Persius/hicric huggingface dataset:
Venous Thromboembolism Risk Calculator

# Venous thromboembolism Risk Stratification for Surgical Patients

## Caprini Score

# Venous thromboembolism Risk Stratification for Non-Surgical Patients

## IMPROVE Score
function calcScore(){
var score = 0;
if(document.forms.checked == 1){
score += 3;
if(document.forms.checked == 1){
score += 2;
if(document.forms.checked == 1){
score += 2;
if(document.forms.checked == 1){
score += 2;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
document.forms.value = score;
if(score == 0){document.forms.value = "0.4%";}
if(score == 1){document.forms.value = "0.6%";}
if(score == 2){document.forms.value = "1%";}
if(score == 3){document.forms.value = "1.7%";}
if(score == 4){document.forms.value = "2.9%";}
if(score >= 5){document.forms.value = "7.2%";}

## IMPROVEDD Score
function calcScore(){
var score = 0;
if(document.forms.checked == 1){score += 3;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 2;
document.forms.value = score;
if(score == 0){document.forms.value = "0.4% at 3542 days; 0.5% at 77 days";}
if(score == 1){document.forms.value = "0.6% at 3542 days; 0.7% at 77 days";}
if(score == 2){document.forms.value = "0.8% at 3542 days; 1.0% at 77 days";}
if(score == 3){document.forms.value = "1.2% at 3542 days; 1.4% at 77 days";}
if(score == 4){document.forms.value = "1.6% at 3542 days; 1.9% at 77 days";}
if(score >= 5 && score <= 10){document.forms.value = "2.2% at 3542 days; 2.7% at 77 days";}

## Padua Score
function calcScore(){
var score = 0;
if(document.forms.checked == 1){
score += 3;
if(document.forms.checked == 1){
score += 3;
if(document.forms.checked == 1){
score += 3;
if(document.forms.checked == 1){
score += 3;
if(document.forms.checked == 1){
score += 2;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
if(document.forms.checked == 1){
score += 1;
document.forms.value = score;
if(score >= 4){document.forms.value = "High risk for VTE";}
if(score < 4){document.forms.value = "Low risk for VTE";}
Valproate sodium indications and usage

# Indications and Usage

### Epilepsy
Depacon is indicated as an intravenous alternative in patients for whom oral administration of valproate products is temporarily not feasible in the following conditions:
- Depacon is indicated as monotherapy and adjunctive therapy in the treatment of patients with complex partial seizures that occur either in isolation or in association with other types of seizures. Depacon is also indicated for use as sole and adjunctive therapy in the treatment of patients with simple and complex absence seizures, and adjunctively in patients with multiple seizure types that include absence seizures.
- Simple absence is defined as very brief clouding of the sensorium or loss of consciousness accompanied by certain generalized epileptic discharges without other detectable clinical signs. Complex absence is the term used when other signs are also present.
See Warnings and Precautions (5.1) for statement regarding fatal hepatic dysfunction.

### Important Limitations
Because of the risk to the fetus of decreased IQ, neural tube defects, and other major congenital malformations, which may occur very early in pregnancy, valproate should not be administered to a woman of childbearing potential unless the drug is essential to the management of her medical condition .
Vasoactive intestinal peptide receptor
There are two known receptors for the vasoactive intestinal peptide (VIP) termed VPAC1 and VPAC2. These receptors bind both VIP and pituitary adenylate cyclase-activating polypeptide (PACAP) to some degree. Both receptors are members of the 7 transmembrane G protein-coupled receptor family.
VPAC1 is distributed widely in the CNS, liver, lung, intestine and T-lymphocytes.
VPAC2 is found in the CNS, pancreas, skeletal muscle, heart, kidney, adipose tissue, testis, and stomach.
Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP) receptors are activated by the endogenous peptides VIP, PACAP-38, PACAP-27, peptide histidine isoleucineamide (PHI), peptide histidine methionineamide (PHM) and peptide histidine valine (PHV). PACAP type II receptors (VPAC1 and VPAC2 receptors) display comparable affinity for PACAP and VIP, whereas PACAP-27 and PACAP-38 are >100 fold more potent than VIP as agonists of most isoforms of the PAC1 receptor.
Vertebrobasilar insufficiency overview

# Overview

# Historical Perspective
The concept of vertebrobasilar insufficiency" was first described in 1961 by Niedermeyer.

# Classification
There isn't classification about the VBI yet, but there are three phenotypes of the basilar artery occlusion depending on the modal of initial symptoms.

# Pathophysiology

# Causes
The causes leading to VBI is primarily the vasulcar ones, like atherosclerosis and cardioembolism, etc.  As the vertebral artery is in the cervical vertebra, the orthopedical lesion also contribute to part of the causes.

# Differentiating Myocarditis from other Diseases

# Epidemiology and Demographics

# Natural History, Complications and Prognosis

# Diagnosis

## History and Symptoms

## Laboratory Findings

# Treatment

## Medical Therapy
Voriconazole dosage and administration

# Dosage and Administration

## Instructions for Use in All Patients
VFEND Tablets or Oral Suspension should be taken at least one hour before or after a meal.
VFEND I.V. for Injection requires reconstitution to 10 mg/mL and subsequent dilution to 5 mg/mL or less prior to administration as an infusion, at a maximum rate of 3 mg/kg per hour over 1 to 2 hours.
Do not administer as an IV bolus injection.

## Use of VFEND I.V. With Other Parenteral Drug Products
Blood products and concentrated electrolytes
VFEND I.V. must not be infused concomitantly with any blood product or short-term infusion of concentrated electrolytes, even if the two infusions are running in separate intravenous lines (or cannulas). Electrolyte disturbances such as hypokalemia, hypomagnesemia and hypocalcemia should be corrected prior to initiation of VFEND therapy .
Intravenous solutions containing (non-concentrated) electrolytes
VFEND I.V. can be infused at the same time as other intravenous solutions containing (non-concentrated) electrolytes, but must be infused through a separate line.

## Total parenteral nutrition (TPN)
VFEND I.V. can be infused at the same time as total parenteral nutrition, but must be infused in a separate line. If infused through a multiple-lumen catheter, TPN needs to be administered using a different port from the one used for VFEND I.V.
Recommended Dosing in Adults
- Invasive aspergillosis and serious fungal infections due to Fusarium spp. and Scedosporium apiospermum
See Table 1. Therapy must be initiated with the specified loading dose regimen of intravenous VFEND on Day 1 followed by the recommended maintenance dose regimen. Intravenous treatment should be continued for at least 7 days. Once the patient has clinically improved and can tolerate medication given by mouth, the oral tablet form or oral suspension form of VFEND may be utilized. The recommended oral maintenance dose of 200 mg achieves a voriconazole exposure similar to 3 mg/kg IV; a 300 mg oral dose achieves an exposure similar to 4 mg/kg IV. Switching between the intravenous and oral formulations is appropriate because of the high bioavailability of the oral formulation in adults.
- Candidemia in non-neutropenic patients and other deep tissue Candida infections
See Table 1. Patients should be treated for at least 14 days following resolution of symptoms or following last positive culture, whichever is longer.
- Esophageal Candidiasis
See Table 1. Patients should be treated for a minimum of 14 days and for at least 7 days following resolution of symptoms.
Zolmitriptan dosage and administration

# Dosage and Administration

### 2.1 Dosing Information
The recommended starting dose of zolmitriptan is 1.25 mg or 2.5 mg. The 1.25 mg dose can be achieved by manually breaking the functionally-scored 2.5 mg zolmitriptan tablet in half. The maximum recommended single dose of zolmitriptan is 5 mg.
In controlled clinical trials, a greater proportion of patients had headache response following a 2.5 mg or 5 mg dose than following a 1 mg dose. There was little added benefit from the 5 mg dose compared to the 2.5 mg dose, but adverse reactions were more frequent with the 5 mg dose.
If the migraine has not resolved by 2 hours after taking zolmitriptan, or returns after a transient improvement, a second dose may be administered at least 2 hours after the first dose. The maximum daily dose is 10 mg in any 24-hour period.
The safety of zolmitriptan in the treatment of an average of more than three migraines in a 30-day period has not been established.

### 2.2 Administration of Zolmitriptan Orally Disintegrating Tablets
Instruct patients not to break zolmitriptan orally disintegrating tablets because they are not functionally-scored. Administration with liquid is not necessary.
Orally disintegrating tablets are packaged in a blister pack. Instruct patients not to remove the tablet from the blister until just prior to dosing. Subsequently, instruct patients to peel the blister pack open, and to place the orally disintegrating tablet on the tongue, where it will dissolve and it will be swallowed with the saliva.

### 2.3 Dosing in Patients with Hepatic Impairment
The recommended dose of zolmitriptan in patients with moderate to severe hepatic impairment is 1.25 mg (one-half of one 2.5 mg zolmitriptan tablet) because of increased zolmitriptan blood levels in these patients and elevation of blood pressure in some of these patients. Limit the total daily dose in patients with severe hepatic impairment to no more than 5 mg per day.
The use of zolmitriptan orally disintegrating tablets is not recommended in patients with moderate or severe hepatic impairment because these orally disintegrating tablets should not be broken in half .

### 2.4 Dosing in Patients Taking Cimetidine
If zolmitriptan is co-administered with cimetidine, limit the maximum single dose of zolmitriptan to 2.5 mg, not to exceed 5 mg in any 24-hour period .
4-Hydroxy-5-methoxydimethyltryptamine
4-Hydroxy-5-methoxydimethyltryptamine, or 4-HO-5-MeO-DMT is the 4-hydroxy counterpart of 5-MeO-DMT, or the 5-methoxy counterpart of psilocin.
It is a psychedelic tryptamine but very little is known about it. The only report of it in the chemical literature was a paper published by Marc Julia's group at the Pasteur Institute in 1965.  They only reported the synthesis and physical properties of the compound and it has never been documented or explored in any other way.
Their paper cites a 10 step synthesis of 4-HO-5-MeO-DMT from ortho-vanillin. However, Alexander Shulgin has explained that it could be possible to cultivate 4-HO-5-MeO-DMT in psilocybin mushrooms by adding 5-MeO-DMT to the growing substrate of the fungus. Though this method has never been explored with 5-MeO-DMT, it has been used successfully for changing DET into 4-HO-DET and 4-PO-DET, both of which had never before been found in nature.
In the case of DET the mushrooms yielded only 4-HO-DET or 4-PO-DET respectively, instead of psilocin (4-HO-DMT) and psilocybin (4-PO-DMT), suggesting that the presence of the extraneous N-dialkylated tryptamines competed for the enzymes in the fungus mycelium that would normally produce psilocin. This method thus not only produced new chemical compounds that had never previously been made synthetically, but also rendered the fungus itself completely legal in many countries because of its absence of psilocin or psilocybin, although in countries with stricter drug analogue laws such as the USA or Australia the novel tryptamines produced would also be illegal.
The same process can also be used to make psilocin bearing mushrooms of much higher potency than normal by adding small quantities of DMT to the substrate, to act as feedstock for the production of psilocin. However the amount of DMT added must be carefully controlled, as if too much is added it appears to inhibit the action of the enzyme.
Theoretically, this method would 4-hydroxylate and 4-phosphoryloxylate any tryptamine added to the substrate, opening the possibility of synthesizing as yet undiscovered tryptamines.
ACCP guidelines classification scheme

# Overview
The Grading scheme is used to indicate whether a therapy is recommended or not according to the balance among benefits, risks, burdens, and possibly cost, and the degree of confidence in estimates of benefits, risks, and burdens.

## Grading Scheme Classification
- Grade 1: Strong recommendation
- Grade 2: Weak recommendation

## Level of Evidence
The level of evidence is classified according to the factors that include the study design, the consistency of the results, and the directness of the evidence.
- Grade A: High
- Grade B: Moderate
- Grade C: Low

# Resources
Grading Strength of Recommendations and Quality of Evidence in Clinical Guidelines
Abacavir lamivudine drug interactions

# Drug Interactions
No drug interaction trials have been conducted using EPZICOM Tablets .

## Ethanol
Abacavir: Abacavir has no effect on the pharmacokinetic properties of ethanol. Ethanol decreases the elimination of abacavir causing an increase in overall exposure .

## Interferon- and Ribavirin-Based Regimens
Lamivudine: Although no evidence of a pharmacokinetic or pharmacodynamic interaction (e.g., loss of HIV-1/HCV virologic suppression) was seen when ribavirin was coadministered with lamivudine in HIV-1/HCV co-infected subjects, hepatic decompensation (some fatal) has occurred in HIV-1/HCV co-infected subjects receiving combination antiretroviral therapy for HIV-1 and interferon alfa with or without ribavirin .

## Methadone
Abacavir: The addition of methadone has no clinically significant effect on the pharmacokinetic properties of abacavir. In a trial of 11 HIV-1-infected subjects receiving methadone-maintenance therapy with 600 mg of ZIAGEN twice daily (twice the currently recommended dose), oral methadone clearance increased . This alteration will not result in a methadone dose modification in the majority of patients; however, an increased methadone dose may be required in a small number of patients.

## Trimethoprim/Sulfamethoxazole (TMP/SMX)
Lamivudine: No change in dose of either drug is recommended . There is no information regarding the effect on lamivudine pharmacokinetics of higher doses of TMP/SMX such as those used to treat PCP.
Aggregatibacter actinomycetemcomitans

# Overview
Aggregatibacter actinomycetemcomitans is an oral commensal found also in severe infections in the oral cavity, mainly the periodontium. A. actinomycetemcomitans, previously Actinobacillus actinomycetemcomitans, is a gram negative facultative non motile rod.  It is also associated with non oral infections.

## Nomenclature
Recent studies have shown a phylogenetic similarity of Actinobacillus actinomycetemcomitans and  Haemophilus aphrophilus, Haemophilus paraphrophilus, and Haemophilus segnis suggesting the  new genus Aggregatibacter for them. Now or before, the bacterium still holds the longest binomial nomenclature name of a living thing.

## Importance
It is one of the bacteria which might be implicated in destructive periodontal disease. Although it has been found more frequently in localized aggressive periodontitis,, prevalence in any population is rather high. 
It has also been isolated from actinomycotic lesions (mixed infection with certain Actinomyces species, in particular Actinomyces israelii). 
It possesses certain virulence factors that enable it to invade tissues, such as leukotoxin.

## Virulence Factors
- Leukotoxin; kills PMN's and monocytes.
- Immunosuppression factors that inhibit blastogenesis, antibody production and activate T-suppressor cells
- Inhibition of PMN's functions
- Resistant to complement mediated killing.

## A. actinomycetemcomitans Serotypes
- a strain, for example ATCC 29523, frequently in oral cavity, variable leukotoxin expression.
- b strain Y4, most frequently in localized aggressive periodontitis, leukotoxin expression.
- c strain ATCC 33384, low leukotoxin.
- serotypes d, e
X-linked adrenal hypoplasia congenita

# Overview
X-linked adrenal hypoplasia congenita is a genetic disorder that mainly affects males. It involves many endocrine tissues in the body, especially the adrenal glands.

# Presentation
One of the main characteristics of this disorder is adrenal insufficiency, a reduction in adrenal gland function that results from incomplete development of the gland's outer layer (the adrenal cortex). Adrenal insufficiency typically begins in infancy or in childhood and can cause vomiting, difficulty with feeding, dehydration, extremely low blood sugar (hypoglycemia), and shock.
Affected males may also lack male sex hormones, which leads to underdeveloped reproductive tissues, undescended testicles (cryptorchidism), delayed puberty, and an inability to father children (infertility). These characteristics are known as hypogonadotropic hypogonadism. Females are rarely affected by this disorder, but a few cases have been reported of adrenal insufficiency or a lack of female sex hormones, resulting in underdeveloped reproductive tissues, delayed puberty, and an absence of menstruation.

# Genetics
Mutations in the NR0B1 gene located on the X chromosome (Xp21.3-p21.2) cause X-linked adrenal hypoplasia congenita. The NR0B1 gene provides instructions to make a transcription factor protein called DAX1 that helps control the activity of certain genes. When the NR0B1 gene is deleted or mutated, the activity of certain genes is not properly controlled. This leads to problems with the development of the adrenal glands, two structures in the brain (the hypothalamus and pituitary gland), and reproductive tissues (the ovaries or testes). These tissues are important for the production of many hormones that control various functions in the body. When these hormones are not present in the correct amounts, the signs and symptoms of adrenal insufficiency and hypogonadotropic hypogonadism can result. This condition is inherited in an X-linked recessive pattern.
Agranulocytosis (patient information)
For the WikiDoc page for this topic, click here

# Overview
Agranulocytosis means a failure of the bone marrow to make enough white blood cells (neutrophils). Bone marrow is the soft tissue inside bones that helps form blood cells.

# What are the symptoms of Agranulocytosis?
Persons with this condition are more likely to have fevers and infections.

# What causes Agranulocytosis?
Agranulocytosis may be caused by:
- Autoimmune disorders
- Bone marrow diseases such as myelodysplasia or large granular lymphocyte leukemia
- Chemotherapy and bone marrow transplantation
- Medications such as rituximab, penicillin, captopril, ranitidine, cimetidine, methimazole, and propylthiouracil
- Preparation for bone marrow transplant
Agranulocytosis results in a person not having enough of a specific type of white blood cells, called neutrophils or granulocytes. A low neutrophil count (neutropenia) may also occur when white blood cells are destroyed faster than they can be produced.

# Who is at highest risk?

# Diagnosis

# When to seek urgent medical care?

# Treatment options

# Where to find medical care for Agranulocytosis?

# Prevention of Agranulocytosis

# What to expect (Outlook/Prognosis)?

# Possible complications

# Sources
Allergic reactions during anaesthesia
The incidence of life-threatening hypersensitivity reactions occurring during anaesthesia is around one in 10,000 procedures. Muscle relaxants are involved in over two thirds of the cases. Antibiotic administration is a frequent cause.
The mortality rate from these reactions is about 3-6%.
Successful immediate treatment requires prompt recognition by the attending anaesthetist. Adrenaline (epinephrine) remains the mainstay of treatment, with corticosteroids and antihistamines providing limited benefit in the acute situation.
Subsequent investigation aims to determine the responsible agent to allow its future avoidance. Skin testing is often useful to identify potentially cross-reactive compounds and appropriate therapeutic alternatives. This is done weeks after the initial reaction to allow the immune system to reset itself. However, skin testing can be misleading in giving false positive and false negative results.
Almotriptan dosage and administration

# Dosage and Administration
- Adults and adolescents age 12 to 17 years: 6.25 mg or 12.5 mg single dose; may repeat after 2 hours if headache returns; benefit of second dose in patients who have failed to respond to first dose has not been established; maximum daily dose 25 mg
- Patients with hepatic or severe renal impairment: 6.25 mg starting dose; maximum daily dose 12.5 mg

## Acute Treatment of Migraine Attacks
The recommended dose of Almotriptan (almotriptan malate) in adults and adolescents age 12 to 17 years is 6.25 mg to 12.5 mg, with the 12.5 mg dose tending to be a more effective dose in adults. As individuals may vary in their response to different doses of Almotriptan, the choice of dose should be made on an individual basis.
If the headache is relieved after the initial Almotriptan dose but returns, the dose may be repeated after 2 hours. The effectiveness of a second dose has not been established in placebo-controlled trials. The maximum daily dose should not exceed 25 mg. The safety of treating an average of more than four migraines in a 30-day period has not been established.

## Hepatic Impairment
The recommended starting dose of Almotriptan in patients with hepatic impairment is 6.25 mg. The maximum daily dose should not exceed 12.5 mg over a 24-hour period [seeWarnings and Precautions (5.8) and Clinical Pharmacology

## Renal Impairment
The recommended starting dose of Almotriptan in patients with severe renal impairment is 6.25 mg. The maximum daily dose should not exceed 12.5 mg over a 24-hour period [seeWarnings and Precautions (5.8) and Clinical Pharmacology (
Aminosalicylic acid adverse reactions

# Adverse Reactions
The most common side effect is gastrointestinal intolerance manifested by nausea, vomiting, diarrhea, and abdominal pain.
Hypersensitivity reactions: Fever, skin eruptions of various types, including exfoliative dermatitis, infectious mononucleosis-like, or lymphoma-like syndrome, leucopenia, agranulocytosis, thrombocytopenia, Coombs' positive hemolytic anemia, jaundice, hepatitis, pericarditis, hypoglycemia, optic neuritis, encephalopathy, Loeffler syndrome, vasculitis and a reduction in prothrombin.
Crystalluria may be prevented by the maintenance of urine at a neutral or an alkaline pH.