Persius/hicric huggingface dataset:
Azithromycin (ophthalmic) microbiology

# Microbiology
Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms and interfering with microbial protein synthesis.
Azithromycin has been shown to be active against most isolates of the following microorganisms, both in vitro and clinically in conjunctival infections .
- CDC coryneform group G2
- Haemophilus influenzae
- Staphylococcus aureus
- Streptococcus mitis group
- Streptococcus pneumoniae
The following in vitro data are also available, but their clinical significance in ophthalmic infections is unknown. The safety and effectiveness of AzaSite in treating ophthalmological infections due to these microorganisms have not been established.
The following microorganisms are considered susceptible when evaluated using systemic breakpoints. However, a correlation between the in vitro systemic breakpoint and ophthalmological efficacy has not been established. This list of microorganisms is provided as an aid only in assessing the potential treatment of conjunctival infections.
Azithromycin exhibits in vitro minimal inhibitory concentrations (MICs) of equal or less (systemic susceptible breakpoint) against most (90%) of isolates of the following ocular pathogens:
- Chlamydia pneumoniae
- Chlamydia trachomatis
- Legionella pneumophila
- Moraxella catarrhalis
- Mycoplasma hominis
- Mycoplasma pneumoniae
- Neisseria gonorrhoeae
- Peptostreptococcus species
- Streptococci (Groups C, F, G)
- Streptococcus pyogenes
- Streptococcus agalactiae
- Ureaplasma urealyticum
- Viridans streptococci
Efficacy for this organism was studied in fewer than 10 infections.
Body fat redistribution (BFR) syndrome
Synonyms and keywords: BFR; Body fat redistribution; fat derangement; fat redistribution

# Overview
Body fat redistribution (BFR) syndrome, sometimes called fat derangement, is a medical condition characterized by fat loss (or occasionally fat gain), often in the cheeks or face.  BFR most often occurs in HIV/AIDS patients undergoing antiretroviral therapy.
No firm definition of body fat redistribution syndrome exists as yet.  At least four syndromes have been described that are characterized by the accumulation of fat, and one by the loss of fat; combinations of these may occur in an individual. Gender, age, and pre-therapy body weight appear to influence the severity of BFR in patients.  BFR is distinct from lipodystrophy, which simply refers to fat loss.

# Causes

## Common Causes
- Antiretroviral therapy

## Causes by Organ System

## Causes in Alphabetical Order

# Symptoms
The most common manifestations of body fat redistribution are accumulations of fat in the central body in the form of a fat pad on the back of the neck and an accumulation of visceral fat in the abdomen or belly.  This fat accumulation is accompanied by a loss of subcutaneous fat in the face, arms, legs, and buttocks.
Patient #1: HIV patient developed fat redistribrution syndrome while on HAART

# Adverse effects
Cosmetic concerns may cause patients to refuse or stop treatment.  If severe enough, the fat accumulation may result in sleep apnea or other sleep disorders, migraines, decreased range of motion, discomfort due to pressure on internal organs, and general loss of condition.  Fat loss may result in pain in the buttocks when seated.  Other potential complications resulting from BFR include high cholesterol, high levels of triglycerides, insulin resistance, hyperglycemia, diabetes, gout, and cardiovascular disease.  BFR is also associated with certain metabolic abnormalities such as elevations of plasma sugar and fats, but the precise relationship is unknown.

# Treatment
Treatment of symptoms may include cosmetic surgery such as collagen implants; treatment of the underlying syndrome may include changing from protease inhibitors to an NNRTI.

# Related Chapters
- lipodystrophy
Birmingham Institute of Art and Design
The Birmingham Institute of Art and Design (BIAD) is the largest British university art & design teaching and research centre outside London. It is part of Birmingham City University (formerly Birmingham Polytechnic and the University of Central England in Birmingham).
The main BIAD campus and library is located at Gosta Green, just north of Birmingham city centre, and about three-quarters of a mile from either Birmingham New Street railway station or the Custard Factory quarter.
There are also smaller centres at: Bournville (foundation awards & evening classes) in the suburbs south of the city centre; Margaret Street (Fine Art) in the city centre next to Birmingham Central Library and Birmingham Museum & Art Gallery; and Vittoria Street (Jewellery) in the city's Jewellery Quarter. The International Project Space at Bournville hosts international art exhibitions and residencies. BIAD at Gosta Green is home to User-lab, a research and design laboratory specialising in user-centred design.
The Sunday Times University Guide 2004 stated: "Rated excellent (5) Art and Design". Birmingham City University states that: "BIAD received an excellent Quality Assurance score of 22/24 for Art and Design" from the QAA.
BIAD dates back, in various incarnations, to the year 1843. It reached its full maturity from the 1890s, as the Birmingham Municipal School of Art at Margaret Street, under the leadership of Edward R. Taylor.  BIAD's Archives holds extensive records on the history of art & design in Birmingham, and 20 similar collections have also been deposited with the archives.

# Notable graduates
- Patrick le Quement - Chief of Design, Renault
- Vivien Hoffpauir - Founder and Lead Designer of Vivcore
Blurred vision resident survival guide
Synonyms and Keywords: blurry vision management, blurry vision diagnosis, blurry vision, treatment, blurry vision workup

# Overview
Blurred vision is a very common visual complaint with ophthalmologic or neurologic conditions. It is an inability to see small details clearly and sharply. Decreased visual clarity can develop gradually or suddenly depending on the cause of the symptom. Refractory errors are the major causes of blurred vision complaints. Therefore most of these vision issues can be corrected with glasses. Any disease affecting eyes can cause blurriness in vision. To guide the diagnosis of blurred vision it is important to know the details like duration, progression, near or farsighted, permanent or transient, uniocular or binocular, and associated symptoms.

# Causes

## Life-Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- Eye Trauma
- Glaucoma
- Stroke
- Brain tumor
- Retinal detachment
- Optic neuritis
- Transient ischemic attack

## Common Causes
- Age related macular degeneration
- Cataract
- Diabetic retinopathy
- Myopia
- Migraines
- Dry eyes
- Presbyopia
- Need for corrective lenses
- Uveitis
- iritis
- Adverse effect (medicine)

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of blurred vision according to the American Academy of Ophthalmology guidelines.

# Treatment
Treatment of blurry vision will vary depending on the underlying cause:
- To view the treatment of conjunctivitis click here.
- To view the treatment of optic neuritis click here.
- To view the treatment of iritis click here.
- To view the treatment of macular degeneration click here.
- To view the treatment of keratitis click here.
- To view the treatment of Sjogren's syndrome click here.
- To view the treatment of EOM paralysis  click here.
- To view the treatment of glaucoma click here.
- To view the treatment of presbyopia click here.
- To view the treatment of migraines click here.

# Dos
- Ask the patient for the time of onset and how he/she first noticed the symptoms.
- Ask if the presentation was sudden in onset, or if it was gradual.
- Ask if it occurred with or without pain.
- Ask if the blurry vision was unilateral or bilateral.
- Ask for any associated conditions or events, such as auras before migraines or focal neurologic signs.
- Ask if any history of blunt trauma, penetrating injury, or exposure to a foreign body.
- Ask for the recent use of any medications such as steroids (systemic, injectable, topical, or inhaled), as these may be associated with cataracts, glaucoma, and keratitis.
- Ask for any family history of glaucoma or macular degeneration.
- Ask for any personal history of symptoms similar to the current ones.
- Test eyes one at a time; the patient should have their contact lenses or glasses in place if these are normally worn.

# Don'ts
- Do not use topical corticosteroids regularly, since they may be associated with the development of cataracts, glaucoma, and reactivation of herpes simplex virus infection.
Brain herniation (patient information)
For the WikiDoc page for this topic, click here

# Overview
Brain herniation is a side effect occurs when intracranial pressure (pressure inside the skull) builds up and causes brain tissue and blood vessels to be moved and pressed against the skull. Brain herniation is extremely dangerous and should be treated immediately.

# What are the symptoms of Brain herniation?
Symptoms of Brain herniation include:
- Coma
- Lack of energy and tiredness
- Cardiac arrest (no heartbeat)
- Respiratory arrest (inability to breathe)
- Loss of consciousness
- Loss of brainstem reflexes
blinking
pupil dilation
gag reflex
- blinking
- pupil dilation
- gag reflex

# What are the causes of Brain herniation?
Causes of Brain herniation can include:
- Brain tumors
Metastatic brain tumor
Primary brain tumor
- Metastatic brain tumor
- Primary brain tumor
- Hemorrhage
- Abscess
- Stroke
-  ("water on the brain")

# Who is at highest risk?
People who have suffered a stroke or have a brain tumor are at a high risk of developing Brain herniation.

# Diagnosis
Doctor's will look for physical signs of Brain herniation including:
- Irregular breathing
- Irregular or slow pulse rate
- High blood pressure
- changes in consciousness/alertness
- Problems with brain reflexes and nerve functions

# When to seek urgent medical care?
Call 911 and seek medical treatment immediately if you suspect Brain herniation or you experience any of the symptoms listed above. Brain herniation is a medical emergency and can result in death if left untreated.

# Treatment options
Treatment of Brain herniation involves relieving the pressure and fluid build-up in the brain. Treatment measures may include:
- Placing a shunt in the brain to drain excess fluid
- Taking medications that promote fluid loss from the body
Mannitol or other diuretics
- Mannitol or other diuretics
- Taking corticosteriods (if there is a brain tumor) to reduce swelling
Dexamethasone
- Dexamethasone
- Surgical removal of blood clots or blood to relieve pressure
- Performing endotracheal intubation (putting a tube in the airway) to reduce CO2 levels in the blood by promoting an increased breathing rate

# Where to find medical care for Brain herniation?
Directions to Hospitals Treating Brain herniation

# Prevention of Brain herniation
Prevention of Brain herniation includes:
- treatment of conditions that can lead to brain herniation (stroke, tumors,
- treatment of intracranial pressure

# What to expect (Outlook/Prognosis)?
Brain herniation is a severe condition that can cause stroke and may lead to impaired breathing, impaired neurological functioning, or death. The outlook will depend on where the herniation is located in the brain and how quickly treatment is sought.
If treatment is not sought death is a likely outcome.

# Possible complications
Complications of Brain herniation include:
- Brain death
- Permanent neurological damage

# Sources
Brain stem death (patient information)
For the WikiDoc page for this topic, click here

# Overview
Brain stem is the inner part of the brain that is connected to the spinal cord. It is responsible for regulating most of the automatic functions of the body that are essential for life, including breathing, heartbeat, blood pressure and swallowing. Further more, the brain stem plays a vital role in core functions such as consciousness, awareness and movement. Brain stem death means that the brain stem stops working, not sending messages to the body to control such core functions, at the same time, not receiving messages back from the body. Once brain stem occurs, there is no chance to recover.

# What are the symptoms of Brain stem death?
- No pupillary response to light
- No blanking on corneal touch
- No eye movement on caloric testing
- No grimacing on paiful stimuli
- No cough reflex or gag reflex
- No vestibulo-ocular reponse

# What causes Brain stem death?
- Severe brain swelling after a serious fall or traffic accident or trauma
- Massive cerebral hemorrhage
- Severe or long time of anoxia

# Diagnosis
A series of strict tests need to be carried out by two senior doctors who are not members of transplant team. The tests are done at the patient's bedside. These tests are frequently repeated to confirm that the patient's brain stem has stopped working. All the following criteria need to be met before brain stem death can be pronounced.
- Clinical tests for absent brain stem reflexes
- No pupillary response to light
- No blanking on corneal touch
- No eye movement on caloric testing
- No grimacing on paiful stimuli
- No cough reflex or gag reflex
- No vestibulo-ocular reponse
- Test for confirmation of persistent apnoea. The procedure is the following:
- Preoxygenation with 100% oxygen for 10 minutes
- Allow PaCO2 to rise above 5.0 kPa before test
- Disconnect from ventilator
- Maintain adequate oxygenation during test
- Allow PaCO2 to climb above 6.65 kPa
- Confirm no spontaneous respiration
- Reconnect ventilator

# Diseases with similar symptoms
- Persistent vegetative state (PVS): Patients in a PVS has no feeling mental distress, or physical pain, or awareness of the surroundings. The difference between PVS and brain stem death is whether the core functions are affected. For patients with PVS, there is a slim chance to recover.But for the patients with brain stem death, there is no chance once their brain stem has died. All of the core functions of the body have stopped working and can never be restarted.

# Where to find medical care for Brain stem death?
Directions to Hospitals Treating Brain stem death
Cardiac allograft vasculopathy surgery

# Overview

# Surgery

## Nonpharmacologic Interventions
- Retransplantation
- Percutaneous coronary interventions
- Coronary artery bypass grafting (CABG)
- Transmyocardial revascularization
- Heparin induced/mediated extracorporeal LDL plasmapheresis (HELP)

### Retransplantation
- Retransplantation is the only definitive treatment for CAV. It is associated with satisfactory survival in patients with CAV.
- About 60% of the repeat transplantation procedures performed are due to graft failure secondary to CAV . It is a higher risk procedure and raises significant ethical concerns primarily because of scarcity of heart transplant donors .
- Prognosis: One year survival has improved in recent years, but continues to be inferior compared to primary transplants (79% in re-transplant group compared to 85% in primary transplant group) .

### Percutaneous Coronary Intervention
- This procedure is limited only to a selected group of patients with focal disease in a single artery. Moreover, the number of patients who benefit are small.
- Incidence of re-stenosis is high, ranging from 20 to 60% as reported in various studies.
- Intracoronary stenting appears to have lower rate of re-stenosis as compared to coronary angioplasty alone.
- Concomitant use of high dose immunosuppressive therapy with azathioprine and mycophenolate have shown to significantly reduce the rate of re-stenosis .

### Coronary Artery Bypass Grafting
- Associated with a high perioperative mortality especially in those with distal disease.
- In a retrospective analysis of 12 patients with CAV who underwent CABG, 4 died perioperatively, while only 7 were alive at the end of 9 months post-surgery .

### Transmyocardial Revascularization
- Also known as transmyocardial laser revascularization (TMLR), is a procedure involving creation of transmural channels in the myocardium to enhance blood supply.
- This procedure has been studied in multiple clinical trials in patients with refractory angina and those who are not considered as surgical candidates.
- Mehra and colleagues  first studied the effects of TMLR in patients with diffuse CAV. They reported significant improvement in symptoms and anginal class at 4 and 8 week follow up. However, at 24 month follow up, the procedure showed neither consistent symptomatic improvement nor any change in course of the progression of CAV .

### Heparin Induced/Mediated Extracorporeal LDL Plasmapheresis
- Also known as LDL apheresis.
- Leads to significant reductions in LDL, lipoprotein(a) levels and fibrinogen.
- No effect on HDL levels.
- In a prospective study by Park et al., patients treated with LDL apheresis had a statistically significant increase in intraluminal diameter between 1 year and 2.5 years of follow up. However, long term trials are required to draw firm conclusions.
Cardiac arrest resident survival guide
Synonyms and keywords: cardiorespiratory arrest, cardiopulmonary arrest, circulatory arrest, Advanced life support, ACLS, Basic life support, BLS

# Overview
A cardiac arrest is the abrupt cessation of normal blood flow circulation due to the failure of the heart to contract effectively during systole.

# Causes

## Life Threatening Causes
Cardiac arrest is a life-threatening condition and must be treated as such irrespective of the underlying cause.

## Common Causes
- Arrhythmia
- Cardiomyopathy
- Ischemic heart disease

## Reversible Causes

### H's
- Hypovolemia
- Hypoxia
- Hydrogen ions (acidosis)
- Hyperkalemia or Hypokalemia
- Hypothermia
- Hypoglycemia or Hyperglycemia

### T's
- Tablets or Toxins (tricyclic antidepressants, phenothiazines, beta blockers, calcium channel blockers, cocaine, digoxin, aspirin, acetominophen)
- Cardiac Tamponade
- Tension pneumothorax
- Thrombosis (myocardial infarction)
- Trauma (hypovolemia)

# Management

## Cardiac Arrest Care: Algorithm 1
Adapted from 2010 AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, part 8.

## Cardiac Arrest Care: Algorithm 2
Adapted from 2010 AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, part 8.

## Acute Immediate Post-Cardiac Arrest Care
Adapted from 2010 AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, part 9.

## Do's
- Chronotropic drug infusions are recommended as an alternative to pacing in symptomatic and unstable bradycardia.
- Adenosine is recommended as a safe and potentially effective therapy in the initial management of stable undifferentiated regular monomorphic wide-complex tachycardia.
- If using bag and mask ventilation, use adult mask to deliver at least 600 ml of tidal volume, sufficient to produce chest rise, over at least 1 second.
- Perform a head tilt-chin lift maneuver to open the airway, and ensure there is an airtight seal when using bag mask ventilation.
- Oropharyngeal and nasopharyngeal airways may be used to assist in bag and mask ventilation in unconscious patients.
- Continuous waveform capnography is recommended to confirm the placement of endotracehal tube.
- If the cardiac rhythm changes, shift to the appropriate rhythm based strategy.
- If you are not sure of the defibrillator's recommended energy levels, use maximum output level.

## Dont's
- Do not use atropine in the management of pulseless electrical activity (PEA)/asystole.
- Do not interrupt the compressions or the use of defibrillator to place an advanced airway, secure IV/IO access or deliver drugs.
- Do not hyperventilate the patient.
- Do not use femoral pulse to assess return of spontaneous circulation (ROSC). The pause in compressions should be used to assess pulse.
Catastrophic antiphospholipid syndrome
Synonyms and keywords: CAPS; Asherson's syndrome

# Overview
Catastrophic antiphospholipid syndrome, CAPS, also Ashersons syndrome, is an acute and complex biological process that leads to occlusion of small vessels of various organs. It was first described by Ronald Asherson in 1992. The syndrome exhibits thrombotic microangiopathy, multiple organ failure, and tissue necrosis and is considered an extreme variant of the antiphospholipid syndrome.
CAPS has a mortality rate of about 50 %. With the establishment of a CAPS-Registry more has been learned about this syndrome, yet the cause remains elusive. Infection, trauma, medication, or surgery can be identified in about half the cases as a trigger. It is thought that cytokines are activated leading to a cytokine storm with the potentially fatal consequences of organ failure. Patients exhibit a positive test to antilipid antibodies, typically IgG, and often have a history of lupus or another connective tissue disease. Thrombocytopenia is a common finding.
Clinically, the syndrome can affect many organs systems. Peripheral thrombosis may be encountered affecting veins or arteries. Intraabdominal thrombosis may lead to pain. Renal and pulmonary complications are common. The patient may exhibit skin purpura and necrosis. Cerebral manifestations may lead to encephalopathy and seizures.  Myocardial infarctions may occur. Death may result from multiple organ failure.
Treatments may involve the following steps:
- Prevention includes the use of antibiotics for infection and parenteral anticoagulation for susceptible patients.
- Specific therapy includes the use of  intravenous heparin, corticosteroids, and possibly plasma exchanges, intravenous immunoglobulin.
- Additional steps may have to be taken to manage circulatory problems, renal failure, and respiratory distress.
Cefazolin sodium clinical pharmacology

# Clinical Pharmacology

## Mechanism of Action
Cefazolin is an antibacterial drug .

## Pharmacodynamics
The pharmacokinetic/pharmacodynamic relationship for cefazolin has not been evaluated in patients.

## Pharmacokinetics
Studies have shown that following intravenous administration of cefazolin to normal volunteers, mean serum concentrations peaked at approximately 185 mcg/mL and were approximately 4 mcg/mL at 8 hours for a 1 gram dose.
The serum half-life for cefazolin is approximately 1.8 hours following intravenous administration.
In a study, using normal volunteers, of constant intravenous infusion with dosages of 3.5 mg/kg for 1 hour (approximately 250 mg) and 1.5 mg/kg the next 2 hours (approximately 100 mg), cefazolin produced a steady serum concentration at the third hour of approximately 28 mcg/mL.
Plasma pharmacokinetic parameters of cefazolin in normal volunteers (N=12) following a single 15-minute intravenous infusion of 2 grams of Cefazolin for Injection, USP are summarized in Table below.
Studies in patients hospitalized with infections indicate that cefazolin produces mean peak serum concentrations approximately equivalent to those seen in normal volunteers.
Bile concentrations in patients without obstructive biliary disease can reach or exceed serum concentrations by up to five times; however, in patients with obstructive biliary disease, bile concentrations of cefazolin are considerably lower than serum concentrations (< 1 mcg/mL).
In synovial fluid, the cefazolin concentration becomes comparable to that reached in serum at about 4 hours after drug administration.
Studies of cord blood show prompt transfer of cefazolin across the placenta. Cefazolin is present in very low concentrations in the milk of nursing mothers.
Cefazolin is excreted unchanged in the urine. In the first 6 hours approximately 60% of the drug is excreted in the urine and this increases to 70% to 80% within 24 hours.