Persius/hicric huggingface dataset:
Haemophilus influenzae infection overview

# Overview
Infection with the bacterium Haemophilus influenzae type b (Hib) can result in meningitis and other severe infections (e.g., pneumonia, bacteremia, cellulitis, septic arthritis, and epiglottitis) primarily among infants and children <5 years of age.

# Pathophysiology
Haemophilus influenzae, formerly called Pfeiffer's bacillus or Bacillus influenzae, is a non-motile Gram-negative coccobacillus first described in 1892 by Richard Pfeiffer during an influenza pandemic. It is generally aerobic, but can grow as a facultative anaerobe. H. influenzae was mistakenly considered to be the cause of the common flu until 1933, when the viral etiology of the flu became apparent. Still, H. influenzae is responsible for a wide range of clinical diseases. Transmission is by direct contact with respiratory droplets from nasopharyngeal carrier or case patient.

# Epidemiology and Demographics
During 1980-1990, incidence was 40-100/100,000 children < 5 years old in the United States. Due to routine use of the Hib conjugate vaccine since 1990, the incidence of invasive Hib disease has decreased to 1.3/100,000 children. However, Hib remains a major cause of lower respiratory tract infections in infants and children in developing countries where vaccine is not widely used.

# Risk Factors
Infants and young children, household contacts, and day care classmates are at higher risk of acquiring Haemophilus influenza serotype B infection.

# Prognosis
3%-6% of cases are fatal; up to 20% of surviving patients have permanent hearing loss or other long-term sequelae.

# Diagnosis

## History and Symptoms
Before the availability of the Haemophilus influenzae serotype b (Hib) conjugate vaccine in the United States and other industrialized countries, more than one-half of Hib cases presented as meningitis with fever, headache, and stiff neck. The remainder presented as cellulitis, arthritis, or sepsis. In developing countries, Hib is still a leading cause of bacterial pneumonia deaths in children.

# Treatment

## Medical Therapy
Specific parenteral antibiotic treatment is necessary for invasive Hib disease, and immediate airway stabilization is necessary for epiglottitis. A 4-day course of rifampin eradicates Hib carriage from the pharynx in approximately 95% of carriers.

## Primary Prevention
Haemophilus Influenzae Type b (Hib) Vaccine

## Future and Investigational Therapies
Evaluating the characteristics of Hib vaccines associated with prevention of carriage and invasive disease will facilitate application of this technology to development of conjugate vaccines for other organisms with polysaccharide capsules (such as the meningococcus, pneumococcus, and group B streptococcus). Further evaluation of herd immunity effects may lead to insight into vaccination strategies that optimize protection against invasive disease and transmission of Hib organisms.
Healthcare Common Procedure Coding System

# Overview
The Healthcare Common Procedure Coding System (HCPCS) is a set of health care procedure codes based on the American Medical Association's Current Procedural Terminology (CPT).   Commonly pronounced Hick-Picks.
The Healthcare Common Procedure Coding System (HCPCS) was established in 1978 to provide a standardized coding system for describing the specific items and services provided in the delivery of health care. Such coding is necessary for Medicare, Medicaid, and other health insurance programs to ensure that insurance claims are processed in an orderly and consistent manner. Initially, use of the codes was voluntary, but with the implementation of the Health Insurance Portability and Accountability Act of 1996 (HIPAA) use of the HCPCS for transactions involving health care information became mandatory.
HCPCS includes two levels of codes:
- Level I consists of the American Medical Association's Current Procedural Terminology (CPT) and is numeric.
- Level II codes are alphanumeric and primarily include non-physician services such as ambulance services and prosthetic devices.
The acronym HCPCS originally stood for HCFA Common Procedure Coding System, as the Centers for Medicare and Medicaid (CMS) was previously (before 2001) known as the Health Care Financing Administration (HCFA).
Heart fatty acid binding protein (h-FABP)
Heart fatty acid binding protein (h-FABP) is also a small cytoplasmic protein with kinetics similar to myoglobin that is somewhat more specific for cardiac tissue over skeletal muscle.(1),(2) It, too, appears to be an independent predictor of outcomes in patients with ACS.(3)
References: 
- ref1 pmid=7306088 This is free space so that you can describe the reference if you want
- ref2 pmid=11179265 This is free space so that you can describe the reference if you want
- ref3 pmid=16880323 This is free space so that you can describe the reference if you want
Hydroxyacid oxidase (glycolate oxidase) 1
Hydroxyacid oxidase (glycolate oxidase) 1 is a protein that in humans is encoded by the HAO1 gene.

# Function
This gene is one of three related genes that have 2-hydroxyacid oxidase activity yet differ in encoded protein amino acid sequence, tissue expression and substrate preference. Subcellular location of the encoded protein is the peroxisome. Specifically, this gene is expressed primarily in liver and pancreas and the encoded protein is most active on glycolate, a two-carbon substrate. Glycolate oxidase oxidizes glycolic acid to glyoxylate, and can also oxidize glyoxylate into oxalate. These reactions are central to the toxicity of ethylene glycol poisoning.
The protein is also active on 2-hydroxy fatty acids. The transcript detected at high levels in pancreas may represent an alternatively spliced form or the use of a multiple near-consensus upstream polyadenylation site.
Hyperlipoproteinemia physical examination

# Overview
Hyperlipidemias, particularly familial hypercholesterolemia and familial defective apoB-100, are commonly associated with the findings of xanthoma, xanthelasma and corneal arcus on physical examination.

# Physical Examination

## Skin
- XanthomaDue to deposition of cholesterol in the skin and the tendons, patients with familial hypercholesterolemia or familial defective apoB-100 may have several types of xanthomas, which include:
Planar xanthomas (on hands, elbows, buttocks, or knees), which are diagnostic for the homozygous familial hypercholesterolemia and are distinct from other cutaneous xanthomas because of their yellow-to-orange coloration.
Tuberous xanthomas (on hands, elbows, or knees)
Tendon xanthomas (on extensor tendons of hands or Achilles tendon), which can be detected by careful palpation rather than simple inspection, which reveals diffusely thickened tendon or discreet irregularities along the tendon.
- Planar xanthomas (on hands, elbows, buttocks, or knees), which are diagnostic for the homozygous familial hypercholesterolemia and are distinct from other cutaneous xanthomas because of their yellow-to-orange coloration.
- Tuberous xanthomas (on hands, elbows, or knees)
- Tendon xanthomas (on extensor tendons of hands or Achilles tendon), which can be detected by careful palpation rather than simple inspection, which reveals diffusely thickened tendon or discreet irregularities along the tendon.
- Patients with homozygous familial hypercholesterolemia may have cutaneous xanthomas at birth or by early childhood and other types of xanthomas are usually obvious in the first decade of life, whereas patients with heterozygous familial hypercholesterolemia may develop xanthomas in the third decade of life and later.

## Eyes
- XanthelasmaXanthelasmas occur due to deposition of cholesterol in the eyelids, which may also be present in older patients with normal cholesterol levels.
- Corneal arcusCorneal arcus occurs due to deposition of cholesterol in the cornea, which may also be occasionally present in older adults with normal cholesterol levels. In children, it is suggestive of familial hypercholesterolemia.
Copyleft image obtained courtesy of Wikipedia; Loren A Zech Jr and Jeffery M Hoeg.
Mean corpuscular hemoglobin concentration

# Overview
The mean corpuscular hemoglobin concentration, or MCHC, is a measure of the concentration of hemoglobin in a given volume of packed red blood cell. It is reported as part of a standard complete blood count.

# Differential diagnosis of MCHC
It is diminished ("hypochromic") in microcytic anemias, and normal ("normochromic") in macrocytic anemias (due to larger cell size, though the haemoglobin amount or MCH is high, the concentration remains normal). MCHC is elevated in hereditary spherocytosis.
This count is used to give a rough guide to what shade of red, RBC will be.  (paler=lower than the standard)
Because of the way automated analysers count blood cells, a very high MCHC (greater than about 370 g/L) may indicate the blood is from someone with a cold agglutinin. This means that when their blood gets colder than 37C it starts to clump together. As a result, the analyzer may incorrectly report a low number of very dense red blood cells for blood samples in which agglutination has occurred.
This problem is usually picked up by the laboratory before the result is reported. The blood is warmed until the cells separate from each other, and quickly put through the machine while still warm.
It is calculated by dividing the hemoglobin by the hematocrit. A normal value is 32 to 36 g/dl.
IMITREX tablet dosage forms and strengths

# Dosage Forms and Strengths
25 mg Tablets:	 White, triangular-shaped, film-coated, and debossed with I on one side and 25 on the other.
50 mg Tablets:	 White, triangular-shaped, film-coated, and debossed with IMITREX 50 on one side and a chevron shape (^) on the other.
100 mg Tablets: Pink, triangular-shaped, film-coated, and debossed with IMITREX 100 on one side and a chevron shape (^) on the other.
Ichthyosis vulgaris (patient information)
For the WikiDoc page for this topic, click here

# Overview
Ichthyosis vulgaris is a common skin disorder passed down through families that leads to dry, scaly skin.

# What are the symptoms of Ichthyosis vulgaris?
- Dry skin, severe
- Scaly skin (scales)
- Possible skin thickening
- Mild itching of the skin
The dry, scaly skin is usually most severe over the legs but may also involve the arms, hands, and middle of the body. Persons with this condition may also have many fine lines over the palm of the hand.

# What causes Ichthyosis vulgaris?
Ichthyosis vulgaris is one of the most common of the inherited skin disorders. It may begin in early childhood, before age 4. The condition is inherited in an autosomal dominant pattern. That means you only need to get the abnormal gene from one parent in order for you to inherit the disease.
The condition is often more noticeable in the winter. It may occur along with atopic dermatitis, keratosis pilaris (small bumps on the back of the arms), or other skin disorders.

# Who is at highest risk?
Ichthyosis vulgaris is a genetic disorder, so anyone with a family history of the disorder is at risk.

# When to seek urgent medical care?
Call for an appointment with your health care provider if:
- Symptoms continue despite treatment
- Symptoms get worse
- Skin lesions spread
- New symptoms develop

# Diagnosis
Your doctor can usually diagnose this condition by looking at your skin. Tests may be needed to rule out other possible causes of dry, scaly skin.
Your doctor will ask you if you have a family history of similar skin dryness.

# Treatment options
Your doctor will recommend heavy duty moisturizers. Creams and ointments work better than lotions. Apply these to moist skin immediately after bathing. You should use mild, non-drying soaps.
Your doctor may tell you to use moisturizing creams that contain chemicals that help skin to shed normally, including lactic acid, salicylic acid, and urea.

# Where to find medical care for Ichthyosis vulgaris?
Directions to Hospitals Treating Ichthyosis vulgaris

# What to expect (Outlook/Prognosis)?
Ichthyosis vulgaris can be a nuisance, but it rarely affects your overall health. The condition usually disappears during adulthood, but may return years later.

# Possible complications
A bacterial skin infection may develop if scratching causes openings in the skin.

# Prevention of Ichthyosis vulgaris
If you have this condition, be aware that your children are at risk for developing it.

# Sources
Imipenem cilastatin clinical pharmacology

# Clinical Pharmacology

## Adults

### Intravenous Administration
Intravenous infusion of PRIMAXIN I.V. over 20 minutes results in peak plasma levels of imipenem antimicrobial activity that range from 14 to 24 g/mL for the 250 mg dose, from 21 to 58 g/mL for the 500 mg dose, and from 41 to 83 g/mL for the 1000 mg dose. At these doses, plasma levels of imipenem antimicrobial activity decline to below 1 g/mL or less in 4 to 6 hours. Peak plasma levels of cilastatin following a 20-minute intravenous infusion of PRIMAXIN I.V. range from 15 to 25 g/mL for the 250 mg dose, from 31 to 49 g/mL for the 500 mg dose, and from 56 to 88 g/mL for the 1000 mg dose.
The plasma half-life of each component is approximately 1 hour. The binding of imipenem to human serum proteins is approximately 20% and that of cilastatin is approximately 40%. Approximately 70% of the administered imipenem is recovered in the urine within 10 hours after which no further urinary excretion is detectable. Urine concentrations of imipenem in excess of 10 g/mL can be maintained for up to 8 hours with PRIMAXIN I.V. at the 500mg dose. Approximately 70% of the cilastatin sodium dose is recovered in the urine within 10 hours of administration of PRIMAXIN I.V.
No accumulation of imipenem/cilastatin in plasma or urine is observed with regimens administered as frequently as every 6 hours in patients with normal renal function.
In healthy elderly volunteers (65 to 75 years of age with normal renal function for their age), the pharmacokinetics of a single dose of imipenem 500 mg and cilastatin 500 mg administered intravenously over 20 minutes are consistent with those expected in subjects with slight renal impairment for which no dosage alteration is considered necessary. The mean plasma half-lives of imipenem and cilastatin are 91  7.0 minutes and 69  15 minutes, respectively. Multiple dosing has no effect on the pharmacokinetics of either imipenem or cilastatin, and no accumulation of imipenem/cilastatin is observed.
Imipenem, when administered alone, is metabolized in the kidneys by dehydropeptidase I resulting in relatively low levels in urine. Cilastatin sodium, an inhibitor of this enzyme, effectively prevents renal metabolism of imipenem so that when imipenem and cilastatin sodium are given concomitantly, fully adequate antibacterial levels of imipenem are achieved in the urine.
After a 1 gram dose of PRIMAXIN I.V., the following average levels of imipenem were measured (usually at 1 hour post dose except where indicated) in the tissues and fluids listed:
Imipenem-cilastatin sodium is hemodialyzable. However, usefulness of this procedure in the overdosage setting is questionable. (See OVERDOSAGE.)
Lopinavir ritonavir indications and usage

# Indications and Usage
KALETRA is indicated in combination with other antiretroviral agents for the treatment of HIV-1 infection in adults and pediatric patients (14 days and older).
The following points should be considered when initiating therapy with KALETRA:
- The use of other active agents with KALETRA is associated with a greater likelihood of treatment response .
- Genotypic or phenotypic testing and/or treatment history should guide the use of KALETRA . The number of baseline lopinavir resistance-associated substitutions affects the virologic response to KALETRA .
MICU intern's survival guide vasopressors

# Overview
Shock is a common condition that interns have to encounter in the MICU. Some important ideas to keep in mind while managing shock are: determine the type of shock as the treatment is different for different shocks, norepinephrine can be used as a first line vasopressor in any shock and fluid resuscitation is an important first line management in all type of shocks except cardiogenic shock.

# Norepinephrine

### Mechanism of action
Acts on both alpha1 (vasoconstriction of blood vessels) and beta1 receptors (increases cardiac output).

### Indications
- Septic shock
- Cardiogenic shock - Recent studies have shown that norepinephrine may be better than dopamine in cardiogenic shock due to a decreased risk of tachyarrhythmias.
- In cases where the type of shock is unclear, norepinephrine can be tried as a first line agent.

### Doses
- 1-30 mcg/min.

# Dopamine

### Mechanism of action
- Acts on alpha1 (vasoconstriction of blood vessels), beta1 (increases cardiac output) and dopamine receptors (scattered throughout the body).
- Its action is dose dependent. At low doses it predominantly acts on cardiac receptors (1-10 mcg/min) with less vasoconstriction activities. At higher doses it has both vasoconstriction and cardiac activities.

### Indications
- Cardiogenic shock
- Septic shock - second line treatment for septic shock

### Side-effects
- Arrhythmogenic. Avoid in patients prone to arrhythmias.
- Doses
- 1-20 mcg/min.

# Vasopressin

### Mechanism of action
- Acts by stimulating V1 (vasopressin) receptors in vascular and GI smooth muscles causing contraction. It also has anti-diuretics effect.

### Indications
- Septic shock - second line treatment for septic shock

### Side-effects
- Coronary and splanchnic vasoconstriction. Avoid in NSTEMI (can use in mild troponin leaks but avoid if Trops high 5-10) and gut ischemia.

### Doses
- .03units/min (only vasopressor which is not titrated).

# Phenylephrine

### Mechanism of action
- Acts only on alpha1 receptors (vasoconstriction). No action on cardiac receptors and is cardiac neutral.

### Indications
- Used in neurogenic shock
- Third or fourth line vasopressor in septic shock (refractory to norepinephrine, dopamine, and vasopressin).

### Side-effects
- Can cause reflex bradycardia but not tachycardia.

### Doses
- 20-300 mcg/min

# Dobutamine

### Mechanism of action
- Acts on Beta1 (increases cardiac output) and Beta2 receptor (vasodilatation). Thus, it increases cardiac output but increases the risks for hypotension too.

### Indications
- Cardiogenic shock
- Low output septic shock.

### Side-effects
- Tachyarrhythmias (B1 effect)
- Hypotension (B2 effect)
- In cases of hypotension with dobutamine add another vasopressor with alpha effects (norepinephrine or dopamine) with dobutamine.

### Doses
- 2.5 to 20mcg/kg/min (usually titrated by doctors and not ICU nurses)
Magnesium Hydroxide (patient information)

# Why this medication is prescribed
Magnesium hydroxide is used on a short-term basis to treat constipation.
This medication is sometimes prescribed for other uses; ask your doctor or pharmacist for more information.

# How this medication should be used
Magnesium hydroxide come as a tablet and liquid to take by mouth. It usually is taken as needed for constipation. Follow the directions on the package or on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take magnesium hydroxide exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.
Shake the liquid well before each use.

# Special precautions
Before taking magnesium hydroxide:
- tell your doctor and pharmacist if you are allergic to magnesium hydroxide or any other drugs.
- tell your doctor and pharmacist what prescription and nonprescription medications you are taking, including vitamins.
- tell your doctor if you have or have ever had kidney disease.
- tell your doctor if you are pregnant, plan to become pregnant, or are breast-feeding. If you become pregnant while taking magnesium hydroxide, call your doctor.

# What to do if you forget a dose
This medication usually is taken as needed. If your doctor has told you to take magnesium hydroxide regularly, take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not take a double dose to make up for a missed one.

# Side effects
Magnesium hydroxide may cause side effects. If you experience any of the following symptoms, call your doctor immediately:
- stomach cramps
- upset stomach
- vomiting
- diarrhea
If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online  or by phone .

# Storage conditions needed for this medication
Keep this medication in the container it came in, tightly closed, and out of reach of children. Store it at room temperature and away from excess heat and moisture (not in the bathroom). Throw away any medication that is outdated or no longer needed. Talk to your pharmacist about the proper disposal of your medication.

# Other information
Ask your pharmacist any questions you have about taking this medicine.

# Brand names
- Milk of Magnesia
- Milk of Magnesia-Concentrated
- Phillips Milk of Magnesia
Mothers against decapentaplegic homolog 2
Mothers against decapentaplegic homolog 2 also known as SMAD family member 2 or SMAD2 is a protein that in humans is encoded by the SMAD2 gene. MAD homolog 2 belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways.

# Function
SMAD2 mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the cell nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants encoding the same protein have been observed.
Like other Smads, Smad2 plays a role in the transmission of extracellular signals from ligands of the Transforming Growth Factor beta (TGF) superfamily of growth factors into the cell nucleus. Binding of a subgroup of TGF superfamily ligands to extracellular receptors triggers phosphorylation of Smad2 at a Serine-Serine-Methionine-Serine (SSMS) motif at its extreme C-terminus. Phosphorylated Smad2 is then able to form a complex with Smad4. These complexes accumulate in the cell nucleus, where they are directly participating in the regulation of gene expression.

# Nomenclature
The SMAD proteins are homologs of both the drosophila protein, mothers against decapentaplegic (MAD) and the C. elegans protein SMA. The name is a combination of the two. During Drosophila research, it was found that a mutation in the gene MAD in the mother repressed the gene decapentaplegic in the embryo. The phrase "Mothers against" was added, since mothers often form organizations opposing various issues, e.g., Mothers Against Drunk Driving, or (MADD).  The nomenclature for this protein is based on a tradition of such unusual naming within the gene research community.

# Interactions
Mothers against decapentaplegic homolog 2 has been shown to interact with:
- ANAPC10,
- DAB2,
- EP300,
- FOXH1,
- HDAC1,
- TGIF1,
- Insulin receptor,
- LEF1,
- Myc,
- MEF2A,
- PIAS3,
- PIN1,
- SKI protein,
- SKIL,
- SMAD3,
- SMURF2,
- SNW1,
- STRAP