Persius/hicric huggingface dataset:
Easy bruising resident survival guide
Synonyms and keywords:

# Overview
Easy bruising is the bruising of skin with minor compression or pressure. When small capillaries of the superficial skin rupture from pressure or compression, petechiae occur, sometimes ecchymosis is also seen with insignificant trauma which is a bleed in the deeper layers in the skin. A wide variety of causes lead to easy bruising, some of which are clotting and bleeding disorders, platelet dysfunction, age-related skin changes, and some forms of cancer such as leukemia.

# Causes

## Life threatening causes
- Thrombotic Thrombocytopenic Purpura
- Disseminated intravascular coagulation
- Leukemia
- Severe thrombocytopenia

## Other causes
- Hemophilia A
- Hemophilia B
- Scurvy
- Von Willebrand disease
- Ehlers-Danlos syndrome
- Corticosteroid use
- Anticoagulant therapy
- Idiopathic Thrombocytopenic Purpura
- Henoch-Schonlein Purpura
- Vitamin K deficiency
- Liver disease
- Systemic Lupus Erythematosus
- Glanzmann Thrombasthenia
- Bernard-Soulier syndrome
For a full list of causes of easy bruising, click here.

# Diagnosis
The algorithm below summarises approach to the different causes of easy bruising.

# Diagnostic clues
Shown below is a table summarizing different findings in easy bruising and their interpretation.

# Treatment
The goal of treatment of easy bruising is to identify and treat the underlying disorder. 

# Do's
- Order a peripheral smear for all patients to rule out presence of shistocytes in conditions like TTP/HUS, DIC which need emergency treatment.
- Educate patients about red flag signs signs wherever appropriate such as epistaxis, hematemesis, melena, lethargy, pale and clammy hands and feet, oliguria or anuria.
- Early vaccination in all patients with hemophilia.
- Educate patients with bleeding disorders about wearing a medical identification tag in case of trauma or if emergency surgery is needed.
- Consider Vitamin C and Vitamin K supplementation.
- Appropriate measures to increase factor levels or platelets before any dental procedures or surgeries such as factor infusion, cryoprecipitate, fresh frozen plasma, platelet or blood transfusions.
- Regular follow up with factor levels, platelet count and response to therapy.
- Hepatitis C, Hepatitis B and HIV screening in patients who have received blood transfusions in the past.

# Dont's
- Avoid contact sports.
- Avoid repeated pricks for investigations/ blood sample collection in patients with hemophilia or other bleeding disorders.
- Transfusion is contraindicated in TTP.
- Do not prescribe aspirin or other NSAIDs during phases of active bleeding.
Echo in double-outlet right ventricle

# Double Outlet Right Ventricle
Double Outlet Right Ventricle occurs when both great arteries arise predominantly from the right ventricle (usually defined as both great arteries arising >50% from the right ventricle).

### Echo functions in DORV
- Evaluation of relationship of the great arteries and right ventricle
Possible orientations: normal, side-by-side (aorta to the right of the pulmonary artery)
- Possible orientations: normal, side-by-side (aorta to the right of the pulmonary artery)
- Evaluation of the ventricular septal defect
- Doppler evaluation of pressure gradients and presence of valvular regurgitation
- Associated anomalities, especially pulmonic stenosis but also:
Atrial Septal Defect
Subaortic Stenosis
Patent Ductus Arteriosus
Mitral valvular abnormalities
- Atrial Septal Defect
- Subaortic Stenosis
- Patent Ductus Arteriosus
- Mitral valvular abnormalities
- Evaluation after repair

### Special Echo techniques in DORV
- Optimal views:
Parasternal long axis
Subcostal coronal view
Parasternal short axis
- Parasternal long axis
- Subcostal coronal view
- Parasternal short axis
Erythromycin warnings and precautions

# Warnings
The safe use of Akne-mycin during pregnancy or lactation has not been established.

# Precautions
Akne-mycin is for topical use only and should be kept out of the eyes, nose and mouth.
The use of antibiotic agents may be associated with the overgrowth of antibiotic resistant organisms. If this occurs, administration of the drug should be discontinued and appropriate measures taken.
Ethambutol hydrochloride how supplied

# How Supplied
MYAMBUTOL (Ethambutol Hydrochloride) Tablets USP
100 mg - round, convex, white, film coated tablets engraved with M6 on one side are supplied as follows:
NDC 68850-010-01 - Bottle of 100
400 mg  round, convex, white, scored, film coated tablets engraved with M to the left and 7 to the right of the score on one side are
supplied as follows:
NDC 68850-012-01 - Bottle of 100
NDC 68850-012-02 - 10 Blister-Packs x 10 tablets
Store at controlled room temperature 20 to 25C (68 to 77F).
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
Manufactured by Patheon Inc., Ontario, Canada.
For STI Pharma LLC.
Distributed by X-GEN Pharmaceuticals, Inc., Big Flats, NY 14814.
Myambutol is a registered trademark of STI Pharma LLC.
Revised November 2008
Famciclovir dosage and administration

# Dosage And Administration
FAMVIR may be taken with or without food.

## Dosing Recommendation in Immunocompetent Adult Patients
Herpes labialis (cold sores): The recommended dosage of FAMVIR for the treatment of recurrent herpes labialis is 1500 mg as a single dose. Therapy should be initiated at the first sign or symptom of herpes labialis (e.g., tingling, itching, burning, pain, or lesion).
Genital herpes:
Recurrent episodes: The recommended dosage of FAMVIR for the treatment of recurrent episodes of genital herpes is 1000 mg twice daily for 1 day. Therapy should be initiated at the first sign or symptom of a recurrent episode (e.g., tingling, itching, burning, pain, or lesion).
Suppressive therapy: The recommended dosage of FAMVIR for chronic suppressive therapy of recurrent episodes of genital herpes is 250 mg twice daily.
Herpes zoster (shingles): The recommended dosage of FAMVIR for the treatment of herpes zoster is 500 mg every 8 hours for 7 days. Therapy should be initiated as soon as herpes zoster is diagnosed.

## Dosing Recommendation in HIV-Infected Adult Patients
Recurrent orolabial or genital herpes: The recommended dosage of FAMVIR for the treatment of recurrent orolabial or genital herpes in HIV-infected patients is 500 mg twice daily for 7 days. Therapy should be initiated at the first sign or symptom of a recurrent episode (e.g., tingling, itching, burning, pain, or lesion).

## Dosing Recommendation in Patients with Renal Impairment
Dosage recommendations for adult patients with renal impairment are provided in Table 1 .
Familial partial lipodystrophy type 1
Synonyms and keywords: Familial partial lipodystrophy, Kobberling type; Kobberling type familial partial lipodystrophy.

# Overview
Kobberling type familial partial lipodystrophy is a member of the group of lipodystrophy syndromes characterised by anomalies of adipose tissue distribution and often associated with severe insulin resistance manifested by hyperinsulinemia (insulin levels above 20mUI/l), carbohydrate intolerance or diabetes, hypertriglyceridemia with low levels of high-density lipoproteins (HDL) and arterial hypertension. Acanthosis nigricans, hepatic steatosis and polycystic ovary syndrome are also frequent.

# Pathophysiology

## Genetics
The mode of transmission is autosomal dominant

# Causes
The underlying cause of the disease is unknown.

# Epidemiology and Demographics
Kobberling type familial partial lipodystrophy is rare, with only 16 patients reported between 1975 and 2003.

# Natural History, Complications and Prognosis
The risk of cardiovascular disease is probably increased but the long-term prognosis is unknown, particularly for cases with early diagnosis and treatment.

# Diagnosis
The syndrome is characterised clinically by a loss of subcutaneous adipose tissue in the lower members but accumulation of truncal fat, a normal distribution of facial adipose tissue and, most prominently, arterial hypertension. Diabetes and hypertriglyceridemia, leading to a risk of acute pancreatitis, has been resported in the majority of cases. As the clinical and biological picture is nondistinctive, the syndrome may remain unrecognised, particularly given the absence of genetic confirmation for the disease and the frequency of android obesity in the general population.

# Treatment
In principle, treatment of the insulin resistance should follow the same guidelines as those used for other forms of insulin resistance: physical exercise, insulin-sensitising medication (metformin or glitazones), insulin (or preferably insulin analogues), antihypertensives, follow-up and treatment of the hypertriglyceridemia.
High cholesterol physical examination

# Overview
Elevated cholesterol does not lead to specific symptoms unless it has been longstanding. Some types of hypercholesterolemia lead to specific physical findings: xanthoma (thickening of tendons due to accumulation of cholesterol), xanthelasma palpabrum (yellowish patches around the eyelids) and arcus senilis (white discoloration of the peripheral cornea).

# Physical Examination
Elevated cholesterol does not lead to specific physical examination signs unless it has been longstanding. Some types of hypercholesterolemia lead to specific physical findings:
- Head, eyes, ears, nose throat (HEENT):
Arcus senilis (white discoloration of the peripheral cornea)
xanthelasma palpabrum (yellowish patches around the eyelids).  Shown below is an image depicting xanthelasma.
- Arcus senilis (white discoloration of the peripheral cornea)
- xanthelasma palpabrum (yellowish patches around the eyelids).  Shown below is an image depicting xanthelasma.
- Heart and Lungs: Congestive heart failure and rales due to ischemia or myocardial infarction (heart attack)
- Extremities:
- Xanthoma (thickening of tendons due to accumulation of cholesterol)
- Reduced femoral, posterior tibial, and dorsalis pedis pulses and femoral bruit due to peripheral artery disease (PAD)
- Neurologic exam: Signs of either transient ischemic attacks (TIAs) or cerebrovascular accidents/Strokes
Holocarboxylase synthetase deficiency
Holocarboxylase synthetase deficiency is an inherited disorder in which the body is unable to use the vitamin biotin effectively. This disorder is classified as a multiple carboxylase deficiency, a group of disorders characterized by impaired activity of certain enzymes that depend on biotin.  The signs and symptoms of holocarboxylase synthetase deficiency typically appear within the first few months of life, but the age of onset varies.  Affected infants often have immunodeficiency diseases, difficulty feeding, breathing problems, a skin rash, hair loss (alopecia), and a lack of energy (lethargy). Immediate treatment and lifelong management (using biotin supplements) may prevent many of these complications. If left untreated, the disorder can lead to delayed development, seizures, and coma. These medical problems may be life-threatening in some cases.
This condition is inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered.
Mutations in the HLCS gene cause holocarboxylase synthetase deficiency. The HLCS gene makes an enzyme, holocarboxylase synthetase, that attaches biotin to other molecules. Biotin, a B vitamin, is found in foods such as liver, egg yolks, and milk. It is essential for the normal production and breakdown of proteins, fats, and carbohydrates in the body. Mutations in the HLCS gene reduce the activity of holocarboxylase synthetase, preventing cells from using biotin effectively and disrupting many cellular functions. These defects lead to the serious medical problems associated with holocarboxylase deficiency.
This article incorporates public domain text from The U.S. National Library of Medicine
Hydrops fetalis (patient information)
For the WikiDoc page for this topic, click here

# Overview
Hydrops fetalis is a serious condition in which abnormal amounts of fluid build up in two or more body areas of a fetus or newborn.

# What are the symptoms of Hydrops fetalis?
- Symptoms depend on the severity of the condition.
- Mild forms may cause:
- Liver swelling
- Change in skin color (pallor)
- More severe forms may cause:
- Breathing problems
- Bruising or purplish bruise-like spots on the skin
- Heart failure
- Severe anemia
- Severe jaundice
- Total body swelling

# What causes Hydrops fetalis?
- There are two types of hydrops fetalis: Immune and nonimmune. The exact cause depends on which form a baby has.
- Immune hydrops fetalis is a complication of a severe form of Rh incompatibility. Rh compatibility causes massive red blood cell destruction, which leads to several problems, including total body swelling. Severe swelling can interfere with how the body organs work.
- Nonimmune hydrops fetalis occurs when a disease or medical condition disrupts the body's ability to manage fluid.
- There are three main causes for this type: heart or lung problems, severe anemia (thalassemia), and genetic defects, including Turner syndrome.
- The number of babies who develop immune hydrops fetalis has dramatically decreased since the introduction of the medicine RhoGAM, which is used to treat pregnant mothers at risk for Rh incompatibility.

# Diagnosis
- An ultrasound done during pregnancy may show:
- High amounts of amniotic fluid
- Abnormally large placenta
- Fluid that leads to swelling in the unborn baby's belly area and organs, including the liver, spleen, heart, or lung area
- An amniocentesis and frequent ultrasounds will be done to determine the severity of the condition.

# Treatment options
- Treatment depends on the cause. During pregnancy, treatment may include:
- Medicine to cause early labor and delivery of the baby
- Early cesarean delivery if condition gets worse
- Giving blood to the baby while still in the womb (intrauterine fetal blood transfusion)
- Treatment for a newborn may include:
- Direct transfusion of packed red blood cells (compatible with the infant's blood type) and an exchange transfusion to rid the baby's body of the substances that are destroying the red blood cells
- Using a needle to remove extra fluid from around the lungs and belly area
- Medicines to control heart failure and help the kidneys remove extra fluids
- Methods to help the baby breathe, such as a breathing machine

# Where to find medical care for Hydrops fetalis?
Directions to Hospitals Treating Hydrops fetalis

# What to expect (Outlook/Prognosis)?
- Hydrops fetalis often results in death of the infant shortly before or after delivery.
- The risk is highest among the most premature babies and those who are severely ill at birth.

# Possible complications
Brain damage called kernicterus may occur.

# Prevention
Rh incompatibility, which can lead to this condition, can be prevented if the mother takes a medicine called RhoGAM at certain times during and after pregnancy.

# Source
IDSA guidelines classification scheme

# Strength of Recommendations

## Class A
Good evidence to support a recommendation for or against use.

## Class B
Moderate evidence to support a recommendation for or against use.

## Class C
Poor evidence to support a recommendation.

# Quality of Evidence

## Level of Evidence I
Evidence from 1 properly randomized, controlled trial.

## Level of Evidence II
Evidence from 1 well-designed clinical trial, without randomization; from cohort or case-controlled analytic studies (preferably from >1 center); from multiple time-series; or from dramatic results from uncontrolled experiments.

## Level of Evidence III
Evidence from opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees.

# Applying Strength of Recommendations and Quality of Evidence

# IDSA Updated Guidelines Classification Scheme 2016

# Level of Evidence
Based on the different variables taken into account the level of evidence is rated by IDSA as follows:

## Factors favoring higher level of confidence:
- Randomized trails
- Large Effect
- Dose Response
- All plausible confounding and bias would reduce a demonstrated effect or would suggest a spurious effect if no effect was observed.

## Factors favoring low level level of confidence:
- Observational Studies
- Risk of Bias
- Inconsistency
- Indirectness
- Imprecision
- Publication Bias

## Based on these considerations of the level of confidence the level of evidence is rated as follows:
- Strong
- Moderate
- Low
- Very Low

# Strength of Recommendation

## Determinants of Strength of Recommendation
- Quality of Evidence
- Balance between benefits, harms and burdens
- Patients values and preferences
- Resources and cost

## Implication of Strength of Recommendation

### Strong Recommendation
- Population : Most people in this situation would want the recommended course of action and only a small proportion would not.
- Healthcare workers: Most people should receive the recommended course of action.
- Policy makers: The recommendation can be adopted as a policy in most situations.

### Weak Recommendation
- Population : Majority of the people in this situation would want the recommended course of action, but many would not .
- Healthcare workers: Be prepared to help people to make a decision that is consistent with their values/decision aids and shared decision making.
- Policy makers: There is a need for substantial debate and involvement of stakeholders.

# IDSA 2016 Guidelines
Insulin-like growth factor 2 receptor
Insulin-like growth factor 2 receptor (IGF2R), also called the cation-independent mannose-6-phosphate receptor (CI-MPR) is a protein that in humans is encoded by the IGF2R gene. IGF2R is a multifunctional protein receptor that binds insulin-like growth factor 2 (IGF2) at the cell surface and mannose-6-phosphate (M6P)-tagged proteins in the trans-Golgi network.

# Structure
The structure of the IGF2R is a type I transmembrane protein (that is, it has a single transmembrane domain with its C-terminus on the cytoplasmic side of lipid membranes) with a large extracellular/lumenal domain and a relatively short cytoplasmic tail. The extracellular domain consists of a small region homologous to the collagen-binding domain of fibronectin and of fifteen repeats of approximately 147 amino acid residues. Each of these repeats is homologous to the 157-residue extracytoplasmic domain of the mannose 6-phosphate receptor. Binding to IGF2 is mediated through one of the repeats, while two different repeats are responsible for binding to mannose-6-phosphate. The IGF2R is approximately 300 kDa in size; it appears to exist and function as a dimer.

# Function
IGF2R functions to clear IGF2 from the cell surface to attenuate signalling, and to transport lysosomal acid hydrolase precursors from the Golgi apparatus to the lysosome. After binding IGF2 at the cell surface, IGF2Rs accumulate in forming clathrin-coated vesicles and are internalized. In the lumen of the trans-Golgi network, the IGF2R binds M6P-tagged cargo. The IGF2Rs (bound to their cargo) are recognized by the GGA family of clathrin adaptor proteins and accumulate in forming clathrin-coated vesicles. IGF2Rs from both the cell surface and the Golgi are trafficked to the early endosome where, in the relatively low pH environment of the endosome, the IGF2Rs release their cargo. The IGF2Rs are recycled back to the Golgi by the retromer complex, again by way of interaction with GGAs and vesicles. The cargo proteins are then trafficked to the lysosome via the late endosome independently of the IGF2Rs.

# Interactions
Insulin-like growth factor 2 receptor has been shown to interact with M6PRBP1.

# Evolution
The insulin-like growth factor 2 receptor function evolved from the cation-independent mannose 6-phosphate receptor and is first seen in Monotremes. The IGF-2 binding site was likely acquired fortuitously with the generation of an exonic splice site enhancer cluster in exon 34, presumably necessitated by several kilobases of repeat element insertions in the preceding intron. A six-fold affinity maturation then followed during therian evolution, coincident with the onset of imprinting and consistent with the theory of parental conflict.
Interleukin 10 receptor, beta subunit
Interleukin 10 receptor, beta subunit is a subunit for the interleukin-10 receptor. IL10RB is its human gene.
IL10RB has also recently been designated CDW210B (cluster of differentiation W210B).
The protein encoded by this gene belongs to the cytokine receptor family. It is an accessory chain essential for the active interleukin 10 receptor complex. Coexpression of this and IL10RA proteins has been shown to be required for IL10-induced signal transduction. This gene and three other interferon receptor genes, IFAR2, IFNAR1, and IFNGR2, form a class II cytokine receptor gene cluster located in a small region on chromosome 21.
IMITREX tablet nonclinical toxicology

# Nonclinical Toxicology

### Carcinogenesis, Mutagenesis, Impairment of Fertility
Carcinogenesis: In carcinogenicity studies in mouse and rat, sumatriptan was administered orally for 78 and 104 weeks, respectively, at doses up to 160 mg/kg/day (the high dose in rat was reduced from 360 mg/kg/day during week 21). There was no evidence in either species of an increase in tumors related to sumatriptan administration. Plasma exposures (AUC) at the highest doses tested were 20 and 8 times that in humans at the maximum recommended human dose (MRHD) of 200 mg/day.
Mutagenesis: Sumatriptan was negative in in vitro(bacterial reverse mutation , gene cell mutation in Chinese hamster V79/HGPRT, chromosomal aberration in human lymphocytes) and in vivo (rat micronucleus) assays.
Impairment of Fertility: When sumatriptan (5, 50, 500 mg/kg/day) was administered orally to male and female rats prior to and throughout the mating period, there was a treatment-related decrease in fertility secondary to a decrease in mating in animals treated with doses greater than 5 mg/kg/day (less than the MRHD on a mg/m2 basis). It is not clear whether this finding was due to an effect on males or females or both..

### Animal Toxicology and/or Pharmacology
Corneal Opacities: Dogs receiving oral sumatriptan developed corneal opacities and defects in the corneal epithelium. Corneal opacities were seen at the lowest dose tested, 2 mg/kg/day, and were present after 1 month of treatment. Defects in the corneal epithelium were noted in a 60week study. Earlier examinations for these toxicities were not conducted and noeffect doses were not established. Plasma exposure at the lowest dose tested was approximately 2 times that in humans at the MRHD.