Persius/hicric huggingface dataset:
Varices and variceal bleed resident survival guide

# Overview
Gastroesophageal varices are portosystemic collaterals resulting from portal hypertension which is a complication of cirrhosis.  Gastroesophageal varices are prone to rupture leading to life threatening hemorrhage.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.  Variceal bleed is a life-threatening condition and must be treated as such irrespective of the causes.

## Common Causes
- Cirrhosis

# Management

## Non Bleeding Varices in Cirrhosis
Shown below is an algorithm depicting the screening and prophylaxis management of non bleeding varices in cirrhosis based on the  practice guidelines approved by American Association for the Study of Liver Diseases (AASLD) and American College of Gastroenterology (ACG).
 Varices at high risk of bleeding:
- Cirrhosis with Child-Pugh class B or C severity.
- Presence of red wale marks on varices visualized on endoscopy.
 Varices not at high risk of bleeding:
- Cirrhosis with Child-Pugh class A severity.
- No red wale marks on varices.

## Actively Bleeding Varices
Shoen below is an algorithm depicting the management of actively bleeding varices based on the  practice guidelines approved by American Association for the Study of Liver Diseases (AASLD) and American College of Gastroenterology (ACG).
- Balloon tamponade should be used as a temporizing measure (maximum 24 hours) in patients with uncontrollable bleeding for whom a more definitive therapy is planned.

# Do's
- Use either propranolol or nadolol when non selective beta blockers are indicated.
- If a patient is placed on beta blocker, its dose should be adjusted to the maximum tolerated dose.
- When endoscopic variceal ligation (EVL) is done, repeat EVL every 1 to 2 weeks until complete obliteration of varices.  Follow up with EGD after 1 to 3 months and every 6 to 12 months thereafter to screen for varices recurrence.
- Vasoconstrictive pharmacotherapy should be initiated as soon as variceal bleeding is suspected and should be continued for 3 to 5 days after the diagnosis of bleeding varices is established.

# Dont's
- In patients with small varices, who are on beta blockers, follow up with EGD is not recommended.
- Beta blockers are not recommended to prevent variceal development in cirrhotic patients with no varices.
- Nitrates, sclerotherapy and shunt therapy should not be used to prevent first variceal bleed.
- Don't use beta blockers in acute bleed because it will cause reflex tachycardia that might worsen bleeding.
- Consider transfusion of FFP and platelets in patients with significant coagulopathy and/or thrombocytopenia.
- Don't provide excessive resuscitation with saline solution in variceal bleed.
Azithromycin (ophthalmic) warnings and precautions

# Warnings and Precautions

### Topical Ophthalmic Use Only
NOT FOR INJECTION. AzaSite is indicated for topical ophthalmic use only, and should not be administered systemically, injected subconjunctivally, or introduced directly into the anterior chamber of the eye.

### Anaphylaxis and Hypersensitivity with Systemic Use of Azithromycin
In patients receiving systemically administered azithromycin, serious allergic reactions, including angioedema, anaphylaxis, and dermatologic reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported rarely in patients on azithromycin therapy. Although rare, fatalities have been reported. The potential for anaphylaxis or other hypersensitivity reactions should be considered based on known hypersensitivity to azithromycin when administered systemically.

### Growth of Resistant Organisms with Prolonged Use
As with other anti-infectives, prolonged use may result in overgrowth of non-susceptible organisms, including fungi. If super-infection occurs, discontinue use and institute alternative therapy. Whenever clinical judgment dictates, the patient should be examined with the aid of magnification, such as slit-lamp biomicroscopy, and where appropriate, fluorescein staining.

### Avoidance of Contact Lenses
Patients should be advised not to wear contact lenses if they have signs or symptoms of bacterial conjunctivitis.
Bypass Angioplasty Revascularization Investigation

# Overview

# Bypass angioplasty revascularization investigation
The two U.S. trials of PTCA versus CABG are the multicenter Bypass Angioplasty Revascularization Investigation (BARI) trial and the single-center Emory Angioplasty Surgery Trial (EAST).
In both trials, a majority of patients had two- rather than three-vessel disease and normal LV function. In the BARI trial, 37% of patients had a proximal LAD lesion. The results of BARI trial at seven year follow-up interval has shown that early and late survival rates have been equivalent for the PTCA and CABG groups. The subgroup of patients with treated diabetes had a significantly better survival rate with CABG. That survival advantage for CABG was focused in the group of diabetic patients with multiple severe lesions.  The biggest difference in late outcomes was the need for repeat revascularization procedures and symptom status. 54% of PTCA patients underwent subsequent revascularization procedures during the five-year follow-up versus 8% of the CABG group. In addition, the rate of freedom from angina was better in the CABG group and fewer patients in the CABG groups needed to take anti-anginal medications.

# Related Chapters
- Chronic stable angina percutaneous coronary intervention versus coronary artery bypass grafting
- Emory Angioplasty Vs Surgery Trial
Carbenicillin indanyl sodium clinical pharmacology

# Clinical Pharmacology
Free carbenicillin is the predominant pharmacologically active fraction of Geocillin. Carbenicillin exerts its antibacterial activity by interference with final cell wall synthesis of susceptible bacteria.
Geocillin is acid stable, and rapidly absorbed from the small intestine following oral administration. It provides relatively low plasma concentrations of antibiotic and is primarily excreted in the urine. After absorption, Geocillin is rapidly converted to carbenicillin by hydrolysis of the ester linkage. Following ingestion of a single 500 mg tablet of Geocillin, a peak carbenicillin plasma concentration of approximately 6.5 mcg/ml is reached in 1 hour. About 30% of this dose is excreted in the urine unchanged within 12 hours, with another 6% excreted over the next 12 hours.
In a multiple dose study utilizing volunteers with normal renal function, the following mean urine and serum levels of carbenicillin were achieved:
Carbenicillin indanyl sodium indications and usage

# Indications and Usage
Geocillin (carbenicillin indanyl sodium) is indicated in the treatment of acute and chronic infections of the upper and lower urinary tract and in asymptomatic bacteriuria due to susceptible strains of the following organisms:
- Escherichia coli
- Proteus mirabilis
- Morganella morganii  (formerly Proteus morganii)
- Providencia rettgeri (formerly Proteus rettgeri)
- Proteus vulgaris
- Pseudomonas
- Enterobacter
- Enterococci
Geocillin is also indicated in the treatment of prostatitis due to susceptible strains of the following organisms:
- Escherichia coli
- Enterococcus (S. faecalis)
- Proteus mirabilis
- Enterobacter sp.
WHEN HIGH AND RAPID BLOOD AND URINE LEVELS OF ANTIBIOTIC ARE INDICATED, THERAPY WITH GEOPEN (CARBENICILLIN DISODIUM) SHOULD BE INITIATED BY PARENTERAL ADMINISTRATION FOLLOWED, AT THE PHYSICIAN'S DISCRETION, BY ORAL THERAPY.
NOTE: Susceptibility testing should be performed prior to and during the course of therapy to detect the possible emergence of resistant organisms which may develop.
To reduce the development of drug-resistant bacteria and maintain effectiveness of Geocillin and other antibacterial drugs, Geocillin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Cordarone tablet how supplied storage and handling

# How Supplied
Cordarone (amiodarone HCl) Tablets are available in bottles of 60 tablets as follows:
200 mg, NDC 0008-4188-04, round, convex-faced, pink tablets with a raised "C" and marked "200" on one side, with reverse side scored and marked "WYETH" and "4188."
Keep tightly closed.
Store at Controlled Room Temperature, 20 to 25C (68 to 77F).
Protect from light.
Dispense in a light-resistant, tight container.
Demeclocycline hydrochloride clinical pharmacology

# Clinical Pharmacology
The absorption of demeclocycline is slower than that of tetracycline. The time to reach the peak concentration is about 4 hours. After a 150 mg oral dose of demeclocycline tablet, the mean concentrations at 1 hour and 3 hours are 0.46 and 1.22 mcg/mL (n = 6), respectively. The serum half-life ranges between 10 and 16 hours.
When demeclocycline hydrochloride is given concomitantly with some dairy products, or antacids containing aluminum, calcium, or magnesium, the extent of absorption is reduced by more than 50%.
Demeclocycline hydrochloride penetrates well into various body fluid and tissues. The percent of demeclocycline hydrochloride bound to plasma protein is about 40% using a dialysis equilibrium method and 90% using an ultra-filtration method. Demeclocycline hydrochloride, like other tetracyclines, is concentrated in the liver and excreted into the bile where it is found in much higher concentrations than in the blood. The rate of demeclocycline hydrochloride renal clearance (35 mL/min/1.73 m2) is less than half that of tetracycline. Following a single 150 mg dose of demeclocycline hydrochloride in normal volunteers, 44% (n = 8) was excreted in urine and 13% and 46%, respectively, were excreted in feces in two patients within 96 hours as active drug.
Differentiating celiac disease from other diseases

# Overview
Celiac disease must be differentiated from other diseases presenting as chronic diarrhea. Common differentials of celiac disease include lactose intolerance, cystic fibrosis, Crohns disease,  laxative overuse, hyperthyroidism and irritable bowel syndrome.

# Differentiating Celiac Disease from Other Diseases
Celiac disease must be differentiated from other diseases presenting as chronic diarrhea (diarrhea for more than 2 weeks) and abdominal pain and discomfort.
The table below summarizes the diseases that cause malabsorption, diarrhea and abdominal pain.
Abbreviations:
WBC: White blood cells; Plt: Platelets, Hgb: Hemoglobin, IgE: Immunoglobulin E, IgA: Immunoglobulin A 
Abbreviations:
WBC: White blood cells; Plt: Platelets, Hgb: Hemoglobin, IgE: Immunoglobulin E, IgA: Immunoglobulin A
Distal embolization and loss of side branch case 1

# Distal Embolization and Loss of Side Branch
Shown below is a pre-intervention angiogram with occlusion at the anastomosis between SVG and obtuse anterior branch of obtuse marginal branch of the LCX.
Shown below is a post-intervention angiogram with occlusion of the obtuse marginal branch  after intervention on the lesion described above depicting loss of side branch.
Shown below is a post-intervention angiogram with occlusion at the distal part of obtuse anterior branch of the obtuse marginal branch depicting distal embolization.
Ebstein's anomaly of the tricuspid valve treatment

# Treatment

## Pharmacological Management
Ebstein's cardiophysiology typically presents as an (antidromic) AV nodal reentrant tachycardia with associated pre-excitation. In this setting, the preferred pharmacological treatment agent is procainamide. Since AV-blockade may promote conduction over the accessory pathway, drugs like beta blockers, calcium channel blockers and digoxin are contraindicated.
If there is atrial fibrillation with pre-excitation, treatment options include procainamide, flecainide, propafenone, dofetilide and ibutilide since these medications slow conduction in the accessory pathway causing the tachycardia and should be administered before considering electrical cardioversion. Intravenous amiodarone may also convert atrial fibrillation and/or slow the ventricular response.

## Mechanical and Device Based Therapy
The protracted natural history of this disease in contrast to the uncertainty of long-term results of surgical intervention supports the policy of postponing surgical intervention until the onset of disability.

## Surgery may include
- Tricuspid valve repair or replacement (when possible repair is preferable to replacement as it is associated with a lower mortality rate and fewer complications).
- Atrial septal defect repair.
- Right atrial plication (unclear whther this improves right ventricular function).
- Cardiac defibrillator implantation.
- Accessory pathways may require surgical intervention or ablation.
Hospital mortality at the Mayo for valve reconstruction is 6.7%. Only 1.6% in the Mayo series required reoperation. Long term follow up in the Mayo series showed 92% to have Class I or II symptoms and a 10 year mortality rate of 8%.
Generally, surgical treatment improves the exercise intolerance from NYHA-FC III or IV to NYHA-FC I or II.
Regardless of severity of the Ebsteins Anomaly and type of treatment, risk of sudden death remains an important issue in patients with Ebstein's anomaly.
Ectonucleotide pyrophosphatase/phosphodiesterase 1
Ectonucleotide pyrophosphatase/phosphodiesterase family member 1 is an enzyme that in humans is encoded by the ENPP1 gene.

# Function
This gene is a member of the ecto-nucleotide pyrophosphatase/phosphodiesterase (ENPP) family. The encoded protein is a type II transmembrane glycoprotein comprising two identical disulfide-bonded subunits. This protein has broad specificity and cleaves a variety of substrates, including phosphodiester bonds of nucleotides and nucleotide sugars and pyrophosphate bonds of nucleotides and nucleotide sugars. This protein may function to hydrolyze nucleoside 5' triphosphates to their corresponding monophosphates and may also hydrolyze diadenosine polyphosphates. Mutations in this gene have been associated with Generalized arterial calcification of infancy, ossification of the posterior longitudinal ligament of the spine (OPLL), Hypophosphatemic rickets autosomal recessive 2 (ARHR2), and insulin resistance.

# Interactions
Ectonucleotide pyrophosphatase/phosphodiesterase 1 has been shown to interact with Insulin receptor.
Epidemiology and Demographics compartment syndrome

# Overview
Compartment syndrome is a painful problem known as the increased intracompartmental pressure (ICP) within a closed osteofascial compartment.

# Epidemiology and Demographics
CS usually develops after severe (such as fractures or crush injury), minor, or even iatrogenic has injuries, and it related mortality rate is almost 50%. Usually the leg and forearm are the most common affected sites, but it can also involves the arm, hand, foot, and buttock. Male are almost 10 times more likely to suffer than female with the mean age of involvement of 30 years and 44 years, respectively. Meanwhile, the closed tibial shaft fracture as the most common cause of CS comprised almost 30% of all cases of CS; and blunt and crushed soft tissue limb trauma while radius ulna shaft fractures are responsible for 25% and 20% of cases, respectively. Also, foot injuries in road traffic accidents account for 6% of CS cases, while this incidence is less common in lower leg injuries .
the prevalence of Abdominal CS ranged from 0.0% to 36.4% and the related mortality rated ranged from 0.0% to 100.0%.
Ethambutol hydrochloride dosage and administration

# Dosage and Administration
MYAMBUTOL should not be used alone, in initial treatment or in retreatment. MYAMBUTOL should be administered on a once every 24-hour basis only. Absorption is not significantly altered by administration with food. Therapy, in general, should be continued until bacteriological conversion has become permanent and maximal clinical improvement has occurred.
MYAMBUTOL is not recommended for use in pediatric patients under thirteen years of age since safe conditions for use have not been established.
Initial Treatment: In patients who have not received previous antituberculous therapy, administer MYAMBUTOL 15 mg/kg (7 mg/ lb) of body weight, as a single oral dose once every 24 hours. In the more recent studies, isoniazid has been administered concurrently in a single, daily, oral dose.

## Retreatment
In patients who have received previous antituberculous therapy, administer MYAMBUTOL 25 mg/kg (11 mg/lb) of body weight, as a single oral dose once every 24 hours. Concurrently administer at least one other antituberculous drug to which the organisms have been demonstrated to be susceptible by appropriate in-vitro tests. Suitable drugs usually consist of those not previously used in the treatment of the patient. After 60 days of MYAMBUTOL administration, decrease the dose to 15 mg/kg (7mg/ lb) of body weight, and administer as a single oral dose once every 24 hours.
During the period when a patient is on a daily dose of 25 mg/kg, monthly eye examinations are advised.
See Table for easy selection of proper weight-dose tablet(s).
Eukaryotic translation initiation factor 4 gamma 1
Eukaryotic translation initiation factor 4 gamma 1 is a protein that in humans is encoded by the EIF4G1 gene.

# Function
The protein encoded by this gene is a component of the protein complex eIF4F, which is involved in the recognition of the mRNA cap, ATP-dependent unwinding of 5'-terminal secondary structure, and recruitment of mRNA to the ribosome. Alternative splicing results in five transcript variants encoding four distinct isoforms. eIF4G serves as a scaffold, interacting with mRNA and the other components of the eIF4F complex, as well as the PABP and eIF3.

# Interactions
Eukaryotic translation initiation factor 4 gamma has been shown to interact with MKNK1, EIF4A1, EIF4E, MKNK2 and PABPC1.
Hyperlipoproteinemia epidemiology and demographics

# Overview
Hyperlipidemia is a common health problem that tends to more often affect the elderly population in developed countries. It is a major cause of disease burden globally as a risk factor for cardiovascular and cerebrovascular diseases.

# Epidemiology and Demographics

## Prevalence
Worldwide, the prevalence of hyperlipidemia is about 39,000 per 100,000 patients.
In developed countries, the prevalence of hyperlipidemia is about 51,000 per 100,000 patients.
In developing countries, the prevalence of hyperlipidemia is about 26,000 per 100,000 patients.

## Age
The prevalence of hyperlipidemia increases with age. It may be present in children and young adults but is seen more frequently in later life.

## Gender
The prevalence of hyperlipidemia among men is about 37,000 per 100,000, and among women is about 40,000 per 100,000. Thus gender is not much associated with an increased risk of hyperlipidemia. However, hyperlipidemia is more common in men younger than 55 years and in women older than 55 years.

## Developed Countries
People in the developed countries have a higher prevalance of hyperlipidemia. The prevalence also increases noticeably according to the income level of the country. In high-income countries, over 50% of adults have raised total cholesterol; more than double the level of the low-income countries.

## Developing Countries
In the past, the incidence and prevalence of hyperlipidemia were low in developing countries in comparison to developed countries. But with the westernization of developing regions in Middle East, India, and Central and South America, the incidence of hyperlipidemia is increasing.
Substance or medication induced psychotic disorder
Synonyms and keywords: Medication-induced psychotic disorder; Substance-induced psychotic disorder; Substance/medication-induced psychotic disorder

# Overview
Substance-induced psychotic disorder is defined as hallucinations and/or delusions that occur soon after substance intoxication or withdrawal and that are not better explained by a psychotic disorder.

# Differential Diagnosis
- Alcohol withdrawal
- Brief psychotic disorder
- Cannabis intoxication
- Delusional disorder
- Flashback hallucinations
- Intoxication with stimulants
- Phencyclidine
- Schizophrenia
- Schizoaffective disorder
- Schizophrenia spectrum
- Delusional disorder
- Meperidine use

# Risk Factors
- Cocaine usage
- Heavy and constant ingestion of alcohol
- History of psychopathic disorder 

# Prognosis
Poor prognostic factors include:
- Depersonalization
- Flashbacks
- Hallucinations
- Marked anxiety
- Persecutory delusions

# Diagnostic Criteria

## DSM-V Diagnostic Criteria for Substance/Medication-induced Psychotic Disorder
- A. Presence of one or both of the following symptoms:
AND
- B. There is evidence from the history, physical examination, or laboratory findings of both (1) and (2):
AND
- C. The disturbance is not better explained by a psychotic disorder that is not substance/medication-induced. Such evidence of an independent psychotic disorder could include the following:
The symptoms preceded the onset of the substance/medication use; the symptoms persist for a substantial period of time (e.g., about 1 month) after the cessation of acute withdrawal or severe intoxication: or there is other evidence of an independent non-substance/medication-induced psychotic disorder (e.g., a history of recurrent non-substance/medication-related episodes).
AND
- D. The disturbance does not occur exclusively during the course of a delirium.
AND
- E. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
Note: This diagnosis should be made instead of a diagnosis of substance intoxication or substance withdrawal only when the symptoms in Criterion A predominate in the clinical picture and when they are sufficiently severe to warrant clinical attention.
N-terminal prohormone of brain natriuretic peptide
The N-terminal prohormone of brain natriuretic peptide (NT-proBNP or BNPT) is a prohormone with a 76 amino acid N-terminal inactive protein that is cleaved from the molecule to release brain natriuretic peptide.
Both BNP and NT-proBNP levels in the blood are used for screening, diagnosis of acute congestive heart failure (CHF) and may be useful to establish prognosis in heart failure, as both markers are typically higher in patients with worse outcome. The plasma concentrations of both BNP and NT-proBNP are also typically increased in patients with asymptomatic or symptomatic left ventricular dysfunction and is associated with coronary artery disease and myocardial ischemia.

# Blood levels
There is no level of BNP that perfectly separates patients with and without heart failure.
In screening for congenital heart disease in pediatric patients, an NT-proBNP cut-off value of 91 pg/mL could differentiate an acyanotic heart disease (ACNHD) patient from a healthy patient with a sensitivity of 84% and specificity of 42%. On the other hand, an NT-proBNP cut-off value of 318 pg/mL is more appropriate in differing patients with congenital nonspherocytic hemolytic disease (CNHD) from healthy patients, with 94% sensitivity and 97% specificity. An NT-proBNP value of 408 pg/mL has been estimated to be 83% sensitive and 57% specific in differentiating patients with ACNHD from patients with CNHD

# Test usage in a clinical setting

## Canada
While discussed in Canadian medical journals in the mid to late 2000s, the test is not widely used. It was only approved for use in Alberta in February 2012.

# Test usage in the life insurance industry
The test has been widely used in the life insurance industry to screen applicants as part of the routine requirements when applying for a life insurance policy. It is also inexpensive and can be measured from blood samples routinely drawn as part of the application process. The test can be used to evaluate for a number of health conditions.