answer is surely give O neg",
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"comment": "laparoscopy no more definitive its tvus",
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"comment": "I understand that we still do fluid first, but how do we know that this isn't ruptured?",
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"comment": "Group and save and crossmatch takes timme, followed by setting up transfusion. fluids are faster. (though in reality both would be done in clinical practice) ",
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"explanation": "# Summary\n \n \nEctopic pregnancy is a gynaecological emergency, referring to a fertilised ovum that has implanted anywhere outside the endometrial cavity. This may present with pelvic pain, shoulder tip pain, abnormal vaginal bleeding, and haemodynamic instability if ruptured. Diagnosis is confirmed by positive pregnancy test and a transvaginal ultrasound that has located the pregnancy outside the uterine cavity. Management strategies include conservative management, medical management with methotrexate, and surgical management, the choice of which depends on the patient's presentation and level of risk.\n \n \n \n# Definition\n \nAn ectopic pregnancy refers to a fertilised ovum that has implanted outside the endometrial cavity, usually in the fallopian tubes. This is a gynaecological emergency. \n \n \n \n \n# Epidemiology\n\n \nThe estimated incidence of ectopic pregnancies in the UK is 1.1%. The risk is higher in women with a history of pelvic inflammatory disease, genital infection, pelvic surgery, an intrauterine device in situ, assisted reproduction, previous ectopic pregnancy, or endometriosis.\n \n \n \n \n# Aetiology \n \n \nEctopic pregnancy usually presents in the 6-8th week of pregnancy, but can occur earlier or later. They can occur anywhere outside the endometrial cavity, but most commonly in the fallopian tube. \n\nRisk of an ectopic increases with conditions that impair the passage of a fertilised egg into the uterine cavity, or with conditions that cause the fertilised egg to implant prematurely. However, most ectopics are not associated with any risk factor. \n \nSpecific risk factors include: \n \n - Pelvic inflammatory disease and previous STIs\n - Pelvic surgery\n - Having an intrauterine device e.g. copper coil or Levonorgestrel-releasing intrauterine system (e.g. Mirena) in situ\n - Assisted reproduction e.g. IVF\n - Previous ectopic pregnancy\n - Endometriosis\n \n \n \n# Signs and Symptoms\n \nClinical features of ectopic pregnancy may include:\n \n \n - Pelvic pain, which may be unilateral to the side of the ectopic\n - Shoulder tip pain - If the ectopic pregnancy bleeds, the blood can irritate the diaphragm causing shoulder tip pain\n - Abnormal vaginal bleeding e.g. missed period or intermenstrual bleeding\n - Haemodynamic instability caused by blood loss if the ectopic ruptures, resulting in syncope/fainting\n - Abdominal examination may reveal unilateral tenderness\n - Cervical tenderness (chandelier sign) on bimanual examination\n \n \n# Differential Diagnosis\n\n1. **Miscarriage:** will also present with bleeding following a positive pregnancy test. However, less likely to have shoulder tip pain, beta-hCG levels will not be as high as in an ectopic (and will fall), and TV USS may show intrauterine pregnancy (if not yet completely expelled). \n\n\n2. **Pelvic inflammatory disease:** presents with abdominal pain and cervical tenderness, and may have bloody vaginal discharge. However, pregnancy test will be negative and inflammatory markers raised. Can be confirmed with positive swab. \n\n\n3. **Ovarian torsion:** also presents with abdominal pain, usually unilateral. Less likely to present with vaginal bleeding and will have negative pregnancy test. \n\n# Investigations\n \nThe investigations for ectopic pregnancy include:\n\n**Bedside**\n\n- Pregnancy test (to confirm pregnancy) \n\n \n**Bloods**\n\n* FBC (check for anaemia)\n* Serum beta-hCG (will help guide management)\n\n**Imaging**\n\n - Transvaginal ultrasound (to locate the pregnancy)\n \n \n# Management\n \n \nThere are three management options for ectopic pregnancy:\n \n \n **Conservative:**\n \n \n - This is an option for a small number of women with an ectopic pregnancy who have minimal or no symptoms, who are considered low risk (usually because there is a plateau or drop in beta-hCG levels indicating self-resolution of the ectopic). \n - These patients require close follow-up with serial repeat b-hCG tests. If the levels do not decrease at a satisfactory rate, medical/surgical management is recommended.\n \n \n**Medical:**\n \n \n - Involves administration of a one-off dose of methotrexate\n - Criteria for methotrexate treatment include: \n - No significant pain\n - Low hCG level (below 1500 IU/L)\n - Unruptured ectopic pregnancy measuring below 35mm and with no visible heartbeat\n - Ability to attend follow-up\n - Adherence to avoiding pregnancy for a period following treatment\n - No intrauterine pregnancy (confirmed on an ultrasound scan). \n - If the initial dose of methotrexate fails to treat the ectopic pregnancy, a second dose of methotrexate or surgical management may be indicated\n \n\n**Surgical:**\n \n - Recommended as first-line option if: \n - Patient is unable to attend follow-up\n - Serum hCG level of 5000 IU/L or higher \n - Adnexal mass of 35mm or greater\n - Foetal heartbeat is visible on ultrasound scan\n - Patient is in significant pain\n - Patient is haemodynamically unstable\n - Also offered second line in cases where medical manamgement has failed \n - The preferred surgical management is a **salpingectomy**, where the fallopian tube containing the ectopic pregnancy is removed. For patients with only one patent fallopian tube (e.g. due to previous PID or ectopic, or past removal of a fallopian tube), a **salpingotomy** may be performed instead, where only the ectopic pregnancy is removed and the ends of the fallopian tube are re-attached. \n - There is a risk with salpingotomy that not all the tissue may have been removed, and so serial serum b-hCG measurements are performed to exclude any remaining trophoblastic tissue within the fallopian tube\n - Offer **anti-D immunoglobulin** to all rhesus-negative women who have had surgical management of ectopic pregnancy. \n \n\n**Borderline Cases: Choosing Between Medical and Surgical Management**\n\n* There are some women who may be offered a choice of either methotrexate or surgical management as first-line.\n* This applies to women who: \n * Have a serum hCG level between 1500 IU/L and 5000 IU/L\n * Are able to return for follow up\n * Have no significant pain\n * Have an unruptured ectopic pregnancy with an adnexal mass smaller than 35 mm with no visible heartbeat.\n * Have no intrauterine pregnancy (confirmed on an ultrasound scan). \n \n\n# NICE Guidelines \n \n [Click here for NICE CKS on ectopic pregnancy ](https://cks.nice.org.uk/topics/ectopic-pregnancy/) \n \n# References\n\n\n[NHS UK - Ectopic pregnancy](https://www.nhs.uk/conditions/ectopic-pregnancy/)\n \n[Patient Info - Ectopic pregnancy](https://patient.info/doctor/ectopic-pregnancy-pro)",
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"explanation": "# Summary\n\nThe International Normalised Ratio (INR) is a measure of blood coagulation, typically monitored in patients on anticoagulant therapy. High INR can result from an overdose of anticoagulant medication, drug interactions, dietary changes, and medical conditions such as liver failure or infection. The assessment of high INR includes a thorough patient history, complete blood count, and clotting screen. Management strategies are determined by the presence of active bleeding and the INR level, with a general focus on withholding anticoagulants and administering vitamin K. Re-evaluation of patient compliance and understanding of dosage regimens is also crucial.\n\n# Definition\n\nInternational normalised ratio (INR) is a measure of blood coagulation and is commonly monitored in patients on warfarin at high risk of thromboembolic events (e.g. those with prosthetic heart valves, atrial fibrillation, or those being treated for a thromboembolic event (e.g. DVT or PE).\n\n# Causes \n\n- Overdose of anticoagulant medication\n- Drug interaction (e.g. antibiotics, antifungals, Aspirin, Amiodarone)\n- Herbal products\n- Increase in alcohol consumption\n- Decrease in consumption of foods containing vitamin K\n- Liver failure\n- Infection\n\n# Assessment\n\n- History\n - Dosing history of anticoagulant\n - Concurrent illness\n - Change in medications\n - Change in diet/lifestyle (including alcohol and tobacco use)\n - History of any falls/injuries\n - History of blood loss\n - Haemoptysis\n - Haematemesis\n - Melaena\n - Bleeding from the gums\n- Examination\n \t- Evidence of bleeding\n - Overt blood loss\n - Bruising\n- Bloods\n - Full blood count to check for concurrent anaemia, signs of infection\n - Clotting screen to check for other clotting abnormalities\n\n\n# Management of high INR\n\nManagement depends on the presence of active bleeding and INR level.\n\nIf concerned regarding head injury and intracranial haemorrhage, consider CT head.\n\n- Major bleeding\n - Stop anticoagulants\n - Administer IV vitamin K\n - Administer prothrombin complex (preferred to FFP)\n- Minor bleeding\n - Stop anticoagulants\n - Administer IV vitamin K\n - Repeat INR after 24 hours, may need further vitamin K\n- No bleeding with INR > 8\n - Stop anticoagulants\n - Administer IV or oral vitamin K\n - Repeat INR after 24 hours\n- No bleeding with INR > 5\n - Withhold 1-2 doses of anticoagulant\n - Review maintenance dose of anticoagulant\n\nIt is important to also assess compliance and ensure the patient understands their dosing regime.\n\n# NICE Guidelines\n\n- [NICE Treatment Summary: Oral anticoagulants](https://bnf.nice.org.uk/treatment-summary/oral-anticoagulants.html)\n- [NICE British National Formulary (BNF): Warfarin Sodium](https://bnf.nice.org.uk/drug/warfarin-sodium.html)\n",
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"explanation": "This is a rare cause of anaemia in rheumatoid arthritis. This is unlikely as reticulocyte count is not raised",
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"explanation": "This is a common cause of anaemia in rheumatoid arthritis patients. This would typically present as normochromic normocytic anaemia",
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"explanation": "# Summary \n\nMacrocytic anaemia is a type of anaemia characterized by the presence of larger-than-normal red blood cells (RBCs). It can be classified into megaloblastic and non-megaloblastic types. Megaloblastic anemia is primarily associated with impaired DNA synthesis, often due to deficiencies in vitamin B12 or folate, leading to the enlargement of RBC precursors and hypersegmented neutrophils on blood film. Non-megaloblastic macrocytic anaemia can be caused by various factors, and sometimes a patient may present with non-megaloblastic macrocytosis, without anaemia such as in pregnancy. Key investigations include FBC, blood film and measurement of specific vitamins such as folate and B12, and management centres on the underlying cause of the anaemia. For example, vitamin supplementation in B12/folate deficiency.\n\n\r\n# Definition\n\nMacrocytic anaemia refers to a condition in which red blood cells are larger than normal. It can be further classified into two main categories: megaloblastic and non-megaloblastic. Megaloblastic macrocytic anaemia is characterized by slow or impaired DNA synthesis, leading to delayed maturation of RBCs and, notably, hypersegmented neutrophils on blood film. Non-megaloblastic macrocytic anaemia may manifest as macrocytosis without the presence of anaemia.\n\n\n\r\n# Epidemiology \n\nThe epidemiology of macrocytic anaemia varies depending on the underlying cause. Megaloblastic macrocytic anaemia is often associated with vitamin B12 or folate deficiencies and is more prevalent in older adults. Non-megaloblastic macrocytic anaemia, on the other hand, can occur at any age and may be linked to factors such as alcohol consumption or pregnancy.\n\n\r\n# Classification\n\nMorphologically, macrocytic anaemia is usually typified by large RBCs due to abnormal RBC development, giant metamyelocytes and hypersegmented neutrophils (in the peripheral circulation). Macrocytic anaemia may be megaloblastic or non-megaloblastic.\n\n## Causes of megaloblastic anaemia \n\n* **B<sub>12</sub> deficiency** \n * reduced intake (eg. dietary) \n * reduced absorption (eg. pernicious anaemia, inflammatory bowel disease, gastrectomy)\n* **Folate deficiency**\n* Drugs\n * hydroxycarbamide (previously called hydroxyurea)\n * azathioprine\n * cytosine arabinoside\n * azidothymidine\n\n\n## Causes of non-megaloblastic/normoblastic macrocytic anaemia\n\n* Liver disease\n* Alcohol \n* Hypothyroidism\n* Myelodysplastic syndrome\n* Hypothyroidism\n* Pregnancy (usually a mild macrocytosis)\n\n\r\n# Signs and Symptoms \n\n- Fatigue and Weakness\n- Pallor\n- Shortness of Breath\n- **Glossitis and \"Beefy Tongue\":** A distinctive sign of megaloblastic anaemia, glossitis, is the inflammation of the tongue, giving it a swollen and reddened appearance, often referred to as a \"beefy tongue.\"\n- **Neurological Symptoms:** Severe vitamin B12 deficiency can affect the nervous system, leading to neurological symptoms such as paresthesias (tingling and numbness), ataxia (impaired coordination), and cognitive impairment.\n- Symptoms of associated conditions:\n\t- **Autoimmune Conditions:** Megaloblastic anemia, particularly pernicious anemia, is associated with autoimmune conditions such as autoimmune thyroid disease, type 1 diabetes, and autoimmune gastritis. Therefore, patients may present with features of these conditions.\n\t- **Hypothyroidism Symptoms:** In cases where megaloblastic anaemia is secondary to hypothyroidism, patients may exhibit classic hypothyroidism symptoms like fatigue, weight gain, cold intolerance, and changes in skin and hair.\n\n# Differential Diagnosis\n\n\n- **Megaloblastic Anaemia (Vitamin B12 or Folate Deficiency):** The primary differential diagnosis within the realm of macrocytic anaemia is megaloblastic anaemia, specifically caused by vitamin B12 or folate deficiency. Careful evaluation of vitamin levels, clinical symptoms, and peripheral blood smears can aid in the distinction.\n\n- **Non-Megaloblastic Macrocytic Anaemia:** Macrocytosis, without the typical features of megaloblastic anemia, may result from various non-megaloblastic causes, including alcohol consumption, liver disease, or pregnancy. These cases may present as isolated macrocytosis without the broader clinical picture of anaemia.\n\n- **Haemolysis:** Haemolytic anaemias, both inherited and acquired, can lead to an increase in reticulocyte count and macrocytosis, albeit for different reasons. Evaluating markers of haemolysis, such as elevated bilirubin levels or increased lactate dehydrogenase, can assist in distinguishing haemolytic anaemias from megaloblastic anaemias.\n\n- **Liver Disease:** Patients with liver disease, particularly alcohol-related liver disease, can exhibit macrocytosis. Evaluation of liver function tests and consideration of underlying liver pathology is necessary in such cases.\n\n- **Medications:** Certain medications, such as antiretroviral drugs and chemotherapy agents, can cause macrocytosis. A thorough medication history is important in identifying potential drug-induced macrocytosis.\n\n- **Bone Marrow Disorders:** In rare cases, macrocytic anaemia can be associated with underlying bone marrow disorders, including myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPNs). A bone marrow biopsy may be warranted to evaluate these conditions.\n\n\r\n\r\n# Investigations \n\n* Investigations all patients should have include:\n\t* Full Blood Count (FBC): This reveals anaemia and macrocytosis. The presence of hypersegmented neutrophils in the blood film is characteristic of megaloblastic anemia.\n\t* Haematinics: Serum vitamin B12 and folate levels should be assessed to identify deficiencies.\n\t* Blood Film: A peripheral blood smear can show macrocytosis and the presence of hypersegmented neutrophils.\n* Specific tests to investigate for underlying causes include:\n\t* TFTs to look for hypothyroidism\n\t* LFTs to assess liver function\n\t* Antibodies to intrinsic factor +/- gastric parietal cells, seen in pernicious anaemia\n\t* Markers of haemolysis - bilirubin, DAT testing, LDH\n\n# Management\n\n* **Megaloblastic Anaemia:** In pernicious anemia, intramuscular hydroxocobalamin is typically administered to replace vitamin B12. \n* It is important to address vitamin B12 deficiency before folate replacement (if both are deficient) to avoid exacerbating neurological symptoms and precipitating subacute degeneration of the spinal cord (SACD). \n* In cases of folate deficiency, oral folate supplements are provided.\n* **Non-Megaloblastic Anaemia:** The management of non-megaloblastic macrocytic anemia depends on the underlying cause, such as addressing alcohol consumption or providing support during pregnancy.\n\n# NICE Guidelines\n\n[NICE CKS - B12/Folate-deficiency anaemia](https://cks.nice.org.uk/topics/anaemia-b12-folate-deficiency/)\r\n\r\n\n\n",
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"question": "A 70 year old lady is admitted with an acute polyarthritic flare of her hands and knees. She has a past medical history of rheumatoid arthritis and migraines. Her regular medications include methotrexate, prednisolone and ibuprofen.\n\n\nBloods on admission are as follows:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|101 g/L|(M) 130 - 170, (F) 115 - 155|\n|Platelets|400x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|108 fL|80 - 96|\n|Ferritin|170 μg/L|12 - 200|\n|Iron|20 μmol/L|(M) 14 - 31, (F) 11 - 30|\n|Transferrin saturation|28 %|(M) 16 - 50 (F) 16 - 40|\n\n\n - White cell count and neutrophils normal\n - Reticulocyte count normal\n\n\nWhat is the most likely cause of her anaemia?",
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"explanation": "Effective pain control is key in the management of acute chest crises. Opioid analgesia can be started and titrated according to the pain ladder",
"id": "32028",
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"explanation": "This patient has a productive cough and acute chest crisis in the context of sickle cell anaemia. Recommended treatment in acute chest crises would be intravenous broad spectrum empiric coverage with a third generation cephalosporin for bacterial coverage and a macrolide for atypical organism cover",
"id": "32032",
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"explanation": "This may be considered later down the line if the patient is failing to maintain oxygen saturations on increasing levels of oxygen. Frequent oxygen monitoring, incentive spirometry and arterial blood gases should be done to monitor progression in such patients",
"id": "32031",
"label": "d",
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"comment": "Typical exam question, where every option seems right...",
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"comment": "stem doesn't exclude infections cause does it ? \n",
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"comment": "no, it doesn't. You would definitely give an abx, but not oral as the last answer suggests - IV.",
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"explanation": "# Summary\n\nSickle cell anaemia (SCA) is an autosomal recessive condition in which a point mutation in the beta chain on chromosome 11 leads to the production of HbS (rather than HbA). HbS polymerises when deoxygenated leading to sickled red blood cells. These cells are fragile and sticky, causing vaso-occlusive crises leading to pain and ischaemia of vital organs. The most common acute presentation is painful vaso-occlusive crises, while the most dangerous is acute chest crises. Diagnosis is typically made postnatally in the UK via a national screening programme but otherwise presents with progressive anaemia in early life. Investigations may reveal microcytic anaemia with variable degrees of haemolysis, and a definitive diagnosis is achieved with haemoglobin electrophoresis +/- genetic testing. Management strategies include high-flow oxygen, IV fluids and analgesia for acute crises, hydroxycarbamide, regular exchange transfusions, vaccinations and antibiotics for chronic disease management.\n\n# Definition\n\nSickle cell anaemia (SCA) is a genetic condition where normal haemoglobin (where variable HbS is present) tends to form abnormal haemoglobin molecules (HbS) upon deoxygenation leading to distortion of RBCs.\n\n# Epidemiology\n\nSickle cell disease is common among individuals of Central and West African descent, where having the carrier (trait) status confers some protection against malaria. \n\n# Pathophysiology \n\n- HbS is produced when the glutamic acid at the 6th position of the β chain is replaced by valine \n- In its deoxygenated state, HbS undergoes polymerisation, forming crystals that cause polymers to form, which in turn leads to the development of RBCs with a sickle shape \n- The abnormal shape of the RBCs causes clotting in the microvasculature, which precipitates vaso-occlusive crises, leading to ischaemia of vital organs and pain\n- Deformation of the RBCs leads to chronic haemolysis, which decreases the body's nitric oxide – typically needed for vasoregulation – and this leads to chronic complications such as pulmonary hypertension and leg ulcers\n\n## Inheritance \n\n- Sickle cell anaemia (HbSS) is an autosomal recessive condition. The most predominant and most severe form, homozygous HbS, represents just one of the sickle cell disease syndromes.\n- Other forms of sickle cell disease involve the coinheritance of HbS with other haemoglobin variants.\n - Most commonly HbC or β-thalassaemia, leading to the HbSC or HbS-βthal forms of sickle cell disease.\n\n## Mechanism of hyposplenism\n\nIn addition, sickled red cells commonly sequester in the spleen, where they undergo phagocytosis by the reticular endothelial system, leading to extravascular haemolysis\n\n- Initially, this leads to splenic congestion and splenomegaly\n- This is followed by splenic infarction, leading to hyposplenism\n- Because of splenic compromise, there is reduced immune function \n - Individuals with sickle cell disease are prone to bacteraemia – the spleen is necessary for phagocytosis of encapsulated bacteria. This means there is vulnerability to encapsulated organisms such as Haemophilus influenzae type B.\n - Affected individuals should have up to date vaccinations for S. pneumoniae, H. influenzae B and N. meningitidis.\n\n\n# Signs and Symptoms\n\n## Vaso-occlusive crises\n\nPainful vaso-occlusive crises are the most common acute presentation of sickle cell anaemia\n\n- Primarily caused by microvascular obstruction due to RBC sickling and inflammation\n- May be triggered by local hypoxia (eg. in cold weather)\n\n## Acute chest crisis\n\nAcute chest crises are the most dangerous acute presentation\n\n- 3% mortality rate, causing 25% of sickle cell-related deaths \n- The cause is often unknown (maybe infectious)\n- Patients present with tachypnoea, wheeze, and cough, with hypoxia and pulmonary infiltrates on chest X-ray\n\n## Other complications \n\n- Splenic infarction and subsequent immunocompromise\n- Sequestration crisis\n- Osteomyelitis\n- Stroke\n- Dactylitis\n- Poor growth\n- Chronic renal disease\n- Gallstones\n- Retinal disorders\n- Priapism\n- Pulmonary fibrosis and pulmonary hypertension\n- Iron overload from repeated blood transfusions\n- Red cell aplasia (due to parvovirus B19 infection in the presence of chronic haemolytic anaemia)\n\n**Clinical severity** is highly variable: some patients have few symptoms; others have severe and frequent crises, haemolytic anaemia and end-organ damage\n\n- This is due to a range of factors such as the amount of HbF (foetal haemoglobin) – higher levels of HbF reduce the severity of clinical complications\n- Patients with Hb SC disease have milder anaemia and suffer fewer crises than people with Hb SS disease \n- Patients with Hb SC disease are however more prone to sickle cell retinopathy \n - Ophthalmological review is needed annually for all patients with Hb SC disease\n\n# Investigations\n\n- Bedside - peak flow, which is essential for monitoring patients with chest crisis\n- **FBC** may show microcytic anaemia with variable degrees of haemolysis \n - Reticulocytosis and unconjugated hyperbilirubinemia may be noted\n\n- Typical **blood film** findings include: \n - characteristic sickle cells\n - target cells\n - reticulocytosis with polychromasia \n - features of functional hyposplenism (Howell–Jolly bodies, nucleated red cells)\n\nDefinitive diagnosis is with **haemoglobin electrophoresis** +/– genetic testing. However, many labs use high-performance liquid chromatography (HPLC) and/or isoelectric focusing (IEF) instead of HB electrophoresis. \n\n[lightgallery]\n\n## Screening for sickle cell disease\n\n- Sickle cell disease in the UK is typically diagnosed postnatally (by the national screening programme)\n- Additionally, all patients of African or Caribbean descent should have a sickle cell test prior to surgery \n- Otherwise, it can present with progressive anaemia in early life when levels of foetal haemoglobin (which contains γ-chains) fall and are replaced by HbS (containing the variant β-globin)\n\n# Management \n\n## Acute sickle cell crisis\n\nTreatments include: \n\n- High-flow oxygen \n- IV fluids and analgesia\n- Top-up transfusions – required in some severe cases\n\nNote: ABO-compatible red cells matched for Rhesus and Kell antigens should be given as this will inhibit the development of antibodies that can otherwise complicate future transfusions.\n\n\n## Chronic sickle cell disease\n\n* **Hydroxycarbamide** if frequent crises occur\n * Increases foetal haemoglobin concentrations – needs to be balanced with risks of marrow suppression, reduced fertility and risk of teratogenicity\n\n* Alternatively regular exchange transfusions may be required for frequent sickle cell crises, acute chest syndrome, priapism and stroke prevention \n* **Vaccinations** and **antibiotic prophylaxis** – in view of hyposplenism and subsequent immunocompromise\n* Newer therapies include: \n * crizaniluzumab (p-selectin inhibitor) for treatment of pain crises \n * voxelotor (haemoglobin oxygen-affinity modulator) for haemolytic complications\n\n* Bone marrow transplant and gene-editing techniques are now becoming possible curative options for some patients\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on sickle cell](https://cks.nice.org.uk/topics/sickle-cell-disease/)",
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"question": "A 19 year old male is admitted with a 1 day history of sudden onset severe chest pain and productive cough. He has a known history of sickle cell disease.\n\nVitals on admission:\n\n- T 38.5°C\n- BP 100/60\n- Pulse 105\n- Respiratory rate 25\n- SpO<sub>2</sub> 98% on 4L oxygen\n\nCXR reveals bilateral lower zone shadowing. What is the next best step?",
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"explanation": "This may be useful in evaluating for malignancy or metastatic lesions, which is less likely given the 2 week history of constitutional symptoms",
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"explanation": "This may be useful to evaluate for stroke, however the patient is likely to have experienced a transient ischaemic attack and the scan would most likely be unremarkable in the absence of any lasting neurological deficits. Cerebral infarcts may be one of the complications of infective endocarditis, but this investigation would not help in confirming the underlying diagnosis",
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"comment": "Lord have mercy",
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"comment": "This is total BS, if he has a prosthetic valve one can assume that he is on anticogulants and thus a TIA needs to be investigated with a CT to exclude hemorrhage.. ",
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"comment": "Wrong. PET looks at cellular activity. Please spend more time on the wards.",
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"comment": "Can someone explain why you would do a trans-oesophageal echo in this patient as opposed to the normal transthoracic echo?",
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"explanation": "# Summary\r\n\r\nInfective endocarditis (IE) is a rare infection of the inner surface of the heart (endocardium), usually the valves. Various risk factors contribute to its development, including age, sex, intravenous drug use, poor dentition, valvular disease, congenital heart disease, prosthetic valves, and certain medical conditions like HIV. Symptoms can be diverse and non-specific including fevers, night sweats, weight loss, and myalgia. Diagnosis is based on the modified Duke Criteria, which include major and minor criteria. Treatment involves prolonged courses of intravenous antibiotics, and surgical intervention may be necessary in certain cases. Complications can be severe, and without appropriate treatment, IE can lead to heart failure and death. Prevention through antibiotic prophylaxis is no longer recommended.\r\n\r\n# Definition \r\n\r\nInfective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves. \r\n\r\n# Epidemiology \r\n\r\nInfective endocarditis is a rare disease, impacting approximately 2-6 per 100,000 people every year. There are many risk factors implicated in the development of IE. \r\n\r\nRisk factors for IE: \r\n\r\n* Age >60 years\r\n* Male sex\r\n* IVDU: predisposition to _Staph. aureus_ infection and right-sided valve disease e.g. tricuspid endocarditis.\r\n* Poor dentition and dental infections\r\n* Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. \r\n* Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.\r\n* Prosthetic valves\r\n* Previous history of infective endocarditis\r\n* Intravascular devices: central catheters and shunts.\r\n* Haemodialysis\r\n* HIV infection\r\n\nAntibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. However, the evidence for this is inconclusive, and **NICE therefore do not advise antibiotic prophylaxis for IE.**\r\n\r\n# Pathophysiology\r\n\r\nA damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis. \r\n\r\n# Classification \r\n\r\nIE can be considered according to different classification systems. \r\n\r\n## Acute vs. Subacute vs. Chronic IE \r\n\r\nIE can be considered according to duration of symptoms. \r\n\r\n* *Acute IE*: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to *S.aureus* infection. \r\n* *Subacute IE*: patients has signs or symptoms for 6 weeks up to 3 months. \r\n* *Chronic IE*: patients has signs or symptoms that persist for longer than 3 months. \r\n\r\n## Valve Type \r\n\r\nIE can be considered according to the type of valve involved. \r\n\r\n- *Native-valve endocarditis*: patient without prosthetic valve implant. \r\n- *Prosthetic-valve endocarditis*: \r\n\t- Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. \r\n\t- Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections. \r\n\r\n# Common organisms \r\n\r\nThe most common organisms involved in infective endocarditis (in order of incidence) are:\r\n\r\n* _Staph. aureus_: now the most common cause of IE. Coagulase positive.\r\n* _Strep. viridans_: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. \r\n* Enterococci\r\n* Coagulase negative _staphylococci_ e.g. _staph. epidermidis_: common culprit of prosthetic valve endocarditis. \r\n* _Strep. bovis_: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.\r\n* Fungal \r\n* HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. \r\n* Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE). \r\n\r\n# Symptoms\r\n\r\nClinical features of IE are diverse and variable. It may present acutely with a rapid deterioration or it can present subacutely/chronically with non-specific symptoms. \r\n\r\n* Common presenting symptoms: \r\n\t* Fever: most common symptom. \r\n\t* Night sweats \r\n\t* Anorexia \r\n\t* Weight loss \r\n\t* Myalgia\r\n\r\n* Others: \r\n\t* Headache \r\n\t* Arthalgia\r\n\t* Abdominal Pain \r\n\t* Cough \r\n\t* Pleuritic pain \r\n\r\n# Signs\r\n\r\n**Systemic signs**: \r\n\r\n* Febrile \r\n* Cachectic \r\n* Clubbing\r\n* Splenomegaly \r\n\r\n**Cardiac**: \r\n\r\n* Murmur: fever + new murmur is infective endocarditis until proven otherwise. \r\n* Bradycardia: aortic root abscess tracks down to the AVN causing heart block. \r\n\r\n**Vascular phenomena**: \r\n\r\n* Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. \r\n* Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. \n* Splinter haemorrhages\r\n\r\n**Immunological phenomena**: due to immune-complex deposition. \r\n\r\n* Osler's nodes: painful pulp infarcts on end of fingers. \r\n* Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. \r\n* Glomerulonephritis: identified on urine dip. \r\n\r\n# Differential Diagnoses\r\n\r\n* Non-infectious endocarditis/Nonbacterial thrombotic endocarditis (NBTE)\r\n\t* Similarities: both present with new murmurs and both may have constitutional symptoms including fevers and weight loss. \r\n\t* Differences: blood cultures will likely be positive in infective endocarditis and may identify microorganisms that are commonly associated with IE. NBTE is often associated with advanced malignancy (pancreatic cancer and marantic endocarditis), SLE (Libman Sacks endocarditis) or hypercoagulable states and will not have positive blood cultures. \r\n\r\n* Rheumatic Fever\r\n\t* Similarities: may both present with similar symptoms including fever, heart murmur and joint pain. \r\n\t* Differences: rheumatic fever is an autoimmune response triggered by a Group A strep infection and ASOT titres may be high. In comparison, infective endocarditis will likely have positive blood cultures that identify a particular micro-organism. \r\n\r\n\r\n# Modified Duke Criteria \r\n\r\nFor the diagnosis of IE, the modified Duke Criteria needs to be followed. \r\n\r\nA useful mnemonic to remember the criteria is **'BE FIVE PM'**:\r\n\r\n* Major Criteria: \r\n\t* **B**lood Cultures\r\n\t* **E**vidence of Endocardial Involvement: **E**cho\r\n\r\n* Minor Criteria: \r\n\t* **F**ever\r\n\t* **I**mmunological phenomena\r\n\t* **V**ascular phenomena\r\n\t* **E**chocardiogram minor criteria\r\n\t* **P**redisposing features\r\n\t* **M**icrobiological evidence that does not meet major criteria. \r\n\r\nFor a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present. \r\n\r\n## Major Criteria \r\n\r\n**Blood culture positive for IE**\r\n\r\n* 2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). \r\n* Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). \r\n* Single positive blood culture for Coxiella burnetti or positive antibody titre\r\n\r\n**Evidence of endocardial involvement with imaging positive for IE**\r\n\r\n* Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. \r\n* Abnormal activity around site of prosthetic valve implantation on PET-CT\r\n* Paravalvular lesions on cardiac CT\r\n\r\n## Minor Criteria \r\n\r\n* **Fever**: >38.0 degrees celsius. \r\n* **Immunological phenomena**: Roth spots, Olser's nodes, immune complex-mediated glomerulonephritis, positive rheumatoid factor.\r\n* **Vascular phenomena**: Evidence of septic embolis (splenic infarct/abscess), Janeway lesions, conjunctival haemorrhages, mycotic aneurysm, intracranial haemorrhage. \r\n* **Echocardiogram minor criteria**: not meeting above criteria. \r\n* **Predisposing features**: known valvular disease, IVDU, prosthetic valves etc. \r\n* **Microbiological evidence that does not meet major criteria**: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE\r\n\r\n# Investigations\r\n\r\nBedside:\r\n\r\n- **ECG**: increasing prolongation of PR interval suggests development and worsening of aortic root abscess. \n- **Urine dip**: look for haematuria which may suggest development of glomerulonephritis. \r\n\r\nBlood tests:\r\n\r\n- **Routine bloods**: significant elevation of inflammatory markers and acute phase response is in line with infective endocarditis. If subacute/chronic process there may be a normocytic anaemia. \r\n- **Blood cultures**: required as per the modified Duke criteria. At least 3 sets of blood cultures taken at different times and sites. \r\n\r\nImaging:\r\n\r\n- **Echocardiogram**: \r\n\t* **1st line**: transthoracic echocardiogram \r\n\t* **2nd line**: transoesophageal echocardiogram; more invasive, but better view of mitral valve lesions and aortic root abscesses. It is the most sensitive diagnostic test. \r\n- **PET CT**: used to look for evidence of septic emboli. \r\n\r\n# Management\r\n\r\n## Medical \r\n\r\nMainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term. \r\n\r\nExamples of antibiotic choice demonstrated below: \r\n\r\n**Blind Therapy** when the organism and sensitivities are not yet known: \r\n\r\n* Native valve: amoxicillin (+/- gentamicin) \r\n* Pen-allergy/MRSA: vancomycin (+/- gentamicin) \r\n* Prosthetic valve: vancomycin + rifampicin + gentamicin \r\n\r\n**Native Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin \r\n* 2nd line: vancomycin + rifampicin \r\n\r\n**Prosthetic Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin + rifampicin + gentamicin \r\n\r\n\r\n**Strep viridans IE**\r\n\r\n* 1st line: benzylpenicillin \r\n* 2nd line: vancomycin + gentamicin \r\n\r\n**HACEK IE**: 1st line: ceftriaxone \r\n\r\n## Surgical \r\n\r\nDespite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: \r\n\r\n* Haemodynamic instability\r\n* Severe heart failure\r\n* Severe sepsis despite antibiotics/failed medical therapy\r\n* Valvular obstruction\r\n* Infected prosthetic valve\r\n* Persistent bacteraemia\r\n* Repeated emboli\r\n* Aortic root abscess\r\n\r\n**Common exam question**: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess\r\n\r\n# Complications\r\n\r\nComplications of infective endocarditis can also be the initial presenting complaint\r\n\r\n* Acute valvular insufficiency causing heart failure\r\n* Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)\r\n* Embolic complications causing infarction of kidneys, spleen or lung\r\n* Infection e.g. osteomyelitis, septic arthritis\r\n\r\n\r\nWithout timely and appropriate treatment, IE can rapidly lead to heart failure and death. The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high. \r\n\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Prophylactic Antibiotics in IE](https://www.nice.org.uk/guidance/cg64/ifp/chapter/infective-endocarditis)\r\n\r\n# References \r\n\n[American Heart Association Summary on Heart Valves and Endocarditis](<https://www.heart.org/en/health-topics/heart-valve-problems-and-disease/heart-valve-problems-and-causes/heart-valves-and-infective-endocarditis#:~:text=What%20is%20infective%20endocarditis%3F,greater%20risk%20of%20developing%20it.>)",
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"question": "A 75 year old male presents with a 2 week history of fatigue and night sweats. On admission, he had a transient episode of word finding difficulty which resolved within an hour. On auscultation of the chest, an opening click at S1 and an ejection systolic murmur is heard loudest at the apex. There are no residual neurological deficits. He has a past medical history of rheumatic heart disease and a prosthetic mitral valve replacement one year ago.\n\nSerial blood cultures have been negative so far. Transoesophageal echocardiogram (TOE) showed no vegetations and a functional prosthetic mitral valve with no leaks or stenoses. He has been started on IV antibiotics for 2 weeks with persistently raised inflammatory markers. Which is the next best investigation to evaluate the underlying cause?",
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"explanation": "The NNT is calculated by taking the reciprocal of the absolute risk reduction. In this case, it would be 1/(22.4% - 14%) = 1/(8.4%) = 12",
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"name": "The number needed to treat (NNT) to prevent one cardiovascular event on rosuvastatin is 8",
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"explanation": "The relative risk reduction is calculated by taking the difference between the absolute risk in the control and therapeutic groups and dividing it by the absolute risk of the control group. In this case, it would be (22.4 - 14) / 22.4 = 37.5%",
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"name": "The relative risk reduction of cardiovascular events for patients on rosuvastatin is 37.5%",
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"explanation": "Confidence interval (CI) is a measure of how confident the study's authors are that the true population value lies within a particular range, and it is usually 95%. If the confidence interval does not include the null hypothesis value (for relative risk, this value is 1), we can say a statistically significant difference exists. In this case, as the CI is from 0.75 - 1.10 and includes 1, there is no significant reduction in death from all causes",
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"name": "The absolute risk reduction (ARR) of death from non-cardiovascular causes is 0.88",
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"explanation": "Confidence interval (CI) is a measure of how confident the study's authors are that the true population value lies within a particular range, and it is usually 95%. If the confidence interval does not include the null hypothesis value (for relative risk, this value is 1), we can say a statistically significant difference exists. In this case, as the CI is from 0.75 - 1.10 and includes 1, there is no significant reduction in death from all causes",
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"explanation": "# Definition\n\nRisk in medical statistics refers to the probability of an outcome (either good or bad) occurring within a studied population. There are several different types of risk that are often used in medical studies.\n\n# What is Risk/Prevalence?\n\nThis is simply the probability of an event occurring within a defined population.\n\n# What is Risk Ratio (RR)?\n\nThe risk ratio (also known as relative risk) is the probability of an event occurring in an exposed group compared to the probability occurring in a non-exposed group.\n\nThe risk ratio is calculated by finding the ratio of incidence of a disease amongst the exposed population and the incidence amongst the non-exposed population.\n\nRisk ratios are used in cohort studies and in interventional studies in which the experimenter intervenes at some point during the study, such as in randomised controlled trials and pre-post studies.\n\nHowever, in cross-sectional studies and case-control studies, the incidence of the disease in the exposed and unexposed populations cannot be found, since the data only provides the cases and controls.\n\nConsequently,the risk ratio cannot be calculated for case-control studies and cross-sectional studies. Instead, an odds ratio must be found.\n\n# What is Absolute Risk Reduction (ARR)?\n\nThe absolute risk reduction is the absolute difference in the risk between the control group and the experimental group. It tells you in absolute terms how much an intervention changes an outcome of interest.\n\n# Calculation of Absolute Risk Reduction\n\nIt is calculated as follows:\n\n_ARR = Risk(control group) - Risk(experimental group)_\n\nA given ARR is generally considered significant if the 95% confidence interval does not cross 0.\n\nARR can then be used to calculate the number needed to treat (NNT).\n\n# What is Relative Risk Reduction (RRR)?\n\nThe relative risk reduction can be thought of as the proportional reduction in risk bestowed by the intervention compared to the control situation. It is more useful in helping you understand the efficacy of an intervention when the absolute risk of outcomes are rare (for example when considering the benefits of a statin for reducing MI in a given population).\n\n# Calculating RRR\n\nIt is calculated as follows:\n\n_RRR = 1 - [Risk(Experimental group) / Risk(Control group)]_\n\nA given RRR is generally considered significant if the 95% confidence interval does not cross 1.",
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"question": "A 50-year-old gentleman is admitted to the Cardiology ward having suffered a myocardial infarction. He is started on numerous medications for secondary prevention and has done some reading up whilst recuperating on the ward. In particular, he some questions regarding rosuvastatin as he has heard that it is a highly effective drug.\n\n\nHe would like to discuss a study he read in a journal. The data is as follows:\n\n\n|Outcome|Rosuvastatin group<br />(N=2500)|Placebo group<br />(N=2500)|Relative Risk <br />(95% CI)|\n|---------------------------------------|--------------------------------|---------------------------|----------------------------|\n|Cardiovascular events (including death)|350 (14%)|560 (22.4%)|0.63 (0.59 - 0.72)|\n|Death from non- cardiovascular causes|110 (4.4%)|125 (5.0%)|0.88 (0.80 - 1.05)|\n|Death from any cause|270 (10.8%)|325 (13.0%)|0.83 (0.75 - 1.10)|\n\n\n _N (Total number of people in the group), CI (Confidence Interval)_\n\n\nWhich of the following is true based on the data above?",
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"explanation": "The diamond shows the pooled result of all the studies. The vertical line indicates the line of no effect, i.e. the point at which there is statistically no significant difference between the control and intervention group. The width of the diamond illustrates the length of the confidence interval. Therefore, if the diamond touches the vertical line, it means that the overall result is **not** statistically significant",
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"explanation": "This describes a prospective cohort study, a longitudinal study that observes participants over a period of time to see whether they develop the outcome in question. This would not be suitable in this case as the disease is very rare, and the time taken to develop the condition may be very long",
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"name": "A study involving two groups of patients, one infected with human immunodeficiency virus (HIV) and the other without. The groups are then followed up over a period of 5 years to determine whether or not they develop Castleman disease",
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"explanation": "This is a retrospective cohort study, which is useful for tracking the development of a disease with a long latency period. It is different from a prospective cohort study in that study groups are not followed up in the future. It would not be suitable in this case as the disease is very rare",
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"name": "A study involving previously collected data to investigate whether there was an association between patients infected with human immunodeficiency virus (HIV) and their development of Castleman disease over a five year period",
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"name": "A study involving two groups of patients, one with and one without Castleman disease. The groups are then compared to examine their exposure to possible causal factors such as human immunodeficiency virus (HIV) and human herpesvirus 8 (HHV-8)",
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"name": "A study looking at the prevalence of Castleman disease in all males aged 20-50 years old in London and finding out whether they have been exposed to human herpesvirus 8 (HHV-8)",
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"explanation": "This is a case report, which involves an in-depth study of one to a few individuals with the disease. It is typically used to analyse unusual presentations of disease or unexpected responses to treatment, and is useful with respect to rare or emerging diseases. However, as the sample size is very limited, it would not provide as much data on the various causes of the disease compared to a case-control study",
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"comment": "I thought that causality couldn't be inferred from case-control studies? Also, the requirement to know that Castleman disease is rare seems like an unnecessary knowledge requirement in a Q that is testing study design",
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"explanation": "**Observational Study**\n\nA type of study in which participants in two or more groups are observed without the addition of an intervention. This is in contrast to randomised controlled trials where researchers look at the effects of a specific intervention in the study groups.\n\n**Cohort studies**\n\nCohort studies are one type of observational study. This study design involves examining groups of people over a period of time, where one group is exposed to a certain risk factor and the other group is not in order to establish links between exposure and a health related outcome such as the development of disease.\n\nThese designs are usually prospective in nature however, can be conducted retrospectively by looking back at data already collected, such as hospital records. These studies are useful to measure incidence and risk however, they are prone to confounding factors and are often costly.\n\n**Case-control studies**\n\nCase-control studies examine an association between an outcome and exposure to a risk factor. The studies recruit participants based on the presence of an outcome from the outset of the study. Once cases are recruited, suitable controls are identified and selected for the study. Controls are participants without the outcome of interest. Data of exposure to a risk factor is recorded retrospectively for each of the participants and then compared between cases and controls.\n\nThese studies are more suited to investigate rare conditions as individuals with the outcome of interest are identified at the outset. Other advantages of case-control studies are that they are much quicker to carry out relative to cohort studies and are relatively inexpensive.\n\n**Bradford-Hill Criteria**\n\nThe Bradford-Hill criteria include 9 established viewpoints to help determine if observed epidemiologic associations are causal.\nHill advised that his following viewpoints of an association be considered in attempting to distinguish casual from non-casual associations: strength, consistency, specificity, temporality, biologic gradient, plausibility, coherence, experimental evidence and analogy.\n\n**Strength** - strong associations are more likely to be casual than weak associations (which may be explained by other factors or be affected by undetected biases.)\n\n**Consistency** - refers to the repeated observation of an association in different populations under different circumstances. Lack of consistency does not rule out a casual association, because some effects are produced by causes only under unusual circumstances.\n\n**Specificity** - The criterion of specificity requires that a cause leads to a single effect, not multiple effects. Hill's discussion of this criterion is with reservation, and many authors regard this criterion as useless and misleading on the basis that many outcomes can happen from one variable (e.g. smoking may cause lung cancer, COPD, other forms of cancer, interstitial lung disease..)\n\n**Temporality** - Temporality refers to the necessity that the cause precede the effect in time.\n\n**Biologic gradient** - Biologic gradient refers to the presence of a mono-tone (unidirectional) dose responsive curve. However, like specificity, the acknowledgement that disease frequency may be caused by different exposures shows that the existence of a monotonic association is neither necessary nor sufficient for a causal relation.\n\n**Plausibility** - Plausibility refers to the biologic plausibility of the hypothesis, an important concern but one that is far from objective or absolute.\n\n**Coherence** - implies that a cause and effect interpretation for an association does not conflict with what is known of the natural history and biology of the disease. On the other hand, presence of conflicting information may indeed undermine a hypothesis, but one must always remember that the conflicting information may be mistaken or misinterpreted.\n\n**Experimental evidence** - it is not clear what was meant by this criterion, however, it may have referred to errors when collecting data.\n\n**Analogy** - Analogy provides scientists with a source of more elaborate hypotheses about the associations under study; absence of such analogies only reflects lack of imagination or experience, not falsity of the hypothesis.\n\n[Source: https://www.rtihs.org/sites/default/files/26902%20Rothman%201998%20The%20encyclopedia%20of%20biostatistics.pdf]",
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"learningPoint": "A case-control study, a type of retrospective observational study, is ideal for studying rare diseases or outcomes with a small population size. It allows researchers to examine a wide range of exposure factors from patients' histories to identify potential associations between exposures and the disease.",
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"question": "A university professor would like to conduct a study to investigate the causes of Castleman disease, a disease involving enlarged lymph nodes in the body.\n\nWhich is the most appropriate study design he should select?",
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"explanation": "This may be indicated for primary prevention of cardiovascular disease, however his lipid panel is normal",
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"explanation": "This would be indicated for the management of essential hypertension in patients >55 years old or in Afro-Caribbeans. However, ACE inhibitors are specifically indicated for albuminuria in diabetes",
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"explanation": "Lisinopril is an angiotensin converting enzyme inhibitor (ACE inhibitor) which are the drug class of choice in preventing progression of albuminuria and diabetic nephropathy. They are superior to diuretics and calcium channel blockers in this case",
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"comment": "NICE says you only get ramipril if diabetic AND CKD or ACR >30\nthis does not fall under this",
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"comment": "you start ACEi if ACR >3 ",
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"comment": ">30mg/g OR >3mg/mmol - check your units",
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"comment": "HE DOES NOT HAVE HYPERTENSION!!!!",
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"explanation": "# Summary\n\nType 2 Diabetes Mellitus is a chronic metabolic disorder characterised by pancreatic beta-cell insufficiency and insulin resistance. The resulting hyperglycaemia leads to symptoms such as polyuria, polydipsia and if chronic can have microvascular and macrovascular complications. Key investigations include random and fasting blood glucose, 2-hour glucose tolerance, and HbA1C tests, and diagnosis is based on the results of these +/- symptoms. Management of type 2 diabetes primarily revolves around lifestyle modifications, hypoglycaemic agents, and insulin therapy when necessary, as well as reducing risks for serious complications such as cardiovascular and cerebrovascular disease. Other complications from chronic hyperglycaemia involve the gastrointestinal system, nervous system, peripheral arteries, foot infections, sexual dysfunction, and cardiac system. \n\n# Definition\n\nType 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.\n\n# Epidemiology\n\nT2DM generally manifests in adults, and it is often associated with a strong familial predisposition. It accounts for approximately 90-95% of all diagnosed cases of diabetes.\n\n# Aetiology\n\nT2DM results from a combination of genetic and environmental factors. Known contributors include:\n\n- Poor dietary habits\n- Lack of physical activity\n- Obesity\n\n# Signs and symptoms\n\nIndividuals with T2DM may initially be asymptomatic, but over time, they may develop:\n\n- Polyuria\n- Polydipsia\n- Unexplained weight loss\n- Blurry vision\n- Fatigue\n\n# Differential diagnosis\n\nThe primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:\n\n- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.\n- MODY (Maturity Onset Diabetes of the Young):\n\t- MODY 3 is the commonest cause, occurring due to a mutation in HNF1A. It is characterised by a very high blood sugar (10-20), and is very sensitive to sulphonylureas (e.g. gliclazide.) Insulin is the next line of treatment if it doesn't respond.\n\t- MODY 2 is the second commonest cause, occurring due to a glucokinase mutation. Blood sugars rarely rise above 7-8, over many years. Patients are generally well with few complications and the diabetes often responds to diet alone.\n\t- MODY 5 is associated with HNF1 beta mutation, and is associated with pancreatic atrophy, renal cycsts (causing palpable kidneys), epidydymal cysts, a bicornuate uterus, and abnormal LFTs\n- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).\n\n# Investigations\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l\n- Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\n# Management\n\nManagement of T2DM involves patient education, lifestyle modifications, pharmacological interventions, and close monitoring of glucose levels:\n\n- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation\n- Pharmacological interventions: \n\t- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.\n\t- If on monotherapy HbA1c >58mmol/mol consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).\n\t- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.\n- Close Monitoring: Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.\n\n\n**Insulin Therapy**\n\nNICE guidance recommends basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.\n\nLong acting insulin analogues include Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).\n\nMixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.\n\n**Blood Pressure targets in Diabetes**\n\n- Blood pressure control needs to be strict in diabetes because these patients are at higher risk of macro- and microvascular complications.\n- NICE Hypertension Guidance [CG136] sets the same blood pressure targets as those who do not have diabetes, however in diabetics with HTN, ACE-inhibitors are first line as they are reno-protective\n\n# Complications\n\nComplications of diabetes are diverse, affecting multiple systems:\n\n### Macrovascular:\n\n* **Cardiac Complications** - diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.\n* **Peripheral Arterial Disease (PAD)** - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).\n* **Cerebrovascular disease** - patients with diabetes are at significantly increased risk of TIAs and stroke and as such it is paramount to address the main risk factors (lipids, BP, smoking, obesity) for these as a broader part of management\n\n\n### Microvascular:\n\n* **Diabetic retinopathy** - characterised by vascular occlusion and leakage in the retinal capillaries, leading to potential sight loss if unmanaged, it is the leading cause of visual loss in adults. See separate section.\n* **Diabetic nephropathy** - a leading cause of chronic kidney disease, it is characterised by proteinuria. Prevention of this complication is achieved with ACE inhibitors/ARBs (by managing blood pressure) and SGLT-2 inhibitors.\n\t* Histological changes include Kimmelstiel-Wilson nodules which are the spherical, eosinophilic, sclerotic nodules characteristic of nodular diabetic glomerulosclerosis \n* **Diabetic neuropathy** - the primary causative factor is chronic hyperglycaemia, which leads to several distinct types neuropathy. See separate section.\n\t* **Autonomic Neuropathy** - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.\n\t* **Gastrointestinal Complications: Gastroparesis** - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.\n\t* **Foot Complications: Diabetic Foot Infections** - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.\n* **Sexual Dysfunction** - caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.\n\n# 'Sick day' rules\n\n1. **Temporary Medication Adjustments**: During acute illness, consider temporarily stopping certain medications until the person is eating and drinking normally for 24–48 hours. \n\t- **Angiotensin-Converting Enzyme Inhibitors (ACEIs), Diuretics, and NSAIDs**: Stop treatment if there is a risk of dehydration to reduce the likelihood of acute kidney injury (AKI).\n\n3. **Metformin**: Stop treatment if there is a risk of dehydration to lower the risk of lactic acidosis.\n\n4. **Sulfonylureas**: Be cautious, as they may increase the risk of hypoglycemia, especially if dietary intake is reduced.\n\n5. **SGLT-2 Inhibitors**: Check for ketones and stop treatment if acutely unwell and/or at risk of dehydration due to the risk of euglycemic diabetic ketoacidosis (DKA).\n\n6. **GLP-1 Receptor Agonists**: Stop treatment if there is a risk of dehydration to reduce the risk of AKI.\n\n7. **Insulin Therapy**: Do not stop insulin treatment; instead, consider adjusting the dose with guidance from the specialist diabetes team.\n\n8. **Blood Glucose Monitoring (if indicated)**: \n - Increase monitoring frequency to at least every 3–4 hours, including overnight.\n - Adjust insulin doses based on results.\n - Continue careful monitoring until blood glucose levels return to baseline.\n - Seek urgent medical advice if blood glucose remains uncontrolled.\n\n9. **Ketone Monitoring (Blood or Urinary)**: \n - Check ketone levels regularly (at least every 3–4 hours, including overnight).\n - Seek immediate medical advice if urine ketone level is greater than 2+ or blood ketone level is greater than 3 mmol/L.\n\n10. **Maintain Normal Meal Pattern**: Encourage maintaining regular meals and fluids, including carbohydrates, if appetite is reduced.\n\n11. **Fluid and Carbohydrate Replacement**:\n - If unable to eat or vomiting, replace meals with carbohydrate-containing drinks (e.g. fruit juices, sugary drinks).\n - Adjust fluid intake based on blood glucose levels (sugar-free fluids for high levels, sugary fluids for low levels).\n\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on T2DM](https://cks.nice.org.uk/topics/diabetes-type-2/)\n",
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"question": "A 60 year old male is admitted to the general medical ward with a 2 day history of atypical chest pain. Serial troponin levels are normal and ECG shows no dynamic changes. He is a current smoker and has a past medical history of childhood asthma.\n\nHis observations are as follows:\n\n- Pulse 70\n- BP 125/80\n- SpO<sub>2</sub> 100%\n- Temperature 36.5°C\n\nBloods are sent off for cardiovascular risk factor screening and are as follows:\n\n- HbA1c 7.2%\n- Fasting glucose 7.8\n- Lipid panel unremarkable\n\nUrine albumin creatinine ratio shows microalbuminuria.\n\nHe is started on metformin by the consultant on the ward round. Which other medication should be started?",
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"explanation": "This is most likely to cause diabetic glomerulosclerosis, which shows Kimmelsteil-Wilson nodules (nodules of hyaline material) on biopsy",
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"explanation": "This woman has nephrotic syndrome, characterised by oedema, proteinuria and hypoalbuminaemia. The thickened glomerular basement membrane with subepithelial deposits is characteristic of membranous nephropathy as a cause of her nephrotic syndrome. Causes of membranous nephropathy include autoimmune disease and infection such as hepatitis B and hepatitis C. A renal biopsy would show a spike and dome pattern on a silver stain",
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"name": "Hepatitis B virus",
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"explanation": "This is most likely to cause focal segmental glomerulosclerosis, which would show focal scarring and areas of collagen sclerosis",
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"name": "HIV",
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"explanation": "This is most likely to cause mesangiocapillary glomerulonephritis, which may lead to nephrotic or nephritic syndrome. This would appear as double contouring of the capillary walls or a \"tram track\" appearance on electron microscopy",
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"explanation": "This is most likely to cause minimal change glomerulonephritis, the most common cause of nephrotic syndrome in children. This would appear as podocyte effacement on electron microscopy",
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"comment": "19% seriously?? jesus you guys need to spend more time on the wards",
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"comment": "Ok Tom ",
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"comment": "I got this right but I though HIV could also cause membranous nephropathy?",
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"comment": "more often it causes focal segmental glomerulosclerosis?",
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"explanation": "# Summary\n\nNephrotic syndrome refers to the clinical triad of proteinuria, hypoalbuminemia and peripheral oedema. It occurs due to increased permeability of the glomerular basement membrane, which occurs either due to a variety of both primary (idiopathic) or secondary diseases. Renal biopsy is the key investigation to differentiate between causes and should be considered in all adults. Other investigations include a urine dip and protein:creatinine ratio, LFTs for albumin and investigations for an underlying cause such as myeloma or diabetes. First-line management is usually with steroids; other immunosuppressants may need to be added. Management options for oedema include lifestyle changes (low salt diet, fluid restriction) and/or diuretics.\n\n# Definition\n\nNephrotic syndrome occurs when there is excessive loss of protein in the urine, leading to hypoalbuminemia and peripheral oedema. Other resulting features include hyperlipidaemia, abnormal coagulation and immunodeficiency. \n\n# Aetiology\n\nThe common underlying pathology leading to nephrotic syndrome is damage to the glomerular basement membrane leading to excessive leakage of protein into the urine.\n\nThere are a wide variety of conditions that may lead to nephrotic syndrome which may be classified as either primary (idiopathic) or secondary (due to another underlying disease) - these include:\n\n- **Minimal change disease** causes the majority of cases of nephrotic syndrome in young children\n- It is usually idiopathic but may rarely be associated with lymphoma or NSAID use\n- Glomeruli are normal under light microscopy\n- Electron microscopy shows diffuse effacement of the podocyte food processes\n- Steroid responsiveness is characteristic\n- **Focal segmental glomerulosclerosis** may be primary or secondary to conditions including HIV, extensive nephron loss or drugs (e.g. heroin)\n- Biopsy shows sclerosis of segments of the glomerular tuft, only affecting some glomeruli\n- **Membranous nephropathy** is the leading cause of nephrotic syndrome in older people\n- Biopsy shows thickening of the glomerular basement membrane without cellular proliferation\n- A classic \"spike and dome\" appearance is described where subepithelial immune deposits are interspersed with new basement membrane growth\n- Most cases are primary; usually associated with PLA2R antibodies\n- Others may be secondary to malignancy, infections, autoimmune disease or drugs\n- **Membranoproliferative glomerulonephritis** is also referred to as membranoproliferative glomerulonephritis\n- It can present with nephrotic or nephritic syndrome\n- It may be idiopathic or secondary to infections such as hepatitis C or systemic lupus erythematosus\n- **Diabetic nephropathy** may affect patients with longstanding type 1 or 2 diabetes\n- It tends to be a progression from microalbuminuria, especially if untreated\n- Patients are at risk of end-stage renal disease\n- Biopsy shows thickening of the glomerular basement membrane, mesangial expansion and Kimmelstiel-Wilson nodules\n- **Amyloidosis**, especially AA amyloid due to chronic inflammation\n- AL amyloid (due to light chain deposition) and hereditary amyloidosis can also cause nephropathy\n- On biopsy, amyloid deposits stain with Congo red and display apple green birefringence under polarized light\n- **Multiple myeloma** can present with a variety of renal manifestations, with proteinuria and renal insufficiency the most common\n- Nephrotic syndrome occurs in a minority of cases and may be due to a number of underlying mechanisms\n- **Lupus nephritis** i.e. renal involvement due to systemic lupus erythematosus\n- Class V (membranous lupus nephritis) is the most likely to cause nephrotic syndrome\n- This is characterised histologically by subepithelial immune complex deposition\n- **Medications** are a rarer cause of nephrotic syndrome, including:\n- Bisphosphonates\n- NSAIDs\n- D-penicillamine\n- Probenecid\n- Tolbutamide\n\n# Classification\n\nThe diagnosis of nephrotic syndrome requires the presence of all of:\n\n- Proteinuria > 3.5 grams/24 hours\n- Serum albumin < 30 grams/litre\n- Peripheral oedema\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n- Frothy urine due to proteinuria\n- Swelling of the face and body\n- Weight gain due to fluid retention\n- Fatigue\n- Lethargy\n- Anorexia\n\n**Signs include:**\n\n- Oedema - typically peripheral and periorbital\n- Muehrcke's lines refers to paired white transverse lines across the nails that may occur secondary to hypoalbuminemia\n- Signs of hyperlipidaemia such as xanthelasma (yellow plaques over the eyelids)\n- Signs of pleural effusion e.g. dull bases to percussion with decreased air entry\n\nPatients may also present with signs and symptoms of complications e.g. infection, thrombosis.\n\n# Differential Diagnosis\n\n- **Heart failure** is a common cause of peripheral oedema; typically however patients cannot lie flat due to breathlessness and so facial oedema is unusual; proteinuria is not a feature\n- **Cirrhosis** is commonly complicated by fluid accumulation, usually in the form of ascites; although ascites may occur in nephrotic syndrome it is less common than fluid accumulation in the peripheries and face; proteinuria is not a feature\n- **Chronic kidney disease** may present with fluid retention, especially in patients with end-stage renal disease - it may coexist with nephrotic syndrome however renal function is often preserved\n- **Medications** may cause peripheral oedema including calcium channel blockers, NSAIDs and corticosteroids\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dipstick** looking for proteinuria; glycosuria may be present in diabetes but haematuria is not usually seen\n- **Urine protein:creatinine ratio** should be over 2 or **24 hour urine collection** should show proteinuria >3.5g/day\n\n**Blood tests:**\n\n- **LFTs** to confirm hypoalbuminemia\n- **U&Es** for renal function (significant impairment is unusual)\n- **FBC** may show anaemia in persistent nephrotic syndrome\n- **Vitamin D** may be low as this is lost in urine\n- **Bone profile** may show hypocalcemia secondary to decreased calcium absorption due to vitamin D deficiency\n- **Coagulation screen** is usually normal although there is a hypercoagulable state wiht increased risk of thromboembolism\n- **HbA1c** or **fasting glucose** for diabetes\n- **Lipid profile** often shows dyslipidemia\n- **CRP** and **ESR** may be raised due to an underlying inflammatory, malignant or infectious process\n- **Myeloma screen** i.e. immunoglobulins and serum protein electrophoresis if myeloma is suspected\n- **Autoimmune screen** e.g. for suspected systemic lupus erythematosus (antinuclear antibody, complement levels etc.)\n- **Infection screen** i.e. hepatitis B and C serology, HIV testing\n\n**Imaging tests:**\n\n- **Chest X-ray** if there are clinical signs of pleural effusion\n- **US KUB** (kidneys, ureters and bladder) if there is renal impairment to assess for obstruction and any structural abnormalities of the kidneys\n- Imaging may be required to diagnose complications, such as a **CT pulmonary angiogram** for suspected pulmonary embolism or **doppler ultrasound** of the limbs for suspected deep vein thrombosis\n\n**Special tests:**\n\n- **Renal biopsy** is the key investigation to diagnose the cause of nephrotic syndrome - this is important both for prognosis and to guide management \n- Biopsy is usually indicated in adults, however in children there are specific indications e.g. if not responsive to steroids\n\n# Management\n\n**Conservative:**\n\n- Restrict salt intake to <2g/day\n- Fluid restriction to <1.5L/day \n- Weight should be monitored, with a target of 1-2 kg weight loss per day until the patient reaches their predicted \"dry weight\" (i.e. weight when not oedematous)\n- Dietary changes (e.g. avoiding a high protein diet, limiting fat intake) may be advised and dietician input may be indicated\n- Mechanical thromboprophylaxis (TEDS) to reduce risk of venous thromboembolism\n\n**Medical:**\n\n- **Corticosteroids** are usually first-line for management of nephrotic syndrome - these should be weaned after remission is achieved\n- Other immunosuppressive drugs (e.g. ciclosporin, cyclophosphamide, mycophenolate mofetil or rituximab) may be added as steroid sparing agents or for severe or refractory cases\n- Diuretics are used to treat significant peripheral oedema, usually furosemide but potassium sparing and thiazide diuretics may be added as adjuncts\n- Risk of thromboembolism should be assessed and prophylactic anticoagulation considered\n- Antihypertensives may be required to maintain a normal blood pressure; ACE inhibitors and angiotensin II receptor blockers may also help to reduce proteinuria\n- Ensure patients are up to date with vaccinations (however live vaccines should not be given to patients who are immunocompromised)\n- In some cases hyperlipidaemia may require treatment with statins \n- Patients taking steroids may require co-administration of proton pump inhibitors for gastric protection and consideration of bone protection\n\n**Surgical:**\n\n- If nephrotic syndrome results in end-stage renal failure, renal replacement therapy may be required either with dialysis or renal transplantation\n\n# Complications\n\n- **Increased risk of infection** as immunoglobulins are lost in urine\n- **Venous thromboembolism** due to urinary loss of anti-thrombotic proteins such as antithrombin III\n- **Hyperlipidaemia** due to increased hepatic production of lipoproteins to compensate for hypoalbuminemia - this may also present with lipiduria (which may cause urine to appear milky) \n- **Acute kidney injury** may occur due to excessive diuresis or renal vein thrombosis\n- **Chronic kidney disease** may occur secondary to the underlying cause of nephrotic syndrome (e.g. diabetes, amyloidosis)\n- **Medication side-effects** especially with chronic steroid use (e.g. osteoporosis, psychiatric effects)\n- **Hypothyroidism** due to urinary losses of T4 and T3 with their binding proteins\n- **Vitamin D deficiency** as this is also lost in urine\n- **Anaemia** may result from persistent nephrotic syndrome as iron bound to transferrin and erythropoietin are lost in urine\n\n# Prognosis\n\nPrognosis varies between subtypes, for example minimal change disease rarely progresses to end-stage renal failure (1% of cases), whereas 50% of patients with FSGS will do over 5-10 years.\n\nMortality has been greatly reduced with the use of steroids and immunosuppression.\n\nRelapses are common and may require repeated courses of steroids or escalation to other immunosuppressive medications.\n\n# References\n\n[KDIGO Guidelines on Glomerular Diseases](https://kdigo.org/guidelines/gd/)\n\n[Patient UK - Nephrotic syndrome](https://patient.info/doctor/nephrotic-syndrome-pro)\n\n[Radiopaedia - Nephrotic syndrome](https://radiopaedia.org/articles/nephrotic-syndrome?lang=gb)",
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"learningPoint": "Hepatitis B infection is associated with membranous nephropathy (MN), a kidney disorder characterized by the thickening of the glomerular basement membrane. The association occurs due to immune complex deposition in the kidneys, which can lead to proteinuria and nephrotic syndrome.",
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"question": "A 53 year old lady is admitted with a 2 week history of bilateral lower limb swelling. Albumin is 21g/L (normal range 35-50 g/L) and she has proteinuria of 6.5g/24h. She is referred to the nephrologist who decides to get a renal biopsy. This reveals a diffusely thickened glomerular basement membrane with IgG and C3 subepithelial deposits.\n\nWhich of the following is the most likely underlying cause of her condition?",
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"explanation": "This is a possible differential, as this may cause a bilateral facial palsy. However the progression of muscle weakness in myasthenia gravis is typically descending from the extraocular muscles to the face and limb girdle. Deep tendon reflexes are not affected. The clinical course is also longer in myasthenia gravis and may occur over months to years",
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"explanation": "Guillain-Barré Syndrome (GBS) typically presents with a symmetrical ascending flaccid paralysis of the lower limbs that later spreads to the trunk and may later affect the respiratory muscles. Areflexia may also be present. Bilateral facial nerve palsy can occur in Guillian Barre Syndrome. Miller Fisher syndrome is a valid differential. However, it should be remembered that Miller Fisher syndrome is extremely rare and it is still much more likely to encounter patients with GBS who have atypical features",
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"explanation": "Miller Fisher syndrome (MFS) presents as a triad of ataxia, areflexia and ophthalmoplegia. In this case, the predominant symptoms are of symmetrical ascending weakness, which has now likely extended to involve the chest muscles. You might also expect evidence of opthalmoplegia which is absent in this case. Bilateral facial nerve palsy can occur in Guillian Barre Syndrome. Miller Fisher syndrome is a valid differential. However, it should be remembered that Miller Fisher syndrome is extremely rare and it is still much more likely to encounter patients with GBS who have atypical features",
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"explanation": "This is a possible differential here and may also present with respiratory dysfunction. However, this tends to follow a more acute onset compared to GBS, and focal neurological symptoms such as weakness are not typically symmetrical. Stroke, as an upper motor neurone pathology, is also unlikely to cause hyporeflexia",
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"explanation": "This is an unlikely differential here, as it typically presents with confusion, ataxia and ophthalmoplegia (nystagmus is a common finding). This patient does not present with altered mental status and does not appear to have risk factors for thiamine deficiency, e.g. chronic alcoholism, malnutrition, malabsorption or gastrointestinal disease",
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"comment": "The question implies that the weakness started in the face and progressed to arms and then legs which is the opposite of GBS and was very confusing",
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"comment": "Agreed",
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"comment": "exactly!",
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"comment": "yes, it's atypical GBS, but it does happen and more commonly than miller fisher",
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"comment": "if it was atypical GBS, why didn't they give an explanation that mentions that it is atypical? Literally says here that GBS presents with a symmetrical ascending flaccid paralysis of the lower limbs, with 0 mention of any atypical presentations",
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"explanation": "## Summary\n\nGuillain-Barré Syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy characterised by a rapid, progressive, ascending symmetrical weakness, often preceded by infection. Diagnosis is largely clinical but supported by specific investigations such as lumbar puncture and nerve conduction studies. Treatment is mainly supportive, with options for disease-modifying treatments like intravenous immunoglobulins (IVIG) or plasmapheresis in severe cases.\n\n## Definition\n\nGBS is an ascending inflammatory demyelinating polyneuropathy, typified by an acute onset of bilateral and roughly symmetric limb weakness. \n\n## Epidemiology\n\nThe prevalence of GBS is approximately 1-2 cases per 100,000 worldwide.\n\n## Aetiology\n\nGBS typically occurs 1-3 weeks following an infection, with common culprits being Campylobacter, mycoplasma, and Epstein-Barr Virus (EBV). \n\n40% of cases, however, are idiopathic. \n\nOther potential triggers include infections such as CMV, HIV, Hepatitis A, or following certain vaccinations such as for tetanus, rabies, or swine flu.\n\n## Signs and symptoms\n\nNeurological decline often progresses over days to weeks.\n\nClinical features of GBS include:\n\n- Progressive ascending symmetrical limb weakness (usually starting with the lower limbs)\n- Lower back pain due to radiculopathy\n- Paraesthesia, often preceding motor symptoms\n- Potential respiratory muscle involvement in severe cases\n- Potential cranial nerve involvement leading to diplopia, facial droop\n- **Lower motor neurone** signs in the lower limbs: hypotonia, flaccid paralysis, areflexia\n- Cranial nerve signs: ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy\n- Potential autonomic dysfunction (e.g., arrhythmia, labile blood pressure)\n\n## Variants\n\nSeveral variants of GBS exist, each presenting with unique characteristics:\n\n- Paraparetic variant\n - Primarily affects the lower limbs\n\n- Miller-Fisher syndrome\n - Presents with ataxia, ophthalmoplegia, and areflexia\n - Associated with **anti-GQ1B antibodies**\n\n- Pure motor variant\n - Ascending weakness without sensory involvement\n\n- Bilateral facial palsy with paraesthesias\n - Affects the cranial nerves\n\n- Pharyngeal-brachial-cervical weakness\n - Results in weakness of the upper limbs\n - Associated with **anti- GT1a antibodies**\n- Bickerstaff's Brainstem Encephalitis\n - Presents with encephalitis, ophthalmoplegia, and ataxia\n\nIt's worth noting that these variants rarely present purely as described, and there's often overlap in clinical presentation.\n\n\n## Differential diagnosis\n\n- Vascular: occasionally, brainstem strokes may present similarly\n- Infective/Inflammatory: \n - Polio: asymmetrical weakness from myelitis\n - Lyme disease\n - CMV\n - HIV\n - TB\n - Transverse myelitis \n - Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) \n - Myasthenia gravis\n- Traumatic/Structural:\n - Spinal cord compression\n- Metabolic:\n - Porphyrias: may result in an acute neuropathy\n - Electrolyte derangements: hypokalaemia, hypophosphataemia, hypermagnesaemia\n\t\n\n## Investigations\n\nInvestigations for GBS include:\n\n- Monitoring of forced vital capacity (FVC) for respiratory muscle involvement\n- Cardiac monitoring for autonomic instability\n- Blood tests, including arterial blood gas (ABG)\n- Serological tests: Anti-ganglioside antibodies\n- Lumbar puncture: may show **albuminocytological dissociation** \n\t- Increased level of protein (albumin) without a corresponding increase in white blood cells (cytology)\n- Nerve conduction studies\n\t- May show prolongation or loss of the F wave\n- Identification of the underlying cause: stool cultures, serology, CSF virology\n\n## Management\n\nManagement of GBS is primarily supportive and includes:\n\n- Regular monitoring of FVC\n\t- Early involvement of intensive care is essential if any reduction in FVC as deterioration may be rapid\n- Venous thromboembolism (VTE) prophylaxis: TEDS + LMWH\n- Analgesia: NSAIDs or opiates for radiculopathy-related back pain\n- Management of cardiac arrhythmias as per ALS guidelines\n- Careful use of antihypertensives due to potential autonomic dysfunction\n- Consideration of enteral feeding in those with unsafe swallow\n\nSpecific medical management for those with significant disability (e.g., inability to walk) include:\n\n- Intravenous immunoglobulin (IVIG) over a 5-day course\n- Plasmapheresis, which has similar efficacy to IVIG but is associated with more side effects.\n\n## Prognosis\n\nWhile GBS can be life-threatening, particularly when respiratory muscles are affected or in the presence of autonomic dysfunction, the majority of patients experience full recovery. \n\nHowever, residual fatigue and weakness can persist in some patients. Certain variants of GBS, like Miller-Fisher syndrome, generally have a good prognosis with full recovery being the norm. \n\nPrognostic indicators include speed of onset, severity at nadir, age and the presence of preceding diarrhoeal illness.\n\n## References\n\n1. Van den Berg, B., Walgaard, C., Drenthen, J., Fokke, C., Jacobs, B. C., & Van Doorn, P. A. (2014). Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nature Reviews Neurology, 10(8), 469-482.\n\n2. Yuki, N., & Hartung, H. P. (2012). Guillain–Barré syndrome. New England Journal of Medicine, 366(24), 2294-2304.\n\n3. Hughes, R. A., & Cornblath, D. R. (2005). Guillain-Barré syndrome. The Lancet, 366(9497), 1653-1666.\n\n4. Willison, H. J., Jacobs, B. C., & Van Doorn, P. A. (2016). Guillain-Barré syndrome. The Lancet, 388(10045), 717-727.\n",
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"question": "A 20-year-old male presents to Accident & Emergency with a one-week history of bilateral facial weakness and progressively weak arms and legs. Prior to this, he had an acute diarrhoeal illness which has since settled. He has no other past medical history.\n\nHis Glasgow coma scale (GCS) score is 15. On examination, he has a bilateral facial palsy, bilateral symmetrical lower and upper limb weakness and reduced tendon reflexes.\n\nHe has a sudden onset desaturation whilst on the general medical ward and is transferred to the intensive care unit for intubation and ventilation.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "The main priority is to initiate antiplatelet treatment with aspirin. The blood pressure is not dangerously high at this point and she does not have any serious concomitant medical issues requiring strict BP control (e.g. hypertensive encephalopathy, nephropathy or cardiac failure). In patients with a TIA who have recovered to their neurologic baseline and have no other evidence of infarction, anti-hypertensive treatment may be reinitiated",
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"explanation": "While this patient does have a history of gastroesophageal reflux, the priority is to start her on an antiplatelet therapy (i.e. aspirin). She may require a H2 receptor antagonist such as ranitidine as an adjunct",
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"explanation": "This is only recommended in acute ischaemic stroke within 4.5 hours of onset, where intracranial haemorrhage has been excluded on brain imaging. In this case, the patient has a transient ischaemic attack which would not warrant this",
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"explanation": "The patient has suffered a transient ischaemic attack (TIA) on a background of non-valvular atrial fibrillation (AF). In this case, as AF is likely the underlying cause of the TIA, anticoagulation (rivaroxaban) is superior to aspirin in stroke prevention. Therefore, aspirin would not be the best choice in this scenario.",
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"explanation": "NICE recommend commencing anticoagulant in secondary care for people with ischaemic stroke or TIA and paroxysmal, persistent, or permanent atrial fibrillation or atrial flutter. The choice of anticoagulant is a DOAC in non-valvular AF. ",
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"comment": "How can the neuro exam be fine if he's had a stroke then?",
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"comment": "TIA",
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"comment": "ONLY after a CT scan has been done!!! this is wrong. he cannot be given aspirin until haemorrhagic ruled out",
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"comment": "you don't CT for TIA",
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"comment": "Yeah as above TIA can only be caused by a thrombus, a bleed cannot appear then disappear in the same way",
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"comment": "So if someone comes in with a suspected TIA you will immediately give Aspirin 300mg + refer to TIA clinic where they will get either an urgent carotid doppler or a weighted MRI (preferred) to determine the territory of ischaemia",
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"comment": "If a patient with a transient ischemic attack (TIA) has atrial fibrillation (AF), immediate CT head imaging is recommended to rule out hemorrhage before starting anticoagulation therapy. This is because AF increases the risk of stroke, and anticoagulation is often necessary to prevent further events. However, it's crucial to ensure there is no bleeding before initiating anticoagulation",
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"comment": "During the exam, if I too can't find a word for 15 mins I'll go to A&E",
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"comment": "i put rivarox but the aspirin answer doesnt really explain why aspirin is wrong",
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"comment": "I believe it is due to the presense of AF in this patient, if the patient were not in AF i think 300mg aspirin would be the correct answer, hope this helps\n",
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"explanation": "# Summary\n\nA Transient Ischaemic Attack (TIA), colloquially known as a \"mini-stroke\", represents a sudden focal neurological deficit of vascular origin, characterised by symptom resolution typically within an hour. The absence of an acute infarct on imaging differentiates it from a stroke. Key signs and symptoms include speech difficulty, or arm/leg weakness or sensory changes. Important differential diagnoses include focal seizures, migraine, and intracranial bleeding. Investigations primarily involve neuroimaging, while management aims at reducing future stroke risk with lifestyle changes, control of vascular risk factors, and initiation of antiplatelet therapy. NICE guidelines recommend immediate referral for individuals with suspected TIA for assessment within 24 hours.\n\n# Definition\n\nA transient ischaemic attack (TIA) is a sudden-onset focal neurological deficit with a vascular aetiology, typically resolving symptoms within less than 1 hour. \n\n# Epidemiology\n\nTIA is a significant health concern worldwide due to its association with future stroke risk. \n\nThe incidence is 230 cases per 100000 person-years.\n\nRisk factors include:\n \n* Hypertension\n* Diabetes mellitus\n* High cholesterol\n* Atrial fibrillation\n* Carotid stenosis\n* Smoking\n* Family history of cardiovascular disease/stroke\n* History of cardio-embolic events\n\n# Signs and Symptoms\n\nPatients typically present with a sudden onset of focal neurological deficits which may include:\n\n- Speech difficulty (dysphasia)\n- Arm or leg weakness\n- Sensory changes \n- Ataxia, vertigo or loss of balance\n- Visual disturbance: Homonymous hemianopia, diplopia \n\nSymptoms of TIA are transient, with most resolving within 1 hour.\n\n# Differential Diagnosis\n\nIn assessing for a TIA, clinicians should consider the following differential diagnoses:\n\n- **Stroke**: Persistent symptoms with evidence of ischaemia on MRI imaging\n- **Focal motor seizures**: These might be suggested by positive symptoms preceding the weakness, such as shaking.\n- **Migraine with aura**: Characterized by a preceding aura which may present with visual disturbances, tingling, or numbness, followed by headache.\n\n\n# Investigations\n\nTo confirm the diagnosis and assess the extent of vascular disease, the following investigations are generally recommended:\n\n- Neuroimaging \n\t- The preferred modality is MRI to assess for any evidence of ischaemia, haemorrhage or consider alternative pathologies\n- Carotid ultrasound (looking for carotid stenosis\n- Echocardiogram (looking for cardiac thrombous)\n- 24 hour tape (looking for atrial fibrillation)\n- Blood tests (including glucose, lipid profile, clotting factors)\n\n\n# Management\n\nPatients who have had a suspected TIA should be referred for immediate assessment, ideally to be seen **within 24 hours** of onset of symptoms. The aim of management is to reduce the future risk of stroke and includes:\n\n- Lifestyle modifications (smoking cessation, regular exercise, healthy diet)\n- Control of vascular risk factors (hypertension, diabetes, dyslipidaemia)\n- Initiation of antiplatelet therapy (e.g., aspirin, clopidogrel) unless contraindicated\n- In selected cases, endarterectomy or stenting of the carotid artery might be indicated:\n\t- > 70% stenosis according European Carotid Surgery Trialists' Collaborative Group criteria (ECST) or\n\t- > 50% according to North American Symptomatic Carotid Endarterectomy Trial criteria (NASCT)\n\n# References\n\n[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/management/suspected-transient-ischaemic-attack/)",
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"question": "A 65-year-old woman presents to the emergency department with temporary word finding difficulty that lasted for 15 minutes, occurring approximately 2 hours ago. Past medical history includes hypertension and gastroesophageal reflux disease.\n\nObservations on triage were:\n\n- Temperature 36.5°C\n- Pulse 90\n- Blood pressure (BP) 170/85\n- SpO2 98% on room air\n\nAn electrocardiogram shows non-valvular atrial fibrillation. On examination, she has no neurological deficits.\n\nWhich of the following is the next best step in initial management?",
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"explanation": "This patient has a history suggestive of multiple sclerosis, clinically isolated neurological deficits separated in time. The MRI confirmed several hyperintensities in the periventricular white matter. The next investigation is CSF examination, looking for the typical finding of oligoclonal bands, the presence of which gives a definitive diagnosis of MS",
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"explanation": "Anti-aquaporin 4 (AQP4) antibodies are specific for neuromyelitis optica spectrum disorders (NMOSD). Testing would be recommended in patients with long segments of spinal cord demyelination with or without optic neuritis, and in patients with recurrent optic neuritis with normal brain imaging",
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"explanation": "While B12 deficiency can lead to neurological signs, it would not lead to abnormal findings on MRI, nor would symptoms resolve as spontaneously and rapidly",
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"comment": "Question: which investigation most likely to give definitive diagnosis.\nAnswer: CT head, goes onto explain why unnecessary test.\n...? ",
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"explanation": "# Summary\n\nMultiple Sclerosis (MS) is a chronic, inflammatory, autoimmune disease of the central nervous system, characterised by the demyelination and axonal loss of neurons. Key symptoms include sensory disturbance, optic neuritis, internuclear ophthalmoplegia, cerebellar ataxia, and spastic paraparesis. Diagnosis largely involves the use of clinical history, MRI findings, and CSF analysis, aligning with the McDonald criteria. Management of MS involves both acute and chronic strategies, with glucocorticoids commonly used for acute attacks, and a combination of disease-modifying therapies (DMTs) and symptomatic treatments used in the long-term.\n\n# Definition\n\nMultiple sclerosis is a chronic autoimmune disease, primarily involving the central nervous system, which is marked by the degeneration of the insulating covers of nerve cells in the brain and spinal cord, leading to demyelination and eventual axonal loss.\n\n# Epidemiology\n\nMS predominantly affects females with a current ratio of 2.3:1 and a mean onset age of 30 years.\n\n# Aetiology\n\nThe exact cause of multiple sclerosis remains unknown. However, a combination of genetic and environmental factors, including potential viral pathogens, are believed to be contributing factors. \n\nPathologically, CD4-mediated destruction of oligodendroglial cells and a humoral response to myelin binding protein are key features of the disease.\n\n# Signs and Symptoms\n\nMultiple sclerosis can cause a wide range of symptoms depending on the affected area of the brain or spinal cord, but common presentations include:\n\n- Sensory disturbance, marked by patchy paraesthesia\n- Optic neuritis, characterised by loss of central vision, loss of red desaturation and painful eye movements\n- Internuclear ophthalmoplegia, a lesion in the medial longitudinal fasciculus of the brainstem\n- Subacute cerebellar ataxia\n- Spastic paraparesis, as seen in transverse myelitis, including Lhermitte's sign.\n- Bladder and bowel disturbance\n\n\n# Classification\n\nMultiple sclerosis may be divided into two groups:\n\n- Relapsing-remitting (which may become secondarily progressive)\n- Primary progressive.\n\nRelapsing remitting MS makes up 80% of disease at presentation, compared with primary progressive which is <10%.\n\nThe remaining 10% fall into a difficult to classify intermediate group of progressive-relapsing disease.\n\n# Differential Diagnosis\n\nDiseases that should be considered in differential diagnosis include:\n\n- **Neuromyelitis optica (Devic's disease)**: Characterised by optic neuritis and transverse myelitis.\n- **Systemic lupus erythematosus (SLE)**: Presents with multisystem involvement, including the CNS. Symptoms may include fatigue, joint pain, rash, and fever.\n- **Lyme Disease**: Early signs and symptoms include fever, chills, headache, fatigue, muscle and joint aches, and swollen lymph nodes. Later signs and symptoms may involve the nervous system.\n- **Neurosarcoidosis**: Symptoms include seizures, hearing loss, facial palsy, and psychiatric symptoms.\n- **Vitamin B12 Deficiency**: Presents with weakness, tiredness, or lightheadedness, heart palpitations and shortness of breath, pale skin, constipation, loss of appetite, nerve problems like numbness or tingling, and mental problems like depression, memory loss, or behavioral changes.\n\n\n# Investigations\n\nThe diagnosis of multiple sclerosis is based on at least two of:\n\n- Clinical history/examination\n- Imaging findings\n - Typically these are periventricular white matter lesions seen on MRI **disseminated in time and space**\n\n[lightgallery]\n\n- Oligoclonal bands in the CSF\n - These reflect various immunoglobulins seen on CSF electrophoresis and indicate the presence of an auto-immune process in the CNS.\n - They are very sensitive for multiple sclerosis although they can also be found in other auto-immune and infectious conditions including Lyme disease, SLE and neurosarcoid.\n - Visual evoked potential can help further characterise the diagnosis in patients presenting with optic neuropathy\n\n## McDonald criteria for Diagnosis\n\nThe McDonald criteria (last revised in 2017) is the generally accepted standard for diagnosis:\n\n| Clinical Presentation | Additional Data Needed |\n| ------------------------------------------------------------ | ------------------------------------------------------------ |\n| 2 or more attacks (relapses) <br />2 or more objective clinical lesions | None; clinical evidence will suffice (additional evidence desirable but must be consistent with MS) |\n| 2 or more attacks<br />1 objective clinical lesion | Dissemination in space, demonstrated by:<br /> MRI _or_ <br />A positive (cerebrospinal fluid) CSF and 2 or more MRI lesions consistent with MS _or_ <br />Further clinical attack involving different site |\n| 1 attack <br />2 or more objective clinical lesions | Dissemination in time, demonstrated by: <br />MRI _or_ <br />Second clinical attack |\n| 1 attack<br />1 objective clinical lesion (monosymptomatic presentation) | Dissemination in space demonstrated by: MRI or positive CSF and 2 or more MRI lesions consistent with MS **and** <br />Dissemination in time demonstrated by: MRI or second clinical attack |\n| Insidious neurological progression suggestive of MS (primary progressive MS) | One year of disease progression (retrospectively or prospectively determined) and TWO of the following: <br />a. Positive brain MRI (nine T2 lesions or four or more T2 lesions with positive visual evoked potentials [VEP) <br />b. Positive spinal cord MRI (two focal T2 lesions) <br />c. Positive CSF |\n\n# Acute management\n\n- An acute attack of multiple sclerosis should be treated with glucocorticoids involving local neurology services\n- 1g of intravenous methylprednisolone every 24 hours for 3 days is a typical regimen\n- Infections must first be excluded\n\t- \tAlways ensure to check routine bloods and urine dip to rule out any intercurrent infection.\n\t- While these interventions does not appear to affect long term outcome, it does appear to reduce the duration and severity of individual attacks.\n\n\n# Chronic management\n\nManagement of patients with multiple sclerosis should be led by a multidisciplinary team approach of neurologists, physiotherapists, occupational therapists, psychologists and many other allied healthcare professionals.\n\nThere are two groups of drugs used in the long term management of _relapsing remitting multiple sclerosis_: disease modifying therapies (DMTs) and symptomatic therapies.\n\nThe former group may be divided into three:\n\n- First-line injectables such as beta-interferon and glatiramer\n- New oral agents such as dimethyl fumarate, teriflunomide and fingolimod\n- Biologics such as natalizumab and alemtuzumab.\n\nAs a general rule, increasingly effective treatments are associated with increasingly significant side effects.\n\nThe extent to which long-term use of DMTs reduces risk of secondary progressive MS is not yet clearly established.\n\nSymptomatic therapies include:\n\n- Physiotherapy\n- Baclofen and Botox for spasticity\n- Modafinil and exercise therapy for fatigue\n- Anticholinergics for bladder dysfunction\n- SSRIs for depression\n- Sildenafil for erectile dysfunction\n- Clonazepam for tremor\n\n# Prognosis\n\nThe prognosis of multiple sclerosis (MS) can vary widely among individuals, and several risk factors have been identified that are associated with a worse prognosis. These risk factors may include:\n\n1. **Age at onset**: Onset of MS at an older age, typically over 40, is associated with a worse prognosis.\n2. **Male gender**: Men with MS often experience a more severe and rapidly progressing form of the disease compared to women.\n3. **Primary Progressive MS**: This form of MS is characterised by a steady and continuous worsening of symptoms without distinct relapses and remissions. It tends to have a worse prognosis compared to relapsing forms of the disease.\n4. **High relapse rate**: Frequent relapses and a higher relapse rate can indicate a more aggressive form of the disease, which may lead to greater disability over time.\n5. **Rapid accumulation of disability**: A quick accumulation of physical disability in the early stages of the disease is associated with a less favorable prognosis.\n7. **High lesion load**: A higher burden of lesions (plaques) in the brain and spinal cord on MRI scans is associated with a worse prognosis.\n8. **Cognitive impairment**: Cognitive dysfunction, such as memory problems and difficulties with thinking and processing information, can indicate a worse prognosis.\n10. **Comorbid conditions**: The presence of other medical conditions, such as depression or cardiovascular disease, can complicate the management of MS and lead to a worse prognosis.\n11. **Smoking**: Smoking has been associated with an increased risk of developing MS and may also contribute to a worse prognosis.\n\n\nIt's important to note that while these risk factors are associated with a worse prognosis, the course of MS is highly variable, and individual experiences can differ significantly. Early diagnosis, appropriate treatment, lifestyle modifications, and a strong support system can help improve the prognosis and quality of life for people living with MS. \n\n# NICE Guidelines\n\n[NICE Guidelines for Multiple Sclerosis](https://www.nice.org.uk/guidance/ng220)\n\n[NICE CKS for Multiple Sclerosis](https://cks.nice.org.uk/topics/multiple-sclerosis/)",
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"question": "A 29 year old female presents to the GP with a 5-day history of clouding of vision and difficulty differentiating colours. She has a past history of a 2-week period of left upper limb weakness that spontaneously resolved without intervention.\n\nAn MRI reveals several hyperintensities in the periventricular white matter at various regions.\n\nWhat investigation is most likely to give a definitive diagnosis?",
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"explanation": "This would suggest an S1 radiculopathy, which would involve loss of plantarflexion, weakness of leg extension and knee flexion and loss of the ankle jerk reflex. Sensation would be reduced on the posterior aspect of the leg and the lateral edge of the foot",
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"explanation": "This would suggest a sciatic nerve lesion or S1 level lesion. Peripheral neuropathy and cauda equina syndrome may also result in a loss of the ankle jerk reflex; however, this is more likely to present with bilateral foot drop. In common peroneal nerve lesions, the ankle deep tendon reflex is intact",
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"explanation": "This would suggest an L5 radiculopathy or anterior horn cell dysfunction, which would also present with loss of dorsiflexion and eversion, but would also affect foot inversion, internal rotation and abduction of the hip. Patients typically present with back pain radiating down the lateral aspect of the leg",
"id": "32096",
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"comment": "S1 is sole and shin (weak plantar flex can dorsiflex)",
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"explanation": "# Summary\n\nFoot drop is a condition characterized by weakness or paralysis of the foot dorsiflexion and eversion. It can associated with systemic conditions, trauma, or focal neurological lesions. \n\n# Definition\n\nFoot drop, also known as drop foot, is a gait abnormality characterized by the inability or difficulty in lifting the front part of the foot, resulting in dragging of the foot or a high-stepping gait. This condition is typically a symptom of an underlying neurological, muscular, or anatomical pathology.\n\n# Aetiology\n\nFoot drop may be caused by several factors:\n\n- Common peroneal nerve lesions: The most common cause of foot drop is disease or trauma affecting the common peroneal nerve, particularly where it loops over the fibula's head on the knee joint's lateral aspect.\n- L5 root lesion (radiculopathy): Foot drop can be a symptom of this condition, characterized by loss of **inversion** and sensory loss over the L5 dermatome. Lumbosacral disc herniation is the most common cause of this type of foot drop.\n- Distal motor neuropathy: This condition is often associated with foot drop, accompanied by glove and stocking sensory disturbance and loss of all movements of the foot.\n- Small cortical lesions: Foot drop can be associated with small cortical lesions, often presenting with other upper motor neuron features.\n- Other causes: Intrinsic cord disease, partial sciatic nerve disease, and myopathy may also mimic foot drop, although these are less common.\n\n# Signs and Symptoms\n\nKey motor findings in foot drop include:\n\n- Weakness or paralysis of dorsiflexion and eversion of the foot\n- Difficulty in lifting the front part of the foot\n- A high-stepping gait or foot dragging\n\nIn specific aetiologies, additional symptoms may be present:\n\n- In L5 root lesions, loss of **inversion** (a tibial nerve function not lost in common peroneal nerve lesions), sensory loss over the L5 dermatome, and sciatica-type shooting leg pain.\n- In distal motor neuropathy, glove and stocking sensory disturbance, and loss of all foot movements.\n\n\n# Investigations\n\nInvestigations for foot drop typically involve:\n\n- Neurological examination: To assess the strength, sensation, and reflexes in the lower limbs.\n- Electromyography (EMG) and Nerve Conduction Studies (NCS): To evaluate the electrical activity in the muscles and nerves.\n- Imaging studies: MRI or CT scans of the spine or brain may be ordered to identify potential causes such as disc herniations, spinal cord injuries, or small cortical lesions.\n- Blood tests: To identify potential underlying conditions such as diabetes or other systemic diseases.\n\n# Management\n\nIn most cases of common peroneal nerve palsy, the condition resolves spontaneously with lifestyle modifications avoiding the underlying cause of pressure or damage to the nerve.\n\nOther menaagement options include:\n\n- Physiotherapy: To strengthen the foot and leg muscles and improve gait.\n- Orthotic devices: Such as braces or ankle-foot orthoses (AFOs) to support the foot and ankle.\n- Medication: For underlying conditions that may cause foot drop such as diabetes\n- Surgery: In some cases, decompression surgery or nerve grafts may be necessary.",
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"explanation": "In cerebral venous sinus thrombosis, recurrent seizures are more likely to develop in those who present with seizures and in those with supratentorial brain lesions on imaging. This would not be appropriate in the initial management, but may be considered later on for seizure prophylaxis",
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"explanation": "This usually occurs after 20 weeks gestation and would involve hypertension with proteinuria. Symptoms may include headache, visual disturbances, epigastric pain and marked oedema. Proteinuria 1+ in this scenario may suggest preexisting renal disease as she is at an early gestational stage",
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"explanation": "This usually occurs in the 3rd trimester, and patients may have abdominal pain, pruritus and features of cholestasis (pale stools, dark urine, steatorrhoea). In pregnancy, ALP levels are usually raised by about 1.5 to 2 times the normal level, as is the case in this question",
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"explanation": "This usually occurs after 20 weeks gestation and would involve hypertension with proteinuria. Symptoms may include headache, visual disturbances, epigastric pain and marked oedema. Proteinuria 1+ in this scenario may suggest preexisting renal disease as she is at an early gestational stage",
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"comment": "Does anyone know why she has an elevated ALP?\n",
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"comment": "Can be raised in normal pregnancy apaz ",
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"comment": "My understanding is that ALP is produced by the placenta so levels can go up during pregnancy",
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"comment": "Why does she have low platelets?",
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"explanation": "# Summary\n\nHyperemesis gravidarum is a severe form of nausea and vomiting that occurs before 20 weeks of gestation, often requiring hospital admission. Key signs and symptoms include relentless vomiting, dehydration, and metabolic disturbances. It is typically diagnosed through exclusion. Differential diagnoses involve various infections, gastrointestinal issues, metabolic conditions, drug toxicity, and molar pregnancy. Investigations may include urine tests, blood tests, and ultrasound. Management strategies encompass fluid and electrolyte replacement, anti-emetic medications, thiamine and folic acid supplementation, antacids, and venous thromboembolism prophylaxis.\n\n\n# Definition\n\n\nHyperemesis gravidarum is a condition characterized by severe nausea and vomiting, commencing before the 20th week of gestation. It is intense enough to necessitate hospital admission and is diagnosed through the process of exclusion.\n\n\n# Differential Diagnosis\n\n\n\nDifferential diagnoses for severe vomiting during pregnancy include:\n\n- Infections: Gastroenteritis, urinary tract infection, hepatitis, and meningitis\n- Gastrointestinal problems: Appendicitis, cholecystitis, bowel obstruction\n- Metabolic conditions: Diabetic ketoacidosis, thyrotoxicosis\n- Drug toxicity\n- Molar pregnancy: Characterized by abnormally high levels of beta-hCG due to gestational trophoblastic disease, which can cause severe nausea and vomiting\n\n\n# Management\n\n\nManagement of hyperemesis gravidarum primarily includes supportive care, such as:\n\n- Fluid replacement therapy to correct dehydration\n- Potassium chloride to address hypokalaemia resulting from excessive vomiting\n- Anti-emetic medications, including cyclizine (first line), or prochlorperazine. In severe cases, ondansetron (2nd line), metoclopramide (2nd line) or domperidone may be utilized.\n- Thiamine and folic acid supplementation to prevent the onset of Wernicke's encephalopathy\n- Antacids to alleviate epigastric discomfort\n- Thromboembolic (TED) stockings and low molecular weight heparin to mitigate the increased risk of venous thromboembolism due to a combination of pregnancy, immobility, and dehydration.\n\n# Complications\n\nPotential complications of hyperemesis gravidarum include:\n\n- Gastrointestinal problems: Mallory-Weiss tears, malnutrition, and anorexia\n- Dehydration leading to ketosis and venous thromboembolism\n- Metabolic disturbances, such as hyponatraemia, Wernicke's encephalopathy, kidney failure, and hypoglycaemia\n- Psychological sequelae, including depression, PTSD, and resentment towards the pregnancy\n- Severe conditions may impact the foetus due to maternal metabolic disturbance, leading to low birth weight, intrauterine growth restriction, and premature labour.\n",
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"question": "A 30-year-old primigravida at seven weeks gestation presents with a ten-day history of morning nausea and vomiting, often unable to tolerate breakfast but managing a light lunch.\n\n\nObservations: Temperature 37.0°C, pulse 90, blood pressure 140/90, respiratory rate 20, SpO2 99% on room air\n\n\n\nLiver function tests:\n\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Albumin|40 g/L|35 - 50|\n|Alanine Aminotransferase (ALT)|21 IU/L|10 - 50|\n|Aspartate Aminotransferase (AST)|32 IU/L|10 - 40|\n|Alkaline Phosphatase (ALP)|210 IU/L|25 - 115|\n|Bilirubin|7 µmol/L|< 17|\n|Gamma Glutamyl Transferase (GGT)|20 U/L|9 - 40|\n\n\n\n\nFull blood count:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|121 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|6.5x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|110x10<sup>9</sup>/L|150 - 400|\n\n\nUrine dip:\n\n\n\n - protein negative\n - blood negative\n - nitrites negative\n - leucocytes negative\n - ketones negative\n\n\n\nClinical examination reveals a soft and non-tender pregnant abdomen appropriate for gestational age.\n\n\n\nWhich of the following is the most likely differential?",
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"explanation": "This is typical of glucose-6-phosphate dehydrogenase (G6PD) deficiency. In HELLP syndrome, the usual finding is schistocytes and burr cells, which are fragmented red blood cells indicating microangiopathic haemolytic anaemia",
"id": "32111",
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"explanation": "Haptoglobin level is a specific marker of haemolysis, and a level of ≤25mg/dL would suggest haemolysis which occurs in HELLP syndrome",
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"explanation": "This is a normal physiologic finding in pregnancy. In HELLP syndrome, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are typically elevated ≥2 times the upper limit of normal",
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"comment": "RBC is broken down into LDH and Hb\nHb is carried in the blood by haptoglobin\nLow levels of haptoglobin imply it's saturated by Hb\n\nAlso, haptoglobin is reduced in haemochromatosis\nIt is an acute phase reactant (like ferritin), and will be raised in states of inflammation and infection",
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"comment": "To make it simple:\nIn HELLP you get haemolysis.\nHaemolysis --> More free Haemoglobin --> More Haptoglobin binds to Haemoglobin to prevent toxic effects --> Less serum haptoglobin available",
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"explanation": "# Summary\n\nHELLP syndrome is a severe pregnancy complication characterized by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). It typically manifests during the third trimester and is part of a spectrum of hypertensive disorders of pregnancy, including preeclampsia. Key signs and symptoms include headache, nausea/vomiting, epigastric pain, right upper quadrant abdominal pain, blurred vision, and peripheral edema. Investigations may include blood tests and ultrasound scans. The definitive treatment is usually the delivery of the baby, with some mothers also requiring blood transfusions or steroids during pregnancy.\n\n\n# Definition\n\n\nHELLP syndrome is a complication of pregnancy characterized by the presence of hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). It often manifests during the third trimester and is considered part of a spectrum of hypertensive disorders of pregnancy, which also includes preeclampsia.\n\n\n# Epidemiology\n\n\n\nHELLP syndrome is relatively rare, affecting approximately 0.5-0.9% of all pregnancies. However, it is a significant cause of maternal and perinatal morbidity and mortality.\n\n\n# Aetiology\n\n\n\nThe exact cause of HELLP syndrome is unknown. However, it is believed to be related to abnormal placentation, endothelial cell injury, and a generalized inflammatory response. Genetic predisposition and immune maladaptation may also play roles.\n\n\n# Signs and Symptoms\n\n\n\nPatients with HELLP syndrome may present with:\n\n- Headache\n- Nausea and/or vomiting\n- Epigastric pain\n- Right upper quadrant abdominal pain due to liver distension\n- Blurred vision\n- Peripheral edema\n\n\n# Differential Diagnosis\n\n\n\nThe differential diagnoses for HELLP syndrome include acute fatty liver of pregnancy, idiopathic thrombocytopenic purpura, and thrombotic thrombocytopenic purpura. These conditions can also present with similar signs and symptoms such as thrombocytopenia, liver dysfunction, and neurological symptoms.\n\n# Complications\n\nMaternal complications include:\n\n- Organ failure\n- Placental abruption\n- Disseminated intravascular coagulopathy (DIC).\n\nFoetal complications include:\n\n- Intrauterine growth restriction\n- Preterm delivery\n- Neonatal hypoxia\n\n\n# Investigations\n\n\nInvestigations for HELLP syndrome may include:\n\n- Full blood count to assess for low platelet count and evidence of hemolysis\n- Liver function tests to assess for elevated liver enzymes\n- Coagulation studies to evaluate for disseminated intravascular coagulation\n- Ultrasound scans to assess for liver abnormalities and placental abruption\n\n# Management\n\n\nThe definitive treatment for HELLP syndrome is usually the delivery of the baby. In some cases, mothers may also require blood transfusions to manage anemia and thrombocytopenia or steroids to accelerate lung maturation in the fetus prior to delivery. After delivery, supportive care and close monitoring are essential.",
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"question": "A 38 year old pregnant female at 32 weeks gestation presents to Maternity Triage with mild upper abdominal pain, vomiting and blurred vision. Her observations are normal, and cardiotocograph reveals no abnormalities with the foetus. Urinalysis is normal.\n\nWhich one of the following laboratory findings is most likely in HELLP (haemolysis, elevated liver enzymes, and low platelets) syndrome?",
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"explanation": "The most likely drug to be used here is acetazolamide, a carbonic anhydrase inhibitor. The patient has idiopathic intracranial hypertension, with the typical features of raised intracranial pressure (headache, tinnitus, papilloedema, visual loss). The treatment involves carbonic anhydrase inhibitors to decrease the rate of cerebrospinal fluid production",
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"explanation": "This is the mechanism of action of sumatriptan, which may be used in the treatment of acute migraine. However, this would not be effective here as the headache is secondary to idiopathic intracranial hypertension",
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"explanation": "This is the mechanism of action of prednisolone. Steroids are not recommended for use in idiopathic intracranial hypertension as their withdrawal can cause severe rebound intracranial hypertension with visual loss, and may worsen weight gain, which is a risk factor for the condition. It may, however, be useful as a temporary measure prior to surgery in the setting of acute visual loss",
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"explanation": "## Summary\n \n\nIdiopathic Intracranial Hypertension (IIH), also known formerly as benign intracranial hypertension or pseudotumor cerebri, is a condition characterised by increased intracranial pressure in the absence of a detectable cause. It predominantly affects young, overweight women and can lead to serious consequences such as permanent visual loss if left untreated. The mainstay of management includes weight loss, acetazolamide and symptomatic management of headaches. Severe cases may require surgical intervention, particularly if there is evidence of progressive visual loss.\n \n\n## Definition\n \nIIH is a disorder of unidentified cause which leads to increased intracranial pressure, typically with an opening pressure above 25 cmH2O on lumbar puncture. \n \nIt has been previously referred to as benign intracranial hypertension, though it is not benign, and pseudotumor cerebri, which can cause confusion as it is not related to an identifiable structural lesion.\n \n## Epidemiology\n \n\nThis condition most frequently occurs in young and obese women, with a sex ratio of approximately 9:1 favoring women. \n \n## Aetiology\n \n\nThe aetiology of IIH remains uncertain. There are some reported associations with several drugs, including:\n \n\n - Oral contraceptive pill\n - Steroids\n - Tetracycline\n - Vitamin A\n - Lithium\n \n\n\n## Signs and Symptoms\n \n\nClassic symptoms of IIH include:\n \n\n - Non-pulsatile, bilateral headaches, typically worse in the morning or after bending forwards. Some patients may also experience morning vomiting.\n - Visual disturbances, such as transient visual darkening or loss, likely due to optic nerve ischaemia. \n - Bilateral papilloedema seen on fundoscopy, indicating increased intracranial pressure.\n - 6th nerve palsy: horizontal diplopia\n \n\nIf untreated, permanent visual damage may result, with 1-3% of patients experiencing vision loss within a year of onset. \n \n\n## Differential Diagnosis\n \n\nDifferential diagnoses for IIH mainly include other causes of increased intracranial pressure or morning headaches, such as:\n \n\n - Brain tumour: Symptoms include new onset or change in pattern of headaches, headaches that gradually become more frequent and more severe, unexplained nausea or vomiting, vision problems, such as blurred vision, double vision or loss of peripheral vision, gradual loss of sensation or movement in an arm or a leg, difficulty with balance, speech difficulties, confusion in everyday matters, personality or behaviour changes, and seizures, especially in someone who doesn't have a history of seizures.\n - Venous sinus thrombosis: Presents with a headache, seizures, abnormal vision, and various neurological symptoms such as weakness, loss of sensation, and decreased level of consciousness. \n - Sleep apnoea: Characterized by excessive daytime sleepiness, loud snoring, observed episodes of stopped breathing during sleep, abrupt awakenings accompanied by gasping or choking, awakening with a dry mouth or sore throat, morning headache, difficulty concentrating during the day, experiencing mood changes, such as depression or irritability, high blood pressure, and nighttime sweating.\n - Migraines: Characterised by nausea, vomitting, phonophobia and photophobia. Usually without visual loss or postural headache.\n \n\n## Investigations\n \n\nSeveral investigations are used to diagnose IIH and rule out other causes of raised intracranial pressure:\n \n\n - Ophthalmoscopy, which typically shows bilateral papilloedema. A referral to ophthalmology for a detailed visual field assessment may be warranted.\n - Imaging studies such as CT and MRI of the head may show signs of increased intracranial pressure. An MRI Venogram may be performed to rule out secondary causes, particularly venous sinus thrombosis.\n - Lumbar puncture is a key diagnostic tool, typically revealing an opening pressure above 20 cmH2O. An abnormal CSF profile may suggest a different diagnosis.\n \n\n## Management\n \n\nManaging IIH effectively includes:\n \n\n - Encouraging weight loss as the first-line and best-supported intervention for managing IIH.\n - Carbonic anhydrase inhibitors such as acetazolamide can be used, but are often poorly tolerated due to side effects like peripheral paraesthesia.\n - Topiramate and candesartan are also commonly used alternatives.\n - More invasive procedures such as therapeutic lumbar punctures, surgical CSF shunting or optic nerve sheath fenestration may be necessary for resistant cases to prevent progressive visual loss.\n \n\n## Prognosis\n \n\nThe prognosis of Idiopathic Intracranial Hypertension (IIH) varies among patients. \n \n\nMost patients have a benign course, but a small proportion may develop severe visual impairment or blindness. \n \n\nVisual outcome can often be favourable if the disease is diagnosed and treated early. The visual morbidity mainly results from the delay in diagnosis or inadequate treatment which can lead to irreversible damage.\n \n\nWeight loss has been associated with remission and can potentially result in a better prognosis. Even a modest weight loss can lead to a significant reduction in intracranial pressure. In some patients, weight gain has been linked with worsening symptoms and increased intracranial pressure.\n \n\n## References\n \n\n 1. Friedman, D. I., Liu, G. T., & Digre, K. B. (2014). Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology, 81(13), 1159–1165. [Link](https://doi.org/10.1212/WNL.0b013e31824e9821)\n 2. Mollan, S. P., Davies, B., Silver, N. C., Shaw, S., Mallucci, C. L., Wakerley, B. R., Krishnan, A., Chavda, S. V., Ramalingam, S., Edwards, J., Hemmings, K., Williamson, M., Burdon, M. A., Hassan-Smith, G., Digre, K., Liu, G. T., Jensen, R. H., & Sinclair, A. J. (2018). Idiopathic intracranial hypertension: consensus guidelines on management. Journal of Neurology, Neurosurgery & Psychiatry, 89(10), 1088–1100. [Link](https://doi.org/10.1136/jnnp-2017-317440)\n 3. Wall, M. (2010). Idiopathic Intracranial Hypertension. Neurologic Clinics, 28(3), 593–617. [Link](https://doi.org/10.1016/j.ncl.2010.03.003)",
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"question": "A 45-year-old woman presents to Accident & Emergency with a one-week history of persistent headache. She was worried as she started experiencing bilateral blurring of vision in the past day. She also reports hearing the sound of 'rushing water' in both ears. Fundoscopy reveals bilateral swelling of the optic discs.\n\nThe consultant reviews her and decides to start her on medication. What is the mechanism of action of the most likely drug used?",
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"explanation": "HIV is one of the systemic causes of eye disease, including HIV retinopathy, cytomegalovirus (CMV) retinitis, herpes simplex virus (HSV) keratitis or retinitis and toxoplasmosis. CMV retinitis tends to be the most common HIV-related eye condition, causing loss of central vision, blind spots, floaters or flashing lights. Fundoscopy typically shows a \"pizza pie\" appearance due to haemorrhagic retinal necrosis",
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"explanation": "This may be done to investigate ankylosing spondylitis. This may cause anterior uveitis, which leads to acute-onset painful vision loss with photophobia, red eye and a constricted pupil. Slit lamp may reveal a hypopyon in the anterior chamber and white precipitates on the cornea. This is not the case here, as the visual loss is painless with no red eye",
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"explanation": "The patient has sudden onset painless monocular vision loss with a fundoscopy finding suggestive of central retinal artery occlusion. This is usually due to thromboembolism, obstructing blood flow to the retinal artery. Workup for cardiovascular risk factors and a possible thromboembolic cause should be done, including investigations for stroke. The patient is hypertensive and a current smoker, both of which are contributing risk factors as well",
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"explanation": "This would be appropriate if suspecting acute anterior ischaemic optic neuropathy, which may occur due to giant cell arteritis (arteritic) or atherosclerosis (non-arteritic). Presenting symptoms include a sudden onset painless monocular vision loss with deterioration of colour vision, and fundoscopy reveals unilateral optic disc oedema with flame-shaped haemorrhages. In giant cell arteritis, erythrocyte sedimentation rate (ESR) would be raised, and temporal artery biopsy is the gold standard investigation",
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"explanation": "This may be done if suspecting multiple sclerosis, which is the top cause of optic neuritis. Patients usually have painless monocular vision loss over hours to days with colour desaturation. Fundoscopy may show a swollen, blurred optic disc. Lumbar puncture would demonstrate oligoclonal bands in the cerebrospinal fluid",
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"comment": "GCA is also a possible cause of central retinal artery occlusion??",
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"comment": "In hindsight, I think the lack of Hx pointing towards GCA + the risk factors of cardioembolic cause would suggest an ECHO is the most correct answer -sucks to suck though because I also got this wrong!",
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"explanation": "# Summary\n\nCentral Retinal Artery Occlusion (CRAO) is an ocular condition marked by sudden, painless vision loss that typically occurs within seconds. The condition is less common than retinal vein occlusion and results in faster deterioration of vision. Key signs and symptoms include a pale retina with a cherry red spot at the macula, carotid bruits, hypertension, atrial fibrillation, diabetes mellitus, smoking, or hyperlipidaemia. Key investigations include fundoscopy and patient history and examination. Management involves treating the primary cause and may include anticoagulant therapy or ocular massage.\n\n# Definition\n\nCentral Retinal Artery Occlusion (CRAO) is a serious ocular condition characterized by a sudden, painless loss of vision. This abrupt vision loss typically occurs over seconds and is due to the occlusion of the central retinal artery.\n\n\n# Epidemiology\n\nCRAO is less common than retinal vein occlusion. However, it is associated with a faster rate of vision deterioration.\n\n\n# Pathophysiology\n\nThe retina receives its blood supply from two sources:\n\n1. Central retinal artery: \n\n - The internal carotid artery's first branch is the ophthalmic artery, which subsequently branches to the central retinal artery\n\n - The central retinal artery enters the eye at the optic disc, then branches into the superior and inferior retinal arteries, before branching into temporal and nasal subdivisions, which each supply a quadrant of the retina\n\n\n2. Choriocapillaries:\n - The peripheral retina receives its blood supply from the capillaries of the choroid, which are branches of the ciliary artery\n\n\nTherefore, the more proximal an occlusion is, the worse the effect on vision:\n\n- Occlusion of the retinal artery before branching is termed **central retinal artery occlusion** (CRAO)\n- Occlusion after branching is termed **branch retinal artery occlusion** (BRAO)\n\nPatients often present with the 'cherry red spot' finding on fundoscopy (see below) and this refers to the fact that the macula/fovea (responsible for central vision) are spared in CRAO. This is because the macula is supplied by the cilioertinal artery which is usually not affected in CRAO.\n\n# Aetiology\n\nCRAO is essentially a stroke that affects the eye, so it has similar risk factors and pathophysiology.\n\nOften the specific aetiology of a CRAO remains unclear, but the most common causes are:\n\n- Atherosclerosis – roughly 80% of cases\n- Embolism – carotid, cardiac or aortic\n- Inflammatory (e.g. GCA, SLE)\n- Thrombophilia (e.g. protein S or C deficiency, antiphospholipid syndrome)\n\n\n# Signs and Symptoms \n\n- In CRAO, patients present with sudden-onset painless loss of vision that typically occurs over seconds – in almost all cases, vision is reduced to counting fingers. \n- Patients may also report a history of amaurosis fugax.\n\nThe classic examination finding is a pale retina with a 'cherry red spot' at the macula. Patients may also have a relative afferent pupillary defect.\n\n[lightgallery]\n\nPatients should also be examined/investigated for risk factors for CRAO including: \n\n- Carotid bruits\n- Hypertension\n- Atrial fibrillation\n- Diabetes mellitus\n- Smoking\n- Hyperlipidaemia\n\n# Differential Diagnosis\n\nDifferential diagnoses for CRAO should include other conditions that can cause sudden vision loss. These may include:\n\n- Retinal Vein Occlusion: Characterised by sudden, painless vision loss, floaters, and decreased peripheral vision.\n- Retinal Detachment: Presenting with flashing lights, floaters, or a shadow in the peripheral vision.\n- Optic Neuritis: Symptoms may include pain, vision loss, and abnormalities in colour vision.\n- Ischemic Optic Neuropathy: Characterised by sudden, painless vision loss and a pale, swollen optic disc.\n\n# Investigations\n\n- Primary investigations for CRAO involve fundoscopy and a thorough patient history and examination. \n- Imaging techniques such as optical coherence tomography (OCT) and fluorescein angiography may also be utilized.\n\n# Management \n\nThe reversibility of damage to the retina decreases with time. Therefore, the window of time in which treatment is likely to be beneficial is short. Evidence to date suggests that, beyond 90–100 minutes, vision is unlikely to improve with treatment.\n\nThe aim of treatment in the acute setting is to reperfuse the ischaemic retina as quickly as possible. Some centres will advocate the following methods, but there is no proven benefit in the literature:\n\n- Ocular massage – aiming to dislodge the embolus\n- Vasodilation with isosorbide dinitrate\n- Anterior chamber paracentesis – aiming to reduce IOP to help dislodge the embolus\n\nLong-term management consists of secondary prevention of further ischaemic end-organ damage.\n\n# Prognosis \n\nThe visual prognosis is unfortunately very poor with CRAO as the neural layer of the retina atrophies swiftly without a blood supply. Only 30% of patients will have any improvement in vision after presentation.\n\n# Branch Retinal Artery Occlusion\n\nBRAO presents similarly to CRAO, but only some of the visual field is lost because only some of the retinal blood supply is occluded.\n\nManagement is the same as for CRAO and mainly consists of long-term secondary prevention.\n\n# References\n\nDenniston AK, Murray PI. Oxford Handbook of Ophthalmology. Fourth Edition. Oxford University Press. 2018.\n\n[Further information on Patient.co.uk](https://patient.info/doctor/retinal-artery-occlusions)\n",
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"question": "A 75-year-old male presents to the Emergency Department with sudden vision loss in his right eye. His past medical history includes hypertension, and he is a smoker.\n\nHis right eye is painless, and there is no conjunctival redness. Fundoscopy reveals a red spot at the macula.\n\nWhich of the following tests are most appropriate in investigating the underlying cause?",
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"explanation": "This is a beta-blocker that would be contraindicated in patients with asthma, COPD, heart block and severe heart failure, to name a few conditions. It may cause bronchoconstriction in a patient with asthma",
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"label": "c",
"name": "Timolol",
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"explanation": "This is a cycloplegic that dilates the pupil and is used in anterior uveitis to prevent the formation of posterior synechiae. It would worsen glaucoma as it exacerbates angle closure",
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"explanation": "This patient is presenting with acute angle closure. The immediate management of this includes pilocarpine eye drops, acetazolamide (contraindicated in this case), analgesia and an anti-emetic if needed.",
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"explanation": "This is an alpha agonist that reduces aqueous secretion and increases outflow through the trabecular meshwork. It is contraindicated in patients taking monoamine oxidase inhibitors (selegiline in this case) due to the risk of hypertensive crisis",
"id": "32126",
"label": "d",
"name": "Brimonidine",
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"explanation": "This is a carbonic anhydrase inhibitor, which is contraindicated in those with sickle cell disease, as it may precipitate a vaso-occlusive crisis by exacerbating sickling of cells. In the absence of contraindications, IV acetazolamide may be given in acute glaucoma to lower intraocular pressure",
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"comment": "I'm flabbergasted ",
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"comment": "This case sounds like acute angle closure in which case they use pilocarpine first line. \nI’m pretty sure they sure latanoprost for open angle closure glaucoma instead. ",
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"comment": "why would acetazolamide be contraindicated in this case ??",
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"comment": "Acetazolamide is not advised for patients with sickle cell disease as it can cause metabolic acidosis, increasing the likelihood of red blood cell sickling and may trigger a vaso-occlusive crisis. Additionally, its diuretic effect can lead to dehydration, further heightening the risk of sickling episodes.",
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"explanation": "# Summary\n\nPrimary angle closure glaucoma (PACG) is a severe ocular condition primarily affecting older individuals, particularly those of Asian ethnicity or with hypermetropia. Key signs and symptoms include systemic discomfort, nausea, headaches, ocular pain, blurred vision, and a fixed-dilated pupil. Immediate referral to ophthalmology is necessary to prevent progression of visual loss. Key investigations include intraocular pressure measurement and ophthalmological examination. Management includes the prompt reduction of intraocular pressure via a combination of pharmaceutical interventions, and potentially a peripheral iridectomy.\n\n# Definition\n\nPrimary Angle Closure Glaucoma (PACG) is a type of glaucoma characterized by the blockage or narrowing of the drainage angle formed by the cornea and the iris, resulting in a sudden increase in intraocular pressure. \n\n# Pathophysiology\n\nIn health, aqueous humour, which is produced by the ciliary body, flows through the pupil and leaves the eye via the trabecular meshwork.\n\nThe trabecular meshwork is a circular structure that lies in the anterior chamber angle, which is where the cornea meets the iris.\n\nPprimary angle-closure glaucoma occurs when the iris blocks the drainage angle, which causes a rise in IOP and subsequent damage to the optic nerve. **Primary angle closure** is the term used to describe when the iris blocks the drainage angle but there is no evidence of optic nerve damage.\n\n# Epidemiology\n\nPACG predominantly affects older individuals, with an incidence rate of approximately 0.4% in individuals over 40 years of age in the UK.\n\n# Risk Factors\n\n* Hyperopia (long-sightedness) and short axial length of the eyeball\n* Age – the lens grows with age and can push the iris forwards into the angle\n* Ethnicity – Asian or Inuit populations\n* Pupillary dilatation – either iatrogenically (eg. topical mydriatics or systemic alpha-adrenergic agonists) or owing to the patient being in a dimly lit environment (eg. watching television in a dark room) \n\n\n# Signs and Symptoms\n\n## Symptoms\n\n- **Pain** – an extremely painful eye that develops rapidly, with pain spreading throughout the orbit\n- **Blurred vision** – can progress to vision loss\n- **Haloes** – patients will often describe coloured haloes around lights\n- **Systemically unwell** – nausea and vomiting are very common presenting symptoms\n\n\n## Signs\n\n- **Red eye** – ciliary flush with a hazy cornea\n- **Mid-dilated or fixed pupil** \n- **Closed iridocorneal angles** on gonioscopy\n- **Corneal oedema**\n- **Raised IOP** (defined as >21 mmHg) – the globe may feel hard on palpation\n\n\n# Differential Diagnosis\n\nThe main differential diagnoses for PACG include other types of glaucoma, such as open-angle glaucoma, as well as other ocular emergencies like acute anterior uveitis and retinal detachment. The key presenting signs and symptoms of these conditions are:\n\n- Open-angle glaucoma: Gradual loss of peripheral vision, usually in both eyes, and tunnel vision in the advanced stages.\n- Acute anterior uveitis: Red, painful eye, blurred vision, photophobia, and a small, irregular pupil.\n- Retinal detachment: Sudden appearance of floaters, flashes of light in the periphery, and a shadow or curtain over a portion of the visual field.\n\n# Investigations\n\nIn cases of suspected PACG, the following investigations are typically performed:\n\n- Gonioscopy - assessing angle between iris and cornea \n- Tonometry - measurement of intraocular pressure\n- Ophthalmological examination\n\n# Management\n\nAcute angle-closure glaucoma is an emergency and requires urgent admission and referral to ophthalmology.\n\n## Medical management\n\nThe intra-ocular pressure (IOP) must be reduced as soon as possible to prevent further damage to the optic nerve and preserve vision. Medical management consists of:\n\n- IOP-lowering agents e.g. a combination of beta blockers, pilocarpine, and IV acetazolamide.\n- Rarely intravenous hyperosmotics (eg. mannitol) may be added if there is no improvement in IOP\n- Analgesia and antiemetics\n\nThe aim of medical management is to stabilise or reduce the IOP while awaiting formal ophthalmological assessment and definitive surgical intervention.\n\n## **Surgical management**\n\n- **Peripheral iridotomy** – a laser is used to make a hole in the peripheral iris to allow free flow of aqueous – the contralateral eye is treated prophylactically as it is predisposed to PACG\n- **Surgical iridectomy** – rarely used nowadays, but still carried out when a laser iridectomy is not possible\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on glaucoma](https://cks.nice.org.uk/topics/glaucoma/)\n\n\n\n",
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"question": "A 50-year-old woman presents to the Emergency Department with sudden onset severe pain in her right eye. Her past medical history includes severe asthma, sickle cell disease and depression. She only takes selegiline. She has nausea and vomited once on the way to the hospital. On inspection, she has right conjunctival redness, and her right pupil reacts poorly to light.\n\nWhich of the following medications should be started?",
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"explanation": "If median nerve injury occurs more proximally at the elbow (most commonly due to a supracondylar fracture of the humerus), this may result in a hand of benediction (inability to flex the 2nd and 3rd fingers when making a fist) and paralysis of the flexors and pronators of the forearm. Sensation to the palmar aspect of the lateral 3.5 fingers may also be affected",
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"explanation": "Isolated musculocutaneous nerve lesions are rare. This would result in weakness of elbow flexion and forearm supination, weak biceps tendon reflex and sensory loss over the lateral surface of the forearm",
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"explanation": "This is most commonly damaged by direct trauma to the shoulder or proximal humerus, such as in fracture of the surgical neck of the humerus or shoulder dislocation. It would result in regimental badge numbness (over the inferior portion of the deltoid) and inability to abduct the affected shoulder due to deltoid and teres minor muscle weakness",
"id": "32132",
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"name": "Axillary nerve",
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"explanation": "This is golfer's elbow, which results from medial epicondylitis. The ulnar nerve may be compressed as it passes through the ulnar groove, which lies posterior and lateral to the medial epicondyle, resulting in numbness and/or tingling in the 4th and 5th fingers",
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"explanation": "This is most likely to be affected in tennis elbow, which results from lateral epicondylitis as the radial nerve travels anterior to the lateral epicondyle to enter the forearm. Pain is exacerbated in resisted wrist extension or supination. It may lead to radial nerve entrapment syndrome, causing wrist drop, loss of sensation to the anatomical snuff box and radial 3.5 digits on the dorsum of the hand",
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"explanation": "# Summary\n\nMedial epicondylitis, also known as 'golfer's elbow', is a condition resulting from tendinopathy of the wrist flexor tendons attaching to the medial epicondyle of the distal humerus. Patients typically present with gradual-onset medial elbow pain, which is exacerbated by activity, especially wrist flexion, and may also report wrist flexion weakness. The diagnosis is primarily clinical. Key investigations may include physical examination, MRI, and ultrasound. Management strategies predominantly involve conservative measures such as rest and guided rehabilitation, with surgical debridement as a potential course of action for cases unresponsive to six months of non-surgical treatment.\n\n# Definition\n\nMedial epicondylitis, or 'golfer's elbow', is a condition that arises due to tendinopathy of the wrist flexor tendons, which attach to the medial epicondyle of the distal humerus. The primary tendons involved include the flexor carpi radialis, pronator teres, palmaris longus, flexor digitorum superficialis, and flexor carpi ulnaris.\n\n# Epidemiology\n\nMedial epicondylitis most commonly affects individuals between 20 and 50 years of age. The condition is more prevalent in athletes or those involved in repetitive activities that stress the involved tendons. Despite its moniker \"golfer's elbow,\" it can affect individuals from various occupations and recreational backgrounds.\n\n# Aetiology\n\nMedial epicondylitis typically results from overuse and strain of the muscles and tendons involved in wrist flexion and forearm pronation. It often occurs due to repetitive strain, especially in sports like golf, but it can also arise from occupational activities that involve repetitive wrist flexion or twisting motions.\n\n# Signs and Symptoms\n\nPatients generally report a gradual onset of medial elbow pain that worsens with activity, particularly during wrist flexion. Additional symptoms may include weakness of wrist flexion and a decreased range of motion in the affected arm.\n\n# Differential Diagnosis\n\nThe main conditions to consider in the differential diagnosis include:\n\n- **Lateral Epicondylitis ('Tennis Elbow')**: Characterised by pain and tenderness over the lateral aspect of the elbow, exacerbated by wrist extension.\n- **Olecranon Bursitis**: Presents with swelling and pain at the back of the elbow.\n- **Cubital Tunnel Syndrome**: Marked by numbness or tingling in the ring and little fingers, weakness in the hand, and pain on the inside of the elbow.\n- **Ulnar Neuropathy**: Symptoms can include numbness and tingling in the fourth and fifth fingers, elbow pain, and weakness of the hand.\n\n# Investigations\n\nThe diagnosis of medial epicondylitis is primarily clinical. Physical examination can reveal pain and tenderness at the medial epicondyle, exacerbated by resisted wrist flexion and forearm pronation. If the clinical presentation is unclear, imaging modalities such as MRI or ultrasound may be utilized to confirm the diagnosis and assess the extent of the lesion.\n\n# Management\n\nMedial epicondylitis is generally managed conservatively with rest and guided rehabilitation, which can include physical therapy, pain management with NSAIDs, and corticosteroid injections. Surgical debridement of damaged tissue may be indicated in cases which do not respond to six months of non-surgical management.\n\n# External links\n\n- [Physiopedia: Medial Epicondyle Tendinopathy](https://www.physio-pedia.com/Medial_Epicondyle_Tendinopathy)\n- [Ortho Bullets: Medial Epicondylitis (Golfer's Elbow)](https://www.orthobullets.com/shoulder-and-elbow/3083/medial-epicondylitis-golfers-elbow)",
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"question": "A 30-year-old male presents to his GP with a two-month history of persistent right elbow pain. He describes a tingling sensation in the 4th and 5th fingers. On examination, the pain is aggravated by wrist flexion and pronation of the arm.\n\nWhich single nerve is involved?",
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"explanation": "This is an early finding in compartment syndrome",
"id": "32136",
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"explanation": "The patient has developed compartment syndrome due to significant trauma causing bleeding and raised intracompartmental pressure within the limb. Late findings may also include the absence of distal pulses, and hypoesthesia. The patient would require an urgent fasciotomy to relieve the pressure within the compartment. It is important to remember always to have a high index of suspicion for compartment syndrome as clinical signs may be varied, and consider urgent referral for any patient with a tense, painful muscle compartment",
"id": "32133",
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"explanation": "Tingling sensations in the limb are an early finding in compartment syndrome and would suggest ischaemic nerve dysfunction. Sensory deficits would typically precede motor deficits, i.e. weakness of the limb",
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"explanation": "# Summary\n \nCompartment syndrome occurs when an increase in pressure in a closed anatomical compartment causes local tissue ischaemia. Typically the increase in pressure is secondary to inflammation caused by a traumatic injury, usually a fracture. Key signs and symptoms include severe pain out of keeping with the associated injury, particularly during passive stretching, pallor, limb paralysis, pulselessness, and paraesthesia. Rapid diagnosis is crucial to prevent complications of limb loss, loss of function and rhabdomyolysis causing renal failure. Diagnosis is clinical however compartment pressures may be measured at the bedside or during surgery. Definitive management is urgent fasciotomy, with IV fluids and analgesia both important. \n\n# Definition\n \nCompartment syndrome refers to the condition that results when inflammation of injured muscle causes an increase in pressure within a fascial compartment. As the pressure rises, circulation is cut off leading to tissue ischaemia and necrosis. \n \n# Aetiology\n\nThe majority of cases of compartment syndrome occur secondary to fractures, with tibial, forearm and wrist fractures carrying the highest risk. \n\nOther causes include:\n\n- Crush injuries\n- Excessive exercise\n- Constrictive dressings or plaster casts\n- Prolonged immobilisation\n- Reperfusion of ischaemic limbs\n\n# Signs and Symptoms\n\nThe classic symptom of compartment syndrome is severe pain that is typically out of proportion to the initial injury. On examination, passive stretching of the affected muscles exacerbates the pain.\n\nOther signs and symptoms occur sequentially as the increasing pressure initially compresses veins, followed by nerves then arteries:\n\n- Paraesthesia\n- Pallor \n- Pulselessness\n- Paralysis\n- Coolness of the affected limb\n- The area may feel tense on palpation\n\n\n# Differential Diagnosis\n \n- **Deep vein thrombosis** also causes pain and may be associated with immobility and inflammation after injury, however the affected area is usually warm, erythematous and swollen\n- **Cellulitis** also causes localised pain and may be associated with injury; the patient may also be systemically unwell, however skin is erythematous and warm to touch \n- **Acute limb ischaemia** can both result from compartment syndrome and may also lead to compartment syndrome after reperfusion, however they are not always associated and are managed differently. Symptoms and signs of pain, paraesthesia, pallor, pulselessness, paralysis and \"perishing\" coldness of the limb are classic but the significant pain of compartment syndrome and a preceding injury may not be seen.\n\n# Investigations\n\nCompartment syndrome is a clinical diagnosis, however it is possible to measure intra-compartmental pressures directly (for example in atypical presentations). Normal compartment pressures are 0-8mmHg; in compartment syndrome these are often above 40mmHg. A difference between the patient's diastolic blood pressure and the compartment pressure of under 30mmHg is suggestive of compartment syndrome.\n\nOther useful tests include:\n\n- **CK** is often elevated due to ischaemic muscle damage\n- **U&Es** may be deranged secondary to rhabdomyolysis\n- **FBC**, **LFTs**, **clotting** and **group and saves** should be done in preparation for surgery\n- An **ECG** should also be done in preparation for surgery; arrhythmias may occur secondary to rhabdomyolysis\n\n# Management\n\n- Urgent surgical referral for immediate fasciotomies is the key management - surgery should occur within an hour of deciding to operate\n- This involves making surgical incisions through the fascia to relieve the pressure in the affected compartment\n- These incisions are left open and further operations may be required to debride necrotic tissues - a re-exploration should be performed at 24-48 hours\n- Remove any circumferential dressings or casts\n- Elevate the limb to the level of the heart to maximise perfusion\n- Resuscitate with IV fluids and supplementary oxygen to maintain perfusion and oxygenation\n- Ensure adequate analgesia is given (usually IV opioids); avoid regional anaesthesia as this may mask symptoms\n- Close monitoring including the neurovascular status of the limb is crucial\n- Ensure other injuries are addressed; intensive care input may be required especially if serious complications arise (e.g. renal failure secondary to rhabdomyolysis)\n\n# Complications\n \n- **Rhabdomyolysis** due to ischaemia of muscles, which may lead to renal failure and arrhythmias as well as death\n- **Limb amputation** may be required if there is extensive necrosis of tissues\n- **Volkmann contracture** refers to an ischaemic contracture which causes a flexion deformity of a limb due to ischaemic injury of its deep tissues\n\n# References\n\n[British Orthopaedic Assocation - Diagnosis and Management of Compartment Syndrome of the Limbs](https://www.boa.ac.uk/static/0d37694f-1cad-40d5-b4c1032eef7486ff/de4cfbe1-6ef3-443d-a7f2a0ee491d2229/diagnosis%20and%20management%20of%20compartment%20syndrome%20of%20the%20limbs.pdf) \n\n[Life in the Fast Lane - Compartment Syndrome](https://litfl.com/compartment-syndrome-ccc/)\n\n[Radiopaedia - Acute Compartment Syndrome](https://radiopaedia.org/articles/acute-compartment-syndrome?lang=gb)\n\n[Patient UK - Compartment Syndrome](https://patient.info/doctor/compartment-syndrome-pro)",
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"question": "A 40-year-old motorcyclist is involved in a road collision accident and sustains a displaced tibial shaft fracture. He undergoes closed reduction, and his leg is immobilised in a long cast. A few hours after the procedure, he complains of severe pain in the affected limb that seems disproportionate to clinical findings.\n\nGiven the most likely complication that has occurred, which of the following is considered a late finding in his condition?",
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"explanation": "This patient has presented with diabetic ketoacidosis, meeting the criteria of hyperglycaemia, acidosis and ketonaemia. A resuscitation fluid bolus of maximum 10-20ml/kg 0.9% normal saline should be given initially. It should not exceed this amount due to the increased risk of cerebral oedema. Subsequently, the maintenance fluid volumes should be calculated, and the volume deficit gradually replaced over the next 48 hours. The initial resuscitation fluid bolus should be subtracted from the maintenance fluid volume if the patient is not in shock",
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"explanation": "This is reserved for symptomatic hyponatraemia with a depressed level of consciousness and a high risk of cerebral oedema, which may occur if fluid administration is given too rapidly. **This should not be given without discussing with a senior first!** In diabetic ketoacidosis, the sodium levels should always be corrected for hyperglycaemia",
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"explanation": "This **should not** be given to children and young people with diabetic ketoacidosis. It should only be reserved for special situations in which the patient has compromised cardiac contractility caused by life-threatening hyperkalaemia or severe acidosis, and only after discussion with a senior. The initial metabolic acidosis should resolve upon treatment with intravenous fluids and an insulin infusion",
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"explanation": "This would be a suitable maintenance fluid regimen. Maintenance fluid volumes for children in DKA can be calculated as reccommended by the BPSED DKA guideline as: 100ml/kg/day for the first 10kg of bodyweight, 50ml/kg/day for weight between 10-20kg and then 20ml/kg/day for each additional kg above 20kg. For a 40kg boy, it would be (100ml x 10kg) + (50ml x 10kg) + (20ml x 20kg) = 1000ml + 500ml + 400ml = 1900ml over 24 hours",
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"explanation": "This would be one of the treatments for hyperkalaemia. However, this should not be given as a fixed rate insulin infusion would be started for the initial management of diabetic ketoacidosis, which would drive potassium into cells and cause the K levels to fall. Potassium replacement should be added to bags of maintenance fluid unless the patient has K levels above the upper limit of normal",
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"comment": "explanation sounds like 1900ml over 24 hours is correct?\n",
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"comment": "think its describing that as an appropriate maintenance dose, but that this patient requires a bolus first as they are significantly dehydrated",
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"comment": "how do you work out they are significantly dehydrated?",
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"comment": "@relapse sclerosis electrolyte imbalances, urea, and just general clinical presentation",
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"comment": "40kg at 5 years old? Dude must be a giant. ",
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"comment": "i think explanation is wrong, rapid correction of hyponatremia causes central pontine myelinolysis, not cerebral oedema. the latter is if you correct hypernatraemia too quickly which this patient is not at risk of",
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"comment": "that is what I thought initially but apparently it is pseudohyponatraemia. Hyponatremia in DKA is often pseudohyponatremia, meaning the sodium level appears low on lab tests but is not truly low in the body. This occurs due to:\n\nHyperglycemia: High blood glucose levels cause water to shift out of cells and into the bloodstream (osmotic effect), diluting the sodium concentration. For every 100 mg/dL increase in blood glucose above normal, serum sodium decreases by approximately 1.6–2.4 mEq/L.\nCorrected Sodium Calculation: To determine the true sodium level, you can use the following formula:\nCorrected Sodium\n=\nMeasured Sodium\n+\n0.016\n×\n(\nGlucose\n−\n100\n)\nCorrected Sodium=Measured Sodium+0.016×(Glucose−100)\nThis adjustment accounts for the dilutional effect of hyperglycemia.",
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"comment": "Cerebral oedema is a well-recognised and potentially fatal complication of diabetic ketoacidosis (DKA) in children. Its mechanism is not fully understood, but it is thought to arise from rapid fluid shifts caused by a sudden decrease in serum osmolality during treatment.",
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"explanation": "# Summary\n \n\nDiabetic ketoacidosis (DKA) is a serious complication often associated with type 1 diabetes, characterised by hyperglycaemia, ketonaemia, and acidosis. Key signs and symptoms include fruity-smelling breath, vomiting, dehydration, abdominal pain, hyperventilation, and altered mental status. Investigations include blood glucose and ketone measurements, blood gas analysis, urea and electrolytes, and possibly blood cultures if infection is suspected. Management strategies largely depend on the patient's condition, including hydration and insulin administration via various routes and in various volumes based on severity. The major complication is cerebral oedema, a rare but potentially fatal condition that might be caused by rapid correction of dehydration with IV fluids.\n \n\n# Definition\n \n\nDiabetic ketoacidosis (DKA) is a severe and life-threatening medical complication characterised by hyperglycaemia, acidosis and ketonaemia.\n\nIt is defined by acidosis (bicarbonate < 15 mmol/l or pH <7.3) and ketones >3.0 mmol/L. \n \n\n# Epidemiology\n \n\nDKA is most commonly seen in individuals with type 1 diabetes. However, it can occur in those with type 2 diabetes under extreme stress or illness. The condition can be the first presentation of diabetes, especially type 1 diabetes in children and young adults.\n\nIt is more common in children under 5. \n \n\n# Aetiology\n \n\nDKA can be precipitated by several factors, including infection, dehydration, stress, burns, fasting, or untreated type 1 diabetes. It is important to note that fever is not a typical part of DKA presentation. A raised temperature could indicate an underlying infection that may have triggered the DKA.\n\nRisk factors include:\n\n- Previous episodes of DKA \n- Peripubertal and adolescent girls \n- Comorbidities including psychiatric disorders\n- Difficult home life\n- Insulin pump therapy \n\n\n# Classification\n\n- Mild: pH 7.1-7.29 or bicarbonate < 15 mmol/L. Dehydration 5%\n- Moderate: pH 7.1-7.19 or bicarbonate < 10 mmol/L. Dehydration 5%\n- Severe: pH <7.1 or bicarbonate < 5 mmol/L\n \n\n# Signs and Symptoms\n \n\nPatients with DKA may present with:\n \n\n - Fruity-smelling breath (due to the presence of acetone)\n - Vomiting\n - Dehydration secondary to polydipsia and polyuria \n - Abdominal pain\n - Deep, sighing respiration (Kussmaul respiration)\n - Signs of hypovolaemic shock\n - Altered mental status, including drowsiness or coma\n \n\n# Differential Diagnosis\n \n\nThe main differential diagnoses for DKA in children include:\n \n - **Lactic Acidosis**: This may present with rapid breathing, abdominal pain, and altered mental status. The patient may have a history of severe illness or sepsis, hepatic failure or metformin use.\n - **Starvation Ketosis**: This usually presents with weight loss, nausea, and clear mental status. The condition is mild, with low-level ketonaemia.\n - **Inborn errors of metabolism**: Tend to present earlier in life with metabolic disturbances or failure to thrive. \n - **Sepsis**: The child will be generally unwell, with a high or low temperature, hypotension and tachycardia. \n \n\n# Investigations\n \n\nDiagnosis of DKA involves assessment of clinical features along with:\n \n\n - Blood glucose (>11.1mmol/L)\n - Blood ketones (>3mmol/L)\n - Urea and electrolytes\n - Blood gas analysis\n - Urinary glucose and ketones\n - Blood cultures (if evidence of infection)\n - Cardiac monitoring/ECG (for any ischaemic changes or changes secondary to hypokalaemia)\n \n\nNote that hyperglycaemia may not always be present in DKA.\n \n\n# Management\n \n\nManagement of DKA should be based on the A to E approach followed by the following treatments: \n\n - IV fluids (initial bolus of 10ml/kg 0.9% NaCl, even if the patient is shocked) given over 15 minutes.\n - Repeat as needed to restore circulation\n - At 40 ml/kg then discuss with a senior for consideration for inotropes \n - Insulin infusion at 0.1 units/kg/hour 1 hour after starting IV fluids\n\n\nFluids:\n\n- Further fluids, following initial boluses should contain 40 mmol/l potassium chloride to protect against hypokalaemia. \n- Total fluid required = deficit + maintenance\n- Hourly rate = [(Deficit - initial bolus) / 48 hours ] + maintenance per hour \n- Deficit \n - A 5% fluid deficit is assumed for children with mild or moderate DKA\n - A 10% fluid deficit is assumed for children with severe DKA\n - Deficit should be replaced over 48 hours alongside maintenance fluids \n- Maintenance \n - Calculated by Holliday-Segar formula: 100 ml/kg/day for the first 10 kg, 50 ml/kg/day for the next 10 kg, and 20 ml/kg/day for each additional kg over 20 kgs. \n \nImportant points to consider: \n\n- Monitoring should include hourly blood glucose and ketones, neurological observations and fluid balance. \n- Investigations should be done to determine the cause of the DKA. \n- Many patients will require HDU-level care. \n- Intravenous insulin infusion should not be stopped until 1 hour after subcutaneous insulin has been given.\n- Long-acting insulin should continue to be given.\n\n\n# Resolving DKA\n\nIVF can be stopped once ketosis is resolving and oral fluids are tolerated without nausea or vomiting. \n\nSubcutaneous insulin can be started once ketosis is resolving and should be started at least 30 minutes before stopping intravenous insulin. \n\nDischarge can be considered once a child is eating and drinking, and stabilised on their subcutaneous insulin regime. \n \n\n# Complications\n\n\nImportant complications to monitor for include:\n\n- Cerebral oedema:\n - Can occur several hours after the onset of DKA due to rapid correction of dehydration with IV fluids. \n - Due to the potential risk, fluid deficit correction is recommended to be performed slowly, over 48 hours. \n - Though rare, this complication is fatal in 1 in 4 children. \n - Risk factors include younger age and longer duration of symptoms. \n - Management includes hypertonic (2.7%) sodium chloride and restriction of IV fluids. \n- Hypokalaemia \n- Aspiration pneumonia \n- Venous thromboembolism \n - Thromboembolic prophylaxis is not recommended in children < 16 years \n- Inadequate resuscitation \n- Hypoglycaemia\n - Blood glucose levels can fall rapidly with intravenous insulin, and if blood glucose falls below 14 mmol/L, IV fluids should include glucose. \n\n# Prognosis\n\nEarly detection and treatment results in good outcomes for patients with DKA, with many children discharged within a few days of DKA. Poorer outcomes are associated with delays in treatment and the development of cerebral oedema. \n\n\n# NICE Guidelines\n\n[BNFC Treatment Summaries: Diabetic hyperglycaemic emergencies](https://bnfc.nice.org.uk/treatment-summaries/diabetic-hyperglycaemic-emergencies/) \n \n\n# References\n \n[BSPED Guidelines for Management of DKA in Children](https://www.bsped.org.uk/media/1959/dka-guidelines.pdf)\n \n[Patient Info: Childhood ketoacidosis](https://patient.info/doctor/childhood-ketoacidosis#ref-2)",
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"question": "A 5-year-old boy presents to Accident & Emergency with a one-day history of abdominal pain and vomiting. He weighs 40 kg and has no past medical history of note.\n\n\nObservations on triage: Temperature 36.5°C, pulse 90, blood pressure 100/70, SpO2 98% on room air.\n\n\nOn examination, his abdomen is soft with mild generalised tenderness, and bowel sounds are present.\n\n\nInitial investigations are as follows:\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|124 mmol/L|135 - 145|\n|Potassium|5.5 mmol/L|3.5 - 5.3|\n|Chloride|85 mmol/L|95 - 106|\n|Urea|8 mmol/L|2.5 - 7.8|\n|Creatinine|100 µmol/L|60 - 120|\n|Non-fasting Glucose|30.5 mmol/L|< 6.1|\n|Ketones (Serum)|4 mmol/L|< 0.6|\n\n\nArterial blood gas:\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.15|7.35 - 7.45|\n|PaO₂|12 kPa|11 - 15|\n|PaCO₂|4 kPa|4.6 - 6.4|\n|Bicarbonate|14 mmol/L|22 - 30|\n\n\nWhich is the next most appropriate prescription to administer?",
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"explanation": "This would only be considered in patients with life-threatening haemorrhage, persistent bleeding refractory to treatment or those requiring surgery. The patient is stable; hence this would not be required",
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"label": "c",
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"explanation": "Platelet transfusions are generally reserved for patients with active life-threatening haemorrhage, persistent bleeding refractory to treatment or those requiring surgery. The patient is stable, and hence this would not be required",
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"explanation": "Platelet transfusions are generally reserved for patients with active life-threatening haemorrhage, persistent bleeding refractory to treatment or those requiring surgery. The patient is stable, and hence this would not be required",
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"explanation": "Glucocorticoids may be given to raise the platelet count if it needs to be raised acutely. However, in the absence of any clinically significant bleeding, there is no need for this",
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"explanation": "The patient has immune thrombocytopenic purpura (ITP). Patients usually present with an isolated low platelet count with normal coagulation profile, peripheral blood film and reticulocyte count. The negative DAT rules out autoimmune haemolytic anaemia, which may occur in conjunction with ITP (Evans syndrome). The general approach in stable patients without clinically significant bleeding would be to wait and observe, with safety net advice given to avoid contact sports, blood-thinning medications and to monitor for signs of worsening bleeding",
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"comment": "How do you distinguish this from HSP?",
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"comment": "Dat scan is negative so no haemolytic anemia and in HSP, features include haemolytic anemia, aki and thrombocytopenia i thinkinggg ?",
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"comment": "HSP is an IgA mediated small vessel vasculitis whereas ITP is destruction of platelets. Therefore HSP would present with a palpable rash (ITP would not), as well as more systemic sx e.g. abdominal pain, arthralgia and haematuria. Platelets should not be low in ITP. ",
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"comment": "platelets shouldn't be low in ITP? do you mean HSP?",
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"comment": "thought palpable rash was is HSP not ITP?",
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"comment": "can't agree",
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"comment": "how is 3 days of nosebleeds not clinically significant :((",
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"explanation": "# Summary \n \n\nImmune thrombocytopenic purpura (ITP) is an autoimmune disease characterised by a reduction in circulating platelets. In children, it usually follows a viral infection and is self-limiting. Primary investigation includes Full Blood Count (FBC), blood film and exclusion of differential diagnoses. Management generally involves a 'watch and wait' approach due to the high rate of spontaneous remission. In persistent cases, steroids are employed, and splenectomy may be considered in refractory cases. \n \n\n# Definition\n \n\nImmune thrombocytopenia purpura (ITP) is an autoimmune condition, characterised by a reduction in the number of circulating platelets. It is a type II hypersensitivity reaction whereby the spleen produces antibodies directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.\n \n\n# Epidemiology\n \n\nIn children, ITP often presents as a self-limiting disease following a viral infection in approximately 60% of cases. It affects 4 in 100,000 children per year, with more girls affected than boys and with an average age at onset of 5.7 years. \n \n\n# Aetiology\n \n\nITP in children is often triggered by a viral infection or following immunisation. \n\nSecondary ITP is rare in children but it can be due to:\n\n- Autoimmune conditions (i.e. systemic lupus erythematosus)\n- Infections (i.e. H pylori and CMV)\n- Medications\n- Lymphoproliferative disorders \n \n\n# Signs and Symptoms\n \n\nITP typically presents with:\n \n\n - Easy or excessive bruising (purpura)\n - Superficial bleeding into the skin that appears as a rash of pinpoint-sized reddish-purple spots (petechiae), usually on the lower legs\n - Prolonged bleeding from cuts\n - Spontaneous bleeding from the gums or nose - ITP presents with mucocutaneous bleeding (rather than e.g. haemarthrosis which is often associated with defects in the coagulation cascade like in haemophilia)\n - Blood in urine or stools\n - Unusually heavy menstrual flow in females \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for ITP include aplastic anaemia, leukaemia, and thrombotic thrombocytopenic purpura. These diagnoses can be differentiated by their unique signs and symptoms:\n \n\n - **Aplastic anaemia**: Children would show symptoms of anaemia - including shortness of breath, rapid or irregular heart rate and pallor. They will also have increased bleeding and frequent or prolonged infections.\n - **Leukaemia**: Children will generally be more unwell with fatigue, frequent infections, lymphadenopathy, easy bleeding or bruising and weight loss. \n - **Thrombotic thrombocytopenic purpura**: This is a more severe condition, with purpura, fatigue, fever, thrombocytopenia, haemolytic anaemia, and neurological abnormalities.\n\nIn neonates, hereditary thrombocytopenia or ITP in the mother should be considered. \n \n\n# Investigations\n \nThe primary investigations for ITP include:\n \n\n - Full Blood Count (FBC)\n - Blood film\n - Inflammatory markers to check for active infection\n\nFurther tests may be done to exclude other differential diagnoses:\n\n - Bone marrow examination (biopsy), which is only required if the case appears atypical or there is suspicion of malignancy\n \n\n [lightgallery]\n \n\n# Management\n \n\n * The management of ITP is generally conservative, with a watch-and-wait approach typically adopted due to the high rate of spontaneous remission. \n * Tranexamic acid (TXA) may be used to help blood clot, particularly used for menorrhagia. \n * For persistent cases, steroids (immunosuppressant) can be used for 4-7 days. \n * IVIG can also be used as it is immunomodulatory, reducing antibody production. \n * In cases that prove refractory for 12-24 months, splenectomy may be considered.\n * Platelet transfusions should be avoided unless there is life-threatening bleeding. This is because giving more platelets will increase the rate of platelet destruction.\n\nIbuprofen should be avoided in children with ITP. \n \n \n# Complications\n\nITP is generally mild in children. Serious complications are rare but can include:\n\n- Significant bleeds (affecting 3% of children with ITP)\n- Intracranial haemorrhage in 1 in 300 children with ITP\n\nThese complications typically occur when platelet counts are less than 20, and occur in patients with pre-existing vascular abnormalities. \n\n# Prognosis \n\nITP is generally self-resolving within weeks to months without intervention. However, up to 1 in 5 children will follow a chronic course. If recovery is not achieved by 6 months, a differential diagnosis should be considered, and a bone marrow aspirate may be needed. For some children, ITP can become chronic. \n\nITP is typically an isolated event in children, with only 5% having a recurrence. \n\n \n# NICE Guidelines\n\n[NICE Guidelines on Platelets - abnormal counts and cancer](https://cks.nice.org.uk/topics/platelets-abnormal-counts-cancer/) \n \n\n# References\n\n[ITP Support Association - ITP in children](https://itpsupport.org.uk/itp-in-children/#:~:text=How%20common%20is%20ITP%20and,common%20in%20girls%20than%20boys.)\n\n[Patient Info Immune Thrombocytopenic Purpura](https://patient.info/doctor/immune-thrombocytopenia-pro)",
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"question": "A 10-year-old boy presents to A&E with a 3-day history of nosebleeds and palpable, non-blanching red spots on his arms and legs. (refer to image provided).\n\n\n\n [lightgallery]\n\n\n\nHe has no past medical history of note. He has otherwise been well apart from a recent cold two weeks ago. His mother says that he has not had any recent trauma and does not play any contact sports.\n\n\n\nInvestigations are as follows:\n\n\n\nFull blood count:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|140 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|9x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|55x10<sup>9</sup>/L|150 - 400|\n|Reticulocytes|1 %|0.2 - 2|\n\n\n\n\nCoagulation screen:\n\n\n||||\n|---------------|:-------:|------------------------|\n|Activated Partial Thromboplastin Time (APTT)|30 seconds|22 - 41|\n|Prothrombin Time (PT)|12 seconds|10 - 12|\n|Fibrinogen|0.4 g/dL|1.5 - 4.0|\n\n\n\n\n\nPeripheral blood film:\n\n\n\n - Normal sized platelets, no clumping seen\n\n\n\nDirect antiglobulin test (DAT): Negative\n\n\n\nWhich is the most appropriate management of his condition?",
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"explanation": "# Summary\n \n\nAnaphylaxis is an acute, life-threatening allergic reaction characterised by multi-system involvement, typically involving the skin, respiratory, cardiovascular, and gastrointestinal systems. Triggered primarily by allergens such as certain foods, medications, and insect stings, anaphylaxis requires immediate management with adrenaline and patient monitoring for any rebound symptoms. Investigations commonly involve the measurement of serum mast cell tryptase levels. Upon discharge, patients newly diagnosed with anaphylaxis should be provided with two adrenaline auto-injectors and proper counselling on how to use them.\n \n\n# Definition\n \n\nAnaphylaxis is an acute and severe type 1 hypersensitivity reaction. It is a systemic, potentially life-threatening condition that involves multiple organ systems due to the release of mediators from mast cells and basophils.\n \n\n# Epidemiology\n \n\nAnaphylaxis is relatively uncommon, affecting 1-3 per 10,000 annually. Its incidence appears to be rising, particularly in Western countries. It affects people of all ages and both sexes, though certain groups, such as those with a history of asthma or atopy, are at higher risk.\n \n\n# Aetiology\n \nAs a type 1 hypersensitivity reaction, an allergen reacts with specific IgE antibodies causing a rapid release of histamine and other vasoactive substances. This increases capillary permeability, causing oedema and shock. \n\nCommon triggers of anaphylaxis include:\n \n\n - Animals: Insect stings, animal dander\n - Foods: Nuts, peanuts, shellfish, fish, eggs, milk\n - Medications: Antibiotics, IV contrast media, NSAIDs\n \n\n# Signs and Symptoms\n \n\nThe clinical manifestations of anaphylaxis can vary greatly but are best assessed following the ABCDE approach. \n \n\n - **A**irway: Hoarse voice, lip swelling, stridor indicative of upper airway obstruction and laryngeal oedema \n - **B**reathing: Wheezing, shortness of breath, fatigue, SpO2 < 94%\n - **C**irculation: Tachycardia, hypotension/shock, angioedema, confusion\n - **D**isability: Confusion\n - **E**verything else: \n - Gastrointestinal: Abdominal pain, diarrhoea, vomiting\n - Urticaria \n \n\n [lightgallery]\n \n\n# Differential Diagnosis\n \n\nThe differential diagnoses for anaphylaxis may include:\n \n -**Anaphylactoid Reaction**: These are similar reactions which cause similar mast cell activation but are not due to IgE. \n - **Vasovagal reaction**: Characterised by hypotension, bradycardia, pallor, diaphoresis, and nausea.\n - **Panic attack**: Shortness of breath, tachycardia, sweating, tremors, and feeling of impending doom, but lacks skin involvement.\n - **Asthma exacerbation**: Primarily respiratory symptoms such as wheezing, cough, and breathlessness, without systemic involvement.\n - **Carcinoid syndrome**: Flushing, diarrhoea, abdominal pain, and wheezing due to serotonin release but generally has a more chronic course.\n \n\n# Investigations\n \n\nThe primary investigation in anaphylaxis is the measurement of serum levels of mast cell tryptase, which rises within an hour of onset and can confirm the diagnosis. **However, this should not delay management**\n \nDuring the A to E assessment, investigations may include:\n\n- Pulse oximetry to detect hypoxia\n- Bloods to include:\n\t- Mast cell tryptase: These levels peak 1 hour following anaphylaxis, but remain elevated for up to 6 hours. In children, mast cell tryptase is only indicated if the trigger is believed to be idiopathic or related to venom or drugs. \n\n\n# Management\n \n\nPrompt management of anaphylaxis is crucial and includes:\n \n\n - Immediate administration of adrenaline (1:1000, IM):\n - Child > 12 years: 500 micrograms IM (0.5 mL)\n - Child 6-12 years: 300 micrograms IM (0.3 mL)\n - Child 6 months - 6 years: 150 micrograms IM (0.15 mL)\n - Child < 6 months: 100-150 micrograms IM (0.1-0.15 mL) \n - Removing the trigger if possible\n - Early call for help\n - Placing the patient in a supine position and raising their legs\n - Managing the airway and administering high-flow oxygen when skills and equipment are available\n - Administering IV fluids (10 mL/kg bolus) if patient \n - Attaching the patient to monitoring equipment\n - If no response 5 minutes after IM adrenaline: \n \t- Repeat adrenaline \n - If no improvement despite 2 doses of IM adrenaline \n - Follow refractory anaphylaxis guidelines\n \n\nPost-crisis, patients should be monitored for 6-12 hours after the initial presentation in case of a rebound episode. Children are admitted to hospital under the care of the paediatric medical team. Upon discharge, newly diagnosed patients (and their carers) should receive:\n \n\n - Counselling on the use of adrenaline auto-injectors\n - A supply of two auto-injectors\n - Written advice\n - A referral to the local allergy service for follow-up\n \n# References\n \n\n[UK Resuscitation Council Guidelines](https://www.resus.org.uk/sites/default/files/2020-06/EmergencyTreatmentOfAnaphylacticReactions%20%281%29.pdf)\n\n [A simple summary of managing anaphylaxis in all groups](https://www.resus.org.uk/EasySiteWeb/GatewayLink.aspx??alId=793)\n \n [RCPCH Anaphylaxis Care Pathway](https://www.rcpch.ac.uk/resources/allergy-care-pathway-anaphylaxis)\n \n [Patient Info Anaphylaxis and its treatment](https://patient.info/doctor/anaphylaxis-and-its-treatment)",
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"question": "A 10-year-old boy collapses in the Emergency Department after being administered a dose of amoxicillin for otitis media. He has no other past medical history of note.\n\nHe develops a sudden onset wheeze and shortness of breath.\n\nObservations:\n\n- Temperature 37.5°C\n- pulse 150\n- BP 80/60\n- SpO<sub>2</sub> 88% room air\n\nWhat is the next most important medication to administer?",
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"explanation": "Nebulised adrenaline may be used in acute symptom relief of croup by reducing stridor and work of breathing, as it works by decreasing airway oedema and relieving airway obstruction. However, it would not alter the natural clinical course of croup",
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"explanation": "Salbutamol does not play a role in the management of croup. It would be useful as a bronchodilator in asthma",
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"explanation": "Dexamethasone is the preferred glucocorticoid in the management of croup due to its longer half-life and anti-inflammatory effects. It works by reducing laryngeal mucosal oedema. It has been shown to reduce the overall severity of croup, length of hospital stay and the need for nebulised adrenaline",
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"comment": "what does the xray show?",
"createdAt": 1655315218,
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"comment": "steeple sign",
"createdAt": 1656153482,
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"comment": "what does the xray show?",
"createdAt": 1655315231,
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"comment": "Subglottic narrowing - also known as Steeple Sign",
"createdAt": 1683113776,
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"comment": "how do you tell this from epiglottitis? thank you! ",
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"comment": "thumbprint sign on x-ray",
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"comment": "whoops I thought steeple sign = epiglottitis",
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"comment": "Can be present in both",
"createdAt": 1709278997,
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"explanation": "# Summary\n \n\nCroup (also known as acute laryngotracheobronchitis) is a common childhood infection characterised by a harsh barking cough and inspiratory stridor. It is usually mild and self-limiting, however, some cases may cause severe respiratory distress requiring hospitalisation and supportive treatment. Parainfluenza viruses are the commonest causes, but the diagnosis is a clinical one and as symptoms such as stridor can worsen if the child is distressed, investigations should only be done if necessary. Oral steroids should be given to all children; in moderate to severe cases nebulised adrenaline, supplementary oxygen and airway support may be indicated.\n \n\n# Definition\n \n\nCroup, or acute laryngotracheobronchitis, is an upper respiratory tract infection that in most cases has a viral aetiology. Key symptoms include a barking cough, hoarse voice and inspiratory stridor. \n\n# Epidemiology\n \n\nCroup commonly affects children aged from 6 months old to 3 years old, with the peak incidence at 2 years. It is uncommon after the age of 6.\n\nSimilar to other viral infections, it is commonest in the autumn and winter months and is linked to parainfluenza epidemics. \n\n# Aetiology\n \nThe commonest cause is the parainfluenza virus. Other viral causes include adenovirus, respiratory syncytial virus (RSV), rhinovirus and influenza.\nRarely, bacteria can cause croup (e.g. Mycoplasma pneumoniae).\n\nThe pathophysiology involves infection and resulting inflammation of the subglottic and laryngeal mucosa which causes partial obstruction of the airways leading to respiratory distress and stridor.\n\n# Signs and Symptoms\n\n- The prodromal phase of coryzal symptoms, fever and a non-specific cough usually lasts 12-72 hours.\n- Characteristic symptoms of croup such as the harsh barking cough, hoarse voice or cry and inspiratory stridor then develop - these tend to be worse at night.\n- In severe cases, children may become drowsy and lethargic, or conversely more agitated.\n- The usual course of disease is resolution of symptoms within 48 hours (up to a week at most).\n\nOn examination, look for the following red flags that may indicate impending respiratory failure:\n\n- Signs of respiratory distress e.g. intercostal recessions, accessory muscle usage, tachypnoea\n- Cyanosis\n- Decreased level of consciousness\n- Stridor may decrease due to worsening airway obstruction\n- Decreased air entry on auscultation of the chest\n- Tachycardia\n\n# Differential Diagnosis\n \n\n- **Epiglottitis**: Sudden onset high fever, drooling, and dysphagia are seen without the barking cough of croup. Usually secondary to Haemophilus influenzae B and so significantly rarer since routine immunisation against this.\n- **Bacterial tracheitis**: Suspect if acute deterioration following initial viral symptoms, with high fevers, stridor and respiratory distress.\n- **Foreign body aspiration**: No prodrome or fever, usually sudden onset of choking, cough or wheeze after eating or playing with small objects.\n- **Anaphylaxis**: Rapid onset stridor, possible urticarial rash and facial swelling; suspect if history of previous episodes with allergens or family history of atopy.\n \n\n# Investigations\n \nDiagnosis is clinical, and investigations need to be carefully considered as distressing the child may lead to worsening of symptoms due to agitation.\n\nFurther investigation may include: \n\n- Pulse oximetry should be done to determine if supplementary oxygen is required.\n- Chest X-ray may be of use if a differential diagnosis such as an inhaled foreign body is suspected. \n - In croup, an X-ray may show a steeple sign, where the upper trachea is seen to taper.\n \n\n# Management\n\nClassifying the severity of croup is key to determining appropriate management:\n\n| Severity | Description |\n|------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| Mild | Seal-like barking cough but no stridor or sternal/intercostal recession at rest. |\n| Moderate | Seal-like barking cough with stridor and sternal recession at rest; no (or little) agitation or lethargy. |\n| Severe | Seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy. |\n| Impending respiratory failure | Minimal barking cough, stridor may become harder to hear. Increasing upper airway obstruction, sternal/intercostal recession, asynchronous chest wall and abdominal movement, fatigue, pallor or cyanosis, decreased level of consciousness or tachycardia. The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires. A respiratory rate of over 70 breaths/minute is also indicative of severe respiratory distress. |\n\nMild cases with no stridor or chest wall recessions at rest may be treated at home with a single dose of oral dexamethasone (0.15mg/kg). In children treated at home, families should be safety-netted on signs of deterioration and advised to check on the child regularly and encourage fluids. Paracetamol or ibuprofen can be used for fever and pain.\n\nChildren with any of the following should be considered for hospital admission:\n\n* Stridor and/or sternal recession at rest\n* High fever\n* Respiratory rate > 60\n* Cyanosis\n* Lethargy or agitation\n* Fluid intake < 75% of normal or no wet nappies for 12 hours\n* Aged under 3 months\n* Chronic conditions such as immunodeficiency, chronic lung disease or neuromuscular disorders\n\nManagement is supportive as there is no treatment indicated for the usual causative viruses, and may include:\n\n- Supplementary oxygen if low saturations - consider how best to deliver this so as not to distress the child (e.g. a parent holding an oxygen mask to the face)\n- Steroids for all - if unable to swallow oral dexamethasone or prednisolone can give nebulised budesonide\n- Nebulised adrenaline for temporary symptom relief\n- Anaesthetics +/- ENT input if concerns regarding airway or respiratory failure\n\n# Complications\n\n- Dehydration secondary to poor fluid intake during illness\n- Pneumonia due to secondary bacterial infection \n- Respiratory failure \n- Death is very rare (1 in every 30,000 cases)\n\n# Prognosis\n\nUsually, symptoms resolve within 48 hours but may last longer. Occasionally, severe upper airway obstruction can occur, causing respiratory failure and arrest.\n\n# NICE Guidelines\n\n[NICE CKS: Croup](https://cks.nice.org.uk/topics/croup/)\n\n# References\n \n[BNF Treatment summaries: Croup](https://bnf.nice.org.uk/treatment-summaries/croup/)\n\n[Patient.info: Croup](https://patient.info/doctor/croup-pro)",
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"question": "A 12-month-old girl is brought in by her worried parents to the children's Accident & Emergency department with a three-day history of persistent cough, hoarse voice and shortness of breath.\n\nObservations:\n\n- Temperature 38.5°C\n- pulse 150\n- BP 80/60\n- respiratory rate 40\n- SpO<sub>2</sub> 95% room air\n\nA posterior-anterior chest X-ray is done and is shown below.\n\n[lightgallery]\n\nGiven her most likely diagnosis, which single therapy has been shown to improve disease outcomes?",
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"comment": "The answers for this are muddled? If he's not doing great on salmeterol and beclometasone (LABA + ICS) surely go for a MART. If the salmeterol is a typo and they mean salbutamol then you'd go for a LTRA like montelukast?",
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"comment": "I thought the same but the stem says \"salButamol\" and the answer is montelukast, just unlike the step up from a LABA you dont have to discontinue a SABA.",
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"comment": "all wales national guidelines say to Step 2 of persistent asthma include management with MART or LABA/ICS , so seeing as he has trailed the latter and it hasn't worked, it is reasonable to move to step 3 and commence trail of montelukast for 6 weeks, 10mg nocte ,",
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"explanation": "# Summary\n\nAsthma is the commonest chronic condition in children in the UK, affecting 1 in 11 children. Diagnosis and management, although there are similarities with the adult pathways, have some important differences and vary between young children aged under 5 and those aged above 5. Under 5s are diagnosed clinically, whereas older children the first investigation to offer is FeNO testing. Management is holistic and involves regular reviews, reducing exposure to triggers and ensuring families have a personalised asthma plan with education on how to manage exacerbations. Pharmacological treatment involves a ladder of escalating inhaled medications, as well as considering leukotriene receptor antagonists (an oral medication) in some cases.\n\n# Definition\n\nAsthma is a common condition in children and young people which usually presents with a triad of wheeze, cough and shortness of breath. Symptoms are intermittent and occur in response to triggers, such as dust mites, viral respiratory infections, smoke or exercise. \n\n# Epidemiology\n\nAsthma is the commonest chronic condition in childhood in the UK and affects 1 in 11 children. Unfortunately outcomes in the UK are some of the worst in Europe, with approximately 25-30 children per year dying of asthma. 90% of these deaths are thought to be preventable with better care and tackling the deprivation that contributes to poor outcomes. \n\n# Aetiology \n\nThe characteristic intermittent bronchoconstriction that causes shortness of breath and wheezing can be caused by a variety of triggers, including:\n\n- Air pollution\n- Dust mites\n- Viral respiratory tract infections\n- Exercise\n- Cold air\n- Strong emotions \n- Medications (e.g. NSAIDs)\n \nChildren who have asthma often have other conditions caused by atopy (the tendency to produce an exaggerated IgE mediated response to benign triggers) including allergic rhinitis, eczema or food allergies. There may also be a family history of these conditions. \n\nOther risk factors for paediatric asthma include preterm birth, low birth weight and obesity in childhood. Environmental contributors to the development of asthma include air pollution, exposure to damp or mould in the home and exposure to secondhand smoke. \n\n# Signs and Symptoms\n\nExamination may be normal in between exacerbations, or the following may be found:\n\n- Widespread wheeze on auscultation\n- Chest hyperinflation\n- Signs of respiratory distress during an exacerbation, e.g. tachypnoea, accessory muscle usage\n\n# Differential Diagnosis\n\n- **Respiratory tract infection** - may present with wheeze, cough and difficulty breathing, often accompanied by fever, malaise and coryzal symptoms.\n- **Cystic fibrosis** - lifelong symptoms, as well as respiratory manifestations would have gastrointestinal symptoms and failure to thrive.\n- **Bronchopulmonary dysplasia** - chronic lung disease caused by prematurity, usually presents in babies who required ventilation for respiratory distress syndrome. Presents with respiratory distress and low oxygen saturations in infants, asthma-like symptoms can develop in childhood.\n- **Bronchiectasis** - often follows severe lower respiratory tract infection, persistent productive cough with copious sputum.\n- **Gastro-oesophageal reflux or aspiration** - can present with cough and wheeze due to irritation from gastric contents, may have vomiting and failure to thrive.\n- **Foreign body inhalation** - may mimic asthma symptoms, acute onset and focal wheeze.\n- **Bronchiolitis** - common infection in the under 2s caused by RSV, causes coryzal symptoms, fevers, cough, shortness of breath and wheeze.\n\n# Investigations\n\nChildren under 5:\n\n- In the under 5s, after a detailed history and examination a provisional diagnosis of asthma can be made and treatment initiated based on clinical judgement.\n- This should be reviewed regularly and the diagnosis reconsidered if response to treatment is not as expected.\n\nChildren aged 5 and above:\n\n- At the age of 5, investigations should be offered to aid in diagnosis. If children are unable to perform the tests, these should be offered every 6-12 months with treatment based on clinical impression in the meantime.\n- The first investigation to offer is **FeNO testing** (fractional exhaled nitric oxide) which quantifies eosinophilic inflammation in the airways - if this is 35 parts per billion or more this is diagnostic of asthma.\n- If this is not raised or FeNO testing is not available, offer **spirometry with bronchodilator reversibility** - if this finds reversible obstruction (FEV1 increase of 12% or more from baseline, or an increase 10% or more of the predicted normal FEV1) this is sufficient to diagnose asthma.\n- If spirometry is delayed or not available, advise patients/families to measure peak flow twice daily for 2 weeks - variability over 20% is diagnostic of asthma.\n- If all of FeNO, bronchodilator reversibility and peak flow variability are negative but asthma is still suspected, either take bloods for eosinophil count and total IgE level, or do skin prick testing to the house dust mite:\n - Negative skin prick testing or a normal total IgE level can be used to rule out asthma.\n - A raised IgE and eosinophil count or evidence of sensitisation on skin prick testing are diagnostic of asthma.\n- Children in whom there is ongoing diagnostic uncertainty should be referred to specialist services for further investigations (e.g. a bronchial challenge test).\n\n# Management\n\n- All children and young people should have regular reviews in primary care (at least annually), with monitoring of asthma control using symptoms, peak flow or spirometry.\n- Inhaler technique should be checked and all patients should have an up-to-date personalised asthma action plan with details of current treatments and instructions on what to do in case of an acute asthma exacerbation.\n- Education of both children and caregivers on modifiable risk factors (such as smoke exposure, household chemicals and obesity) is also key.\n\n## Under 5 years old\n\n- For children with suspected asthma and either a history of severe asthma exacerbations or interval symptoms, consider a trial of a twice-daily paediatric low-dose inhaled corticosteroid (ICS) as maintenance therapy with a short-acting beta-2 agonist (SABA) reliever inhaler.\n- If symptoms do not resolve, check adherence and inhaler technique, look for environmental triggers such as mould or smoke exposure, and review the diagnosis of asthma.\n- Refer children who do not respond to treatment and where there is no clear explanation for this to specialist asthma services.\n- If symptoms resolve with treatment, consider stopping inhalers after 8-12 weeks with a planned review of symptoms in 3 months time.\n- If children respond to initial treatment but symptoms recur or they have a significant exacerbation (requiring hospital admission or oral steroids), restart treatment with an ICS and SABA.\n- The ICS may be titrated up to a paediatric moderate dose if required.\n- If this is not sufficient to control symptoms, the next step is a trial of a leukotriene receptor antagonist (LTRA) e.g. montelukast - this should be stopped if ineffective after 8-12 weeks.\n- If asthma is still uncontrolled, children should then be referred to secondary care for further assessment.\n\n## 5 to 11 years old\n\n- As in the under 5s, a twice-daily paediatric low-dose inhaled corticosteroid (ICS) as maintenance therapy with a short-acting beta-2 agonist (SABA) reliever inhaler is the first step in management.\n- If this does not control symptoms, there are two options to step up treatment:\n - A single maintenance and reliever therapy (MART) inhaler may be started, which contains both a paediatric low-dose ICS and a fast-acting long-acting beta-2 agonist (LABA).\n - If the child isn't able to manage a MART regimen, the alternative is adding a LTRA and assessing response to this after 8-12 weeks.\n- The next steps after this are respectively: - Increasing the low-dose ICS in the MART to a moderate-dose ICS\n - Switching the low-dose ICS to a combination inhaler with a low-dose ICS with a LABA, as well as continuing the SABA +/- the LTRA if this was effective \n- For patients on a low-dose ICS//LABA inhaler + SABA +/- LTRA, this could then be increased to a moderate dose ICS if needed\n- If asthma is not controlled at this stage, patients should be referred to specialist services - options include switching to a high dose ICS or adding another medication e.g. theophylline.\n\n## 12 years or older\n\n- Young people from the age of 12 should be managed as per the adult guidelines - please see the separate Asthma chapter for details\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng245/)\n\n# References\n\n[RCPCH - State of Child Health](https://stateofchildhealth.rcpch.ac.uk/evidence/long-term-conditions/asthma)\n\n[Asthma and Lung UK](https://www.asthmaandlung.org.uk/conditions/asthma/child)\n\n\n\n\n\n",
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"explanation": "The patient meets the diagnostic criteria for generalised anxiety disorder. CBT has been shown to be highly effective and should be trialled in all patients before moving on to pharmacotherapy. Other psychological interventions may include counselling, support groups and relaxation training",
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"explanation": "This is a selective serotonin reuptake inhibitor (SSRI), the class of drugs that would be recommended as first-line in the pharmacological treatment of generalised anxiety disorder. However, before escalating to pharmacotherapy, it would be more appropriate to try psychological interventions first",
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"explanation": "This would only be appropriate to use in an acute anxiety attack. It is not recommended for long term use in patients with anxiety as it may result in benzodiazepine dependence",
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"explanation": "This would provide pain relief for her tension headache but would not be addressing the root cause of her problem, which is generalised anxiety disorder",
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"explanation": "This is a specialised form of cognitive behavioural therapy shown to be most effective in treating obsessive compulsive disorder. This would involve exposing patients to situations that provoke their obsessions whilst helping them overcome their compulsive responses. It would not be relevant in treating generalised anxiety disorder in this case",
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"comment": "i know its not an option, but surely check TFTs etc?",
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"comment": "she lost her job cos of her symptoms - this would be enough to start meds",
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"comment": "Surely this stem can't be enough to diagnose her with anxiety?? What if she has idiopathic tension headaches and then suffered with the poor sleep and concentration as a consequence?",
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"comment": "Im losing 50/50s all over the pitch",
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"explanation": "# Summary \n\nAnxiety disorders constitute a range of psychiatric conditions, including generalized anxiety disorder (GAD), specific phobias, panic disorder, obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD). These disorders are typified by excessive fear, worry, and physical symptoms such as insomnia, restlessness, and gastrointestinal symptoms. Key diagnostic steps include history-taking, clinical examination, and the utilization of rating scales like the Beck Anxiety Inventory and the Hospital Anxiety and Depression Scale. Management strategies encompass counseling, cognitive behavioral therapy (CBT), and pharmacotherapy with SSRIs, SNRIs, and benzodiazepines. \n\n\n# Generalised Anxiety Disorder (GAD)\n\nGeneralized Anxiety Disorder (GAD) constitutes a chronic and pervasive condition characterized by excessive, uncontrollable worry extending across various life domains. GAD encompasses physical symptoms such as restlessness, muscle tension, and fatigue, accompanied by cognitive manifestations like difficulty concentrating and disrupted sleep patterns. Prevalent in middle age, affecting 3-5% of the population, GAD's aetiology involves a complex interplay of biological, psychological, and environmental factors. D. Cognitive-Behavioral Therapy and pharmacotherapy, particularly with SSRIs, form integral components of its multifaceted management.\n\n\r\n## Definition\n\n**ICD-11 Criteria:**\n\n- Excessive worry and apprehension.\n- Difficulty controlling worry.\n- Associated symptoms: Restlessness, muscle tension, fatigue.\n- Duration: At least 6 months.\n\n**DSM-V Criteria:**\n\n- Excessive anxiety and worry about various domains.\n- Difficulty controlling worry.\n- Associated symptoms: Restlessness, muscle tension, fatigue, irritability.\n- Duration: At least 6 months.\n\n\r\n## Epidemiology \n\n* Predominantly affects females.\n* Affects up to 10% of the general population.\n* Commonly comorbid with depression, substance misuse, and personality disorder.\n* An onset beyond the age of 35-40 years is more likely indicative of depressive disorder or organic disease.\n* Associated risk factors include lower socioeconomic status, unemployment, divorce, renting rather than owning a home, lack of educational qualifications, and urban living.\n\r\n## Clinical Features\n\n- Psychological: Fears, worries, poor concentration, irritability, depersonalization, derealization, insomnia, night terrors\n- Motor symptoms: Restlessness, fidgeting, a feeling of being on edge\n- Neuromuscular: Tremor, tension headache, muscle ache, dizziness, tinnitus\n- Gastrointestinal: Dry mouth, dysphagia, nausea, indigestion, \"butterflies\" in the stomach, flatulence, frequent or loose bowel movements\n- Cardiovascular: Chest discomfort, palpitations\n- Respiratory: Dyspnea, tight/constricted chest\n- Genitourinary: Urinary frequency, erectile dysfunction, amenorrhea\n\n\r\n## Differential Diagnosis \n\n- Hyperthyroidism - look for goiter, tremor, tachycardia, weight loss, arrhythmia, exophthalmos\n- Cardiac causes - palpitations/arrythmias can either be part of GAD or seperate diagnoses in and of themselves\n- Medication-induced anxiety - e.g. overuse of SABA inhalers/nebulisers such as salbutamol\n- Substance misuse - intoxication – amphetamines; withdrawal – benzodiazepines, alcohol\n- Excessive caffeine intake\n- Depression: anxiety is a common feature of depression and vice versa. Identifying which condition appeared first and which is currently more prominent provides useful diagnostic cues. If both conditions are present, a diagnosis of mixed anxiety and depressive disorder is made.\n- Anxious (avoidant) personality disorder: the patient describes themselves as an anxious person without a recent significant increase in anxiety levels. (Note, this disorder can predispose the individual to anxiety disorders.)\n- Early-stage dementia\n- Early-stage schizophrenia\n\n\r\n## Management \n\n- The majority of patients can be treated in a primary care setting\n- Advice and reassurance can help prevent early or mild problems from worsening (psycho-education)\n- Counselling alone may be highly effective – it addresses patients' worries and provides reassurance about somatic symptoms\n- First line - low-intensity psychological interventions:\n\t- Individual non-facilitated self-help - written/electronic materials that the patient can work through over a period of around 6 weeks, with occasional but minimal therapist contact.\n\t- Individual guided self-help - written/electronic materials that a patient works through with 5–7 weekly or fortnightly face-to-face or telephone sessions (30 minutes each) with a trained practitioner.\n\t- Psychoeducational groups - interactive CBT-guided group sessions consisting of 6 weekly 2-hour sessions\n- Second line: for people with GAD and marked functional impairment, or with GAD that has not improved following the above:\n\t- High-intensity psychological intervention such as CBT or applied relaxation\n\t- Medical management - SSRIs are preferred i.e. sertraline, and if one does not work an alternative can be trialled e.g. escitalopram, paroxetine, or an SNRI (venlafaxine or duloxetine) can be used\n\t\t- In the first week of treatment there may be increased anxiety, agitation, and sleeping problems, and in people aged under 30 years that in a minority of people aged under 30 years, SSRIs and SNRIs are associated with an increased risk of suicidal thinking and self-harm. \n\t\t- **Patients under 30 should therefore have a follow-up appointment within 1 week to monitor progress.**\n\t\t- Symptomatic management with propranolol for palpitations can also be used.\n\n# Panic Disorder\n\nPanic Disorder, a prevalent anxiety disorder, is characterized by the occurrence of recurrent, unexpected panic attacks, each marked by intense fear or discomfort. These episodes prompt persistent worry about future attacks and may lead to avoidance behaviors, altering one's lifestyle to prevent potential episodes. Onset typically arises in adolescence or early adulthood, and the disorder exhibits a lifetime prevalence of 2-5%. Biological, psychological, and environmental factors contribute to its development. Differential diagnosis involves distinguishing panic disorder from other anxiety and medical conditions with overlapping symptoms. Cognitive-Behavioral Therapy, pharmacotherapy (especially with SSRIs), and lifestyle modifications are essential components of its comprehensive management.\n\n## Definition\n\n**ICD-11 Criteria:**\n\n- Recurrent, unexpected panic attacks.\n- At least one attack followed by a month of persistent concern.\n- Avoidance behaviors related to attacks.\n\n**DSM-V Criteria:**\n\n- Recurrent, unexpected panic attacks.\n- Persistent concern about future attacks.\n- Behavioral changes: Avoidance of situations associated with attacks.\n\r\n## Epidemiology \n\n- Prevalence of 1-2% in the general population.\n- 2-3 times more prevalent in females.\n- Bimodal incidence, peaking at ages 20 and 50.\n- Agoraphobia is concurrent in 30-50% of cases.\n- Increased risk of attempted suicide with comorbid depression, alcohol misuse, or substance misuse.\n\r\n## Clinical Features\n\n- Difficulties in breathing.\n- Chest discomfort.\n- Palpitations.\n- Hyperventilation, leading to tingling or numbness in the hands, feet, or around the mouth due to hypocalcemia resulting from increased blood pH and calcium binding to albumin. If extreme, carpopedal spasm (curling of fingers and toes) can occur.\n- Shaking, sweating, dizziness.\n- Depersonalization/derealization.\n- May result in fear of situations where panic attacks occur or lead to agoraphobia.\n- Development of a conditioned fear-of-fear pattern.\n\r\n## Differential Diagnosis \n\n- Other anxiety disorders, such as Generalized Anxiety Disorder (GAD) and agoraphobia.\n- Depression (takes precedence if it predates panic disorder or fulfills diagnostic criteria).\n- Alcohol or drug withdrawal.\n- Organic causes like cardiovascular or respiratory diseases, hypoglycemia, hyperthyroidism. Rarely, pheochromocytoma.\n\n\r\n## Management \n\n- Cognitive Behavioral Therapy (CBT) effective in 80-100% of cases and is the first-line treatment.\n\t- Initial education about the nature of panic attacks and fear-of-fear cycles.\n\t- Cognitive restructuring and detection of logical flaws.\n\t- Interoceptive exposure techniques such as controlled exposure to somatic symptoms (breathing in CO2 and physical exercise).\n\t- Treatment of secondary agoraphobic avoidance through situational exposure and anxiety management techniques.\n- Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line drug treatment (second-line to CBT).\n- Clomipramine, a tricyclic with a similar action on serotonin, is also effective, and propranolol can be used as needed for symptomatic management.\n\n# Phobias\n\nPhobias, encompassing specific phobia, social anxiety disorder (SAD), and agoraphobia, represent a cluster of anxiety disorders characterized by excessive and irrational fears. Specific phobia involves intense anxiety triggered by a specific object or situation, leading to avoidance behavior. Social anxiety disorder revolves around a marked fear of social scrutiny and performance situations, impeding daily functioning. Agoraphobia entails anxiety about situations where escape might be difficult or help unavailable. These conditions, distinct in their triggering stimuli, share common features of avoidance and significant impairment in daily life. Cognitive-Behavioral Therapy, exposure therapy, and pharmacotherapy, in alignment with NICE guidelines, form the cornerstone of their comprehensive management.\n\n\n## Definition\n\n **ICD-11 criteria:** \n- Restricted to highly specific situations such as proximity to particular animals, heights, thunder, flying, exposure to blood, etc.\n\r\n\r\n## Clinical Features\n\nGeneral features of phobias include:\n\n- Usually apparent in early adulthood.\n- Leads to avoidance behavior.\n- Phobias of blood and bodily injury can result in bradycardia and hypotension upon exposure.\n- Severity is dependent on the effect on quality of life (e.g., pilots afraid of flying).\n- Always rule out comorbid depression.\n\n\n\n## Specific Phobias\n\n### Agoraphobia\n\n- **ICD-11 criteria:** Fear of open spaces and associated factors like the presence of crowds or the perceived difficulty of immediate easy escape to a safe place, usually home (may occur with or without panic disorder).\n- Typically begins in 20s or mid-thirties.\n- Onset may be gradual or precipitated by a sudden panic attack.\n- Comorbid depression is common (beware of reliance on drugs and alcohol for coping).\n\n\r\n### Social Phobia/Social Anxiety Disorder (SAD)\n\n- Most common anxiety disorder.\n- **ICD-11 criteria:** Fear of scrutiny by others in relatively small groups (as opposed to crowds), resulting in the avoidance of social situations.\n- Relatively small groups generally consist of around 5-6 people (usually 1-2 is tolerable).\n- May be specific (public speaking) or generalized (any social setting).\n- Physical symptoms include blushing, fear of vomiting.\n- Symptoms include blushing (characteristic), palpitations, trembling, sweating.\n- Can be precipitated by stressful or humiliating experiences, parental death, separation, chronic stress.\n- Genetic predisposition is possible.\n- May lead to alcohol or drug abuse (perpetuating the problem).\n- Mental state examination: may appear relaxed as the phobic object or situation is not present.\r\n\r\n## Management \n\n- CBT is first-line management for all phobias:\n\t- Exposure techniques are the most widely used, aiming for systematic desensitization (using a graded hierarchy approach, for example).\n\t- Flooding (exposing someone with a fear of heights to a tower),\n\t- Modelling (individual observes therapist interacting with phobic stimulus).\n- If ineffective/severe functional impairment, SSRIs are first-line medical management. Propranolol can be used if somatic symptoms predominate.\n\n\r\n# NICE guidelines \n\n[NICE CKS - GAD](https://cks.nice.org.uk/topics/generalized-anxiety-disorder/)\n\r\n# References \n\n3. The British Psychological Society. (2011). Good Practice Guidelines on the use of psychological formulation.\n4. Royal College of Psychiatrists. (2011). Anxiety, panic and phobias.\n5. Mental Health Foundation. (2021). How to manage and reduce stress.\n6. UK Psychological Trauma Society (UKPTS). (2012). Post-traumatic stress disorder.\r\n",
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"question": "A 50-year-old woman presents to her General Practitioner with a two-week history of intermittent tension headache. She describes having poor sleep and concentration for the past year and has had to leave her job as a result. She also has frequent episodes of palpitations accompanied by shortness of breath at rest.\n\nPhysical examination reveals no significant abnormalities. An electrocardiogram shows a normal sinus rhythm.\n\nWhich is the next best course of management?",
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"explanation": "Antipsychotics are more likely to cause postural hypotension, likely secondary to alpha-adrenergic blockade; hence they should be used with caution in the elderly who are at higher risk of falls",
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"explanation": "Antipsychotics are usually associated with hyperprolactinaemia. This is due to their dopamine antagonist effect, which blocks the inhibitory effects of dopamine on the pituitary, thereby increasing its secretion of prolactin. Clinical consequences of elevated prolactin levels include gynaecomastia and galactorrhoea",
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"comment": "On bnf, insomnia is a 'common' side effect of ALL antipsychotic drugs... ",
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"comment": "quetiapine increases the risk of metabolic syndrome - part of that is hypertension?",
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"explanation": "# Summary\n\n\n\n# Typical antipsychotics\n\n- Also known as 'first-generation' antipsychotics, these not only act as antagonists to D2 receptors but also on cholinergic, adrenergic and histaminergic receptors. The most commonly used medication in this class is **Haloperidol**, though other examples include Chlorpromazine and flupentixol. \n- Side effects can therefore be grouped according to receptor blockade (see below).\n\n### Dopamine D2 Receptor Blockade:\n\n1. **Extrapyramidal Symptoms (EPS):**\n - **Acute Dystonia:** Involuntary muscle contractions causing spasms.\n - **Akathisia:** Restlessness and an inability to sit still.\n - **Parkinsonism:** Tremors, rigidity, and bradykinesia (slowed movements).\n - **Tardive Dyskinesia:** Involuntary, repetitive movements, especially of the face.\n\n2. **Hyperprolactinemia:**\n - Elevated levels of prolactin, leading to:\n - Menstrual irregularities in women.\n - Gynecomastia (breast enlargement) in men.\n - Sexual dysfunction in both genders.\n\n### Other Receptors:\n\n1. **Histamine H1 Receptor Blockade:**\n - **Sedation:** Drowsiness and sleepiness.\n\n2. **Alpha-1 Adrenergic Receptor Blockade:**\n - **Orthostatic Hypotension:** A sudden drop in blood pressure upon standing, leading to dizziness or fainting.\n\n3. **Muscarinic Receptor Blockade:**\n - **Anticholinergic Effects:**\n - Dry mouth.\n - Constipation.\n - Blurred vision.\n - Urinary retention.\n\n\n# Atypical antipsychotics\n\n- Also known as 'second-generation' antipsychotics, these are D2, D3 and 5-HT2A antagonists, with less overspill into other receptors. \n- As effective as typical antipsychotics (even slightly better at negative symptoms), and have a more favourable side effect profile with reduced extrapyramidal effects, but increased metabolic side-effects. \n- They are 1st line for new-onset psychosis. Examples include risperidone, quetiapine, olanzapine, aripiprazole and clozapine (see below). \n\n### Dopamine Receptor Blockade:\n\n1. **D2 Receptor Blockade:**\n - **EPS (Extrapyramidal Symptoms):**\n - Atypicals generally have a lower risk of causing EPS compared to typicals.\n - Lower risk of tardive dyskinesia.\n\n### Serotonin Receptor Blockade:\n\n1. **5-HT2A Receptor Blockade:**\n - **Lower Risk of EPS:** Atypicals have a reduced risk of causing EPS due to serotonin receptor blockade.\n\n### Other Receptors:\n\n1. **Histamine H1 Receptor Blockade:**\n - **Sedation:** Although less common than with typicals, some atypicals can cause drowsiness.\n\n2. **Alpha-1 Adrenergic Receptor Blockade:**\n - **Orthostatic Hypotension:** Some atypicals may cause a drop in blood pressure upon standing.\n\n3. **Muscarinic Receptor Blockade:**\n - **Anticholinergic Effects:**\n - Generally less pronounced compared to typicals.\n - Mild dry mouth, constipation, or blurred vision.\n\n### Metabolic Effects:\n\n1. **Weight Gain:**\n - **Common Side Effect:** Atypical antipsychotics, in general, have a higher risk of causing weight gain compared to typicals.\n - **Varying Degrees:** The degree of weight gain can vary among different atypicals.\n\n2. **Dyslipidemia and Glucose Metabolism:**\n - **Increased Risk:** Some atypicals are associated with an increased risk of dyslipidemia and impaired glucose metabolism.\n\n3. **Prolactin Elevation:**\n - **Variable:** Some atypicals may elevate prolactin levels, leading to menstrual irregularities and sexual dysfunction.\n\n### Other side effects:\n\n1. **Seizures:**\n - **Low Risk:** Generally, atypicals have a lower risk of lowering the seizure threshold compared to typicals.\n\n2. **QT Prolongation:**\n - **Potential Risk:** Some atypicals may have a mild effect on the QT interval, but the clinical significance varies.\n\n3. **Increased risk of VTE and stroke in elderly**\n\n### Monitoring\n\n* Weight should be measured at the start of therapy, then weekly for the first 6 weeks, then at 12 weeks, at 1 year, and then yearly.\n* Fasting blood glucose, HbA1c, and blood lipid concentrations should be measured at baseline, at 12 weeks, at 1 year, and then yearly. \n* Prolactin concentrations should also be measured at baseline.\n* Before initiating antipsychotic drugs, an ECG may be required, particularly if there are cardiovascular risk factors (e.g. high blood pressure), if there is a personal history of cardiovascular disease, or if the patient is being admitted as an inpatient.\n* Blood pressure monitoring before starting therapy, at 12 weeks, at 1 year and then yearly during treatment and dose titration of antipsychotic drugs.\n\n# Clozapine\n\n- Clozapine is an atypical antipsychotic that is indicated if there is failure of treatment of 2 other antipsychotic medication, known as treatment-resistant schizophrenia.\n- Treats both positive and negative symptoms, slightly more effective than other antipsychotics.\n- Important side effects include: **agranulocytosis**, neutropenia, reduced seizure threshold, myocarditis, slurred speech (due to hypersalivation), constipation (most common cause of mortality when related to clozapine use).\n\n### Monitoring\n\n- Due to its unique and potentially serious side effect profile, monitoring while on clozapine is very important.\n- Patients should have weekly FBC (to look at white cell counts) for the first 18 weeks of treatment then fortnightly for up to one year, and then monthly.\n- Blood lipids and weight should be measured at baseline, every 3 months for the first year, and then yearly.\n- Fasting blood glucose should be tested at baseline, after one months’ treatment, then every 4–6 months.\n\n\n# Neuroleptic Malignant Syndrome\n\nNeuroleptic Malignant Syndrome (NMS) is a rare, but potentially life-threatening, idiosyncratic reaction to antipsychotic medications, particularly those that block dopamine receptors. It typically occurs as a response to the introduction or an increase in the dosage of neuroleptic medications.\n\n### Clinical Features\n\n1. **Hyperthermia:**\n - Profound elevation of body temperature is a hallmark feature.\n \n2. **Altered Mental Status:**\n - Fluctuating levels of consciousness, ranging from confusion to catatonia.\n\n3. **Autonomic Dysregulation:**\n - Dysautonomia characterized by fluctuations in blood pressure, tachycardia, and diaphoresis.\n\n4. **Rigidity:**\n - Generalized muscle stiffness, often described as \"lead-pipe\" rigidity.\n\n### Differential Diagnosis\n\n- **Malignant Hyperthermia** - a rare, genetic condition triggered by certain medications, often during anaesthesia.\n\n- **Serotonin Syndrome** similar to NMS but associated with serotoninergic medications. Presents with hyperthermia, autonomic dysregulation, and altered mental status.\n\n### Investigations \n\n- Bloods:\n\t- FBC - Monitoring for potential leukocytosis or signs of infection.\n - **Creatine Kinase (CK) Levels:** Markedly elevated CK levels are often observed due to muscle breakdown.\n - Renal and Liver Function Tests: monitoring organ function due to the potential systemic effects.\n \n### Management\n\n1. **Discontinuation of Causative Agent:**\n - Immediate cessation of the implicated neuroleptic medication.\n\n2. **Supportive Care:**\n - Aggressive cooling measures to address hyperthermia, including cooling blankets and IV fluids to prevent renal failure.\n\n3. **Benzodiazepines:**\n - Administering benzodiazepines to manage agitation and muscle rigidity.\n\n4. **Dantrolene:**\n - Consideration of dantrolene, a skeletal muscle relaxant, in severe cases.\n\n5. **Intensive Monitoring:**\n - Continuous monitoring of vital signs, fluid balance, and laboratory parameters.",
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"question": "An 80-year-old gentleman with a background of mixed dementia is admitted to the care of the elderly ward with a urinary tract infection. He has challenging behaviour on the ward, being aggressive to nursing staff and refusing to take his medications. Collateral history from his family reveals that he has also displayed such behaviour at home.\n\nHe is diagnosed as having behavioural and psychological symptoms of dementia and is started on quetiapine.\n\nWhich is the following potential side effects is he at increased risk of with this new medication?",
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"explanation": "Another possible differential is peptic ulcer disease, which may have been caused by non-steroidal anti-inflammatory drugs such as ibuprofen. This is unlikely to cause elevated lipase. The patient also does not have signs of peritonism, which might suggest a perforation",
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"explanation": "This woman has presented with acute pancreatitis secondary to valproate, which is a rare cause of pancreatitis. Lipase is more sensitive in patients with pancreatitis as it has a longer half-life than amylase; thus, lipase levels may remain elevated even after amylase levels have normalised",
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"comment": "Scorpio sting ",
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"comment": "Drugs causing pancreatitis: FAT SHEEP.\n\nFurosemide\nAzathioprine / Asparaginase\nTetracyclines / Thiazides\n\nSulfa drugs, Sodium Valproate, Statins\nHydrochlorothiazides\nEthanol\nEstrogen\nProtease inhibitors.",
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"comment": "my guess paid off ",
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"explanation": "# Summary\n \nAcute pancreatitis refers to inflammation of the pancreas; there are a wide variety of causes and severity ranges from mild and self-resolving pancreatitis to life-threatening multi-organ failure. The main symptom is acute-onset epigastric pain which radiates to the back, which may be accompanied by nausea and vomiting. Diagnosis is primarily with bloods showing an elevated amylase or lipase. Abdominal ultrasound is another important investigation to look for gallstones (the commonest cause of acute pancreatitis). General management includes aggressive fluid resuscitation, analgesia, antiemetics and nutritional support. \n\n# Definition\n\nAcute pancreatitis refers to an inflammatory process affecting the pancreas as well as local or distant tissues and organs in some cases.\n \n\n# Epidemiology\n \n- Acute pancreatitis has an incidence of approximately 30 cases per 100,000 people per year\n- There are many causes as detailed below\n- Half of cases are caused by gallstones, and around a quarter of cases by alcohol\n- 10% of cases are idiopathic\n- The majority of cases (around 80%) are mild and self-limiting, with low mortality rates (1-3%)\n- The 20% of patients with moderate or severe disease have a higher risk of death (estimated at 13-35%)\n\n# Aetiology\n\nCauses of acute pancreatitis can be remembered using the mnemonic GET SMASHED:\n \n - Gallstones \n - Ethanol (alcohol)\n - Trauma\n - Steroids\n - Mumps\n - Autoimmune disease (e.g. systemic lupus erythematosus, Sjogren's syndrome)\n - Scorpion stings\n - Hypercalcaemia, hypertriglyceridemia, hypothermia\n - ERCP\n - Drugs (e.g. thiazides, azathioprine, sulphonamides)\n\nOther causes include blunt abdominal trauma or local surgery, microlithiasis (tiny gallstones and biliary sludge), pancreatic tumours and cholangiocarcinomas and congenital abnormalities such as pancreas divisum. \n\n# Classification\n\nSeverity of pancreatitis is stratified using the Glasgow Score - each of the following scores 1 point and a score of **3 or more** predicts severe pancreatitis:\n\n- PaO2 < 8kPa\n- Age > 55 years\n- Neutrophils > 15\n- Calcium < 2\n- Renal i.e. Urea > 16 \n- Enzymes i.e. LDH > 600 or AST > 200\n- Albumin < 32\n- Sugar i.e. Glucose > 10\n\nThis should be calculated on admission and at 48 hours.\n \n# Signs and Symptoms\n\n- The main symptom of acute pancreatitis is epigastric pain which may radiate to the back\n- Nausea and vomiting are also common symptoms\n- Diarrhoea can occur\n \nOn examination, signs may include:\n\n- Abdominal tenderness\n- Peritonism, rebound tenderness and guarding may be seen\n- Abdominal distension \n- Fevers (which may be due to inflammation or superadded infection)\n- Tachycardia and hypotension if shocked\n- Haemorrhagic pancreatitis may present with Grey-Turner's sign (bruising in the flank area), Cullen's sign (bruising around the umbilicus) or Fox's sign (bruising over the inguinal ligament)\n\n[lightgallery]\n \n[lightgallery1]\n \n# Differential Diagnosis\n \n- **Acute Coronary Syndrome** may present atypically with epigastric rather than chest pain with nausea and vomiting - an ECG should be done to look for ischaemic changes.\n- **Perforated Peptic Ulcer** may present with sudden onset severe abdominal pain with nausea and vomiting and signs of peritonitis; amylase may be raised and a chest X-ray may show air under the diaphragm.\n- **Ruptured Abdominal Aortic Aneurysm** shares features of abdominal pain radiating to the back; patients are typically very unwell with haemodynamic instability. A bedside ultrasound can be done for rapid diagnosis.\n- **Bowel Obstruction** causes abdominal pain and distension with nausea and vomiting, constipation is seen rather than diarrhoea and pain is usually colicky in nature.\n- **Cholecystitis** typically presents with right upper quadrant pain and fever with a positive Murphy's sign on examination, also commonly related to gallstones \n\n# Investigations\n \n**Bedside tests:**\n\n- **ABG** if low oxygen saturations to help with risk stratification (the pO2 is needed for the Glasgow criteria)\n- **ECG** to rule out acute coronary syndrome as a cause of pain\n- **Pregnancy test** in women of child-bearing age to rule out causes of abdominal pain such as ectopic pregnancy\n- **Capillary blood glucose** as hyperglycaemia indicates severe pancreatitis\n\n**Blood tests:**\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** to look for kidney injury; urea is part of the Glasgow criteria\n- **LFTs** are often deranged; a low albumin and high AST indicate severe pancreatitis\n- **Amylase** is the key diagnostic test, with levels over 3x the upper limit of normal indicating acute pancreatitis\n- **Lipase** is not usually measured but can also be used to diagnose pancreatitis - it is more sensitive and specific than amylase\n- **LDH** and a **bone profile** for calcium are also required for the Glasgow criteria with hypocalcaemia being a poor prognostic factor\n- **Blood cultures** in patients with fevers or other signs of infection \n- **Coagulation screen** as a baseline - may be deranged in severe illness\n- **Lipid profile** if hypertriglyceridaemia is suspected as a cause of pancreatitis\n- **Autoimmune markers** if the cause of pancreatitis is unclear\n \n**Imaging:**\n \n- **Abdominal ultrasound** looking for gallstones and duct dilation\n- **Chest X-ray** for complications such as pleural effusions or acute respiratory distress syndrome\n- **CT pancreas with contrast** should be done in patients who are deteriorating or have signs of sepsis or organ failure after 6-10 days - may detect complications such as pseudocysts or necrotising pancreatitis\n- **Magnetic Resonance Cholangiopancreatography (MRCP)** may be required in cases of pancreatitis secondary to gallstones \n \n# Management\n\n**Conservative:**\n\n- Ensure patients with severe pancreatitis (e.g. Glasgow score 3+, hypotension, oliguria, respiratory distress) are referred for intensive care assessment and input\n- Catheterise and monitor input-output\n- Insert an NG tube if significant vomiting\n- If the patient can eat, encourage oral intake as tolerated - they should not be made nil by mouth unless there is another reason for this\n- Enteral nutrition should be started within 72 hours of presentation (e.g. NG feeding) - if this fails parenteral nutrition should be considered\n\n**Medical:**\n\n- IV fluid resuscitation is the mainstay of treatment - crystalloids should be used and should be titrated to achieve an adequate urine output\n- Ensure adequate analgesia is given - opioids may be required\n- Antiemetics for nausea and vomiting\n- Antibiotics should not be given routinely - in some cases (e.g. confirmed pancreatic necrosis) broad-spectrum antibiotics should be given\n- Monitor for and treat any complications\n- For alcohol-related pancreatitis, alcohol withdrawal treatment may be required (i.e. benzodiazepines and pabrinex)\n\n**Surgical:**\n\n- The underlying cause of pancreatitis should be treated; an ERCP may be required for gallstones in cases of jaundice, cholangitis or a dilated common bile duct on imaging\n- Laparoscopic cholecystectomy for gallstone pancreatitis should ideally be done in the same admission unless the patient is not fit for surgery\n- Surgical or interventional management may be required for complications e.g. drainage of large pancreatic pseudocysts or debridement of pancreatic necrosis\n\n# Complications\n\n**Local complications include:**\n\n- A **pancreatic pseudocyst** is a fluid-filled sac that lacks a true epithelial lining (the wall is vascular and fibrotic); typically these form weeks after an episode of acute pancreatitis and can become infected, rupture, haemorrhage or cause compression of surrounding structures\n- **Pancreatic necrosis** occurs due to ischaemia of the pancreas and may become infected causing systemic inflammation and multi-organ failure\n- **Peripancreatic fluid collections** may occur, which can get infected leading to abscess formation\n- **Haemorrhage** from local vessels (e.g. pancreatic or splenic arteries or veins) can occur due to inflammation and enzyme release\n- **Pancreatic fistulae** may form due to pancreatic duct disruption, causing these to communicate with for example the skin, the abdominal cavity or the pleural space\n \n**Systemic complications include:**\n\n- **Acute Respiratory Distress Syndrome (ARDS)** which is a severe lung injury with non-cardiogenic pulmonary oedema and respiratory failure\n- **Acute kidney injury** is a common complication which may require renal replacement therapy; often secondary to intravascular volume depletion due to third spacing \n- **Disseminated intravascular coagulation** \n- **Sepsis** for example secondary to infected pancreatic necrosis\n- **Multi-organ failure** which may lead to death\n- **Hypocalcaemia** occurs due to free fatty acids reacting with serum calcium to form salts, a process called saponification; this can cause tetany if severe\n- **Hyperglycaemia** due to disruptions in insulin production due to pancreatic destruction as well as systemic inflammation\n \n# NICE Guidelines\n\n[NICE CKS - Acute Pancreatitis](https://cks.nice.org.uk/topics/pancreatitis-acute/)\n\n[NICE - Pancreatitis](https://www.nice.org.uk/guidance/ng104/)\n \n# References\n\n[UK guidelines for the management of acute pancreatitis](https://gut.bmj.com/content/54/suppl_3/iii1)\n\n[British Society of Gastroenterology - Practical Guide to Acute Pancreatitis](https://www.bsg.org.uk/clinical-resource/practical-guide-to-the-acute-pancreatitis)",
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"learningPoint": "Valproate can cause drug-induced pancreatitis, and other drugs that can also lead to this condition include azathioprine, mercaptopurine, sulfonamides, tetracyclines, estrogens, calcium channel blockers, and furosemide.",
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"question": "A 60-year-old lady is admitted with a three-day history of sudden onset epigastric pain, nausea and two episodes of vomiting.\n\n\nOn examination, her abdomen is soft and diffusely tender. There is no rigidity or guarding.\n\n\nObservations: temperature 37.0°C, HR 110 bpm, BP 90/60 mmHg, RR 20 bpm, SpO2 99% on room air.\n\n\nHer bloods show:\n\n||||\n|---------------------------|:-------:|--------------------|\n|Albumin|40 g/L|35 - 50|\n|Alanine Aminotransferase (ALT)|21 IU/L|10 - 50|\n|Aspartate Aminotransferase (AST)|32 IU/L|10 - 40|\n|Alkaline Phosphatase (ALP)|110 IU/L|25 - 115|\n|Bilirubin|7 µmol/L|< 17|\n|Gamma Glutamyl Transferase (GGT)|20 U/L|9 - 40|\n|Lipase|432 IU/L|< 101|\n|Amylase|289 U/L|< 220|\n\n\nShe was recently started on a new medication. Which of the following is the most likely cause of her current presentation?",
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"explanation": "This would occur with obstructive lung diseases such as asthma or chronic obstructive pulmonary disease. This is not likely given the clinical history and the fact she is a non-smoker. Sarcoidosis would typically present with a restrictive picture on lung function testing, although it may also be normal",
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"explanation": "This is a test used to detect tuberculosis (TB) infection and would be positive in the context of both latent and active TB. Bronchoalveolar lavage (BAL) may be used in the diagnosis of TB if there are difficulties obtaining induced sputum samples. In TB, BAL is more likely to show caseating (necrotising) granulomas, and cultures would be positive for acid-fast bacilli, which is not the case here",
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"explanation": "# Epidemiology\n\nAround 4,500 people are diagnosed with sarcoidosis in the UK each year representing an annual incidence rate of 7 people per 100,000.\n\n# Definition\n\nSarcoidosis is a multi-system disease characterised by granuloma formation, resulting in widespread inflammatory changes and complications.\n\n# Acute sarcoidosis features\n\nAcute sarcoidosis: fever, polyarthralgia, erythema nodosum, and bilateral hilar lymphadenopathy. This is also known as **Löfgren syndrome**.\n\n# Chronic sarcoidosis features\n\n- Pulmonary (most common manifestation): dry cough, dyspnoea, reduced exercise tolerance. Examination may reveal crepitations.\n\n- Constitutional: fatigue, weight loss, arthralgia, and low-grade fever. General signs include lymphadenopathy and enlarged parotid glands.\n\n- Neurological: meningitis, peripheral neuropathy, bilateral Bell's palsy.\n\n- Ocular: uveitis, keratoconjunctivitis sicca.\n\n- Cardiac: arrhythmias, restrictive cardiomyopathy.\n\n- Abdominal: hepatomegaly, splenomegaly, renal stones.\n\n- Dermatological: erythema nodosum, lupus pernio.\n\n# Investigation\n\nTissue biopsy (eg. lung, lymph nodes) is diagnostic, which typically finds non-caseating granulomas. However, other investigations can point towards a diagnosis of sarcoidosis.\n\n- Bloods: Raised ESR, ACE (not specific or diagnostic) and calcium; reduced lymphocytes.\n\n- Chest x-ray or CT:\n - Stage 1 - bilateral hilar lymphadenopathy (BHL)\n - Stage 2 - BHL with peripheral infiltrates\n - Stage 3 - peripheral infiltrates alone\n - Stage 4 - pulmonary fibrosis\n\n# Management\n\n- Bilateral hilar lymphadenopathy alone - usually self-limiting\n- Acute sarcoidosis - bed rest, NSAIDs\n- Steroid treatment: oral or IV, depending on severity of disease\n- Immunosuppressants: in severe disease",
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"explanation": "This would be able to provide oxygen of up to 6-10 L per minute, which would likely be insufficient for this patient's current requirements in view of the respiratory acidosis. It is also a form of uncontrolled oxygen therapy which would not be appropriate in carbon dioxide retaining patients",
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"comment": "Does anyone know what the threshold is for when you would prescribe high flow o2 over bipap? I know bipap is given to co2 retainers but when someone is hypoxic they say to give o2 - wondering at which sats you would go non-rebreathe? thanks",
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"comment": "from my understanding high flow is what you would give in a patient first presenting with very low 02 stats + being unstable. This patient most likely wasn't acutely unwell in the beginning so was given ventri mask and after that failed the next step would b BiPAP \n",
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"comment": "literally doesn't say anywhere about COPD",
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"explanation": "# Summary\n\nChronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).\n\n# Definition\n\nChronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). \n\n# Epidemiology\n\nIn the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. \n\nAround 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.\n\n# Risk Factors\n\n- Tobacco smoking and passive smoke exposure\n- Marijuana smoking \n- Occupational exposure to dusts and fumes\n- Household air pollution from wood or coal burning\n- Alpha-1 antitrypsin deficiency\n\nPrognosis is variable, with the following factors associated with higher morbidity and mortality:\n\n- Poor exercise tolerance\n- Smoking\n- Low body mass index\n- Multi-morbidity and frailty\n- Exacerbations requiring admission to hospital or frequent exacerbations\n- Severe obstruction on spirometry (as measured by a lower FEV1)\n- Chronic hypoxia\n- Cor pulmonale\n\n# Pathophysiology\n\nChronic Bronchitis:\n\n- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.\nCilia are not able to remove the excess mucus and so it obstructs the small airways.\nOngoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.\n\nEmphysema:\n\n- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. \n- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.\n- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.\n\n# Classification\n\nThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. \n\n| GOLD Grade | Severity | Post-Bronchodilator FEV₁ (% Predicted) |\n|------------|--------------------------|----------------------------------------|\n| 1 | Mild | ≥ 80% |\n| 2 | Moderate | 50-79% |\n| 3 | Severe | 30-49% |\n| 4 | Very Severe | < 30% |\n\n\nThe two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:\n\n| Grade | Description |\n|-------|----------------------------------------------------------------------------------------------------|\n| 0 | I only get breathless with strenuous exercise. |\n| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |\n| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |\n| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |\n| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |\n\n# Signs and symptoms\n\n- Shortness of breath that worsens with exertion\n- Reduced exercise tolerance\n- Chronic productive cough\n- Recurrent lower respiratory tract infections\n- Wheeze\n- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present\n\nExamination may be normal, though signs may include:\n\n- Wheeze or crackles on auscultation\n- Accessory muscle usage\n- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)\n- Cyanosis \n- Hyperinflation of the chest\n- Cachexia\n- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)\n\n# Investigations\n\n- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.\n\n- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history\n- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:\n\t- Right axis deviation\n\t- Prominent P waves in inferior leads\n\t- Inverted P waves in high lateral leads (I, aVL)\n\t- Low voltage QRS\n\t- Delayed R/S transition in leads V1-V6\n\t- P pulmonale\n\t- Right ventricular strain pattern\n\t- RBBB\n\t- Multifocal atrial tachycardia\n\n- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.\n\n[lightgallery1]\n\n- **Sputum culture** - during exacerbations to target antibiotic therapy\n\n# Differential diagnosis\n\n- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.\n- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.\n- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.\n- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.\n- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.\n- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.\n\n# Management of Chronic COPD\n\n**Conservative:**\n\n- Patient education, ensure all patients have a personalised self-management plan\n- Smoking cessation support\n- Nutritional support and dietician referral if malnourished\n- Annual influenza and one-off pneumococcal vaccination\n- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)\n- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques\n\n**Medical:**\n\n\n- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler\n- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). \n- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).\n\nPatients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).\n\nManagement of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:\n\n**Group A**\n \n- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**:\n - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.\n - If symptoms are not controlled, consider switching to a long-acting bronchodilator: \n - **LAMA** or **LABA**, depending on individual tolerance and symptom profile. \n\n**Group B**\n \n- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**: \n - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy. \n - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**. \n\n**Group E**\n \n- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden. \n- **Management**: \n - First-line therapy is **LAMA** for exacerbation prevention. \n - If exacerbations persist, escalate to: \n\t - **Dual therapy (LABA + LAMA)**. \n\t - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**. \n - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**. \n\n\n\n| **Group** | **Phenotype** | **Initial Therapy** | **Escalation Therapy** | \n|-------------|--------------------------------|------------------------------|------------------------------------| \n| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed | LAMA or LABA | \n| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA | LABA + LAMA | \n| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation\t | LAMA | LABA + LAMA or LABA + LAMA + ICS | \n\n\nOther medical treatments that may be considered include:\n\n- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.\n- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.\n- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.\n- Long-term oxygen therapy (LTOT) - see below for more details\n\n\n**Surgical:**\n\n- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. \n- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung. \n\n### Long term oxygen therapy (LTOT)\n\n**The following patients should be referred for assessment for LTOT:**\n\n- Oxygen saturations <92% in air or cyanosis\n- FEV1 <30% predicted (consider referring if <49%)\n- Polycythaemia\n- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)\n\nThis assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. \n\nPatients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):\n\n- PaO2 below 7.3kPa\n- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension\n\n# Complications\n\n## Acute exacerbations\n\n- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. \n- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. \n- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).\n\n- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. \n- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. \n- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.\n\n## Polycythaemia\n\n- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). \n- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. \n\n\n## Cor Pulmonale\n\nCor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.\n\nThe pathophysiology is as follows:\n\n- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.\n- This increases vascular resistance in the lungs.\n- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.\n- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).\n\nPeripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.\n\n## Pneumothorax\n\n- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. \n- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).\n\n## Depression and anxiety\n- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. \n- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. \n- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)\n\n[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)\n\n# References\n\n[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)\n\n[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)\n\n[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)\n\n[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)",
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"question": "A 75-year-old man is admitted to the general medical ward with a 3 day history of worsening shortness of breath and a productive cough with green sputum. He has a past medical history of COPD.\n\n\nOn examination, he has visible accessory muscle use and has widespread coarse crepitations with an expiratory wheeze.\n\n\nObservations:\n\n\n - Temperature 38.5°C\n - pulse 105\n - BP 140/70\n - SpO<sub>2</sub> 89% on 40% O<sub>2</sub> via Venturi mask\n\n\nArterial blood gas:\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.27|7.35 - 7.45|\n|PaO₂|8 kPa|11 - 15|\n|PaCO₂|7.1 kPa|4.6 - 6.4|\n|Bicarbonate|15 mmol/L|22 - 30|\n\n\n\nWhich is the next most appropriate management?",
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"explanation": "The role of inhaled corticosteroids as an adjunct in asthma exacerbations has not been well established. As the patient has already received high dose IV steroids, this would not be of additional benefit",
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"explanation": "The patient has features of a life-threatening asthma attack and would benefit from an early ICU review. Patients with a normal pCO2 are at risk of quick deterioration to type 2 respiratory failure due to exhaustion and hypoventilation. The patient should be assessed for consideration of intubation and mechanical ventilation",
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"explanation": "This would not be appropriate at this stage although the blood gas results seem relatively reassuring. As the patient has a normal pCO2, they are at risk of exhaustion and hypoventilation, and should be considered for early escalation and senior review",
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"explanation": "Uncontrolled oxygen delivery may be dangerous in the deteriorating asthmatic patient as it may cause over-oxygenation and worsening hypercapnia if the patient hypoventilates. Controlled supplementary oxygen should be given to maintain oxygen saturations above 94%, with close pulse oximetry monitoring",
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"explanation": "This is not likely to result in an additional bronchodilator effect compared with inhaled bronchodilators and steroids. It should only be administered after consultation with a senior as it would require close monitoring of levels",
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"explanation": "# Summary\n\nAsthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation. When bronchoconstriction is triggered (an “asthma attack”), patients experience episodes of wheeze, dyspnoea, cough and chest tightness. Initial investigations for all adults with suspected asthma are fractional exhaled nitric oxide (FeNO) or a full blood count looking for eosinophilia. If neither of these are confirmatory, patients should be assessed with spirometry including bronchodilator reversibility. Management involves a stepwise approach to medications, starting with “reliever therapy” (usually short-acting beta-2 agonists such as salbutamol inhalers) in combination with “preventer therapy” medications including inhaled corticosteroids, leukotriene receptor antagonists and long-acting beta-2 agonist inhalers. Allergen avoidance, smoking cessation, regular peak flow monitoring and inhaler technique are all key to good asthma control.\n\n# Definition\n\nAsthma is a common disease in both adults and children, characterised by intermittent \"asthma attacks\" with wheeze, cough, shortness of breath and chest tightness. There are several underlying mechanisms that centre around reversible bronchoconstriction, hyperreactivity and chronic inflammation.\n\n# Epidemiology\n\nIn the UK, approximately 8 million people have been diagnosed with asthma, of which 5.4 million are on treatment. Onset is usually in childhood and some find symptoms remit with age, although relapse is possible after long periods of being well.\n\nOn average, three people die from an asthma attack each day in the UK. The majority of these deaths are preventable, with an estimated 7/10 people with asthma not receiving basic preventative care such as inhaler technique checks and a personalised asthma plan.\n\nPeople experiencing socioeconomic deprivation are more likely to have asthma and to have worse outcomes (e.g. higher rates of hospitalisation). This is multifactorial, with these groups more likely to be exposed to triggers such as smoking and air pollution, and to have lower health literacy and access to healthcare.\n\n# Pathophysiology\n\nAsthma is often associated with a personal and/or family history of atopy, including the atopic triad of asthma, allergic rhinitis, and eczema. In asthma, there is an exaggerated response to a wide range of triggers. These include:\n\n- Cold air and exercise\n- Pollution and cigarette smoke\n- Allergens such as animal dander, dust mites and pollen\n- Irritants such as perfumes, paints or air fresheners\n- Medications such as NSAIDs or beta-blockers\n\nThese trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.\n\nThis inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.\n\n# Risk factors\n\n- Family history of asthma or atopy\n- Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)\n- Exposure to smoke, including maternal smoking in pregnancy\n- Respiratory infections in infancy\n- Prematurity and low birth weight\n- Obesity\n- Social deprivation\n- Occupational exposures (e.g. flour dust, isocyanates from paint)\n\n# Symptoms\n\n- Wheeze\n- Dyspnoea\n- Cough\n- Chest tightness\n\nThe above symptoms should be episodic and usually show **diurnal variation** (worse at night or in the early morning). The patient may be able to identify specific triggers as listed above.\n\n# Signs\n\nIn between asthma exacerbations, clinical examination may be normal. If asthma is poorly controlled or during an exacerbation, signs include:\n\n- Tachypnoea\n- Increased work of breathing\n- Hyperinflated chest\n- Expiratory polyphonic wheeze throughout the lung fields\n- Decreased air entry (if severe)\n\n\n# Differential diagnosis\n\n- **Bronchiectasis** - usually associated with a productive cough, patients get frequent chest infections and coarse crackles rather than wheeze predominate on examination.\n- **Vocal cord dysfunction** - shares many triggers with asthma, inspiration more difficult than expiration, may have stridor.\n- **Chronic obstructive pulmonary disease** - patients usually >35 years old with a significant smoking history, may overlap with asthma in some.\n- **Gastro-oesophageal reflux disease** - microaspiration of stomach acid due to reflux can cause episodes of cough and wheeze which mimic asthma (although these may coexist and reflux can trigger asthma exacerbations). Symptoms are often postural and related to eating.\n- **Eosinophilic Granulomatosis with Polyangiitis** (Churg-Strauss syndrome) - small vessel vasculitis associated with pANCA, aside from asthma symptoms include nasal polyps, sinusitis, purpuric rashes and peripheral neuropathy.\n\n# Investigations \n\n- **FeNO (fractional exhaled nitric oxide) testing:** offer this **or** blood eosinophil count to all adults to confirm eosinophilic airway inflammation, asthma can be diagnosed if this is >50 parts per billion.\n- **Full blood count** to check **eosinophil count:** offer this **or** FeNO first-line to all adults - asthma can be diagnosed if this is above the normal reference range.\n- If neither of these confirm asthma, **spirometry** with **bronchodilator reversibility** should be offered to confirm airway obstruction (i.e. FEV1/FVC<70%). A bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is diagnostic of asthma.\n- If spirometry is delayed or not available, patients may be asked to monitor their peak flow twice a day for 2 weeks and keep a diary of the readings. This is then used to assess **peak flow variability** (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result.\n- If none of the above are confirmatory, patients may be referred to specialist services for a **direct bronchial challenge test**, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.\n\nNote: All of the above tests may be falsely negative in patients treated with inhaled corticosteroids.\n\n# Management of Chronic asthma\n\nThe aim of chronic asthma management is to achieve complete control over symptoms, with no need for rescue medications and no restrictions on physical activity. All patients should have a personalised asthma action plan which should be reviewed at least annually. Components of management include:\n\n## Non-pharmacological\n\n- Teach good inhaler technique and review this regularly\n- Spacer devices can be used to optimise medication delivery\n- Regular peak flow monitoring\n- Smoking cessation\n- Advice on avoiding triggers where possible (e.g. allergens, certain medications)\n- Ensure vaccinations are up to date, including annual influenza vaccination\n- Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected\n\n## Pharmacological\n\n- Prescribe all patients a combination inhaler with a **long-acting beta-2 agonist** (LABA) i.e. formoterol and a low-dose **inhaled corticosteroid** (ICS) i.e. budesonide to use as a reliever inhaler (i.e. PRN) - this is referred to as anti-inflammatory reliever (AIR) therapy.\n- Patients who do not respond adequately to AIR therapy, who are highly symptomatic at presentation or who present with a severe asthma exacerbation should be started on a low-dose **maintenance and reliever therapy inhaler** (MART). MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler (PRN) and as maintenance treatment (usually twice daily).\n- The next step would be increasing the ICS dose from low to **moderate** in the MART inhaler.\n- At this stage if asthma is not controlled, check FeNO and blood eosinophil count and refer to specialist asthma services if either are raised.\n- If neither are raised, consider adding either a **leukotriene receptor antagonist** (LTRA) such as montelukast (this is a tablet taken every night) or a **long-acting muscarinic agonist** (LAMA) such as tiotropium.\n- One of these should be trialled for 8-12 weeks alongside the moderate-dose MART - if asthma is well-controlled it can be continued.\n- If there is some improvement in control but this is still inadequate, the other medication can be trialled in addition (i.e. moderate dose MART + LTRA + LAMA).\n- If control has not improved, stop the medication and try the other one - if this is not successful refer to specialist services.\n- Options in specialist clinics include therapies such as **biologics** (e.g. omalizumab, which targets IgE).\n\nOther than patients who are not responding to treatment, the following situations shold also prompt a secondary care referral:\n\n- Uncertainty regarding diagnosis\n- Suspected occupational asthma\n- Severe or life-threatening asthma requiring admission to hospital\n- Multiple exacerbations requiring oral steroid treatment per year\n\n# Acute asthma\n\nAcute asthma exacerbations are graded in severity as below:\n\n\n| Severity | Clinical Features |\n|-----------------------|-----------------------------------------------|\n| Moderate | PEFR > 50% of predicted or best |\n| | No features of severe/life-threatening asthma |\n| Severe | PEFR 33-50% of predicted or best |\n| | Heart rate > 110 |\n| | Respiratory rate > 25 |\n| | Unable to complete sentences in one breath. |\n| | Accessory muscle use |\n| Life-threatening | PEFR < 33% of predicted or best |\n| | Oxygen saturation < 92% or cyanosis |\n| | Altered conciousness/confusion |\n| | Exhaustion/poor respiratory effort |\n| | Cardiac arrhythmia |\n| | Hypotension |\n| | Silent chest |\n\n\n## Investigations \n\n- **Peak expiratory flow rate (PEFR)** to help assess severity as per the classification above and monitor response to treatment.\n- **Arterial blood gas** if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.\n- **Portable chest X-ray** if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.\n\n## Management \n\n- Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment\n- Titrate oxygen to maintain saturations of 94-98%\n- Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)\n- If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide\n- Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow\n- Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers\n- If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)\n\nFollow up after an acute asthma attack is crucial, with NICE guidelines stating that patients should be reviewed within 2 days of discharge from hospital to assess their symptoms, inhaler technique and current management.\n\n# NICE Guidelines\n\n[NICE - Asthma: diagnosis, monitoring and chronic asthma management](https://www.nice.org.uk/guidance/ng245)\n\n# References\n\n[NICE CKS](https://cks.nice.org.uk/topics/asthma/)\n\n[Report on health inequalities and asthma](https://www.asthmaandlung.org.uk/sites/default/files/2023-03/auk-health-inequalities-final.pdf)\n\n[Guideline on severe asthma in primary care](https://www.pcrs-uk.org/sites/default/files/pcru/articles/2019-Autumn-Issue-18-SevereAsthmaReferral.pdf)\n\n\n\n",
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"question": "A 75 year old lady is admitted to the general medical ward with a 2 day history of worsening shortness of breath and a productive cough. She has a background of asthma since childhood and is known to be poorly compliant with her inhalers.\n\n\nOn examination, she is drowsy and has reduced breath sounds bilaterally.\n\n\nObservations:\n\n\n - Temperature 38.5°C\n - pulse 115\n - BP 110/70\n - respiratory rate 16\n - SpO<sub>2</sub> 96% on 8L oxygen\n\n\nArterial blood gas:\n\n||||\n|--------------|:-------:|------------------|\n|pH|7.37|7.35 - 7.45|\n|PaO₂|11.5 kPa|11 - 15|\n|PaCO₂|5.1 kPa|4.6 - 6.4|\n|Bicarbonate|23 mmol/L|22 - 30|\n\n\nShe has been started on nebulised salbutamol and ipratropium, and has been given IV hydrocortisone and magnesium sulphate. Which is the next most appropriate management?",
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"explanation": "This would not be useful as Mycoplasma lacks a cell wall and would not be visible on Gram stain. Culture would be of low yield as it is a fastidious organism and would take weeks to grow",
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"explanation": "This would not be useful as Mycoplasma lacks a cell wall and would not be visible on Gram stain. Culture would be of low yield as it is a fastidious organism and would take weeks to grow",
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"explanation": "This is more appropriate for detecting Legionella or Pneumococcal antigen, which is not the case here. These are not known to be associated with autoimmune haemolytic anaemia",
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"explanation": "This may be used as an alternative to molecular testing for Mycoplasma. However, it is impractical as the gold standard for diagnosis would require comparison of acute and convalescent serum samples (approximately 4 weeks apart) to detect a rise in IgG titres",
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"explanation": "The patient has Mycoplasma pneumonia complicated by cold agglutinin disease, a form of autoimmune haemolytic anaemia that is associated with Mycoplasma infection. This is shown by the raised reticulocyte count and LDH, raised unconjugated bilirubin and decreased haptoglobin level, which are byproducts of red blood cell breakdown. Mycoplasma is a fastidious organism and difficult to grow in culture, hence molecular testing would be advised",
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"comment": "I thought mycoplasma was a non productive cough?",
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"comment": "Most sources seem to say that mycoplasma pneumonia is picked up via serology. It can be done alongside NAAT but the main method in use is serology. ",
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"comment": "what is the purple discolouration referring to?",
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"comment": "Mycoplasma = serology",
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"explanation": "# Summary \n \nPneumonia is a radiological diagnosis, often due to a lower respiratory tract infection causing inflammation of the alveoli and terminal bronchioles, leading to consolidation of bronchopulmonary segment or lobe. Key signs and symptoms include rapid onset of high fever and productive cough for typical bacterial causes. Key investigations include blood tests, sputum culture, urinary antigen tests, and chest x-ray. Management strategies involve use of antibiotics, assessment of severity using CURB-65 score and inpatient treatment for severe cases.\n \n \n# Definition\n \n- Lower Respiratory Tract Infection/ Pneumonia is caused by infection and subsequent inflammation of the alveoli and terminal bronchioles.\n- This leads to an entire bronchopulmonary segment or lobe becoming consolidated, which means that tissue is filled with inflammatory cells and oedema.\n \n \n# Community Acquired Pneumonia (CAP)\n \n \n## Bacterial Causes\n \n \n- Typicals - so called because of the classical rapid onset of symptoms, including high fever and productive cough;\n- Streptococcus pneumoniae (gram +ve cocci found in pairs, also known as 'Pneumococcus')\n- Staphylococcus aureus\n- Haemophilus influenzae (gram -ve rod, potent beta-lactamase producer)\n- Moraxella catarrhalis (gram -coccus, potent beta-lactamase producer)\n- Atypicals: so called because of the more gradual onset of symptoms, which may be non-specific initially (fever, myalgia, dry cough). The organisms are also intracellular;\n- Mycoplasma pneumoniae\n- Chlamydia pneumoniae\n- Legionella pneumophila\n- Coxiella burnettii\n- Chlamydia psittaci\n \n \n## Viral Causes \n \n- Most commonly Influenza A, which can predispose to superadded Staph aureus (or strep pneumoniae) pneumonia.\n- Others: CMV, HSV, VZV\n \n## Fungal Causes\n \nCan be seen after silver staining and microscopy:\n \n- Candida - dimorphic yeast\n- Aspergillus - fungus with hyphae\n- Cryptococcus - encapsulated yeast\n \n \n## Specific Causes \n \nCOPD: \n \n- Pneumococcus still most common\n- Haemophilus influenzae\n- Morexella catarrhalis\n \nCystic Fibrosis:\n \n \n- Staph aureus\n- Pseudomonas aeruginosa\n- Burkholderia cepacia\n \nCauses in Homeless people: malnourished, alcohol or drug dependent, immunosuppressed:\n \n \n- Mycobacterium tuberculosis\n- Aspiration pneumonia (infection with normal flora of mouth and anaerobes, also consider in any patient with an unsafe swallow or with depressed consciousness)\n- Klebsiella pneumoniae (causes 'red-current jelly' sputum, and commonly causes lung abscess formation and empyema)\n \n \nOccupational/travel situations:\n \n- Aerosols from humidifiers and airconditioning (e.g. at holiday resorts) - Legionella pneumophila.\n- Patients can present with diarrhoea and vomiting, develop hepatorenal syndrome and have a low sodium. Severe pneumonia develops, with other rare complications such as:\n- Pancreatitis\n- Peritonitis\n- Myocarditis, endocarditis, pericarditis\n- Glomerulonephritis\n \n \nClosed populations e.g. schools, offices\n \n- Mycoplasma pneumoniae\n- Extra respiratory symptoms:\n- Erythema multiforme, erythema nodosum\n- Guillain-Barre Syndrome (and rarely other neurological complications e.g. aseptic meningitis, cerebellar disease, transverse myelitis).\n- Cold agglutinin production with haemolytic anaemia\n- Chlamydia pneumoniae\n \n \nZoonotic Causes: \n \n- In Abattoir worker, farmer, vets\n- Coxiella burnettii\n- Brucella spp.\n \n- Animal hide importers/sorters\n- Bacillus anthracis\n- Coxiella burnettii\n \n \n- Following exposure to birds\n- Chlamydia psittaci (causes psittacosis)\n- Exposure to bats/bat droppings\n- Histoplasma capsulatum (a fungus, classically affects cave-explorers)\n \n \n## Investigations\n \n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## CURB-65 \n \n \n- Use the CURB-65 score to aid in deciding the severity of pneumonia and further management based on this\n- Components (1 point for each if present):\n- Confusion +/-\n- Urea >7\n- Respiratory Rate >30\n- Blood pressure: systolic < 90 or diastolic <60\n- More than 65 years old\n \n \nCURB-65 mortality by score:\n \n- 0 or 1 - 1.5%\n- 2 - about 10%\n- 3 or more - 10% or more \n \n \n \n \n## Management\n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input.\n \n- Management based on CURB-65 score:\n- 0/1: home-based care, give oral amoxicillin for 5 days (macrolide e.g. clarithromycin, doxycycline or tetracycline if penicillin allergic).\n- 2: hospital-based care, 7-10 day course of dual antibiotic therapy with amoxicillin (IV or oral) and a macrolide\n- 3: Hospital/ITU-based care, 7-10 day course of dual antibiotic therapy with IV co-amoxiclav/ceftriaxone/tazocin and a macrolide.\n \n \n- Atypical and typical community-acquired pneumonia are both managed in the same way initially.\n- Liaise with microbiology to guide targeted antibiotics following culture results e.g. flucloxacillin for staph aureus pneumonia.\n- A repeat chest x-ray is required after 6 weeks to assess for underlying pathology.\n \n \n## Complications\n \n \n- Pleural effusion\n- Empyema (suspect if persistent, swinging fever with leucocytosis found after antibiotic therapy)\n- Abscess (can be caused by S. pneumoniae, Klebsiella, staph aureus). Can develop pyopneumothorax.\n- Pneumothorax\n- Septicemia\n- Atrial fibrillation\n- Post-infective bronchiectasis\n \n \n \n \n# Hospital Acquired Pneumonia\n \n \n## Definition\n \n \nLower respiratory tract infection that develops more than 48 hours after admission to hospital\n \n \n## Risk Factors\n \n \n- Poor hand hygiene and hospital infection control\n- Intubation and ventilation\n \n \n## Causative Organisms\n \n \n- Pseudomonas aeruginosa\n- E. coli\n- Klebsiella pneumoniae\n- Acinetobacter species (can acquire high potency beta-lactamases, known as ESBLs)\n- Serratia species (can acquire high potency beta-lactamases, known as ESBLs)\n \n \n## Investigations\n \nMay include:\n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## Management \n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input and discussion with microbiology. Empirical antibiotics are guided by severity and likelihood of resistant organisms:\n \n- HAP within 5 days of admission: co-amoxiclav is usually first line for non-severe symptoms\n- HAP more than 5 days after admission (associated with higher risk of resistance) or severe symptoms: tazocin or cephalosporin (e.g. ceftazidime) or quinolone first-line.\n- If MRSA is suspected, add vancomycin\n \n \n# Aspiration Pneumonia \n \n \n- Caused by any cause of depressed consciousness or impairment of the swallowing mechanism\n- Infection caused by mixed aerobic and anaerobic mouth flora, which can cause cavitary pneumonia or empyema\n- Same empirical therapy as for non-aspiration pneumonia, but later antibiotic choice made by pathogen and sensitivities. Metronidazole often added in to cover for anaerobic organisms. Local guidance should be sought.\n \n \n# NICE Guidelines\n \n \n[Click here for NICE CKS on chest infections](https://cks.nice.org.uk/topics/chest-infections-adult/)\n \n[Click here for NICE guidance on antimicrobial prescribing in hospital-acqui",
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"question": "A 75 year old lady is admitted to the general medical ward with a 3 day history of worsening shortness of breath and a productive cough.\n\n\nExamination reveals bibasal coarse crepitations and purplish discoloration of her fingers and toes. \n\nThe patient’s observations include a temperature of 38.5°C, pulse of 90, blood pressure of 110/70 mmHg, respiratory rate of 25, and SpO₂ of 98% on 2L oxygen. \n\n\n\n\nFull blood count:\n\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|95 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|186x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|115 fL|80 - 96|\n|Reticulocytes|5 %|0.2 - 2|\n|Haptoglobin|12 mg/dL|41 - 165|\n\n\n\nLiver function tests:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Albumin|40 g/L|35 - 50|\n|Alanine Aminotransferase (ALT)|21 IU/L|10 - 50|\n|Aspartate Aminotransferase (AST)|32 IU/L|10 - 40|\n|Alkaline Phosphatase (ALP)|110 IU/L|25 - 115|\n|Bilirubin|58 µmol/L|< 17|\n|Conjugated Bilirubin|3.2 µmol/L|0 – 8|\n|Unconjugated Bilirubin|26.5 µmol/L|0.2 – 0.8|\n|Lactate Dehydrogenase|910 IU/L|70 - 250|\n\n\n\n\nChest X-ray: Bilateral patchy consolidation\n\n\n\nGiven the most likely diagnosis and complication that has occurred, which of the following is the most appropriate diagnostic test to find out the causative organism?",
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"explanation": "Pulmonary embolism tends to cause a transudative pleural effusion, and this history here does not indicate PE",
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"explanation": "This patient has an exudative effusion fulfilling Light's criteria, with pleural fluid/serum LDH ratio >0.6 and pleural fluid LDH >2/3 the upper limit of normal serum LDH. Parapneumonic effusions may occur with bacterial pneumonia, and may cause either simple or complicated effusions (including empyema). This would usually show up on pleural tap as purulent pleural fluid with neutrophil predominance, pH <7.3, low glucose and raised LDH. Clinical presentation may be similar to that of pneumonia",
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"explanation": "Whilst malignancy often causes a exudative effusion, this is unlikely given her young age and more recent onset of symptoms",
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"explanation": "In rheumatoid pleurisy, pleural fluid is likely to be low in glucose with raised LDH and pH <7.3, which is rather similar to the pleural fluid results in this patient. However, the history is not suggestive of rheumatoid arthritis",
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"comment": "How is this exudative?? The protein isn't more than 30g/L on either of them?",
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"comment": "Use light's criteria when protein is between 20-30 (some textbooks say 25-35)",
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"comment": "But the protein is only 11 @ myotonia bladder ??",
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"comment": "this question is pure bs. the protein is literally 11g/L. its transudative by definition.",
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"comment": "lights criteria states that if pleural protein/serum protein=<0.5 then that is transudative ",
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"comment": "Also this was misleading - ''She has visited her General Practitioner and has completed a 5 day course of antibiotics with no improvement.'' if her presentation was bacterial pneumonia should have been some improvement ",
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"explanation": "# Summary\n\nA pleural effusion refers to abnormal fluid accumulation in the pleural cavity. There is a wide range of causes, which are classified into transudative and exudative effusions. Transudates include effusions secondary to heart failure or cirrhosis, and typically have low protein levels in the pleural fluid. Exudates include effusions due to malignancy or infection, and have higher protein levels in the fluid. Key investigations include a pleural tap to sample the fluid, chest X-ray to detect an effusion and further imaging and bloods to investigate for underlying causes (e.g. a CT chest if malignancy is suspected). Treatment depends on the underlying cause, but larger effusions or empyemas should be drained. Options for recurrent effusions include pleurodesis or an indwelling chest drain.\n\n# Definition\n\nA pleural effusion is a collection of fluid in the pleural cavity (space between the lung and the chest wall). In health, there is a small volume of serous pleural fluid (10-20ml) which lubricates the pleura and creates surface tension. When larger volumes of fluid accumulate this overwhelms the resorption capacity of the pleura and can impede respiration as the lung cannot expand fully.\n\n# Aetiology\n\nCauses of pleural effusions are classified as either **transudates** (where changes in oncotic and hydrostatic pressure cause fluid to leak from the vasculature) or **exudates** (where inflammation leads to increased microvascular permeability and drainage of pleural fluid may be impaired).\n\n**Examples of transudative causes include:**\n\n- Heart failure\n- Nephrotic syndrome\n- Cirrhosis\n- Hypoalbuminaemia\n\n**Examples of exudative causes include:**\n\n- Pneumonia (a “parapneumonic effusion”) \n- Malignancy\n- Tuberculosis\n- Pulmonary embolism\n- Rheumatoid arthritis\n- Systemic lupus erythematosus \n- Pancreatitis \n- Trauma\n\n# Classification\n\nTransudates are classified as pleural fluid with a protein level less than 25g/L (assuming a normal serum protein).\n\nExudates are classified as pleural fluid with a protein level more than 35g/L.\n\nFor intermediate effusions, **Light’s criteria** are used - if any of the following are true then the effusion is an exudate:\n\n- The ratio of pleural to serum protein is greater than 0.5\n- The ratio of pleural to serum LDH is greater than 0.6\n- The pleural fluid LDH is greater than ⅔ of the upper limit of normal serum value\n\n# Signs and symptoms\n\nPatients may be asymptomatic, especially if their lung function and capacity are normal, and so many effusions are detected incidentally on imaging. \n\nSymptoms as effusions enlarge include:\n\n- Shortness of breath\n- Reduced exercise tolerance\n- Dry cough\n- Pleuritic chest pain\n\nOn examination, signs include:\n\n- Reduced chest expansion on the affected side\n- Dullness to percussion over the effusion\n- Reduced or absent breath sounds over the effusion\n- Loss of vocal resonance over the effusion\n- Large pleural effusions may cause tracheal deviation away from the effusion\n- Respiratory distress (e.g. accessory muscle usage) \n\nSymptoms and signs of an underlying cause of the effusion may also be seen, for example peripheral oedema in a patient with an effusion secondary to congestive cardiac failure. \n\n# Differential diagnosis\n\nOther than the causes listed above, other types of fluid can accumulate in the pleural cavity - these may also be thought of as types of pleural effusion but don’t fit into the transudate/exudate classification and have different causes and management:\n\n- **Haemothorax** - a collection of blood in the pleural cavity, usually secondary to trauma but can occur spontaneously e.g. in the context of malignancy or vascular rupture\n- **Chylothorax** - chylous fluid in the pleural cavity, occurs due to lymphatic duct injury or obstruction (leading to rupture of small collaterals). Common causes include iatrogenic injury during thoracic surgery, traumatic injury or lymphoma.\n- **Empyema** - a collection of pus in the pleural cavity, may be loculated with gas. Usually develop as a complication of pneumonia.\n- **Mesothelioma** - tumour of the pleura, strongly associated with asbestos exposure.\n\n# Investigations\n\n**Bedside investigations:**\n\n- A **pleural tap** should be done in all new suspected exudative effusions, as well as those presumed to be transudates (e.g. bilateral, associated features of heart failure) if they fail to respond to treatment or have atypical features.\n- Pleural fluid is aspirated and sent for cytology, MC&S (microscopy, culture and sensitivity) and biochemistry (pH, protein, LDH and glucose).\n- Paired serum protein and LDH should also be sent.\n- Other investigations may be requested for a suspected underlying cause, e.g. pleural fluid amylase (raised in an effusion secondary to pancreatitis).\n- Pleural fluid cholesterol and triglycerides are raised in a chylothorax.\n- Low glucose is seen in effusions secondary to rheumatoid arthritis, SLE and in empyemas.\n- Complement is also low in effusions secondary to rheumatoid arthritis or SLE.\n- pH<7.2 indicates either infection (e.g. an empyema) or malignancy.\n- Bloody pleural fluid can be seen in malignancy, trauma or PE - haematocrit measurement of the pleural fluid is used to determine if it is a haemothorax.\n- Other bedside tests should be targeted to the underlying cause e.g. sputum AFB for TB, urinalysis looking for proteinuria in suspected nephrotic syndrome.\n\n**Blood tests:**\n\n- FBC - may show a raised WCC suggestive of infection, anaemia or thrombocytosis in malignancy\n- U&E - for baseline renal function especially if diuretic treatment is considered\n- LFTs - may show a low albumin in cirrhosis \n- Clotting - to indicate safety for pleural intervention\n- ANA, rheumatoid factor - if a rheumatological cause such as SLE or rheumatoid arthritis is suspected\n- Serum amylase - if pancreatitis is suspected\n\n**Imaging:**\n\n[lightgallery]\n\n\n- Chest X-ray is the first-line imaging investigation in all patients with a suspected pleural effusion \n- will reveal blunting of the costophrenic angle or white-out of lung (if large)\n\n- Thoracic ultrasound \n- can reveal whether it is simple fluid or septated, which would be consistent with malignancy or infection\n- underlying changes in the lung can also be identified such as consolidation or pulmonary oedema.\n\n- CT scan with contrast \n- can be used to further investigate an underlying cause e.g. malignancy\n\n**Other investigations:**\n\n- Pleural biopsy may also be considered if pleural fluid analysis and imaging do not reveal a diagnosis - samples should be sent for histology and TB culture.\n\n- Echocardiogram in suspected heart failure\n\n- Fibroscan in suspected liver cirrhosis\n\n# Management\n\n**Conservative:**\n\n- Symptom management e.g. analgesia for chest pain\n- Oxygen if low saturations\n- May require resuscitation (use an ABCDE approach) if unstable due to a large effusion \n\n**Medical:**\n\n- Antibiotics for infection - may need a prolonged course for empyema along with drainage\n- Diuretics for pleural effusions secondary to heart failure\n\n**Interventional**\n\n- Ultrasound-guided pleural aspiration may be used for symptomatic relief \n- A chest drain is needed for empyemas and haemothoraxes, and for some larger effusions\n- If pleural effusions are rapidly recurring, the two main options are pleurodesis or a tunnelled indwelling pleural drain\n- Indwelling drains are often used in patients receiving palliative treatment (e.g. of a malignancy) as they can have regular drainage in the community, reducing hospital admissions\n- Pleurodesis can be chemical (where an irritant is injected into the pleural space, sealing it shut via a fibrotic reaction) or surgical via thoracotomy or thoracoscopy\n\n# References\n\n[Radiopaedia - Pleural Effusion](https://radiopaedia.org/articles/pleural-effusion?lang=gb)\n\n[Patient UK - Pleural Effusion](https://patient.info/doctor/pleural-effusion-pro)\n\n[Life in the Fast Lane - Pleural Fluid Analysis](https://litfl.com/pleural-fluid-analysis/)",
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"question": "A 40 year old female is admitted to the general medical ward with a 2 week history of fever, worsening shortness of breath and a productive cough with yellow sputum. She has visited her General Practitioner and has completed a 5 day course of antibiotics with no improvement. She has no other past medical history of note.\n\n\n\nOn examination, she has right sided coarse crepitations with reduced air entry in the right lower zone.\n\n\n\nChest X-ray: Right sided pleural effusion\n\n\n\nThe respiratory registrar performs a diagnostic pleural tap. The results are as follows:\n\n\n\nAppearance - Purulent\nMicroscopy - Neutrophil predominant\npH - 7.28\n\n\n\n||Pleural fluid|Serum|\n|---------------------------|-------------|----------|\n|Protein|11 g/L|28 g/L|\n|Lactate dehydrogenase (LDH)|358 U/L|465 U/L|\n|Glucose|2.8 mmol/L|6.9 mmol/L|\n\n\n\nGiven the pleural fluid results, which is the most likely cause of her pleural effusion?",
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"explanation": "This may be considered if the patient has very poor renal function and is not able to take either non-steroidal anti-inflammatory drugs or colchicine. Blood glucose monitoring should be done whilst on prednisolone, especially since the patient is diabetic, as it usually causes elevated glucose levels in the evening or nighttime",
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"comment": "As this patient has a high temperature, wouldn't you be concerned about septic arthritis?",
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"comment": "Surely this question should be about next step in management i.e. performing joint aspiration to rule out septic arthritis rather than going straight to gout treatment?",
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"comment": "Why is the WCC raised\n",
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"comment": "crystals are DAMPS -> activates innate immune response",
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"explanation": "# Summary\n\nGout is a type of arthritis caused by the accumulation of monosodium urate crystals in and around the joints. It presents acutely with rapid onset of severe pain, swelling and redness of affected joints, with the first metatarsophalangeal joints the most commonly affected. Chronic untreated gout may lead to tophi which are hard nodules made up of monosodium urate crystals that deposit in soft tissues. Gout may be diagnosed clinically, with supportive investigations including a serum urate and synovial fluid analysis looking for monosodium urate crystals. Management of acute gout is with NSAIDs, colchicine or a short course of oral steroids. Urate-lowering therapy with allopurinol or febuxostat should be considered to reduce the risk of further gout flares. \n\n# Definition\n\nGout is a form of arthritis that occurs when monosodium urate crystals deposit in joints. This causes both acute inflammation (gout flares) and in the longer-term, a chronic gouty arthritis with tophi (hard deposits of monosodium urate crystals in soft tissues).\n\n# Epidemiology\n\n- Gout is the most common inflammatory arthritis and prevalence is increasing with time (currently 2.5%)\n- Hyperuricaemia (high urate) is the main risk factor (although most patients with a high urate do not develop gout, and some patients develop gout with a normal urate)\n- Factors that contribute to this include:\n- Older age - typically patients are above the age of 40\n- Male sex (post-menopausal women are also at increased risk)\n- Comorbidities including chronic kidney disease (CKD), diabetes, osteoarthritis, hypertension\n- Excess alcohol consumption\n- Dietary excess of meat, seafood and sugary drinks\n- Overweight or obesity\n- Medications such as thiazide diuretics and ciclosporin\n- Family history of hyperuricaemia and gout\n- Genetic disorders associated with hyperuricaemia such as Lesch-Nyhan or glycogen storage disorders\n- Organ transplant recipients\n- Acute attacks may be triggered by stressors including:\n- Trauma and surgery\n- Intercurrent illness\n- Alcohol excess\n- Sudden excess of protein in the diet\n- Chemotherapy (due to cell breakdown)\n- Urate-lowering medications can cause a flare (as crystals are shed into the joint space)\n\n# Signs and Symptoms\n\nOverlapping clinical syndromes are caused by the deposition of monosodium urate crystals in different tissues:\n\n**Acute gout** \n\n- Commonly presents with a monoarthritis\n- Pain is severe and rapid in onset, reaching a peak within 24 hours \n- Affected joints become swollen, erythematous and tender\n- The first metatarsophalangeal (MTP) joint is the most commonly affected (70% of first attacks)\n- Other common sites include the knees, ankles, midtarsal joints, wrists, elbows and small joints of the hands\n- Systemic features such as fever and malaise may be seen\n- Patients may be tachycardic due to pain\n\n**Tophaceous gout**\n\n- Patients will usually have a history of longstanding recurrent acute gout\n- However in atypical cases patients may present with tophi without previous flares\n- Tophi are firm white nodules of sodium monosulphate crystals under the skin\n- They commonly occur on extensor surfaces of joints such as knees or elbows, the Achilles tendons, backs of hands and feet and on the helices of the ears\n- Usually they are painless however they can become infected, inflamed or ulcerated\n- They may discharge white material onto the skin surface\n- Chronic gouty arthritis may present with tender and stiff joints with reduced range of motion\n\n# Differential Diagnosis\n\n- **Septic arthritis** must be ruled out in patients who are systemically unwell with an acute monoarthritis - urgent synovial fluid analysis is needed if this is suspected\n- **Pseudogout** typically affects the knee and wrists rather than the MTP joint; synovial fluid analysis shows calcium pyrophosphate crystals\n- **Cellulitis** causes erythema, pain and swelling of the skin rather than the joint - patients may be systemically unwell\n- **Trauma** should be asked about in the history as this may cause similar symptoms of pain, difficulty mobilising and swelling\n- **Other inflammatory arthritides** such as rheumatoid arthritis may mimic chronic gouty arthritis\n\n# Investigations\n\n**Bedside tests:**\n\n- **Joint aspiration** is the gold standard diagnostic investigation \n- Needle-shaped monosodium urate crystals with negative birefringence are seen in gout\n- Synovial fluid should also be sent for gram stain and culture to rule out septic arthritis\n- Tophi can be biopsied to look for these crystals\n\n**Blood tests:**\n\n- **Serum uric acid** should be measured in all patients with suspected gout\n- A serum urate of 360 micromol/L or more confirms the diagnosis\n- Levels may be falsely low in an acute attack and so should be repeated 2-4 weeks after the flare has resolved\n- Levels are used to guide urate-lowering therapy if this is initiated as prophylaxis\n- **Screening for risk factors** should be considered:\n- Fasting glucose or HbA1c for diabetes\n- Renal function and urine albumin:creatinine ratio for CKD\n- Lipids for hypercholesterolaemia\n- **Inflammatory markers** with FBC and CRP should be checked if septic arthritis is suspected\n- **Liver function tests** are needed prior to starting febuxostat\n- Patients from Han Chinese, Thai and Korean backgrounds should be screened for **HLA-B5801** prior to starting allopurinol (as this increases the risk of severe cutaneous adverse reactions if present)\n\n**Imaging tests:**\n\n- These may be useful to assess chronic disease or where the diagnosis of acute gout is uncertain\n- X-rays in chronic disease show punched-out periarticular erosions, areas of sclerosis and tophi\n- Ultrasound may show joint effusions, tophi, synovial thickening and erosions\n\n# Management \n\n**Acute gout flares** \n\nThere are three first-line options for treatment of a gout flare:\n\n- NSAIDs e.g. naproxen\n- Give at maximum dose\n- Continue until 1-2 days after resolution of symptoms\n- Consider giving with a PPI for gastric protection\n- Avoid in heart failure, patients at high risk of gastrointestinal bleeding and severe renal failure\n- Colchicine\n- Dosing is 500 mcg 2-4 times per day\n- Continue until pain resolves\n- Dose-dependent side effects include diarrhoea, nausea and vomiting\n- Oral corticosteroids\n- e.g. prednisolone 30mg once a day for 3-5 days\n- Useful in patients with contraindications to both NSAIDs and colchicine\n- An injection of intramuscular, intravenous or intra-articular steroids can also be considered\n- Alongside this, consider other analgesia (e.g. paracetamol) and other non-pharmacological pain relief such as ice packs\n- A combination of the above may be tried if a single agent is ineffective\n- Patients should be advised to keep the affected joint cool and exposed and to rest and elevate the affected limb\n- Patients already on urate lowering treatment should continue this throughout the acute flare\n\n## Prevention\n\nPatients should be followed up 4-6 weeks after an acute episode of gout to think about preventative strategies and assess for risk factors (also see Investigations). \n\nOptimisation of risk factors may include:\n\n- Reducing alcohol consumption\n- Maintaining a balanced diet and healthy weight\n- Investigate and treat for comorbidities such as hypertension or CKD\n- Review medications and consider switching medications such as thiazides that cause hyperuricaemia\n- Where possible, switch antihypertensive medications to losartan or amlodipine, which have modest urate-lowering effects \n- Initiating urate-lowering therapy (see below)\n\nMost patients can be managed in primary care, however the following should prompt referral to or discussion with specialist services:\n\n- Patients with complications of gout\n- Atypical presentations (e.g. aged under 30) or uncertain diagnosis\n- Pregnant patients\n- Stage 3b to 5 CKD\n- Organ transplant recipients\n- Those at risk of adverse effects with standard medical treatment, or if treatment is ineffective or not tolerated\n\nIndications for **urate-lowering therapy** include:\n\n- Multiple or troublesome gout flares\n- Chronic gouty arthritis or tophi\n- Patients taking diuretics\n- CKD stage 3 to 5\n\n**Starting and monitoring urate-lowering therapy (ULT):**\n\n- ULT should be started at least 2-4 weeks after an acute flare if possible as medications can precipitate further attacks\n- Colchicine should be given whilst starting ULT to reduce the risk of a flare (NSAIDs or steroids are second-line)\n- Doses should be uptitrated with monthly monitoring of serum urate levels, aiming for a target of 360 micromol/L\n- A target urate level of 300 micromol/L may be helpful in patients with tophi or chronic arthritis due to gout, or those who continue to have flares despite ULT\n- First-line options are either allopurinol or febuxostat which are both xanthine oxidase inhibitors (so reduce uric acid production)\n- Allopurinol is preferred in patients with significant cardiovascular disease\n- Second line options include uricosuric medications (e.g. probenecid) - these can promote stone formation so should be avoided if there is nephrolithiasis\n\n# Complications\n\n- Chronic gouty arthritis and permanent joint damage\n- Tophi, which may become inflamed or infected\n- Nephrolithiasis due to uric acid precipitation - these are responsible for 8% of renal calculi and are radiolucent\n- Chronic urate nephropathy - urate deposition in the renal interstitium causes inflammation and fibrosis\n- Both allopurinol and febuxostat can cause rashes, which in rare cases may be severe (e.g. Stevens Johnson syndrome or toxic epidermal necrolysis)\n- Increased risk of cardiovascular disease and mortality\n\n# NICE Guidelines\n\n[NICE CKS - Gout](https://cks.nice.org.uk/topics/gout/)\n\n[NICE - Gout: diagnosis and management](https://www.nice.org.uk/guidance/ng219/)\n\n# References\n\n[Patient UK - Gout](https://patient.info/doctor/gout-pro)\n\n[Radiopaedia - Gout](https://radiopaedia.org/articles/gout?lang=gb)",
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"question": "A 70-year-old man is admitted with sudden onset right ankle pain and swelling for 1 day, the third episode this year. His medical history includes type 2 diabetes and chronic kidney disease, likely from diabetic nephropathy.\n\n\nOn examination, his right ankle is erythematous, warm, and tender, with full range of movement.\n\n\n\n\nObservations: Temperature 38.1°C, pulse 90, BP 110/70, respiratory rate 18, SpO<sub>2</sub> 100% on room air\n\n\n\nInitial blood tests are as follows:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|142 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Neutrophils|5.5x10<sup>9</sup>/L|2.0 - 7.5|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\n|Sodium|137 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Chloride|102 mmol/L|95 - 106|\n|Urea|8 mmol/L|2.5 - 7.8|\n|Creatinine|151 µmol/L|60 - 120|\n|eGFR|60 mL/min/1.73m<sup>2</sup>|> 60|\n\n\n\n\n\nX-ray of the right ankle showed no acute fractures or bony erosions.\n\n\n\nWhich of the following is the next most appropriate treatment?",
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"explanation": "This would appear as Gram-negative intracellular diplococci. It is associated with young sexually active adults",
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"explanation": "This would appear as Gram-positive diplococci in clusters. This is seen as purple staining cocci that appear similar to \"bunches of grapes\". S. aureus is a common cause of septic arthritis in otherwise healthy adults and may be associated with prosthetic joint infections",
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"explanation": "# Summary\n\nSeptic arthritis is an infection of the joint characterized by acute inflammation and swelling. It is caused by a bacterial or viral pathogen that infects the synovial fluid. The most commonly implicated organism is Staphylococcus aureus. Noteworthy clinical signs include a tender, swollen joint with reduced mobility, often accompanied by systemic illness. Key investigations include joint aspiration for Microscopy Culture and Sensitivity, along with blood tests showing increased white blood cell count and elevated ESR/CRP. Management typically involves IV antibiotics, joint washout under general anaesthesia, and physiotherapy once the acute infection has resolved.\n\n# Definition\n\nSeptic arthritis is an infection of the joint, specifically the synovial fluid. It is typically caused by a bacterial or viral pathogen and necessitates prompt medical intervention due to the high risk of joint damage and other severe complications.\n\n# Epidemiology\n\nSeptic arthritis has an annual incidence of 4-10 cases per 100,000 patients in Western Europe. It can affect individuals of any age, though certain populations are at a higher risk due to underlying conditions.\n\n# Aetiology\n\nThe most prevalent organism implicated in septic arthritis is Staphylococcus aureus. Other responsible organisms include:\n\n- Gonococcus: primarily in sexually active individuals\n- Streptococcus spp.\n- Gram-negative bacilli\n\nRisk factors contributing to septic arthritis include:\n\n- Pre-existing joint diseases such as rheumatoid arthritis\n- Chronic kidney disease\n- Immunosuppressive states\n- Presence of prosthetic joints\n\n# Signs and Symptoms\n\nThe clinical presentation of septic arthritis usually involves:\n\n- Acute onset of tender, swollen joint\n- Reduced range of joint movement\n- Systemic symptoms such as fever, malaise, or chills\n\n# Differential Diagnosis\n\nDifferential diagnoses for septic arthritis include:\n\n- Gout and pseudogout: characterized by intense joint pain, redness, and swelling, often in the big toe or knee.\n- Osteoarthritis: presents with joint pain, stiffness, and sometimes swelling, generally improving with movement.\n- Rheumatoid arthritis: marked by joint pain, swelling, and stiffness, often symmetrical and worse after rest.\n- Lyme disease: may show erythema migrans rash, flu-like symptoms, and possibly migratory joint pains.\n\n# Investigations\n\nDiagnostic investigations for septic arthritis include:\n\n- Joint aspiration for Microscopy, Culture, and Sensitivity: The aspirate usually appears turbid and yellow, resembling pus.\n- Blood tests: elevated white cell count, high ESR/CRP\n- Blood cultures: to identify causative organisms\n- Imaging: X-ray of the joint may be performed to evaluate for osteomyelitis or other complications.\n\n# Management\n\nThe treatment of septic arthritis involves:\n\n- IV antibiotics guided by local antibiograms and susceptibilities\n- Consideration of joint washout under general anaesthesia to remove infected material\n- Physiotherapy following the resolution of acute infection to restore joint function\n\nComplications of septic arthritis can include:\n\n- Osteomyelitis: infection of the bone\n- Chronic arthritis: persistent joint inflammation\n- Ankylosis: joint fusion resulting in immobility\n\n# References\n\n[Click here for the BNF Treatment Summary for Musculoskeletal infections](https://bnf.nice.org.uk/treatment-summary/musculoskeletal-system-infections-antibacterial-therapy.html)\n\n[Click here for the BMJ Best Practice Summary of Septic Arthritis](https://bestpractice.bmj.com/topics/en-us/486)",
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"question": "A 40 year old gentleman is admitted to the acute medical unit with a 1 day history of sudden onset right ankle pain and swelling. He has no other past medical history.\n\n\n\nOn examination, his right ankle is erythematous, warm and tender on palpation. There is limited active and passive range of movement in the ankle joint due to pain.\n\n\n\nObservations:\n\n\n\n - Temperature 38.5°C\n - pulse 90\n - BP 110/70\n - respiratory rate 18\n - SpO<sub>2</sub> 100% on room air\n\n\n\nInitial blood tests are as follows:\n\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|142 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|16.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\n|Neutrophils|13x10<sup>9</sup>/L|2.0 - 7.5|\n\n\n\nJoint aspiration is done which shows a cloudy yellow fluid with a predominance of neutrophils. The following is seen on Gram stain:\n\n\n\n [lightgallery]\n\n\n\nWhich is the most likely causative organism?",
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"explanation": "This may be found in transient ischaemic attack (TIA) due to carotid thromboembolism, which may result in transient monocular visual loss or amaurosis fugax. A TIA would not explain the frontal headache and joint stiffness",
"id": "32219",
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"explanation": "This patient has giant cell arteritis and polymyalgia rheumatica, which are closely associated. Raised ESR is a characteristic finding. Sudden onset vision loss is a red flag and requires urgent steroid treatment to avoid permanent vision loss",
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"explanation": "Headache may be a symptom of raised intracranial pressure. This may occur due to a wide range of aetiologies, including intracranial haemorrhage, neoplasm, stroke, infections, hydrocephalus. However, the patient does not have any neurological abnormalities so this would be less likely. Idiopathic intracranial hypertension may present with headache and vision loss but this is less likely to be unilateral",
"id": "32221",
"label": "d",
"name": "Raised cerebrospinal fluid (CSF) pressure",
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"explanation": "This is highly specific for rheumatoid arthritis (RA), which is an inflammatory arthritis that may also present with pain and morning stiffness in joints. However, RA is more likely to have peripheral joint involvement, as opposed to axial involvement in polymyalgia rheumatica",
"id": "32222",
"label": "e",
"name": "Anticyclic citrullinated peptide (anti-CCP) antibody positivity",
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"explanation": "This is classically found in ankylosing spondylitis, which may present with neck or back pain with morning stiffness that improves on exercise. However, this is more likely associated with anterior uveitis, which would cause painful visual loss",
"id": "32220",
"label": "c",
"name": "Inflammation of the sacroiliac joints",
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"explanation": "# Summary\n\nGiant cell arteritis (GCA) is a form of vasculitis which affects medium and large arteries. It classically affects the branches of the external carotid artery and the ophthalmic artery, which is often referred to as temporal arteritis. Key signs and symptoms include a temporal headache, jaw claudication, amaurosis fugax, thickening and tenderness of the temporal artery, and scalp tenderness. Systemic symptoms and features of polymyalgia rheumatica are common. The diagnosis is clinical in the first instance, and patients with visual symptoms should be treated immediately with high-dose steroids, however supportive investigations include full blood count, CRP and ESR. Confirmation of the diagnosis is with vascular ultrasound and temporal artery biopsy. Management is with high-dose steroids, with steroid sparing agents considered in patients who relapse when steroids are weaned.\n\n# Definition\n\nGiant cell arteritis (GCA) is a large vessel vasculitis which commonly affects the extracranial external carotid artery branches. Involvement of other vessels may occur, with patients presenting atypically with systemic symptoms and aortic involvement rather than temporal arteritis.\n\n# Epidemiology\n\n- GCA is the most common primary vasculitis \n- Age is an important risk factor - GCA is rare in the under 50s, with cases peaking in those aged 70-79\n- Women are 2-3x more likely to be affected than men\n- Northern European descent is also a risk factor\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n- Headache - usually temporal but may be generalised, occipital or parietal; present in 2/3 of people with GCA\n- Jaw or tongue claudication (pain on chewing food)\n- Amaurosis fugax (transient monocular blindness, often described as a dark curtain descending vertically)\n- Diplopia\n- Changes to colour vision\n- Fatigue\n- Anorexia and weight loss\n- Depression\n- Features of polymyalgia rheumatica e.g. pain and stiffness of shoulders and pelvic girdle\n\n**Signs include:**\n\n- Tenderness, thickening or nodularity of the temporal artery\n- Pulsation of the temporal artery may be reduced or absent\n- Scalp tenderness or necrosis\n- Visual field defect\n- Low-grade fever\n- On fundoscopy: pallor and oedema of the optic disc, \"cotton-wool\" patches and retinal haemorrhages\n- Involvement of extracranial vessels may be associated with arterial bruits, difference in blood pressure between arms and decreased arterial pulses\n\n# Differential Diagnosis\n\n- **Other causes of headaches** e.g. tension headaches, migraines - lack associated features e.g. jaw claudication, less likely to be new in an older patient\n- **Acute angle closure glaucoma** leads to visual loss and headaches, eye will be painful and red and feel hard on palpation\n- **Shingles** leads to pain and systemic features may be present, however a rash typically appears over the affected area within a few days\n- **Transient ischaemic attack** can cause amaurosis fugax, other features such as headache are not usually present\n\n\n# Investigations\n\n**Bedside tests:**\n\n- Urgent ophthalmological assessment for patients with visual symptoms \n\n**Blood tests:**\n\n- **ESR** and **CRP** - raised in GCA\n- **Full blood count** often shows an elevated platelet count and a normochromic normocytic anaemia\n- Baseline bloods for liver and renal function (**LFTs** and **U&Es**) and a **bone profile** for calcium should be considered to screen for alternative diagnoses e.g. other vasculitides\n- Bloods to screen for increased risk of complications with steroids (such as diabetes or osteoporosis) include an **HbA1c**, **vitamin D** and **thyroid function tests** \n\n**Imaging tests:**\n\n- **Doppler ultrasonography** of the temporal and axillary arteries can be used as a confirmatory diagnostic test\n- **Halo sign** refers to hypoechoic wall thickening of the artery imaged\n- This disappears with steroid treatment\n- Stenosis of the vessel may also be visualised\n- **MRI brain** with vessel wall imaging is an alternative\n- GCA is supported by findings of mural inflammation in the superficial temporal arteries\n- MRI can also be used to look for complications such as ischaemic stroke as well as involvement of other arteries\n- **FDG-PET scanning** can be useful to rule out differential such as malignancy or infection\n- In GCA there will be uptake in affected arteries\n- It can be particularly useful to demonstrate involvement of other arteries e.g. the aorta\n- A **DEXA** scan for baseline bone density should be done for patients starting long-term steroids (due to the risk of osteoporosis)\n\n**Invasive tests:**\n\n- **Temporal artery biopsy**\n- This is the definitive investigation for GCA\n- Typical histological features include granulomatous inflammation of arteries with inflammatory cells including multinucleated giant cells\n- Inflammation is often segmental with \"skip lesions\" i.e. normal parts of the artery in between areas of inflammation, and so false negative biopsies can occur\n- Biopsies may remain positive for several weeks after starting steroids\n\n# Management\n\n- Patients with visual loss usually require **IV steroid treatment** e.g. pulsed methylprednisolone\n- All other patients should be treated with **high dose oral steroids**, usually 40-60 mg prednisolone once a day\n- **Safety netting** patients to seek urgent medical attention if they develop visual symptoms or a relapse on steroids is key\n- Patients seen in primary care should be **referred urgently to rheumatology** for confirmation of the diagnosis and ongoing management\n- **Steroids are tapered** gradually once symptoms and raised inflammatory markers have resolved\n- **Steroid sparing agents** such as methotrexate or tocilizumab (an anti-IL6 biologic) may be added to help with steroid tapering e.g. in patients with recurrent relapses or at increased risk of side effects with steroids\n- All patients should be assessed for risk of steroid side effects:\n- Consider gastric protection with a proton pump inhibitor\n- Consider bone protection e.g. vitamin D and calcium supplementation, bisphosphonates\n- Monitor for steroid-induced diabetes, hypertension and glaucoma\n- Advise on immunosuppression e.g. avoiding contact with patients with diseases such as chickenpox if not immune\n- Give patients a blue steroid card and advise them not to suddenly stop steroids due to the risk of adrenal crisis\n- Aspirin is currently **not** recommended for adjunctive treatment of GCA \n\n# Complications\n\n- Loss of vision - may occur in up to 30% of people with GCA (either total or partial)\n- Scalp necrosis\n- Ischaemic stroke\n- Aortic aneurysms - in 10-20% of people with GCA, most commonly in the thoracic aorta\n- Aortic dissection and aortic regurgitation are less common than aneurysms\n- Stenosis of large arteries\n- Increased risk of cardiovascular disease including stroke, myocardial infarction and peripheral arterial disease\n- Side-effects from long-term steroids e.g. osteoporosis and fragility fracture, weight gain, diabetes, gastric ulcers\n\n# Prognosis\n\n- Most patients respond rapidly to steroids - failure to respond should prompt investigations for an alternative diagnosis\n- Up to 50% of people will experience relapsing disease however\n- Most patients require at least 1-2 years of steroid treatment, with an increased risk of relapse if steroids are stopped within a year of diagnosis\n\n# NICE Guidelines\n\n[NICE CKS - Giant Cell Arteritis](https://cks.nice.org.uk/topics/giant-cell-arteritis/)\n\n# References\n\n[British Society for Rheumatology guideline on diagnosis and treatment of giant cell arteritis](https://academic.oup.com/rheumatology/article/59/3/e1/5714024)\n\n[Radiopaedia - Giant Cell Arteritis](https://radiopaedia.org/articles/giant-cell-arteritis?lang=gb)\n\n[Patient UK - Giant Cell Arteritis](https://patient.info/doctor/giant-cell-arteritis-pro)",
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"question": "A 50 year old woman presents with an episode of sudden painless visual loss in her right eye this morning. She also complains of a 2 week history of persistent frontal headache and morning stiffness of the shoulders and hips worse in the past year.\n\nPhysical examination is otherwise unremarkable.\n\nComputed tomography (CT) brain showed no acute intracranial abnormalities.\n\nWhich of the following findings is most likely associated with her condition?",
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"explanation": "This may be useful in looking for metastases, but it would not be useful in diagnosing suspected renal or bladder cancer",
"id": "32225",
"label": "c",
"name": "CT abdomen pelvis",
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"explanation": "This is usually indicated in nephrotic syndrome, acute nephritic syndrome or unexplained acute kidney injury, which is not the case here",
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"explanation": "Guidelines state that any adult >45 years with unexplained visible haematuria without a urinary tract infection should have a 2 week referral for suspected renal or bladder cancer. Cystoscopy with biopsy is the gold standard for diagnosing bladder cancer, as it allows direct visualisation of the bladder",
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"label": "a",
"name": "Flexible cystoscopy",
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"explanation": "This is best used for excluding urinary tract obstruction and can be used to visualise cysts, abscesses, hydronephrosis and other complications of pyelonephritis. It would not be the best in investigating suspected malignancy",
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"label": "b",
"name": "Ultrasound of the kidneys, ureters and bladder",
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"explanation": "This would be useful in looking for gastrointestinal cancer, which should be suspected in a patient with unexplained iron deficiency anaemia, change in bowel habit, melaena and other constitutional symptoms",
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"comment": "If anyone was like me and thought bladder cancer could be excluded on a KUB, then they have a low sensitivity for small cancers so should always be excluded by cystoscopy.",
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"explanation": "# Summary \n\nHaematuria, the presence of blood in the urine, can be divided into macroscopic haematuria, visible to the naked eye, and microscopic haematuria, detectable only through urinalysis. Key causes include conditions affecting the kidney, ureters, and urethra, as well as certain medications and dietary items. Clinically significant signs and symptoms vary based on the underlying cause. Key investigations include urinalysis, urine culture, and urine microscopy, as well as blood tests and imaging of the renal tract. Management strategies depend on the identified cause.\n\n# Definitions\n\n- Macroscopic haematuria: Blood in the urine, visible to the naked eye.\n- Microscopic haematuria: Blood in the urine, detectable only on urinalysis.\n\n\n# Epidemiology\n\nThe prevalence of haematuria varies depending on population characteristics such as age and sex, and the criteria used to define haematuria. In general, haematuria is more common in older individuals and in males. In clinical settings, haematuria is a common finding on urinalysis.\n\n# Aetiology\n\n## Kidney-related causes\n\n- Glomerular: IgA nephropathy, Alport's syndrome, Glomerulonephritis.\n- Non-glomerular: Tumours (Renal cell carcinoma, Wilm's tumour), Nephrolithiasis, Infection, Polycystic kidneys, Trauma, Urethral stricture, Vascular conditions (infarction, renal vein thrombosis), Sickle cell disease, Certain drugs.\n\n## Ureter or Bladder-related causes\n\n- Stones\n- Tumours, particularly **Bladder Cancer**\n- Strictures\n- Infection\n\n## Urethral causes\n\n- Benign prostatic hypertrophy\n- Prostate cancer\n- Prostatitis\n- Trauma\n\n## Other causes\n\n- Menstruation\n- Post-coital\n- Certain medications\n- Viral illness\n\nNB: Anticoagulants doesn’t in itself cause haematuria, it makes any bleeding worse. E.g. renal cancer may present with NVH, but if the patient was taking anticoagulation, this would potentiates the bleeding leading to VH. \n\n# Signs and Symptoms\n\nSigns and symptoms of haematuria are largely dependent on the underlying cause and may include flank pain, abdominal pain, dysuria, frequency, urgency, and systemic symptoms such as fever or weight loss. In cases of macroscopic haematuria, patients may report pink, red, or brown urine.\n\n# Differential Diagnosis\n\nThe differential diagnosis of haematuria includes a broad range of conditions, and the main signs and symptoms of each can help to distinguish between them:\n\n- Glomerular diseases (e.g. IgA nephropathy, Alport's syndrome): Proteinuria, hypertension, oedema.\n- Non-glomerular kidney diseases (e.g. tumours like renal cell carcinoma, Wilm's tumour): Flank pain, mass, haematuria, weight loss.\n- Ureteral stones: Flank pain, haematuria, possibly signs of infection (fever, dysuria).\n- Urethral conditions (e.g. benign prostatic hypertrophy, prostate cancer): Lower urinary tract symptoms (e.g. difficulty urinating, frequency), possibly haematuria.\n- Pseudohaematuria: History of specific drug use or dietary intake. If there is any doubt over the legitimacy of haematuria, a lab sample should be sought. Causes of pseudohaematuria include:\n\t- Medications such as Rifampicin, Chlorzoxazone, Phenazopyridine, Phenothiazine, Doxorubicin, Phensuximide, Phenytoin, Daunomycin\n\t- Dietary items such as berries, beets, rhubarb\n\t- Myoglobin\n\t- Menstruation\n- Haemoglobinuria: Occurs due to haemolysis of red blood cells.\n- Myoglobinuria: Occurs due to muscle breakdown.\n\n# Investigations\n\n- Bedside - urinalysis.\n- Urine culture.\n- Urine microscopy - the type of blood cells seen may indicate the cause; dysmorphic red blood cells suggest glomerular origin, if red cell casts visible this suggests renal origin (precipitate with protein made in renal tubules)\n- Blood tests: Full Blood Count (FBC), Urea and Electrolytes (U+E), Prostate-Specific Antigen (PSA) for men, and coagulation studies.\n- Imaging: Renal tract ultrasound, Computed Tomography of kidneys, ureters, bladder (CT KUB).\n- Cystoscopy.\n- Renal biopsy.\n\n## 2 week wait referral criteria\n\n\n| Bladder cancer | Renal cancer | \n| ------------- |-------------| \n| If they are aged 45 years and over and have: 1) Unexplained visible haematuria without urinary tract infection, or 2) Visible haematuria that persists or recurs after successful treatment of urinary tract infection.| If they are aged 45 years and over and have: 1) Unexplained visible haematuria without urinary tract infection, or 2) Visible haematuria that persists or recurs after successful treatment of urinary tract infection.\r\nIf they are aged 60 years and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test. | |\nConsider non-urgent referral for bladder cancer in people aged 60 years and over with recurrent or persistent unexplained urinary tract infection.| | right-aligned |\n\n# Management\n\nManagement strategies are tailored based on the identified cause. They may include medical management for infections, surgical intervention for stones or tumours, lifestyle modification for certain causes of pseudohaematuria, or further specialist management for complex cases.\n\n# References\n\n[BMJ Best Practice: Assessment of visible haematuria](https://bestpractice.bmj.com/topics/en-gb/316)\n\n[British Association of Urological Surgeons: Haematuria](https://www.baus.org.uk/patients/conditions/2/blood_in_the_urine_haematuria)\n\n[Oxford Medical Education: Haematuria](https://www.oxfordmedicaleducation.com/wp-content/uploads/2015/04/Haematuria.protected.pdf)",
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"question": "A 65 year old gentleman presents to Accident & Emergency with a 5 day history of persistent haematuria. He has a background of atrial fibrillation and is on warfarin.\n\n\nBlood tests are as follows:\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|115 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|9.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\n|Neutrophils|5.5 x10<sup>9</sup>/L|2.0 - 7.5|\n|Sodium|137 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Chloride|102 mmol/L|95 - 106|\n|Urea|8 mmol/L|2.5 - 7.8|\n|Creatinine|95 µmol/L|60 - 120|\n|eGFR|85 mL/min/1.73m<sup>2</sup>|> 60|\n|International Normalised Ratio (INR)|2.1|1.0|\n\n\nUrinalysis showed red blood cells with no evidence of leucocytes or nitrites. Computed tomography (CT) of kidneys, ureters and bladder showed no stones.\n\n\nWhich is the next most appropriate investigation?",
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"explanation": "This would be most appropriate in patients with suspected prostate cancer after taking into account relevant risk factors including age, prostate specific antigen level, DRE findings and comorbidities. However, this method is invasive and may risk missing the cancer depending on the area biopsied",
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"explanation": "If there is a very high clinical suspicion of localised prostate cancer, clinicians should proceed directly to multiparametric MRI as a first-line investigation. This would reduce the risk of unnecessary prostate biopsies",
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"explanation": "This would be useful in investigating causes of obstructive uropathy. However, as prostate cancer is the most likely cause in this scenario given the DRE findings, it is better to proceed with an MRI prostate first",
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"explanation": "This would be useful in watchful waiting for asymptomatic patients in whom hormonal therapy is being deferred or as a staging scan for bone metastases. However, it is not the most useful in making a diagnosis of prostate cancer",
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"explanation": "This may be useful in investigating voiding dysfunction in patients with lower urinary tract symptoms that point towards chronic bladder outflow obstruction. However, it would not be useful in a patient which has a high clinical likelihood of prostate cancer",
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"explanation": "# Summary\n\nProstate cancer is a common malignancy affecting males, particularly in Western societies. It is characterised by abnormal growth of cells in the prostate gland and can be asymptomatic in early stages. Advanced disease may manifest as urinary issues, pelvic discomfort, bone pain, and erectile dysfunction. The primary investigations are digital rectal examination and a urine dip, with PSA (Prostate Specific Antigen) testing, which carries issues of sensitivity and specificity. MRI is a key tool for assessment, alongside a Gleason score for grading biopsy samples. Management ranges from active surveillance for low-grade disease to hormonal therapy and surgery for more advanced cases.\n\n# Definition\n\nProstate cancer is a malignant tumour that arises from the cells of the prostate, a small walnut-sized gland that produces seminal fluid in men. This condition varies greatly in its presentation, with some cases growing slowly and requiring minimal treatment, while others are aggressive and can spread quickly.\n\nThe majority of prostate cancers are adenocarcinomas, and they usually primarily affect the peripheral prostate. They spread lymphatically first via the obturator nodes.\n\n\n# Epidemiology\n\nProstate cancer is responsible for approximately 48,000 new diagnoses each year in the UK, accounting for 13% of all cancer cases. It is the second most prevalent cancer among men globally, preceded only by lung cancer.\n\n\n# Aetiology\n\n### Non-modifiable risk factors\n\n- African ethnicity\n- BRCA gene mutations\n- Family history of prostate cancer\n- Age (risk increases with advancing age)\n\n### Modifiable risk factors\n\nResearch into modifiable risk factors is ongoing. Some potential factors are:\n\n- Obesity\n- Smoking\n- Diet rich in animal fats and dairy products\n\n# Signs and Symptoms\n\nIn its early stages, prostate cancer often produces no symptoms as it affects the peripheral prostate. However, as the disease progresses with local advancement (which can cause compression of the urethra), symptoms may include:\n\n- Urinary symptoms, including difficulty initiating or stopping urination\n- Poor urine stream\n- Haematospermia (blood in semen)\n- Pelvic discomfort\n- Bone pain, potentially indicating metastatic disease\n- Erectile dysfunction\n\n# Differential Diagnosis\n\nSeveral conditions can mimic the symptoms of prostate cancer and should be considered during evaluation:\n\n- Benign Prostatic Hyperplasia (BPH): Characterised by difficulty in urination, increased frequency of urination, nocturia, and potentially, haematuria.\n- Prostatitis: Acute or chronic inflammation of the prostate that can cause pelvic pain, urinary symptoms, and potentially, systemic symptoms such as fever and malaise.\n- Urinary Tract Infection (UTI): Can cause dysuria, urinary frequency, urgency, and potentially, systemic signs of infection.\n- Bladder cancer: May present with haematuria, dysuria, and urinary frequency.\n\n# Investigations\n\n* Initial examination should include a digital rectal examination and a urine dip.\n\t* An asymmetrical hard/craggy/nodular prostate with loss median sulcus is suspicious for malignancy.\n* A PSA blood test may be considered, despite its lack of sensitivity and specificity. This necessitates patient counselling about the potential for over-investigation and over-treatment. Causes of a falsely raised PSA include:\n\t* An active urinary infection or within previous 6 weeks.\n\t* Ejaculation in previous 48 hours.\n\t* Vigorous exercise, for example cycling, in the previous 48 hours.\n\t* Urological intervention such as prostate biopsy in previous 6 weeks.\n\nInterpretation of PSA results:\n\n| Age (years) | Prostate-specific antigen threshold (micrograms/L) |\n|-------------|--------------------------------------------------|\n| Below 40 | Use clinical judgement |\n| 40–49 | More than 2.5 |\n| 50–59 | More than 3.5 |\n| 60–69 | More than 4.5 |\n| 70–79 | More than 6.5 |\n| Above 79 | Use clinical judgement |\n\n\n* **Multi-parametric MRI** is the gold standard radiological investigation, and can show specific areas which can be targetted for biopsy. If metastatic disease is suspected, additional imaging such as CT scans (can show e.g. sclerotic bony lesions) and bone isotope scans may be required.\n* The Gleason grading system is used to assess prostate cancer severity on initial biopsy. It involves analysing the morphological features of prostatic tissue and assigning a score from 1 (normal tissue) to 5 (very poorly differentiated cells). The sum of the two most common scores represents the Gleason score, which has prognostic value.\n\n### 2 week wait referral criteria\n\n- Refer if their prostate feels malignant on DRE.\n- Consider referring a person with possible symptoms of prostate cancer using a suspected cancer pathway referral (for an appointment within 2 weeks) if their PSA level is above the threshold for their age (see above)\n\n# Classification\n\nThe TNM staging system for prostate cancer provides a standardised way to describe the extent of the disease based on three key parameters: tumour size and extent (T), involvement of regional lymph nodes (N), and the presence of distant metastasis (M).\n\n- **T (Tumour):**\n - **T1:** The tumour is not palpable or visible by imaging.\n - T1a: Tumour found incidentally in less than 5% of tissue removed.\n - T1b: Tumour found incidentally in more than 5% of tissue removed.\n - T1c: Identified by needle biopsy due to elevated PSA (prostate-specific antigen) levels.\n - **T2:** The tumour is confined to the prostate.\n - T2a: Tumour involves half or less of one side of the prostate.\n - T2b: Tumour involves more than half of one side but not both sides.\n - T2c: Tumour involves both sides.\n - **T3:** The tumour extends beyond the prostate.\n - T3a: Tumour extends through the prostate capsule.\n - T3b: Tumor invades seminal vesicle(s).\n - **T4:** The tumour invades adjacent structures other than seminal vesicles (e.g., bladder, rectum).\n\n- **N (Lymph Nodes):**\n - **N0:** No regional lymph node involvement.\n - **N1:** Regional lymph node involvement.\n\n- **M (Metastasis):**\n - **M0:** No distant metastasis.\n - **M1:** Distant metastasis present.\n - M1a: Non-regional lymph nodes.\n - M1b: Bones.\n - M1c: Other sites or multiple sites.\n\n\n# Management\n\nHere is a summary table demonstrating management approaches according to TNM staging:\n\n| TNM Stage | Management Options |\n|--------------------------|--------------------------------------------------------|\n| T1 (T1a, T1b, T1c) | Active surveillance (for low-risk cases) |\n| | Watchful waiting |\n| | Radical prostatectomy (for selected cases) |\n| T2 (T2a, T2b, T2c) | Radical prostatectomy (standard treatment) |\n| | External beam radiation therapy |\n| | Brachytherapy (seed implantation) |\n| | Active surveillance (for low-risk cases) |\n| T3 (T3a, T3b) | Hormonal therapy (to delay progression) |\n| | Radical prostatectomy (selected cases) |\n| | External beam radiation therapy |\n| T4 | Hormonal therapy (palliative, delays progression) |\n| | Radiation therapy (palliative) |\n| | Symptomatic management |\n| Not Fit for Radical Prostatectomy | Hormonal therapy (palliative) |\n| Metastatic (M1) | Hormonal therapy (androgen deprivation) |\n| | Chemotherapy (docetaxel, cabazitaxel) |\n| | Targeted therapy (abiraterone, enzalutamide) |\n| | Immunotherapy (sipuleucel-T) |\n\n\n## Active Surveillance\n\nThis approach is suitable for patients with low-grade prostate cancer and involves repeating investigations periodically to monitor disease progression.\n\n## Radiotherapy\n\nRadiotherapy can be used either as a curative measure or for palliation to reduce tumour bulk and associated pain.\n\n## Surgical Management\n\nSurgical removal of the prostate and any affected organs is an option for patients without metastatic disease. Minimally invasive techniques such as robotically assisted laparoscopic prostatectomy (RALP) are becoming more common.\n\n## Hormonal Management\n\nHormonal therapies aim to reduce testosterone levels, slowing the progression of metastatic prostate cancer. This can be achieved with GnRH analogues, androgen antagonists, or GnRH antagonists. \n\nHormonal therapies may cause sexual side effects, including decreased libido, impotence, infertility, and gynecomastia. Metabolic side effects include weight gain, osteoporosis, diabetes, and ischemic heart disease. Haematological side effects include anaemia.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng131)",
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"question": "A 85 year old male is admitted with acute urinary retention. Over the past year, he has been having urinary hesitancy and poor stream with nocturia up to 5-6 times a night. He had an objective 3kg loss of weight in the last year.\n\nDigital rectal examination (DRE) reveals a hard, asymmetrically enlarged prostate. Prostate specific antigen is elevated at 15ng/mL.\n\nWhich of the following is the next most appropriate investigation?",
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"explanation": "This may be considered as a second line to bisphosphonates. It works by increasing renal calcium excretion and reducing bone resorption by osteoclasts. It is useful in rapidly lowering calcium levels, but bisphosphonates would provide a more sustained effect",
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"explanation": "This is a parathyroid hormone analogue used as a second-line treatment for osteoporosis. It should not be used in this scenario as it will exacerbate hypercalcaemia",
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"name": "Furosemide",
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"explanation": "This is a parathyroid hormone analogue used as a second-line treatment for osteoporosis. It should not be used in this scenario as it will exacerbate hypercalcaemia",
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"explanation": "This patient has a likely new diagnosis of multiple myeloma, as evidenced by the anaemia, renal impairment, pathologic fractures and hypercalcaemia. Bisphosphonates are used in hypercalcaemia of malignancy and renal impairment should be considered when choosing a particular agent for initiation",
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"explanation": "This is a calcimimetic that works by increasing the sensitivity of the calcium-sensing receptor on the parathyroid gland, thereby lowering parathyroid hormone and calcium levels. It is typically used in medical therapy of primary hyperparathyroidism where surgery is not suitable. It would be a second-line agent in this scenario",
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"comment": "previous question said myeloma didnt raise ALP as it doesnt increase osteoblast activity. is the raised ALP here from the fractures?",
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"explanation": "# Summary\n\nHypercalcaemia refers to an abnormally high serum calcium, adjusted for serum albumin concentration. A calcium of over 2.6 mmol/L is generally considered high although laboratory reference ranges may vary slightly. The majority of cases are either due to primary hyperparathyroidism or malignancy, with other causes including medications, endocrine diseases such as hyperthyroidism and granulomatous diseases such as sarcoidosis. Mild cases are usually asymptomatic; symptoms can be remembered using the \"stones, bones, groans and moans\" mnemonic (referring to renal stones, bony pain, abdominal pain and psychiatric manifestations such as depression, anxiety and psychosis). Investigations include an ECG, bloods including a parathyroid hormone (PTH) level and a chest X-ray to look for evidence of malignancy or granulomatous disease. Conservative management may be appropriate for mild cases, with treatment of the underlying cause. Patients with moderate, severe or symptomatic hypercalcaemia are usually treated with intravenous fluids initially, followed by an intravenous bisphosphonate if required.\n\n# Definition\n\nThe normal range for serum calcium is approximately 2.2-2.6 mmol/L. This is adjusted for serum albumin levels, which is important as approximately 40% of serum calcium is bound to albumin and so when albumin levels are low, serum calcium will be underestimated. \n\n99% of the body's calcium is stored in the skeleton and is crucial for the mineralisation of bone. It has many other roles in important functions such as muscle contraction, cardiac pacemaker activity, clotting, cell membrane stability and permeability.\n\nHypercalcaemia refers to an adjusted serum calcium of 2.6 mmol/L or higher - this should be repeated for confirmation. \n\n# Aetiology\n\n- Primary hyperparathyroidism (most common cause)\n - Usually due to a solitary parathyroid adenoma \n - Other causes include multiglandular parathyroid hyperplasia, an ectopic adenoma or a parathyroid cancer\n - 10% of cases are genetic (e.g. multiple endocrine neoplasia)\n- Malignancy (second most common cause overall; commonest cause in hospitalised patients)\n - Commonest in breast and lung cancers, myeloma and leukaemia\n - May be paraneoplastic, for example due to tumour secretion of parathyroid hormone-related protein\n - May be due to osteolytic bone metastases causing release of skeletal calcium\n- Granulomatous disease\n - Activated macrophages cause ectopic production of active vitamin D which increases calcium levels\n - Examples include sarcoidosis, tuberculosis, histoplasmosis and inflammatory bowel disease\n- Tertiary hyperparathyroidism\n - Occurs in patients with longstanding secondary hyperparathyroidism due to chronic renal failure \n - Parathyroid hypertrophy leads to excessive PTH secretion outside of normal homeostatic control, causing calcium levels to rise\n - Hypercalcaemia may be exacerbated if patients are also being treated with calcium or vitamin D supplement\n- Medications \n - Excessive calcium supplements\n - Milk-alkali syndrome (hypercalcaemia, metabolic alkalosis and acute kidney injury due to ingesting excessive antacids e.g. calcium carbonate)\n - Excessive vitamin D (including topical vitamin D analogues)\n - Lithium (via stimulation of PTH secretion and renal calcium reabsorption)\n - Thiazides (due to increased calcium reabsorption)\n - Vitamin A (due to bone resorption)\n- Immobility \n - Due to an imbalance in osteoclast and osteoblast activity\n - Usually only occurs if there is increased bone turnover e.g. Paget's disease\n- Hyperthyroidism\n - Approximately 20% of patients have mild or moderate hypercalcaemia\n - Thought to be due to increased bone turnover\n- Adrenal insufficiency\n - More rarely causes hypercalcaemia (approximately 8% of patients with Addison's disease)\n - Thought to be due to reduced renal excretion of calcium as well as dehydration\n- Phaeochromocytoma\n - Tumours may produce ectopic PTH or PTH-related protein\n- Familial hypocalciuric hypercalcaemia\n- Benign autosomal dominant disorder\n- The calcium-sensing receptor is mutated causing an insensitivity to calcium levels\n- This leads to excessive PTH release, with resulting lifelong mild hypercalcaemia and hypophosphataemia\n- Can be differentiated from primary hyperparathyroidism as urinary calcium is low rather than high\n\n# Classification\n\n- **Mild** hypercalcaemia - adjusted serum calcium **2.6-3.0** mmol/L\n- **Moderate** hypercalcaemia - adjusted serum calcium **3.0-3.5** mmol/L\n- **Severe** hypercalcaemia - adjusted serum calcium **> 3.5** mmol/L\n\n# Signs and Symptoms\n\nMild hypercalcaemia is usually asymptomatic and is diagnosed as an incidental finding\n\nA common mnemonic to remember symptoms of hypercalcaemia is \"stones, bones, groans and moans\":\n\n- **Stones** - kidney stones causing renal colic\n- **Bones** - bony pain and skeletal deformities; the underlying disease process (e.g. bone metastases or hyperparathyroidism) may lead to osteoporosis and increased fracture risk\n- **Groans** - gastrointestinal symptoms of nausea, vomiting, constipation, abdominal pain, anorexia and weight loss\n- **Moans** - neuropsychiatric symptoms of drowsiness, confusion, poor concentration and memory, depression, insomnia, anxiety, irritability and psychosis\n\nOther symptoms include:\n\n- Fatigue\n- Lethargy\n- Muscle weakness\n- Thirst and polydipsia\n- Polyuria and nocturia\n- Flushing\n- Pruritus\n\nSigns include:\n\n- Dehydration\n- Hypertension\n- Reduced consciousness\n- Neuromuscular abnormalities - e.g. hypotonia, hyporeflexia, ataxia, decreased power\n- Band keratopathy due to corneal calcium deposits (rare)\n\n# Investigations\n\n**Bedside:**\n\n- **ECG** may show a shortened QTc (the most common abnormality); Osborn (or J) waves may be seen in severe hypercalcaemia and appear as a deflection at the end of the QRS complex\n- **24 hour urinary calcium** will be high or normal in most cases of hypercalcaemia - if this is low familial hypocalciuric hypercalcaemia should be suspected\n- **Urinary albumin:creatinine ratio** in patients with chronic renal impairment \n- **Sputum microscopy and culture for acid-fast bacilli** if tuberculosis is suspected\n\n**Blood tests:**\n\n- **Bone profile** to confirm hypercalcaemia - a single high reading should be repeated\n- **PTH** should be suppressed; if it is normal or high hyperparathyroidism is the most likely cause (with familial hypocalciuric hypercalcaemia a differential)\n- **Full blood count** may show anaemia related to malignancy or chronic disease (e.g. chronic kidney disease)\n- **U&Es** may show renal impairment\n- **ESR** and/or **CRP** to screen for inflammation, for example secondary to malignancy or tuberculosis\n- **LFTs** for albumin; may be deranged if there are liver metastases from cancer; ALP may be raised due to increased bone turnover e.g. in hyperparathyroidism or bone metastases\n- **Thyroid function tests** to rule out hyperthyroidism as\n- **Vitamin D level** to rule out vitamin D toxicity; often low in primary hyperparathyroidism and should be replaced prior to parathyroidectomy to reduce the risk of hungry bones syndrome\n- **Early morning cortisol** to rule out hypoadrenalism\n- **Serum protein electrophoresis**, **serum free light chains** and a **blood film** to screen for myeloma\n- Tumour markers e.g. **prostate-specific antigen (PSA)** in patients with suspected malignancy\n- **Serum ACE** if sarcoidosis is suspected\n\n**Imaging:**\n\n- **Chest X-ray** as an initial screen for malignancy (either a lung primary or metastases) and to look for evidence of sarcoidosis or tuberculosis\n- Further imaging may be indicated if malignancy is suspected, e.g. a **CT chest, abdomen and pelvis**\n- **Dual-energy X-ray absorptiometry (DEXA)** assessment of bone mineral density to look for associated osteoporosis\n- Renal imaging such as an **abdominal X-ray** or **ultrasound** to look for for renal stones or nephrocalcinosis\n\n**Special tests:**\n\n- **Genetic testing** may be offered to patients with suspected familial hypocalciuric hypercalcaemia and those with suspected inherited endocrinopathies (such as multiple endocrine neoplasia syndrome)\n\n# Management \n\n**Conservative:**\n\n- In some cases (e.g. familial hypocalciuric hypercalcaemia) no specific treatment is required\n- Review medications and consider stopping these where possible (e.g. thiazide diuretics, calcium supplements)\n- Advise patients to maintain an adequate fluid intake\n- Patients should be referred to an appropriate specialist in most cases (e.g. endocrinology for suspected primary hyperparathyroidism, or via a two week wait pathway for suspected malignancy)\n- Patients with severe hypercalcaemia require urgent medical treatment and so should be referred to hospital if seen in primary care\n\n**Medical:**\n\n- First line management is with IV fluids - this corrects dehydration, increases calcium excretion and is renoprotective\n- An example regimen would be 4-6 litres of IV normal saline over the first 24 hours with regular fluid balance reviews to adjust as needed\n- Following fluid resuscitation, intravenous bisphosphonates may be given to reduce osteoclast activity (e.g. zoledronate or pamidronate) - this takes 2-4 days to take full effect\n- Patients may be continued on an oral bisphosphonate to help prevent recurrence\n- Denosumab is an alternative for patients who cannot have a bisphosphonate (e.g. due to chronic kidney disease)\n- Calcitonin is a second line option in hypercalcaemia of malignancy (although efficacy is limited)\n- Steroids may be used and are most effective in hypercalcaemia secondary to sarcoidosis or vitamin D toxicity\n- Vitamin D supplementation should be given where required with caution, in order to maintain levels in the normal range\n- Cinacalcet is a second line option for patients with hyperparathyroidism (e.g. if unsuitable for surgery)\n\n**Surgical:**\n\n- Parathyroidectomy is the definitive management for primary hyperparathyroidism\n- Indications to consider surgery include symptomatic hypercalcaemia, end-organ disease (e.g. osteoporosis, renal stones) or a calcium of 2.85 mmol/L or higher\n\n# Complications\n\n- Delirium\n- Coma\n- Arrhythmias e.g. ventricular fibrillation\n- AVP-R (Nephrogenic diabetes insipidus) - due to degradation of aquaporin 2 channels, leading to polydipsia and polyuria\n- Renal impairment (which may be prerenal due to dehydration as well as due to afferent arteriolar vasoconstriction) \n- Renal stones and nephrocalcinosis (calcium salt deposition in the renal parenchyma)\n- Peptic ulcers (as hypercalcaemia triggers increased gastric acid production)\n- Pancreatitis (rarely)\n\n# NICE Guidelines\n\n[NICE CKS - Hypercalcaemia](https://cks.nice.org.uk/topics/hypercalcaemia/)\n\n# References\n\n[BNF - Calcium imbalance](https://bnf.nice.org.uk/treatment-summaries/calcium-imbalance/)\n\n[Patient UK - Hypercalcaemia](https://patient.info/doctor/hypercalcaemia)\n\n[Life in the Fast Lane - Hypercalcaemia ECG Library](https://litfl.com/hypercalcaemia-ecg-library/)\n\n[Royal United Hospitals Bath - Hypercalcaemia guideline](https://www.ruh.nhs.uk/pathology/documents/clinical_guidelines/PATH-016_Investigation_and_Management_of_HYPERCALCAEMIA.PDF)",
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"question": "A 70 year old lady is admitted with a 1 month history of worsening lower back pain. She also reports feeling more fatigued and constipated recently.\n\n\n\nInitial blood tests are as follows:\n\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|102 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|9.1x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|210x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|85 fL|80 - 96|\n|Sodium|137 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Chloride|102 mmol/L|95 - 106|\n|Urea|8 mmol/L|2.5 - 7.8|\n|Creatinine|181 µmol/L|60 - 120|\n|Calcium|3.1 mmol/L|2.2 - 2.6|\n|eGFR|43 mL/min/1.73m<sup>2</sup>|> 60|\n|Albumin|40 g/L|35 - 50|\n|Alanine Aminotransferase (ALT)|21 IU/L|10 - 50|\n|Aspartate Aminotransferase (AST)|32 IU/L|10 - 40|\n|Alkaline Phosphatase (ALP)|266 IU/L|25 - 115|\n|Bilirubin|7 µmol/L|< 17|\n|Gamma Glutamyl Transferase (GGT)|20 U/L|9 - 40|\n\n\n\n\n\nThoracolumbar spine X-rays reveal multilevel compression fractures.\n\n\n\nShe is started on intravenous hydration.\n\n\n\nWhich of the following is the most appropriate treatment to initiate for her hypercalcaemia?",
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"explanation": "This has the highest association with smoking amongst the lung cancers. It typically presents with centrally located lung masses and tends to be associated with Cushing's syndrome due to ectopic production of adrenocorticotropic hormone. It is not likely here as it is very rare in patients who have never smoked",
"id": "32239",
"label": "b",
"name": "Small cell lung carcinoma",
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"explanation": "This is most commonly associated with asbestos exposure and would typically present with bilateral pleural thickening and plaques. This is not likely given her lack of occupational exposure",
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"explanation": "This has the highest association with smoking amongst the lung cancers. It typically presents with centrally located lung masses and tends to be associated with Cushing's syndrome due to ectopic production of adrenocorticotropic hormone. It is not likely here as it is very rare in patients who have never smoked",
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"name": "Large cell carcinoma",
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"explanation": "This is the second most common type of lung cancer and has a strong association with smoking compared to other non-small cell lung carcinomas. It is usually centrally located and originates in the bronchi. Associated paraneoplastic phenomena usually includes hypercalcaemia secondary to secretion of parathyroid hormone related peptide",
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"explanation": "This is the most common type of lung cancer, especially in females and non-smokers. This patient has presented with hypertrophic osteoarthropathy, with clubbing and a painful arthropathy that can be quite similar to inflammatory arthritis. It is most frequently associated with adenocarcinoma",
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"comment": "I thought both adenocarcinoma and squamous cause hypertrophic pulmonary osteoarthropathy. Also hes a lifelong smoker so doesnt it make squamous more likely?",
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"comment": "she's a lifelong non-smoker - got confused by this as well and put squamous too. ",
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"comment": "Isn't HPOA most strongly associated with squamous cell lung cancer",
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"comment": "Radiopaedia says it's associated with non-small cell cancer generally, but \"particularly squamous cell carcinoma\". So I guess this question is trying to point out that as a non-smoker, adeno is more likely? Looked this up after I got it wrong!",
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"comment": "I literally read that as smoker lol, I am so tried ",
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"comment": "who says lifelong non-smoker? either she's a lifelong smoker or she's never smoked :(",
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"explanation": "# Summary\n\nLung cancers are divided into two main subtypes: small cell and non-small cell, with small cell lung cancers being more aggressive and incurable. Types of non-small cell lung cancer include squamous cell and adenocarcinomas, with several rarer subtypes. Most cases of lung cancer are linked to smoking. Lung cancers may present with chest symptoms such as cough, breathlessness or haemoptysis, systemic symptoms of weight loss and anorexia or symptoms of metastatic disease such as bone pain or seizures. Chest X-ray is the initial investigation of choice, followed by CT chest and a biopsy. Staging scans are done after diagnosis to help plan treatment. Management can be curative or palliative depending on the stage of the cancer, the subtype and the patient’s overall health. It may include chemotherapy, radiotherapy, immunotherapy, targeted therapies to specific mutations and surgery. \n\n\n# Definition\n\nLung cancer refers to a primary malignancy arising from the lung parenchyma or the bronchi. Cancers are classified as small cell (SCLC) or non-small cell (NSCLC), with 80% being non-small cell. The main histological subtypes of NSCLC are squamous cell cancers and adenocarcinomas.\n\n# Epidemiology\n\nLung cancer makes up the largest proportion of cancer deaths of any tumour type, with nearly 35,000 deaths per year in the UK (21% of all cancer deaths). It is the second most common cancer in both males and females (after prostate and breast respectively). \n\nIncidence is strongly related to age, with the highest rates in people aged over 75 years old. Although non-smokers can also get lung cancer, 86% of cases are linked to smoking and so the majority of cases are felt to be preventable.\n\n# Aetiology\n\nRisk factors for lung cancer include:\n\n- Tobacco smoking (e.g. cigarettes, pipes, cigars)\n- Passive smoke exposure\n- Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica)\n- Radon exposure\n- Family history of lung cancer\n- Radiation to the chest (e.g. in lymphoma treatment)\n- Air pollution\n- Immunosuppression (e.g. HIV, medications)\n- Increasing age\n\n# Classification\n\nLung cancers are classified by the cell of origin of the malignancy. Small cell cancers come from neuroendocrine cells of the lung. Non-small cell cancers are split into adenocarcinomas (coming from alveolar type 2 epithelial cells), squamous cell carcinomas (coming from basal epithelial cells) and large cell carcinomas (which come from a variety of epithelial cells). There are also rarer subtypes of lung cancer such as sarcomatoid or salivary gland-type lung cancers which come under the NSCLC umbrella.\n\nStaging is also an important way to classify lung cancers depending on how advanced they are. TNM (tumour, node, metastasis) staging is used to describe how large the tumour is and where it has spread to. This can then be used to classify lung cancers into stage 1 to 4, where stage 1 is localised and small (under 4cm), stages 2 and 3 are locally advanced and stage 4 is metastatic. \n\n# Signs and symptoms\n\n**Symptoms include:**\n\n- Persistent cough\n- Haemoptysis\n- Dyspnoea especially on exertion\n- Chest pain\n- Weight loss\n- Recurrent chest infections, or infections resistant to treatment\n- Anorexia\n\n**Signs include:**\n\n- Cachexia\n- Finger clubbing\n- Lymphadenopathy (supraclavicular or persistent cervical)\n- If there is lung collapse due to an obstructing tumour - absent breath sounds, trachea deviated towards side of collapse\n- If there is a malignant pleural effusion - stony dull on percussion, decreased breath sounds over affected area\n\n**Other signs and symptoms related to paraneoplastic presentations of lung cancer:**\n\n- **Cushing syndrome** - usually SCLC producing ectopic ACTH, presents with dorsal cervical fat pads, truncal obesity, hypertension, striae and proximal muscle weakness\n- **Syndrome of inappropriate ADH secretion (SIADH)** - usually SCLC, present with symptoms of hyponatraemia e.g. fatigue, nausea, weakness, confusion or seizures\n- **Lambert-Eaton myasthenic syndrome (LEMS)** - usually SCLC, due to autoantibodies to presynaptic calcium channels at the neuromuscular junction develop proximal muscle weakness that improves with repeated movement, as well as autonomic effects such as dry mouth, lightheadedness, constipation, urinary symptoms and erectile dysfunction\n- **Humoral hypercalcaemia of malignancy** - usually squamous cell carcinomas (SCC) that release parathyroid hormone-related protein (PTHrP) that mimics PTH and causes hypercalcaemia, leading to symptoms of bone pain, constipation, anorexia, abdominal pain, excessive thirst and confusion\n- **Hypertrophic pulmonary osteoarthropathy** - usually adenocarcinomas which cause a periosteal reaction of bones, resulting in clubbing and arthritis especially affecting wrists and ankles\n\n# Differential diagnosis\n\n- Lung metastases from another primary cancer (e.g. breast or colorectal cancer)\n- Mesothelioma (cancer of the pleura, strongly related to asbestos exposure)\n- Tuberculosis \n- Bronchiectasis\n\n# Investigations\n\nIn primary care, patients should be referred on a 2 week wait pathway in the following situations:\n\n- Aged 40+ with unexplained haemoptysis\n- Chest X-ray findings suspicious for lung cancer\n\nUrgent chest X-rays (to be done within 2 weeks) should be done for patients aged 40+ who have one of these symptoms and have ever smoked (or two symptoms if they are never smokers):\n\n- Cough\n- Fatigue\n- Shortness of breath\n- Chest pain\n- Weight loss\n- Anorexia\n\nAn urgent chest X-ray should be considered in patients aged 40+ with any of:\n\n- Persistent/recurrent chest infection\n- Finger clubbing\n- Supraclavicular or persistent cervical lymphadenopathy\n- Thrombocytosis\n- Chest signs consistent with lung cancer (e.g. reduced breath sounds, dullness to percussion)\n\nChest X-ray findings include:\n\n- Lung mass (may be rounded or spiculated, squamous cell carcinomas may cavitate)\n- Consolidation (where there is infection downstream of the tumour obstructing an airway)\n- Bulky hilum (especially squamous cell carcinomas which often arise centrally)\n- Lobar collapse (due to bronchial obstruction, especially squamous cell carcinomas)\n- Pleural effusion\n\n[lightgallery]\n\nOther initial investigations include:\n\n- **Sputum cytology** - low sensitivity but may be of use in patients who decline or cannot have a biopsy\n- **Diagnostic thoracocentesis** - i.e. a pleural tap; if a pleural effusion is present this should be done and the fluid sent for cytology as well as cell count, microscopy, culture, glucose, LDG and protein (to determine whether it is a transudate or exudate)\n- **Blood tests** - including FBC for anaemia and thrombocytosis, U&Es for hyponatraemia and baseline renal function, LFTs for baseline liver function (may be deranged in liver metastases), bone profile for hypercalcaemia, CRP for superadded infection, clotting if interventions planned\n- **CT chest with contrast** - should be done after chest X-ray to better characterise any lesion seen and investigate for local spread\n- **Biopsy** - to confirm the diagnosis and subtype of cancer, may be done percutaneously for peripheral tumours or via bronchoscopy for central masses\n\nOnce a lung cancer is diagnosed, further investigations may include:\n\n- **Spirometry** - to assess lung function to determine if a patient is suitable for surgical intervention\n- **CT chest abdomen and pelvis** - to stage the cancer (determine if there are any metastases)\n- **PET-CT scan** - a more sensitive way to stage the cancer and look for local or distant spread\n- **CT or MRI head** - may be done as part of staging investigations if curative treatment is planned, or if there are symptoms suspicious of intracranial metastases \n\n# Management \n\n**Conservative:**\n\n- **Holistic support** and an **MDT approach** (e.g. clinical nurse specialist involvement, palliative care input for troubling symptoms or end of life care, signpost to support e.g. Macmillan groups)\n- **Smoking cessation**\n- Discussions around **advance care planning** where appropriate\n\n**Medical**\n\n- **Chemotherapy** is first line in most cases of small cell lung cancer and stage 3 or 4 non-small cell lung cancer - this is with palliative intent (i.e. not aiming to cure the disease but to prolong life and improve symptoms). It is also offered to some patients prior to (neoadjuvant) or after (adjuvant) curative surgery.\n- **Immunotherapy** is also used especially in advanced non-small cell lung cancer; this includes medications such as pembrolizumab or atezolizumab (again with palliative intent).\n- Other **targeted therapies** exist for patients with specific mutations, e.g. erlotinib for patients with advanced non-small cell lung cancers with EGFR-TK mutations.\n- **Radiotherapy** may be curative (for example in early non-small cell lung cancer) or palliative - it is often combined with chemotherapy or other treatment modalities.\n- **Supportive therapies** include analgesia, oxygen if hypoxic and opioid treatment for breathlessness.\n\n**Surgical**\n\n- **Lobectomy** is the standard curative therapy for early stage lung cancers (which can be open or thoracoscopic in approach).\n- Some small tumours can be removed with a **wedge resection.**\n- More extensive surgery such as a **pneumonectomy** (removal of a lung) may be required depending on the size and location of the tumour, however patients need to have adequate FEV1 on pre-operative spirometry to be appropriate for surgery (over 2L for a pneumonectomy).\n- All patients undergoing surgery should also have **mediastinal and hilar lymph nodes sampled** (to look for metastases) or **resected** (removed) to reduce the chances of recurrence.\n\n# Complications\n\n**Common sites of metastatic spread include:**\n\n- Lymph nodes\n- Liver - this can cause significant pain due to stretching of the liver capsule\n- Brain - may cause nausea and vomiting, headaches, seizures, personality changes, sensory or motor symptoms, dysphasia or cerebellar symptoms, depending on where in the brain is affected\n- Bones - mostly osteolytic metastases, can cause bony pain and pathological fractures; there is a risk of metastatic spinal cord compression with vertebral metastases\n- Adrenal glands - may cause flank pain and adrenal insufficiency\n- The contralateral lung or elsewhere in the ipsilateral lung\n\n**Local complications include:**\n\n- Horner’s syndrome - due to an apical (Pancoast) tumour, causes ipsilateral anhidrosis, miosis and partial ptosis\n- Superior vena cava obstruction (SCVO) - lung cancer is the commonest cause of SCVO, causing symptoms of breathlessness, dizziness, headache and swelling of the face, neck and arms. This is a medical emergency due to the risk of airway obstruction.\n- Malignant pleural effusion\n- Hoarse voice - secondary to invasion of left recurrent laryngeal nerve\n- Persistent lower respiratory tract infection due to obstructing tumour\n- Raised hemidiaphragm secondary to invasion of phrenic nerve\n- Brachial plexus injury secondary to tumour invasion from a Pancoast tumour\n\n# Prognosis\n\nOverall prognosis is poor, with an average 5 year survival rate of 17%. This is lower for small cell lung cancer and for metastatic cancers, both of which have around a 5% 5 year survival. Small cell lung cancers are aggressive and are usually metastatic at the time of presentation, hence curative treatment is not possible\n\nIn early stage cancers survival is better, with 70% of patients with stage 1 NSCLC undergoing curative surgery surviving 5 years from diagnosis.\n\n# NICE Guidelines\n\n[Lung cancer: diagnosis and management](https://www.nice.org.uk/guidance/ng122)\n\n[NICE CKS - recognition and referral of lung and pleural cancers](https://cks.nice.org.uk/topics/lung-pleural-cancers-recognition-referral/)\n\n# References\n\n[Radiopaedia - lung cancer](https://radiopaedia.org/articles/lung-cancer-3?lang=gb)\n\n[Patient UK - lung cancer](https://patient.info/doctor/lung-cancer-pro)\n\n[Cancer Research UK - lung cancer statistics](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/lung-cancer)",
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"question": "A 75-year-old woman presents with worsening joint pain and swelling in her hands, wrists, and knees, along with deep bone aches that disrupt her sleep. She has lost 5kg over the past year with poor appetite. She has no significant medical history, occupational exposure, or smoking history.\n\n\nOn examination, she has clubbing bilaterally. She has symmetrical polyarthritis of the wrists, metacarpal joints and knees; with pain, swelling and reduced range of motion of the affected joints.\n\n\nX-rays of her tibia and fibula are suggestive of periosteal bone formation.\n\n\nChest X-ray shows a left lower lobe mass. The medical team decides to arrange an interventional radiology guided biopsy of the mass lesion.\n\n\nWhich of the following histology findings are most likely?",
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"explanation": "Syringe drivers are given as continuous subcutaneous infusions over 24 hours. The oral morphine dose needs to be halved for subcutaneous (SC) administration via the syringe driver. The total daily oral morphine dose is (10mg x 3) + (2mg x 3) = 36mg. This would be SC morphine 18mg. As breakthrough doses should be one-sixth to one-tenth of the total daily dose, you should therefore prescribe him 2-3mg every hourly as required. The lower limit of the dose range may be prescribed to avoid concerns of toxicity. If more than 6 doses are required in 24 hours, consider seeking senior advice or review",
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"comment": "1/6 of 36 = 6?",
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"comment": "that would be 24 hr ORAL dose, you need to halve it for SC dose ",
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"comment": "1/6 of 18 is 3??",
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"comment": "which would be the max with possible concerns for toxicity its 1/10 TO 1/6 (eg. 1.8-3), take lower dose to start",
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"comment": "Why is the patient only on 2mg of oral morphine for breakthrough at the start? Shouldn't the patient's breakthrough dose be between 3.6 - 6mg? I think it's a little confusing that after conversion from oral to SC, the breakthrough dose remained at 2mg",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 90 year old gentleman is admitted to the medical ward with an infected sacral sore. He has a background of advanced dementia and previous stroke. During his stay, he develops aspiration pneumonia and his condition begins to deteriorate.\n\nHe is reviewed by the Palliative team who plan to start him on end of life medications via a syringe driver. He is currently on oral morphine 10mg TDS and has required three breakthrough doses of oral morphine 2mg in the past day. What is the most appropriate subcutaneous breakthrough dose he should be prescribed?",
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"explanation": "# Summary\n \n \nPremature ovarian insufficiency (POI) is a condition characterised by menopause in women aged below 40 years. The key signs and symptoms include vasomotor disturbances such as hot flushes and night sweats, sexual dysfunction, and psychological issues. The diagnosis is confirmed by elevated FSH levels, which should be repeated to rule out anomalous results. The main management approach is hormone replacement therapy (HRT) until the age of normal menopause, unless contraindicated.\n \n \n# Definition\n \n \nPremature ovarian insufficiency (POI) is a medical condition characterised by the onset of menopause (ovarian insufficiency) in a woman aged below 40 years. \n \n \n# Epidemiology\n \n \nThe exact prevalence of POI is not known, but it's estimated to affect approximately 1% of women under the age of 40.\n \n \n# Aetiology\n \n \nThe aetiology of POI can be idiopathic or iatrogenic. Iatrogenic causes include invasive procedures or treatments such as ovarian surgery, radiotherapy, or chemotherapy that directly impact the ovaries.\n \n \n# Signs and symptoms\n \nWomen with POI typically develop the same symptoms as those undergoing natural menopause:\n \n \n - Vasomotor symptoms: hot flushes, night sweats\n - Sexual dysfunction: vaginal dryness, reduced libido, problems with orgasm, dyspareunia\n - Amenorrhoea: infrequent or no periods \n - Psychological symptoms: depression, anxiety, mood swings, lethargy, reduced concentration\n \n \n# Differential diagnosis\n \n \nWhen evaluating for POI, it is essential to rule out other conditions that could present with similar symptoms and cause amenorrhea:\n \n \n1. **Hypothyroidism:** presents with fatigue, weight gain, cold intolerance, depression, hair loss. \n2. **Hyperprolactinemia:** irregular menstrual cycles, infertility, breast milk production not related to childbirth or nursing. \n3. **Polycystic Ovary Syndrome (PCOS):** irregular periods, hirsutism, obesity, infertility. Will have raised LH:FSH ratio. \n \n \n# Investigations\n\n**Bedside:**\n \n* Pregnancy test (to rule out pregnancy as cause of amenorrhea)\n\n**Bloods:** \n\n* FSH levels: two samples taken 4-6 weeks apart, showing raised FSH levels is required for diagnosis\n* anti-Mullerian Hormone (AMH) level: may be low, but not required for diagnosis \n* LH level: may be raised, but not required for diagnosis \n\nOther blood tests to rule out alternative causes:\n\n* Prolactin \n* TFTs\n\n\n**Imaging:**\n\nNo imaging is required for diagnosis. However transvaginal ultrasound scan may show small ovaries and poor perfusion. \n \n\n \n# Management\n \n \n - The primary management strategy for women with POI is to offer hormone replacement therapy (HRT) until at least the expected age of menopause, unless the risks of HRT treatment outweigh the benefits. \n - Additionally, psychological support should be provided due to the potential mental health impacts of early menopause.\n - Vaginal oestrogen can also be provided for women experiencing vaginal dryness and subsequent dyspareunia. \n \n \n# Complications \n\n* Osteoporosis: Declines in oestrogen leads to loss of bone mineral density due to disruption in bone remodelling. \n* Cardiovascular disease: Oestrogen has cardioprotective effects, its decline leads to alternations in lipid profiles, inflammatory changes and endothelial dysfunction. \n* Infertility: Ovarian insufficiency leads to impaired development of ovarian follicles and ovulation, leading to infertility. \n \n \n# NICE Guidelines\n \n \n [Click here for the NICE guidelines on the menopause](https://www.nice.org.uk/guidance/ng23)\n \n# References\n\n[British Menopause Society](https://thebms.org.uk/publications/consensus-statements/premature-ovarian-insufficiency/)",
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"question": "A 30 year old female presents to the GP surgery with a 6 month history of amenorrhoea. She is not sexually active and has had no previous pregnancies. Laboratory testing revealed elevated follicle stimulating hormone (FSH) and luteinising hormone (LH). Genetic testing reveals a mutation in the FMR1 gene causing an expansion of a trinucleotide repeat sequence \"CGG\".\n\nWhich of the following diseases is most likely to share the same mode of inheritance?",
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"explanation": "Dapsone inhibits folic acid synthesis and should be given with folate supplementation. It does not affect B12 levels",
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"comment": "weird question. I think very niche too - not high yield memorising Rx of haemolytic anaemia in pt with G6PD",
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"comment": "Does routine HIV testing post-diagnosis of TB not extend to other Mycobacterium infections?",
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"comment": "i tried looking this up and there doesn't seem to be much evidence in favour of TB association with leprosy. however, if you have both, the leprosy might flare more (i guess reasonably so because of the diminished immune response). but there's no guidance to test everyone (i got it wrong as well tho)",
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"explanation": "# Summary\n \n \nLeprosy is a disease endemic in many developing countries. The disease can manifest in various ways depending on host immunology and bacterial virulence. The two main forms are multibacillary (lepromatous) and paucibacillary (tuberculoid) leprosy. Differential diagnoses to consider include inherited diseases, endocrine disorders, and other conditions such as AL amyloidosis. Diagnosis is primarily based on clinical assessment and the presence of acid-fast bacilli in biopsies or smears. Management involves the use of medications such as dapsone, rifampicin, and clofazimine, with close monitoring for potential side effects and immunological complications. \n \n \n# Definition\n \n \nLeprosy is a mycobacterial disease caused by *Mycobacterium leprae* which typically presents with dermatological and neurological manifestations.\n \n# Epidemiology\n \nLeprosy is endemic in a number of developing countries across the world. Most new cases occur in Southeast Asia.\n \nIt is associated with severe morbidity, reduced psychosocial functioning and stigmatisation. While difficult to transmit, it is thought to be spread by the respiratory route via nasal discharge.\n \n# Aetiology\n \n - Leprosy is spread through droplets from the respiratory tract. Prolonged close contact (over months) is required to transmit the disease.\n - Leprosy manifests in a number of different ways owing to a range of factors, the most important being host immunology and bacterial virulence/initial infectious load\n - *M. leprae* grows best at 27–33° so it prefers to grow at **cooler** areas of the body (eg. skin, nerves close to the skin, mucous membranes)\n - There are five types, but broadly it can be classified as lepromatous and tuberculoid leprosy\n - In disseminated lepromatous/multibacillary leprosy, bacteria become widely disseminated due to poor Th1 cell-mediated responses. This causes symmetrical peripheral nerve damage through demyelination of peripheral nerves, as well as classical skin changes.\n - In tuberculoid/paucibacillary leprosy, there is a robust Th1 cell-mediated response, leading to better control by the immune system and milder clinical manifestations.\n \n# Symptoms & Signs\n \nThe clinical features of leprosy exist on a spectrum. At one end is **disseminated lepromatous/multibacillary leprosy**:\n \n - Coppery or hypopigmented anaesthetic patches; ≥5\n - Classic facial changes include nose destruction and ear swellings – leonine faces\n - Nerve thickening may be felt on palpation, with the most commonly affected nerves being the ulnar, median, radial cutaneous, greater auricular, common peroneal and posterior tibial nerves to control of the infection\n \nClinical features of **tuberculoid/paucibacillary leprosy** include a milder form of nerve damage and dermatological manifestations (<5 lesions)\n \nNerve damage in all forms can lead to contractures, ulceration and deformity in the long term\n \n# Differential diagnosis\n \n \nThe differential diagnosis for other causes of thickened peripheral nerves include:\n \n - **Inherited diseases** – Charcot–Marie–Tooth disease, Refsum's disease and neurofibromatosis. These can also cause peripheral neuropathies and cutaneous manifestations alongside a family history.\n - **Acromegaly** - coarsening features & nerve compression (especially carpal tunnel syndrome). Symptoms are more generalised and complications such as diabetes mellitus can develop.\n - **AL amyloidosis** - may be associated with symptoms of multiple myeloma (hypercalcaemia, renal dysfunction, anaemia, bone pain).\n - **Peripheral neuropathy** secondary to diabetes mellitus, alcohol use or, more acutely, Guillain-Barré syndrome. This is usually preceded by poorly controlled diabetes or alcoholism, or by a recent infection (precipitating GBS)\n \n \n# Diagnosis\n \nLeprosy is diagnosed with one or more of the following clinical features and laboratory tests:\n \n - Loss of sensation in a hypopigmented or reddened skin patch\n - Thickened peripheral nerve and sensory loss/weakness in the area supplied by the nerve\n - Slit-skin smear demonstrating acid-fast bacilli with a special stain\n \n \n# Treatment\n \nEarly diagnosis and treatment can reduce illness severity and long-term sequelae.\n \n - Treatment of multibacillary leprosy involves the use of dapsone, rifampicin and clofazimine (an immunosuppressive agent) for at least 12–24 months\n - Patients commenced on medications need to be monitored closely throughout the course of their treatment for immunological complications known as type I and II (erythema nodosum lepromum) reactions, which require hospital inpatient treatment. Treatment should continue with the addition of prednisolone, aspirin or thalidomide under specialist guidance.\n - Side effects of dapsone include methaemoglobinaemia, agranulocytosis, Stevens–Johnson Syndrome and the DRESS syndrome; it can also trigger a haemolytic crisis in G6PD deficiency\n - Clofozamine can cause abnormal skin pigmentation\n - Rifampicin can cause orange secretions and is a cytochrome P450 inducer, hence has several drug interactions\n - Treatment of paucibacillary leprosy involves rifampicin and dapsone for 6 months\n \n \n# References \n \n [BNF: Leprosy treatment summary](https://bnf.nice.org.uk/treatment-summaries/leprosy/#:~:text=Paucibacillary%20leprosy%20should%20be%20treated,is%20sufficient%20to%20treat%20tuberculosis.)\n \n [Click here for the WHO page on leprosy](https://www.who.int/news-room/fact-sheets/detail/leprosy)\n \n \n [Leprosy: review of the epidemiological, clinical, and etiopathogenic aspects - Part 1 - PMC (nih.gov)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008049/)",
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"question": "A 55 year old man presents to his GP with a 6 month history of multiple hypopigmented patches over his torso. He also has multiple burn marks on his hands from accidentally touching hot pans whilst cooking. Nerve conduction studies reveal reduced conduction velocity in the ulnar and median nerves. He is diagnosed with leprosy and started on dapsone.\n\nWhich one of the following tests should be performed before starting treatment?",
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"explanation": "Based on the evidence given, the sensitivity of PSA testing is only 20%, which is not high. This means that some men with low PSA levels might still have prostate cancer. However, lowering the PSA cutoff level may worsen specificity and result in overdiagnosis",
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"explanation": "The PPV is calculated as (True positives)/(True positives + False positives) = 100/ (100 + 300) = 25%. The value of 75% is referring to the negative predictive value",
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"explanation": "The specificity is defined as the proportion of people who test negative among all those who actually do not have the disease. It is calculated as (True negatives)/ (True negatives + False positives) = 1200/ (1200 + 300) = 80%.\n\nThe value of 20% is referring to the sensitivity of the test",
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"explanation": "# Overview \n\nSeveral key parameters can be calculated to help describe how effective a certain test is at diagnosing a condition.\n\n| | Patients with colon cancer | No cancer |\n| ------------------ | :------------------------: | --------: |\n| Biomarker positive | a | b |\n| Biomarker negative | c | d |\n\n# Sensitivity\n\nSensitivity is the proportion of people with the condition who will have a positive result. If, for example, the sensitivity of a test is 80%, out of a hundred people with the condition, only 80 will have a positive test result.\n\nSensitivity = a/(a+c)\n\n# Specificity\n\nSpecificity describes the proportion of people without the disease who will have a negative test. A specificity of 90% can be interpreted as, out of 100 people without the disease, 90 will have a negative test result.\n\nSpecificity = d/(b+d)\n\n# Positive Predictive Value\n\nPositive predictive value (PPV) is the proportion of people with a positive test who actually have the disease. PPV varies with prevalence of disease in a population. The lower the prevalence, the lower the positive predictive value. A PPV of 78% will mean that if 100 people tested positive, 78 people will have the disease.\n\nPPV = a/(a+b)\n\n# Negative Predictive Value\n\nNegative predictive value (NPV) is the proportion of people with a negative test who truly do not have the disease.\n\nNPV varies with prevalence of disease in a population. The lower the prevalence, the higher the negative predictive value. An NPV of 97% will mean that if 100 people tested negative, 97 people will not have the disease.\n\nNPV = d/(c+d)\n\n# False positive rate\n\nThe false positive rate is the proportion of those without the condition who will test positive.\n\nFalse positive rate = 1 - specificity\n\nFalse negative rate = 1 - d/(b+d)\n\n# False negative rate\n\nThe false negative rate is the proportion of those with the condition who will test negative.\n\nFalse negative rate = 1 - sensitivity\n\nFalse negative rate = 1 - a/(a+c)\n",
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"explanation": "This would be part of initial management to maintain patency of the ductus arteriosus, allowing blood to travel from the left to the right side of the heart. However, in this case, the presence of a ventricular septal defect would already allow for left to right shunting of blood",
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"explanation": "This is a surgical procedure done to stabilise patients with severe hypoxaemia due to inadequate mixing between the two parallel circuits in transposition of the great arteries (TGA). A balloon is placed across the atrial septum and used to enlarge the foramen ovale or existing atrial septal defect. However, it is only a temporary measure before corrective surgery for TGA",
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"__typename": "QuestionComment",
"comment": "Sounded like Tet spells to me",
"createdAt": 1647180250,
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"comment": "How can you tell he has both TGA and a VSD and not TOF?",
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"comment": "TOF would be ejection systolic murmur at left upper edge- pulmonary stenosis.",
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"comment": "it honestly sounds like TOF >> TGA with a VSD? the only thing is that a BT shunt is a temp procedure so sure that's not 'definitive' treatment but the stem should really be changed to look more like TGA maybe? the only indication for this to be a tga for me was mom having diabetes but. idk. ",
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"comment": "I still dont 100% agree that this is great description of TGA BUT after doing this paper again, I suppose one can argue and say that in TOF, the murmur is usually of pulmonary stenosis rather than the VSD and the CXR findings of a narrow mediastinum + large heart are also more likely to be TGA because \n\nThe heart appears globular due to an abnormal convexity of the right atrial border and left atrial enlargement and therefore appears like an egg.\n\nThe superior mediastinum appears narrow due to stress-induced thymic atrophy and hyperinflated lungs which give the picture of an egg suspended by a string on a chest radiograph, hence the name egg-on-a-string.",
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"comment": "can wait to perform my first blalock-taussig shunt as an F1",
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"comment": "Anyone not think of ebsteins anamoly, pan-systolic murmur heard at lower left sternal border with signs of right sided heart failure. Any help would be appreciated ",
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"comment": "This is exactly what I thought",
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"explanation": "# Summary\n \nCongenital cardiac disease refers to a variety of heart abnormalities present at birth, often influenced by maternal risk factors such as infectious disease during pregnancy (e.g. rubella), exposure to teratogenic drugs (e.g. thalidomide, isotretinoin, lithium), substance misuse (e.g., alcohol), and poorly controlled type 1 or 2 diabetes. Identification primarily relies on signs and symptoms observed in newborns, with murmurs often being present, with/without cyanosis, and confirmatory investigations such as echocardiography. Management is typically multidisciplinary and can involve medical therapy, interventional procedures, or surgery, depending on the severity and type of heart defect.\n \n \n# Definition\n \n\nCongenital cardiac disease is a general term referring to abnormalities in the heart's structure that arise before birth. These defects can involve the heart walls, heart valves, or the arteries and veins near the heart.\n \n\n# Epidemiology\n \n\nThe global incidence of congenital heart disease is estimated to be around 1% of live births, making it the most common type of congenital disorder. \n \n\n# Aetiology\n \n\nSeveral factors can contribute to the development of congenital heart disease:\n \n\n- Infectious causes: \n - Maternal rubella infection during pregnancy\n- Teratogenic drugs: \n - Exposure to certain medications during pregnancy, such as thalidomide, isotretinoin, and lithium, increases the likelihood of developing congenital heart disease.\n- Substance misuse: \n - Maternal misuse of substances such as alcohol can also lead to this condition.\n- Maternal diabetes: \n - Poorly controlled type 1 and type 2 diabetes during pregnancy\n - Maternal gestational diabetes is not a known risk factor \n- Family history of congenital heart disease\n - Risk is also increased in consanguineous couples \n\n \n# Classification\n\nCongenital heart disease can be divided into cyanotic or acynotic heart disease.\n\nCyanotic Heart Disease:\n\n- Transposition of the great arteries (TGA)\n- Pulmonary and tricuspid atresias\n- Tetralogy of Fallot (ToF)\n- Total anomalous pulmonary venous return \n- Persistent truncus arteriosus\n- Hypoplastic left heart\n\nAcyanotic Heart Disease:\n\n- Ventricular septal defect (VSD)\n- Atrial septal defect (ASD)\n- Patent ductus arteriosus (PDA)\n- Aortic stenosis \n- Pulmonic stenosis \n- Coarctation of the aorta \n- Endocardial fibroelastosis \n \n\n# Signs and Symptoms\n \n\nNewborns with congenital cardiac disease may present with a variety of signs and symptoms, including:\n \n\n - Cyanosis\n - Fast or troubled breathing\n - Fatigue\n - Poor feeding\n - Delayed growth\n - Heart murmur on auscultation\n \n\nThese symptoms can vary widely depending on the type and severity of the heart defect.\n \n\n# Differential Diagnosis\n \n\nIn an infant presenting with the signs and symptoms of congenital heart disease, several conditions should be considered:\n \n\n - **Respiratory distress syndrome**: This condition can cause fast, troubled breathing, and fatigue. However, it is typically associated with prematurity.\n - **Pneumonia**: Can also lead to breathing difficulties and fatigue, but it is often accompanied by fever and abnormal lung sounds on auscultation.\n - **Gastrointestinal disorders**: These can cause poor feeding and delayed growth but are typically accompanied by vomiting, diarrhoea, or abdominal distension.\n \n\n# Investigations\n \n\nWhilst some cases are detected during prenatal scans, many cases are detected after birth. The following investigations are key to diagnosing congenital heart disease:\n \n\n - Pulse oximetry: To detect low oxygen levels in the blood. This should be measured both pre and post-ductal, with > 3% difference being significant. \n - Chest X-ray: Can reveal an enlarged heart or abnormal heart shape.\n - Electrocardiogram (ECG): Can detect abnormal heart rhythms.\n - Echocardiogram: The gold standard in diagnosing congenital heart disease, providing a detailed image of the heart's structure and function.\n \n\n# Management\n \n\nThe management of congenital heart disease is complex and depends on the type and severity of the heart defect.\n\nRed flag features require more urgent management. These features include:\n\n- Lower limb saturations < 96%\n- More than 3% pre/post ductal difference \n- Signs of heart failure or shock\n\n\nIt typically involves a multidisciplinary team and can include:\n\n- Conservative management:\n - For certain defects (i.e. mild atrial septal defects, a watch-and-wait approach may be adopted as many will close by age 1)\n\n- Medical management:\n - Some patients will require medications including diuretics and ACE inhibitors depending on the type of congenital heart disease. \n- Interventional procedures: Catheter-based procedures to repair certain types of heart defects.\n \n- Surgical intervention: For more complex or severe heart defects, surgery may be necessary.\n\n# Complications\n\nDepending on the type and severity of congenital heart disease, potential complications include:\n\n- Learning difficulties\n- Pneumonia \n- Infective Endocarditis \n- Pulmonary hypertension \n- Heart failure \n\nSudden cardiac death is very rare. \n\n# Prognosis\n\nSurgically corrected congenital heart disease, particularly when isolated, has a good prognosis, however, there is still a reduced life expectancy when compared to the general population. \n\n# NICE Guidelines\n\n[NICE Guidelines on Structural Heart Defects](https://www.nice.org.uk/guidance/conditions-and-diseases/cardiovascular-conditions/structural-heart-defects) \n\n \n# References\n \n [NHS Congenital Heart Disease](https://www.nhs.uk/conditions/congenital-heart-disease/#:~:text=Congenital%20heart%20disease%20is%20a,babies%20born%20in%20the%20UK.) \n \n [British Heart Foundation Congenital Heart Disease](https://www.bhf.org.uk/informationsupport/conditions/congenital-heart-disease) \n \n [Patient Info Congenital Heart Disease in Children](https://patient.info/doctor/congenital-heart-disease-in-children) ",
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"question": "A 21-day old baby boy is brought into the Emergency Department by his worried mother as he has been having shortness of breath and irritability during feeds. His weight is on the 5th percentile for his age.\n\nHis mother has diabetes mellitus, but otherwise had an uncomplicated pregnancy and spontaneous vaginal delivery at 38 weeks.\n\nHe is tachypnoeic with accessory muscle use. On examination, there is a pansystolic murmur at the lower left sternal border and hepatomegaly.\n\nAn electrocardiogram shows right axis deviation. Chest X-ray (CXR) reveals a narrow mediastinum and an enlarged heart.\n\nWhich is the most definitive management of his condition?",
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"explanation": "Nebulised bronchodilators would be indicated in asthma. There are no features to suggest asthma such as shortness of breath, wheeze or a prior history of atopy",
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"explanation": "# Summary\r\n\r\nAcute pericarditis is the inflammation of the pericardium, the sac surrounding the heart. It is commonly seen in patients with chest pain following a viral infection, with pain typically relieved by leaning forward. The condition can be caused by various factors including infections (viral, bacterial), malignancies, cardiac causes, radiation, drugs/toxins, and rheumatological diseases. Diagnosis is based on clinical evaluation, ECG findings (ST elevation, PR depression), and imaging such as echocardiogram. Treatment options include NSAIDs, colchicine, and corticosteroids depending on the underlying cause. Complications are rare, and the prognosis is generally excellent with a low risk of long-term sequelae. \r\n\r\n# Definition \r\n\r\nAcute pericarditis is inflammation of the pericardium, the fibroelastic sac that surrounds the heart. Inflammation can also extend to the myocardium (heart muscle), in which case the condition is referred to as perimyocarditis or myopericarditis depending on which is predominant. \r\n\r\n# Epidemiology \r\n\r\nAcute pericarditis is one of the most common causes of pericardial disease and is estimated to occur in approximately 27.7 per 100,000 people annually. \r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology of pericarditis depends on the cause. The causes of pericarditis are discussed below. \r\n\r\n# Causes\r\n\r\nThe classification of pericarditis can be considered according to cause of the pericarditis. \r\n\r\n* Idiopathic\r\n\r\n* Infective causes\r\n\r\n * Viruses - viruses which cause pericarditis are **coxsackie B viruses**, echovirus, CMV, herpesvirus, HIV among other rarer causes.\r\n * Bacteria - staphylococcus, pneumococcus, streptococcus (rheumatic carditis), haemophilus and M. tuberculosis.\r\n * Fungi and parasites (rare)\r\n\r\n* Malignant causes\r\n\r\n * Lung cancer\r\n * Breast cancer\r\n * Hodgkin's lymphoma\r\n\r\n* Cardiac causes\r\n\r\n * Heart failure may cause pericarditis\r\n * Post-cardiac injury syndrome (Dressler's syndrome) including post-traumatic\r\n\r\n* Radiation - often secondary to therapy for other malignancies\r\n\r\n* Drugs and toxin causes\r\n\r\n * Anthracycline chemotherapy (Doxorubicin)\r\n * Hydralazine\r\n * Isoniazid\r\n * Methyldopa\r\n * Phenytoin\r\n * Penicillins (hypersensitivity)\r\n\r\n* Rheumatological disease\r\n\r\n * Systemic lupus erythematous (SLE)\r\n * Rheumatoid arthritis\r\n * Sarcoidosis\r\n * Vasculitides (Takayasu's, Behcet's)\r\n\r\n* Other causes\r\n * Renal failure (uraemia) - indication for emergency dialysis. \r\n * Hypothyroidism\r\n * Inflammatory bowel disease\r\n * Ovarian hyperstimulation\r\n \r\n# Symptoms\r\n\r\n* Pleuritic chest pain: central, worse on inspiration. \r\n* Postural chest pain: worse on lying flat and relieved on leaning forward.\r\n* Fever\r\n\r\n# Signs\r\n\r\n* Pericardial friction rub - high-pitched scratching noise, best heard over the left sternal border during expiration. Pathogonomonic of pericarditis. \r\n* Pericarditis can lead to the development of a pericardial effusion and cardiac tamponade in which case signs such as hypotension, raised JVP and muffled heart sounds (Beck's Triad) may be present. \r\n\r\n# Differential Diagnoses \r\n\r\n* **Acute Coronary Syndrome** \r\n\t* **Similarities**: both present with chest pain. \r\n\t* **Differences**: pericarditic chest pain is often described as sharp, pleuritic in nature, and relieved on sitting forward. In ACS, the chest pain is often described as a squeezing pressure that is not positional. \r\n\r\n\r\n* **Pleuritic Chest Pain e.g. Pulmonary Embolism or Pneumonia** \r\n\t* **Similarities**: both present with pleuritic chest pain. \r\n\t* **Differences**: PE and pneumonia will often present with very different histories and clinical features. Patients with pneumonia will describe a productive cough and fevers, whereas patients who have a pulmonary embolism will describe acute-onset pleuritic chest pain and will likely have risk factors for VTE. \r\n\r\n* **Musculoskeletal Chest Pain** \r\n\t* **Similarities**: various MSK conditions including costochondritis or muscle strains can cause chest pain that resembles pericarditis. These pains may also be positional. \r\n\t* **Differences**: MSK pain is reproducible with palpation or certain movements. \r\n\r\n\r\n* **Gastro-oesophageal Reflux Disease (GORD)** \r\n\t* **Similarities**: chest pain seen in GORD may be similar to that seen in pericarditis. Those with GORD may describe that symptoms are worse on lying flat, similar to pericarditis. \r\n\t* **Differences**: pericarditic pain is often described as sharp, whereas GORD discomfort may be described as a burning sensation that is worse with certain foods and bending over. \r\n\r\n\r\n# Investigations\r\n\r\nThe diagnosis of pericarditis is often clinical, but the following investigations can help aid diagnosis. \r\n\r\n## Bedside\r\n\r\n**1st line** = ECG \r\n\r\nECG features include: \r\n\r\n* Widespread saddle ST elevation (not following vascular territories) and PR depression. \r\n\r\nECG changes can sometimes evolve over weeks:\r\n\r\n* 1-3 weeks: normalisation of ST changes, T wave flattening\r\n* 3-8 weeks: flattened T waves become inverted\r\n* 8+ weeks: ECG returns to normal\r\n\r\n[lightgallery]\r\n\r\n## Bloods \r\n\r\n* Serial troponins: tend not to peak as in an MI, but tend to stay consistently elevated in the acute phase. \r\n* Inflammatory markers: raised inflammatory markers (WCC, CRP and ESR) are in keeping with an acute pericarditis. \r\n* Viral serology: may help to identify cause of the acute pericarditis. \r\n\r\n## Imaging\r\n\r\n* Echocardiogram - used to assess for pericardial effusion and distinguish between pericarditis and MI (e.g. looking for the absence of regional wall motion abnormalities). \r\n* Angiogram - shows normal coronary arteries (which excludes MI).\r\n* Cardiac MRI - in atypical cases, cardiac MRI can be used to visualise inflammation of the pericardium. \r\n\r\n# Management\r\n\r\n## Idiopathic or Viral Pericarditis \r\n\r\n**1st line**: exercise restriction, NSAIDS (+ PPI) for 1-2 weeks and colchicine for 3 months\r\n\r\n**2nd line**: colchicine (SE: diarrhoea, use in caution in those with renal or hepatic impairment). \r\n\r\n**3rd line**: corticosteroids (for those who cannot tolerate or refractory to NSAIDS). \r\n\r\n## Bacterial Pericarditis \r\n\r\n**1st line**: IV antibiotics +/- pericardiocentesis if purulent exudate present. \r\n\r\nRare cases - pericardectomy may be performed if adhesions or recurrent tamponade occurs. \r\n\r\n## Non-Infective Pericarditis \r\n\r\n**1st line**: corticosteroids (due to the risk of reactivation and if infection has been ruled out). \r\n\r\n# Complications\r\n\r\nComplications are rare but include cardiac tamponade and pericardial effusion requiring pericardiocentesis. In the long term patients occasionally develop constrictive pericarditis.\r\n\r\n# Prognosis \r\n\r\nAcute pericarditis has an excellent prognosis with less than 0.5% going on to develop long-term sequelae (e.g. constrictive pericarditis). \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines on Cardiac Causes of Chest Pain](<https://cks.nice.org.uk/topics/chest-pain/diagnosis/cardiac-causes/>)\r\n\r\n# References\r\n\r\n[UptoDate Article on Acute Pericarditis: Treatment and Prognosis](<https://www.uptodate.com/contents/acute-pericarditis-treatment-and-prognosis>)",
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"comment": "if there was only one or two vessels would stents be the best option? or would CABG still be preferred?",
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"comment": "Why not a PCI?",
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"comment": "AFAIK the choice to perform PCI vs CABG depends on many factors and may be influenced by the surgeon themselves as they may have a preference in terms of expertise. Generally in \"multivessel\" disease, CABG is the preferred option but there are instances where PCI could be used you are correct.\n\nI believe the highest yield takeaway from the question is that the patient is diabetic. Diabetic patients have far more extensive and complex disease of their coronary arteries compared to non diabetic patients. If multi-vessel disease occurs in a diabetic then CABG is strongly preferred over PCI.",
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"comment": "but would you attempt it in an acute setting though? i thought cabg would be done in a subacute setting",
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"explanation": "# Summary\r\n\r\nA coronary artery bypass graft (CABG) is a revascularisation technique used to treat coronary artery disease. It uses harvested blood vessels from other parts of the body to bypass narrowed coronary arteries thus improving blood flow to the heart. It should be considered in those whose symptoms are not controlled by optimal medical management and in those who have complex 3 vessel disease. CABG has an excellent prognosis, with a 5-year survival estimated at 92%. \r\n\r\n# Definition \r\n\r\nA coronary artery bypass graft (CABG) is a revascularisation technique used to treat coronary artery disease. A surgeon uses a healthy blood vessel, usually veins taken from the leg or chest, and attaches it to the heart so blood can get round the narrowed coronary artery. \r\n\r\n# Indication \r\n\r\nRevascularisation with coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) must be considered in patients with: \r\n\r\n* Symptoms which are not controlled by optimal medical management.\r\n* Complex 3 vessel disease and/or significant left main stem on CTCA. \r\n\r\nPCI may be more cost-effective than CABG. However, CABG confers a mortality benefit in patients who are >65 years old, have diabetes, or who have complex 3 vessel disease (with or without left main stem stenosis). \r\n\r\n# Procedure\r\n\r\nWith the patient under general anaesthetic, a midline sternotomy incision is made and the chest is opened. The heart may be placed 'on-pump' or the surgery may be'off-pump'. Blood vessels are usually either harvested from the legs (long saphenous vein) or from the chest (internal mammary artery). These blood vessels are then attached to the heart to bypass narrowed coronary arteries. The procedure often takes between 3-6 hours. Most people make a full requires within 12 weeks. \r\n\r\n# Identifying CABG patients \r\n\r\nCommon signs include: \r\n\r\n* Midline sternotomy scar\r\n* Harvest scars - longitudinal graft scar on either leg. \r\n* No 'click' that you would expect with metallic valve replacement. \r\n\r\n# Complications\r\n\r\nCommon post-operative complications include post-operative bleeding, arrhythmias (most commonly atrial fibrillation), low output cardiac syndrome (requiring inotropes), and midline sternotomy wound infection. \r\n\r\nLong-term complications include narrowing of grafted vessels that require further treatment.\r\n\r\n# Prognosis \r\n\r\nOverall survival at 5 years is estimated at 92%. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidance for CABG](<https://www.nice.org.uk/guidance/IPG377>)\n\r\n[NICE Guidance on Stable Angina](<https://www.nice.org.uk/guidance/cg126>)\r\n\r\n# References\r\n\r\n[2020 Article on the Role of Revascularisation in Stable Angina](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305572/)",
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"question": "A 61-year-old man with a background of type 1 diabetes and hypertension presents with a 30-minute history of chest pain radiating to the left jaw, which is unrelieved by rest or glyceryl trinitrate (GTN). He has anterolateral ST elevation on his ECG and is sent for urgent coronary angiography.\n\nCoronary angiography shows significant stenosis of the left anterior descending, left circumflex and right coronary artery.\n\nWhich of the following is the best step in management?",
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"explanation": "This patient has obstructive shock due to pericardial fluid that is reducing ventricular filling and thereby causing reduced cardiac output. Fluid challenges are more useful in the initial management of hypovolaemic (e.g. blood loss) and distributive shock (e.g. sepsis) but would not be as useful in this context",
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"explanation": "Inotropes act to increase myocardial contractility and thereby increase cardiac output. They may be considered, but definitive management with pericardiocentesis should not be delayed",
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"explanation": "Thoracocentesis is a procedure that aims to remove fluid or air from the pleural space. An emergency thoracocentesis is used for urgent decompression of a tension pneumothorax",
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"explanation": "Cardiac tamponade is a medical emergency caused by the accumulation of fluid in the pericardial space, leading to reduced ventricular filling and haemodynamic compromise. Management is with pericardiocentesis which aims to remove the pericardial fluid",
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"explanation": "Although the patient has a raised JVP, they are not in congestive cardiac failure or pulmonary oedema. The raised JVP indicates increased right atrial pressure due to the pericardial fluid causing strain on the heart. As the patient is not fluid overloaded, there would be no benefit of giving diuretics. In this case, it would likely drop the patient's blood pressure further",
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"comment": "Good question but the wording isn’t clear - surely it should be best next step in management as pericardiocentesis is not necessarily definitive (fluid can reaccumulate in the pericardium if inflammation doesn’t clear up)",
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"comment": "This definitive thing got me all kinds of confused.",
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"explanation": "# Summary\n \nCardiac tamponade is a life-threatening emergency that occurs when fluid (or occasionally gas or malignant tissue) accumulates in the pericardial sac, compressing the heart and impairing cardiac filling. It is often caused by trauma leading to bleeding into the pericardial sac, but may also result from pericarditis or malignancy. Beck's triad refers to the classical findings of a raised jugular venous pressure (JVP), hypotension and muffled heart sounds. Diagnosis can be reached rapidly with an echocardiogram. Pericardiocentesis is the usual emergency treatment. \n\n# Definition\n \nCardiac tamponade refers to the compression of the heart by fluid accumulation (often blood, occasionally gas or malignant tissue) in the pericardial sac. This compression impairs cardiac filling during diastole, compromising cardiac output and rapidly leading to cardiac arrest if untreated. \n \n# Aetiology\n \nThe commonest cause of acute cardiac tamponade is trauma, especially penetrating injuries. These may occur in road traffic accidents.\n\nIatrogenic causes (e.g. cardiothoracic surgery) can also lead to blood tamponading the heart. \n\nOther causes include:\n\n- Pericarditis, which may be secondary to:\n - Malignancies\n - Myocardial infarction\n - Infections e.g. HIV, tuberculosis\n - Connective tissue diseases\n - Radiation\n - Chronic kidney disease\n- Aortic dissection\n- Medications (e.g. minoxidil, hydralazine)\n- Cardiac perforation during diagnostic procedures\n- Pneumopericardium (e.g. secondary to a gastropericardial fistula)\n\n# Signs and Symptoms\n\nThe presentation of cardiac tamponade varies depending on the underlying cause and on how acutely it has developed. \n\nSymptoms include:\n\n- Fatigue\n- Dyspnoea\n- Cold and clammy peripheries due to hypoperfusion\n- Confusion due to reduced cardiac output\n\nSigns include:\n\n- Beck's triad (raised jugular venous pressure, hypotension and muffled heart sounds)\n- Pulsus paradoxus (a decrease in systolic blood pressure by more than 10 mmHg during inspiration)\n- Tachycardia\n- Tachypnoea\n- Altered mental state\n- Hepatomegaly\n- Pericardial friction rub\n- Cyanosis\n- JVP shows an absent Y descent (due to reduced diastolic filling of the ventricles)\n\n# Differential Diagnosis\n\n- **Acute heart failure** - overlapping features of dyspnoea and peripheral oedema, pulmonary oedema can occur in tamponade. Can be distinguished with echocardiography (showing ventricular dysfunction in heart failure).\n- **Constrictive pericarditis** occurs when the pericardium is rigid or thickened (rather than fluid in the pericardial sac). It is usually chronic rather than acute, pericardial calcification may be seen on chest X-ray and Kussmaul's sign may be seen (when venous distention and pressure paradoxically increase in inspiration - rare in tamponade).\n- **Pulmonary embolism** also causes sudden onset dyspnoea, associated with pleuritic chest pain and may have haemoptysis. Can also lead to cardiac arrest if massive; distinguished with echocardiography in the emergency setting and CTPA if stable enough for CT.\n- **Tension pneumothorax** can also result from trauma and lead to rapid cardiac arrest, also causes acute dyspnoea but can be distinguished with examination findings of unilateral hyperresonance and reduced breath sounds, tracheal deviation to the contralateral side. \n \n\n# Investigations\n\n**Bedside tests:**\n\n- **ECG** may show electrical alternans, where the height of QRS complexes alternate due to movement of the heart in the pericardial space \n\n**Blood tests:**\n\n- **Full blood count and CRP** looking for raised inflammatory markers in infective or inflammatory causes of tamponade\n- **U&Es** as uraemia may cause pericarditis leading to tamponade\n- **Coagulation screen** is important if attempting interventions such as pericardiocentesis\n- **HIV testing** if this is a suspected cause of pericarditis\n- **Group and Save** especially if bleeding is the cause of tamponade\n- **Troponin** may be elevated in cardiac trauma or myocardial infarction\n\n**Imaging:**\n\n- An **echocardiogram** is the usual diagnostic test, looking for a pericardial effusion and evidence of impaired cardiac function\n- **Chest X-ray** may show cardiomegaly; the epicardial fat pad sign may be seen (suggestive of pericardial effusion)\n- **CT** sometimes detects evidence of tamponade (e.g. in the context of trauma)\n\n**Other tests:**\n\n- If the cause of tamponade is not clear, fluid drained from a pericardial effusion should be sent for culture and cytology\n\n# Management\n\n- Call for help - alert cardiology and intensive care\n- Supportive therapies e.g. oxygen, IV fluids and inotropes\n- Avoid positive-pressure ventilation as this may decrease venous return, worsening cardiac output\n- Perform **pericardiocentesis** (aspirating pericardial fluid, usually at the bedside under echocardiography guidance)\n- Open surgical drainage may be required in some cases e.g. ongoing intrapericardial bleeding\n- Options for recurrent tamponade include percutaneous balloon pericardiotomy, pericardiodesis or pericardiectomy\n- Treat the underlying cause e.g. infection, repair of traumatic injuries\n \n# References\n\n[Radiopaedia - Cardiac Tamponade](https://radiopaedia.org/articles/cardiac-tamponade)\n\n[Patient UK - Cardiac Tamponade](https://patient.info/doctor/cardiac-tamponade)\n\n[European Society of Cardiology - Cardiac Tamponade](https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Cardiac-tamponade-a-clinical-challenge)",
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"question": "A 45-year-old man with a diagnosis of myocarditis is assessed following an episode of hypotension on the ward. On assessment, he is tachycardic and tachypnoeic with a blood pressure of 90/50 mmHg. He has a raised jugular venous pressure (JVP) and his heart sounds are difficult to auscultate.\n\nAn urgent bedside ECHO shows cardiac tamponade.\n\nWhich of the following is the best definitive step in management?",
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"explanation": "This would be a treatment option for a patient with native valve streptococcal endocarditis. Benzylpenicillin would not work for staphylococcal species",
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"explanation": "MRSA indicates that the staphylococcus aureus species are resistant to β-lactam antibiotics. In this case, for a patient with confirmed MRSA and without any prosthetic heart valves, the BNF advises treatment with vancomycin and rifampicin for 4 weeks",
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"explanation": "This is the empirical treatment for native valve endocarditis. As MRSA has been cultured, this regime needs to be escalated to vancomycin (and gentamicin) as amoxicillin will not cover MRSA",
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"explanation": "MRSA indicates that the staphylococcus aureus species are resistant to flucloxacillin. IV flucloxacillin for 4-6 weeks would be the treatment of methicillin-susceptible Staphylococcus aureus in a patient with native valve (i.e. no prosthetic valves) endocarditis",
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"comment": "was gonna be one or the other",
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"explanation": "# Summary\r\n\r\nInfective endocarditis (IE) is a rare infection of the inner surface of the heart (endocardium), usually the valves. Various risk factors contribute to its development, including age, sex, intravenous drug use, poor dentition, valvular disease, congenital heart disease, prosthetic valves, and certain medical conditions like HIV. Symptoms can be diverse and non-specific including fevers, night sweats, weight loss, and myalgia. Diagnosis is based on the modified Duke Criteria, which include major and minor criteria. Treatment involves prolonged courses of intravenous antibiotics, and surgical intervention may be necessary in certain cases. Complications can be severe, and without appropriate treatment, IE can lead to heart failure and death. Prevention through antibiotic prophylaxis is no longer recommended.\r\n\r\n# Definition \r\n\r\nInfective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves. \r\n\r\n# Epidemiology \r\n\r\nInfective endocarditis is a rare disease, impacting approximately 2-6 per 100,000 people every year. There are many risk factors implicated in the development of IE. \r\n\r\nRisk factors for IE: \r\n\r\n* Age >60 years\r\n* Male sex\r\n* IVDU: predisposition to _Staph. aureus_ infection and right-sided valve disease e.g. tricuspid endocarditis.\r\n* Poor dentition and dental infections\r\n* Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. \r\n* Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.\r\n* Prosthetic valves\r\n* Previous history of infective endocarditis\r\n* Intravascular devices: central catheters and shunts.\r\n* Haemodialysis\r\n* HIV infection\r\n\nAntibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. However, the evidence for this is inconclusive, and **NICE therefore do not advise antibiotic prophylaxis for IE.**\r\n\r\n# Pathophysiology\r\n\r\nA damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis. \r\n\r\n# Classification \r\n\r\nIE can be considered according to different classification systems. \r\n\r\n## Acute vs. Subacute vs. Chronic IE \r\n\r\nIE can be considered according to duration of symptoms. \r\n\r\n* *Acute IE*: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to *S.aureus* infection. \r\n* *Subacute IE*: patients has signs or symptoms for 6 weeks up to 3 months. \r\n* *Chronic IE*: patients has signs or symptoms that persist for longer than 3 months. \r\n\r\n## Valve Type \r\n\r\nIE can be considered according to the type of valve involved. \r\n\r\n- *Native-valve endocarditis*: patient without prosthetic valve implant. \r\n- *Prosthetic-valve endocarditis*: \r\n\t- Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. \r\n\t- Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections. \r\n\r\n# Common organisms \r\n\r\nThe most common organisms involved in infective endocarditis (in order of incidence) are:\r\n\r\n* _Staph. aureus_: now the most common cause of IE. Coagulase positive.\r\n* _Strep. viridans_: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. \r\n* Enterococci\r\n* Coagulase negative _staphylococci_ e.g. _staph. epidermidis_: common culprit of prosthetic valve endocarditis. \r\n* _Strep. bovis_: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.\r\n* Fungal \r\n* HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. \r\n* Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE). \r\n\r\n# Symptoms\r\n\r\nClinical features of IE are diverse and variable. It may present acutely with a rapid deterioration or it can present subacutely/chronically with non-specific symptoms. \r\n\r\n* Common presenting symptoms: \r\n\t* Fever: most common symptom. \r\n\t* Night sweats \r\n\t* Anorexia \r\n\t* Weight loss \r\n\t* Myalgia\r\n\r\n* Others: \r\n\t* Headache \r\n\t* Arthalgia\r\n\t* Abdominal Pain \r\n\t* Cough \r\n\t* Pleuritic pain \r\n\r\n# Signs\r\n\r\n**Systemic signs**: \r\n\r\n* Febrile \r\n* Cachectic \r\n* Clubbing\r\n* Splenomegaly \r\n\r\n**Cardiac**: \r\n\r\n* Murmur: fever + new murmur is infective endocarditis until proven otherwise. \r\n* Bradycardia: aortic root abscess tracks down to the AVN causing heart block. \r\n\r\n**Vascular phenomena**: \r\n\r\n* Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. \r\n* Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. \n* Splinter haemorrhages\r\n\r\n**Immunological phenomena**: due to immune-complex deposition. \r\n\r\n* Osler's nodes: painful pulp infarcts on end of fingers. \r\n* Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. \r\n* Glomerulonephritis: identified on urine dip. \r\n\r\n# Differential Diagnoses\r\n\r\n* Non-infectious endocarditis/Nonbacterial thrombotic endocarditis (NBTE)\r\n\t* Similarities: both present with new murmurs and both may have constitutional symptoms including fevers and weight loss. \r\n\t* Differences: blood cultures will likely be positive in infective endocarditis and may identify microorganisms that are commonly associated with IE. NBTE is often associated with advanced malignancy (pancreatic cancer and marantic endocarditis), SLE (Libman Sacks endocarditis) or hypercoagulable states and will not have positive blood cultures. \r\n\r\n* Rheumatic Fever\r\n\t* Similarities: may both present with similar symptoms including fever, heart murmur and joint pain. \r\n\t* Differences: rheumatic fever is an autoimmune response triggered by a Group A strep infection and ASOT titres may be high. In comparison, infective endocarditis will likely have positive blood cultures that identify a particular micro-organism. \r\n\r\n\r\n# Modified Duke Criteria \r\n\r\nFor the diagnosis of IE, the modified Duke Criteria needs to be followed. \r\n\r\nA useful mnemonic to remember the criteria is **'BE FIVE PM'**:\r\n\r\n* Major Criteria: \r\n\t* **B**lood Cultures\r\n\t* **E**vidence of Endocardial Involvement: **E**cho\r\n\r\n* Minor Criteria: \r\n\t* **F**ever\r\n\t* **I**mmunological phenomena\r\n\t* **V**ascular phenomena\r\n\t* **E**chocardiogram minor criteria\r\n\t* **P**redisposing features\r\n\t* **M**icrobiological evidence that does not meet major criteria. \r\n\r\nFor a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present. \r\n\r\n## Major Criteria \r\n\r\n**Blood culture positive for IE**\r\n\r\n* 2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). \r\n* Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). \r\n* Single positive blood culture for Coxiella burnetti or positive antibody titre\r\n\r\n**Evidence of endocardial involvement with imaging positive for IE**\r\n\r\n* Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. \r\n* Abnormal activity around site of prosthetic valve implantation on PET-CT\r\n* Paravalvular lesions on cardiac CT\r\n\r\n## Minor Criteria \r\n\r\n* **Fever**: >38.0 degrees celsius. \r\n* **Immunological phenomena**: Roth spots, Olser's nodes, immune complex-mediated glomerulonephritis, positive rheumatoid factor.\r\n* **Vascular phenomena**: Evidence of septic embolis (splenic infarct/abscess), Janeway lesions, conjunctival haemorrhages, mycotic aneurysm, intracranial haemorrhage. \r\n* **Echocardiogram minor criteria**: not meeting above criteria. \r\n* **Predisposing features**: known valvular disease, IVDU, prosthetic valves etc. \r\n* **Microbiological evidence that does not meet major criteria**: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE\r\n\r\n# Investigations\r\n\r\nBedside:\r\n\r\n- **ECG**: increasing prolongation of PR interval suggests development and worsening of aortic root abscess. \n- **Urine dip**: look for haematuria which may suggest development of glomerulonephritis. \r\n\r\nBlood tests:\r\n\r\n- **Routine bloods**: significant elevation of inflammatory markers and acute phase response is in line with infective endocarditis. If subacute/chronic process there may be a normocytic anaemia. \r\n- **Blood cultures**: required as per the modified Duke criteria. At least 3 sets of blood cultures taken at different times and sites. \r\n\r\nImaging:\r\n\r\n- **Echocardiogram**: \r\n\t* **1st line**: transthoracic echocardiogram \r\n\t* **2nd line**: transoesophageal echocardiogram; more invasive, but better view of mitral valve lesions and aortic root abscesses. It is the most sensitive diagnostic test. \r\n- **PET CT**: used to look for evidence of septic emboli. \r\n\r\n# Management\r\n\r\n## Medical \r\n\r\nMainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term. \r\n\r\nExamples of antibiotic choice demonstrated below: \r\n\r\n**Blind Therapy** when the organism and sensitivities are not yet known: \r\n\r\n* Native valve: amoxicillin (+/- gentamicin) \r\n* Pen-allergy/MRSA: vancomycin (+/- gentamicin) \r\n* Prosthetic valve: vancomycin + rifampicin + gentamicin \r\n\r\n**Native Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin \r\n* 2nd line: vancomycin + rifampicin \r\n\r\n**Prosthetic Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin + rifampicin + gentamicin \r\n\r\n\r\n**Strep viridans IE**\r\n\r\n* 1st line: benzylpenicillin \r\n* 2nd line: vancomycin + gentamicin \r\n\r\n**HACEK IE**: 1st line: ceftriaxone \r\n\r\n## Surgical \r\n\r\nDespite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: \r\n\r\n* Haemodynamic instability\r\n* Severe heart failure\r\n* Severe sepsis despite antibiotics/failed medical therapy\r\n* Valvular obstruction\r\n* Infected prosthetic valve\r\n* Persistent bacteraemia\r\n* Repeated emboli\r\n* Aortic root abscess\r\n\r\n**Common exam question**: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess\r\n\r\n# Complications\r\n\r\nComplications of infective endocarditis can also be the initial presenting complaint\r\n\r\n* Acute valvular insufficiency causing heart failure\r\n* Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)\r\n* Embolic complications causing infarction of kidneys, spleen or lung\r\n* Infection e.g. osteomyelitis, septic arthritis\r\n\r\n\r\nWithout timely and appropriate treatment, IE can rapidly lead to heart failure and death. The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high. \r\n\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Prophylactic Antibiotics in IE](https://www.nice.org.uk/guidance/cg64/ifp/chapter/infective-endocarditis)\r\n\r\n# References \r\n\n[American Heart Association Summary on Heart Valves and Endocarditis](<https://www.heart.org/en/health-topics/heart-valve-problems-and-disease/heart-valve-problems-and-causes/heart-valves-and-infective-endocarditis#:~:text=What%20is%20infective%20endocarditis%3F,greater%20risk%20of%20developing%20it.>)",
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"question": "A 35-year-old man with no previous past medical history presents with a 3-week history of intermittent fevers and night sweats. There are no localising symptoms of infection.\n\nOn examination, he is tachycardic and febrile with an early diastolic murmur noted over the left sternal edge.\n\nHe is treated empirically for infective endocarditis. Blood cultures subsequently grow methicillin-resistant staphylococcus aureus (MRSA).\n\nWhich of the following is the best antimicrobial regime?",
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"explanation": "Flecainide can be used in WPW in patients who are not suitable for or who refuse accessory pathway ablation",
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"explanation": "This patient has a history and ECG findings consistent with symptomatic Wolff-Parkinson-White (WPW) syndrome. This is a condition in which there is a congenital accessory pathway through which there can be aberrant conduction and pre-excitation of the ventricles.\n\nKey ECG findings are a short PR interval and a broad QRS complex with a slurred upstroke (known as a delta wave).\n\nDefinitive management is a referral to an electrophysiologist for ablation of the accessory pathway",
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"explanation": "# Summary\r\n\r\nWolff-Parkinson-White (WPW) syndrome is a congenital pre-excitation syndrome characterised by the presence of an abnormal accessory electrical pathway between the atria and ventricles. This pathway predisposes individuals to arrhythmias, including supraventricular tachycardias (SVTs) that can potentially lead to ventricular fibrillation. Diagnosis is based on electrocardiogram (ECG) findings such as delta waves, short PR interval, and broadened QRS complex. Management options include conservative monitoring, medical treatment with anti-arrhythmics, and definitive treatment through radiofrequency ablation of the accessory pathway. Emergency management of tachyarrhythmias in WPW syndrome varies based on patient stability and the specific rhythm present. Successful ablation has a high cure rate of 95%.\r\n\r\n# Definition \r\n\r\nWPW syndrome is a congenital pre-excitation syndrome that occurs due to the presence of an accessory electrical pathway between the atria and ventricles. It predisposes patients to supraventricular tachycardias, specifically an AVRT. \r\n\r\n# Epidemiology \r\n\r\nThe prevalence of WPW syndrome is approximately 100-300 per 100,000 people. Men are more commonly affected than women, with the ratio being approximately 2 to 1. \r\n\r\n# Classification \r\n\r\nWPW syndrome can be classified as Type A or Type B dependent on where the aberrant pathway is. \r\n\r\nType A \r\n\r\n* Pathway between the left atrium and ventricle. \r\n\r\nType B \r\n\r\n* Pathway between the right atrium and ventricle. \r\n\r\n\r\n# Symptoms and Signs\r\n\r\nPatients may present with:\r\n\r\n* No symptoms - WPW is often asymptomatic\r\n* Palpitations\r\n* Dizziness\r\n* Syncope\r\n\r\nThere are often no signs on examination unless the patient is currently experiencing a paroxysmal episode of SVT. \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n**1st line = ECG** \r\n\r\n* Delta waves (slurred upstroke in the QRS) \r\n* Short PR interval (<120ms) \r\n* Broadened QRS complex \r\n* If a re-entrant circuit has developed the ECG will show a narrow complex tachycardia. \r\n\r\n[lightgallery]\r\n\r\nIf a patient is experiencing paroxysmal symptoms a 24 hour tape may be used for continuous monitoring. \r\n\r\n## Bloods \r\n\r\nRoutine bloods including TFTs should be completed to investigate non-cardiac causes of tachycardia. \r\n\r\n## Imaging\r\n\r\n* Echocardiogram: to assess for structural cardiac disease and to assess ventricular function. \r\n* Cardiac catheterisation - electrophysiological studies can help map the location of the accessory pathway and identify a focus for ablation. \r\n\r\n# Long-Term Management\r\n\r\n## Conservative \r\n\r\nWPW syndrome may just be monitored if asymptomatic. The majority of patients identified with ECG findings of pre-excitation do not develop tachyarrhythmias. \r\n\r\n## Medical \r\n\r\nAnti-arrhythmics may be used if a patient is having paroxysmal SVT. Medications include amiodarone and sotalol. These are contraindicated in structural heart disease. \r\n\r\n**Contraindications in WPW**: medications that block the AVN are contraindicated in WPW. If you block the AVN, more electrical activity is conducted down the accessory pathway prediposing to dangerous arrhythmias. Digoxin, adenosine, and non-dihydropyridine calcium-channel blockers (verapamil and diltiazem) are therefore contraindicated. \r\n\r\n## Interventional and Surgical \r\n\r\nDefinitive management of WPW syndrome is radiofrequency ablation of the accessory pathway. Rarely, surgical (open heart) ablation can be performed in complex cases. \r\n\r\n# Emergency Management\r\n\r\n**If a patient with WPW presents with a tachyarrhythmia manage as follows:** \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):*\r\n\r\n* **1st line** = **synchronised DC cardioversion**\r\n\r\n*If the patient is stable they are managed according to the rhythm:*\r\n\r\n* In WPW patients with a narrow complex tachycardia with a short PR interval management is as per SVT management guidelines. \r\n\t* **1st line = vagal manouevres:** Valsalva manouevre or carotid sinus massage. \r\n\t* **2nd line = adenosine**\r\n\r\n* In WPW patients with a broad complex tachycardia, atrial fibrillation, or atrial flutter\r\n\t* **1st line = IV anti-arrhythmics:** procainamide or fleicanide as they help prevent rapid conduction through the accessory pathway. \r\n\t* **2nd line = DC cardioversion**\r\n\r\n# Complications\r\n\r\nDue to the accessory pathway in WPW, if a patient develops atrial fibrillation this can pass to ventricles, bypassing the AVN, and causing ventricular fibrillation and cardiac arrest. \r\n\r\n# Prognosis \r\n\r\nIt is estimated that there is a 95% success rate if WPW syndrome is treated with ablation. If radiofrequency ablation is successful, the WPW is considered cured. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidance on Palpitations](<https://cks.nice.org.uk/topics/palpitations/diagnosis/assessment/#:~:text=Wolff%2DParkinson%2DWhite%20(WPW)%20syndrome.&text=Slight%20widening%20of%20the%20QRS,syndrome%20can%20cause%20paroxysmal%20tachycardia.>)\r\n\r\n# References \r\n\n[Patient UK Information on WPW Syndrome](<https://patient.info/doctor/wolff-parkinson-white-syndrome-pro>)",
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"question": "A 23-year-old man presents to his General Practitioner (GP) with two brief episodes of syncope that were preceded by palpitations. He was admitted the previous year with palpitations which were found to be due to supraventricular tachycardia (SVT) that responded to initial management with vagal manoeuvres.\n\nClinical examination is unremarkable and his observations are normal. An ECG shows a short PR interval and a widespread slurred upstroke on the QRS complexes.\n\nWhich of the following is the best step in management?",
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"comment": "I thought you SHOULD give a non-dihydropyridine as it acts on the heart directly, compared to non-rate limiting CCBs which would cause widespread vasodilation and so induce tachycardia as a reflex...which would worsen the angina? no?",
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"comment": "on research, is this correct to assume then:\n- give a non-dihydro. as first line if BB contraindicated\n- give a dihydro. if must be given with a BB as second line, due to risk of heart block (if non-dihydro. given in conjunction with a BB)\n...is this correct? any help would be great cheers",
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"comment": "Yep - you've got it",
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"explanation": "# Summary\r\n\r\nStable angina, characterised by chest pain triggered by myocardial ischemia, is most commonly caused by coronary artery disease. Typical anginal chest pain is described as an exertional chest discomfort that may radiate to the jaw/neck/arm and that is alleviated by rest (<5 minutes) or with GTN spray. Diagnosis involves investigations such as ECG, blood tests, and CT coronary angiogram. Management includes conservative measures to optimise cardiovascular risk factors, medical treatment with anti-anginal medications, and revascularisation options like coronary artery bypass graft or percutaneous coronary intervention in cases not controlled by medical therapy.\r\n\r\n# Definition \r\n\r\nTypical anginal chest pain is defined by the following 3 features:\r\n\r\n1. Constriction/heavy discomfort to chest that may radiate to the jaw/neck/arm.\r\n2. Brought on by exertion.\r\n3. Alleviated by rest (<5 minutes) or GTN spray. \r\n\r\n3/3 features = typical angina pain \r\n\r\n2/3 features = atypical angina pain\r\n\r\n0-1/3 features = non-anginal pain \r\n\r\n# Epidemiology \r\n\r\nA 2020 Health Survey for England estimated prevalence in all UK adults as 3%, increasing to a prevalence of 10–12% in women aged 65–84 years and 12–14% in similarly aged men. \r\n\r\n# Pathophysiology\r\n\r\nStable angina occurs as a result of a mismatch of myocardial oxygen supply and demand. Most commonly, stable angina is due to coronary artery disease. Coronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. When demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. \r\n\r\nOther rarer causes of stable angina include anaemia, aortic stenosis, or hypertrophic cardiomyopathy.\r\n \r\n# Classification \r\n \r\nStable angina pain can be considered by its limitations on day-to-day activity:\r\n\r\n* Class I: no angina with normal physical activity. Strenuous activity may cause symptoms. \r\n* Class II: angina pain causes slight limitation on normal physical activity. \r\n* Class III: angina causes marked limitation on normal physical activity. \r\n* Class IV: angina occurs with any physical activity and may occur at rest (see unstable angina). \r\n\r\n# Symptoms and Signs\r\n\r\n* Central, constricting chest pain that radiates to neck/jaw/arm. \r\n* Exertional chest pain that is relieved on rest/GTN. \r\n* Associated symptoms: nausea, vomiting, clamminess or sweating. \r\n\r\nStable angina may have no clinical signs on examination at rest.\r\n\r\n# Differential Diagnoses \r\n\r\n* **Acute Coronary Syndrome (ACS)** \r\n\t* **Similarities**: cardiac-sounding chest pain as a presenting complaint for both. Similar patient profile with significant risk factors for coronary artery disease. \r\n\t* **Differences**: stable angina only occurs on exertion and is alleviated by rest. ACS chest pain occurs at rest. \r\n\r\n* **Gastro-oesophageal reflux disease (GORD)** \r\n\t* **Similarities**: both may present with central chest discomfort/pain. \r\n\t* **Differences**: discomfort in stable angina commonly described as a squeezing or pressure-like pain brought on by exertion. GORD-related chest discomfort often described as a burning sensation that is triggered by certain foods, alcohol, or lying down. \r\n\r\n* **Costochondritis** \r\n\t* **Similarities**: both present with chest pain. \r\n\t* **Differences**: costochondritis refers to inflammation of the cartilage connecting ribs to the sternum. The pain is described as sharp and can be reproduced by pressing on the chest wall. \r\n\r\n* **Pleuritic Chest Pain e.g. Pulmonary Embolism, Pneumonia** \r\n\t* **Similarities**: both present with chest pain or discomfort. \r\n\t* **Differences**: pleuritic chest pain is often described as sharp and worse on inspiration. Pleuritic chest pain will also be accompanied by clinical features relating to the underlying cause e.g. productive cough, fevers, risk factors for VTE, or a hot swollen calf. \r\n\r\nOther differential diagnoses include anxiety, aortic dissection (radiates to the back), and other causes of musculoskeletal chest pain. \r\n\r\n# Investigations\r\n\r\nOnce atypical/typical anginal pain is suspected: \r\n\r\n**Routine investigations in primary care**: \r\n\r\n* ECG - to assess for ischaemic changes or previous MI. \r\n* Bloods - FBC and TFTs (to exclude anaemia and hyperthyroidism respectively which can exacerbate angina symptoms).\r\n* Consider cardivascular risk factors: hypertension, hypercholesterolaemia, diabetes mellitus, smoking. \r\n\r\n**1st line investigations**\r\n\r\n* CT coronary angiogram (CT CA)- indicated if typical/atypical angina pain or if ECG shows ischaemic changes in chest pain with <2 angina features.\r\n\r\n**2nd line investigations** \r\n\r\nIf CTCA is inconclusive the patient may undergo functional imaging: \r\n\r\n* Stress echocardiogram \r\n* Myocardial perfusion SPECT \r\n* Cardiac MRI\r\n\r\n**3rd line investigations**\r\n\r\nInvasive coronary angiography can be performed if there are inconclusive results from non-invasive testing.\r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\nConservative management involves the optimisation of cardiovascular risk factors to reduce the atherosclerotic process. \r\n\r\n* Smoking cessation\r\n* Glycaemic control\r\n* Hypertension\r\n* Hyperlipidaemia\r\n* Weight loss\r\n* Alcohol intake \r\n\r\n## Medical management \r\n\r\n* Secondary prevention: aspirin 75mg OD and statin 80mg ON. \r\n* GTN spray for symptom relief: inform patient of side-effects (headache, flushing, dizziness) and to repeat dose if pain not stopped after 5 minutes. \r\n\r\n*Emergency help should be sought if pain not subsided after 2 doses of GTN as this may indicate acute coronary syndrome.* \r\n\r\n**Anti-anginal medications**\r\n\r\n**1st line** = beta-blocker (bisoprolol) OR calcium channel blocker (verapamil or diltiazem). *Do not combine due to risk of heart block*. \n\nIf taking a beta-blocker and symptoms are uncontrolled, switch to, or add, a long-acting dihydropyridine calcium-channel blocker (CCB), such as amlodipine, modified-release nifedipine. If taking a non-dyhydropyridine calcium channel blocker already, switch to a beta blocker.\r\n\r\nIf neither can be tolerated, consider a long-acting nitrate (ISMN), ivabradine, nicorandil or ranolazine. \r\n\r\n**2nd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker (amlodipine or nifedipine)\r\n\r\n**3rd line** = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker AND long-acting nitrate.\r\n\r\nA 3rd medication should only be added if the patient is symptomatic despite 2 anti-anginal drugs. At this stage, revascularisation with PCI or CABG must be considered. \r\n\r\n## Revascularisation\r\n\r\nRevascularisation with coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) must be considered in patients with: \r\n\r\n* Symptoms which are not controlled by optimal medical management.\r\n* Complex 3 vessel disease and/or significant left main stem on CTCA. \r\n\r\n# NICE Guidelines\n\r\n[NICE Guidance on Cardiac-Sounding Chest Pain](<https://www.nice.org.uk/guidance/cg95/chapter/Recommendations>) \r\n\n[NICE Guidance on Stable Angina](<https://www.nice.org.uk/guidance/cg126/chapter/Guidance>) \r\n\r\n# References\r\n\r\n[Patient UK Information on Stable Angina](<https://patient.info/doctor/stable-angina-2>) ",
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"question": "A 56-year-old man with a history of angina presents to his GP with central chest pain on exercise that is now occurring more frequently. The pain usually lasts a few minutes and is relieved by sublingual glyceryl trinitrate (GTN) spray. He denies any pain at rest, and an ECG shows no ischaemic changes.\n\nHis only current medications anti-anginal medication is bisoprolol which has been up-titrated to the maximum tolerated dose.\n\nWhich of the following is the next step in management?",
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