Persius/hicric huggingface dataset:
Imerslund-Grasbeck syndrome
Assistant Editor-in-Chief: Robert Shafton

# Overview
Imerslund-Grasbeck syndrome or Imerslund-Najman-Grasbeck syndrome or Imerslund-Grasbeck disease (IGS or INGS) is an autosomal recessive, familial form of vitamin B12 deficiency caused by malfunction of the receptor located in the terminal ileum.

# Signs and symptoms
Defined as those seen in any macrocytic, megaloblastic anemia:
- Anemia
- Glossitis
- Cheilosis
- Tabes dorsalis
- Peripheral neuropathy
- Pancytopenia
- Methylmalonyl CoA-emia
- Hypersegmented neutrophils and large RBCs
- Increased MCV (Mean Corpuscular Volume), decreased Hgb/Hct (indicating anemia), and decreased value of vitamin B12
- Proteinuria
- Reversal of all symptoms except neurological symptoms, by IV injection of vitamin B12.

# Genetics
Autosomal recessive pattern of inheritance. The suspected chromosome is 14.

# Treatment
Injection of IV vitamin B12. Early administration is helpful in reversal of few symptoms.
Gynecologic ultrasonography

# Background
Gynecologic ultrasonography or Gynecologic  sonography refers to the application of medical sonography to the female pelvic organs, specifically the uterus, the ovaries, the Fallopian tubes, as well as the bladder,the adnexa, the Pouch of Douglas, and any findings in the pelvis of relevance outside of pregnancy.
The examination can be performed transabdominally, generally  with a full bladder which acts as an acoustic window to achieve better visualization of pelvis organs, or transvaginally with a specifically designed vaginal transducer. Transvaginal imaging utilizes a higher frequency imaging, which gives better resolution of the ovaries, uterus and endometrium (the fallopian tubes are generally not seen unless distended), but is limited to depth of image penetration. whereas larger lesions reaching into the abdomen are better seen transabdominally.  Having a full bladder for the transabdominal portion of the exam is helpful because sound travels through fluid with less attenuation to better visualize the uterus and ovaries which lies posteriorly to the bladder.  The procedure is regarded as not painful, noninvasive, and relatively safe as no radiation is used. Scans are performed by health care professionals call sonographers, or gynecologists trained in ultrasound.
Gynecologic sonography is used extensively:
- to assess pelvic organs,
- to diagnose and manage gynecologic problems including endometriosis,leiomyoma, adenomyosis, ovarian cysts and lesions,
- to identify adnexal masses, including ectopic pregnancy,
- to diagnose gynecologic cancer
- in infertility treatments to track the response of ovarian follicles to fertility medication (i.e. Pergonal).
Through transvaginal sonography ovarian cysts can be aspirated. This technique is used to obtain human eggs (oocytes)  through sonographic directed transvaginal puncture of ovarian follicles in IVF.
Sonohysterography is a specialiced procedure by which fluid, usually sterile saline, is installed into the uterine cavity, and gynecologic  sonography performed at the same time. The procedure delineates intrauterine pathology such as polyps, Asherman's syndrome, or submucous leiomyoma.
Hemorrhagic gastroenteritis
Synonyms and keywords: HGE

# Overview
Hemorrhagic gastroenteritis (HGE) is a disease of dogs characterized by sudden vomiting and bloody diarrhea.  The symptoms are usually severe, and HGE can be fatal if not treated.  HGE is most common in young adult dogs of any breed, but especially small dogs such as the Toy Poodle and Miniature Schnauzer.  It is not contagious.

# Cause
The cause is uncertain.  Suspected causes include abnormal responses to bacteria or bacterial endotoxin, or a hypersensitivity to food.  Pathologically there is an increase in the permeability of the intestinal lining and a leakage of blood and proteins into the bowel.  Clostridium perfringens has been found in large numbers in the intestines of many affected dogs.

# Signs and symptoms
Profuse vomiting is usually the first symptom, followed by depression and bloody diarrhea with a foul odor.  Severe hypovolemia (low blood volume) is one of the hallmarks of the disease, and severe hemoconcentration (a very high hematocrit) is considered necessary for diagnosis.  The progression of HGE is so rapid that hypovolemic shock and death can occur within 24 hours.  Disseminated intravascular coagulation (DIC) is a possible sequela of HGE.

# Diagnosis
Symptoms of HGE and canine parvovirus (CPV) are similar enough that they need to be differentiated.  HGE is different from CPV in that there is no fever or low white blood cell count, and that there is a high hematocrit.  A negative fecal parvovirus test is sometimes necessary to completely rule out CPV.  Other potential causes of vomiting and diarrhea include gastrointestinal parasites, bacterial infections including E. coli, Campylobacter, or Salmonella, protozoal infections such as coccidiosis or giardiasis, and gastrointestinal cancer.

# Treatment
The most important aspect of treatment of HGE is intravenous fluid therapy to replace lost fluid volume.  The vomiting and diarrhea are treated symptomatically and will usually resolve after one to two days.  Antibiotics targeting C. perfringens are also used.  With prompt, aggressive treatment, the prognosis is good.  There is less than 10 percent mortality with treatment, but 10 to 15 percent of cases will recur.
HIV resident survival guide
Synonyms and keywords:

# Overview
Human Immunodeficiency Virus, the agent causing Acquired Immunodeficiency Syndrome, is one of the leading infectious burdens globally and the fifth leading cause of disability in people of all ages. Belonging to the family of Retroviridae, it particularly infects the immune system cells such as CD4+ T cells, dendritic cells and macrophages. It has 2 serotypes with HIV-1 being most virulent and pathogenic. It is transmitted via sexual fluids(vaginal and semen), blood by percutaneous inoculation, Placenta(vertical transmission from mother to fetus) and breast  milk. Due to competency of Antiretroviral therapy, it is now considered as a chronic illness seen most commonly in mono-sexual men. Initially, the symptoms are nonspecific until it develops into the last stage AIDS where the patient present with opportunistic infections due to suppressed immunity. It is diagnosed by PCR, ELISA, western blot and Rapid antigen testing. ART and vaccines have shown promising results in treatment and prevention respectively. As prevention is the foundation, CDC recommends screening mono-sexual men, pregnant women, drug abusers ad sexually active heterosexuals. Despite better treatment, it remains a serious disease that requires more effort by health care providers in terms of surveillance and education.

# Classification
WHO and CDC classify the HIV infected individuals on the basis of CD count:
- STAGE A- Asymptomatic (CD count > 500/l)
- STAGE B- Mild symptoms to symptoms of AIDS-related complex (CD count between 400/l and 200/l)
- STAGE C- AIDS defining illness (CD count <200/l)

## DISEASE PRESENTATION IN WEEKS

## DISEASE PRESENTATION IN MONTHS AND YEARS
Patients develop opportunistic infections and neoplasms when CD count becomes <200/l.

# Diagnosis
Patient with high suspicion of having HIV in a highly prevalent region should have following diagnostic approach.
Abbreviations: RDTs: Rapid diagnostic tests; EIAs: enzyme immunoassays; CLIAs: chemiluminescence immunoanalysers;ELAs: electrochemiluminescence immunoanalysers;HIV: Human immunodeficiency virus

# Treatment
The most effective treatment regimen is HAART that includes combination of 2 NRTIs and 1 drug from different class.
Abbreviations: HIV: Human immunodeficiency virus; NRTIs: nucleoside reverse transcriptase inhibitor; NNRTIs: non nucleoside reverse transcriptase inhibitor;TDF: tenofovir disoproxil fumarate;TAF: tenofovir alafenamide;CCR5: C-C motif chemokine receptor 5

# Do's
- HLAB*5701 testings should be performed before starting Abacavir.
- Monitor CBC with differentials when prescribing zidovudine.
- Monitor GFR when starting TAF or TDF.

# Don'ts
- Do not give Tenofovir in renal impairment or bone disease.
- Do not give nevirapine in hepatic impairment.
Hantzsch Pyridine synthesis
The Hantzsch pyridine synthesis or Hantzsch dihydropyridine synthesis is a multi-component organic reaction between an aldehyde such as formaldehyde, 2 equivalents of a -keto ester such as ethyl acetoacetate and a nitrogen donor such as ammonium acetate or ammonia. The initial reaction product is a dihydropyridine which can be oxidized in a subsequent step to a pyridine. The driving force for this second reaction step is aromatization.
A 1,4-dihydropyridine dicarboxylate is also called a 1,4-DHP compound or a Hantzsch compound. These compounds are an important class of calcium channel blockers and as such commercialized in for instance nifedipine, amlodipine or nimodipine.
The reaction has been demonstrated to proceed in water as reaction solvent and with direct aromatization by ferric chloride or potassium permanganate in a one-pot synthesis.
The Hantzsch dihydropyridine synthesis is found to benefit from microwave chemistry.

# Knoevenagel-Fries modification
The Knoevenagel-Fries modification allows for the synthesis of unsymmetrical pyridine compounds .
Hepatocyte nuclear factor 4
HNF4 (Hepatocyte Nuclear Factor 4) is a nuclear receptor protein mostly expressed in the liver, gut, kidney, and pancreatic beta cells that is critical for liver development.  In humans, there are two isoforms of HNF4, HNF4 and HNF4, encoded by two separate genes HNF4A and HNF4G respectively.

# Ligands
HNF4 was originally classified as an orphan receptor that exhibits constitutive transactivation activity apparently by being continuously bound to a variety of fatty acids. The existence of a ligand for HNF4 has been somewhat controversial, but linoleic acid (LA) has been identified as the endogenous ligand of native HNF4 expressed in mouse liver; the binding of LA to HNF4 is reversible.
The ligand binding domain of HNF4, as with other nuclear receptors, adopts a canonical alpha helical sandwich fold and interacts with co-activator proteins.
HNF4 binds to the consensus sequence AGGTCAaAGGTCA in order to activate transcription.

# Pathology
Mutations in the HNF4A gene have been linked to maturity onset diabetes of the young 1 (MODY1).
This seems to be caused by HNF4-a's  role in the synthesis of SHBG, which is known to be severely diminished in patients with insulin-resistance.
Hosaka-Cohen Transformation
Hosaka-Cohen Transformation is a mathematical method of converting a particular two-dimensional scalar magnetic field map to a particular two-dimensional vector map. The scalar field map is of the component of magnetic field which is normal to a two-dimensional surface of a volume conductor; this volume conductor contains the currents producing the magnetic field. The resulting vector map, sometimes called an arrowmap roughly mimics those currents under the surface which are parallel to the surface, which produced the field. Therefore, the purpose in performing the transformation is to allow a rough visualization of the underlying, parallel currents.
The transformation was proposed by Cohen and Hosaka of the Biomagnetism group at MIT, then used by Hosaka and Cohen to visualize the current sources of the magnetocardiogram.
Each arrow is defined as
where z of the local x, y, z coordinate system is normal to the volume conductor surface, x-circumflex and y-circumflex are unit vectors, and Bz is the normal component of magnetic field. This is a form of  2-dimensional gradient of the scalar quantity Bz and is rotated by 90 degrees from the conventional gradient.
Almost any scalar field, magnetic or otherwise, can be displayed in this way, if desired, as an aid to the eye, to help see the underlying sources of the field.

# Notes
-  Cohen, D., Hosaka, H. (1976) Part II:  Magnetic field produced by a current dipole. Journal of Electrocardiology ; 9: 409-417.
-  Hosaka, H., Cohen, D. (1976) Part IV:  Visual determination of generators of the magnetocardiogram. Journal of Electrocardiology ; 9: 426-432.

# Further reading
- Koch, H. (2004) Recent advances in magnetocardiography. Journal of Electrocardiology 37: 117-122.
Hyperlipoproteinemia causes

# Overview
The causes of hyperlipoproteinemia are either familial, acquired or idiopathic.  Familial (primary) causes are mainly due to genetic abnormalities and a few examples include familial hypercholesterolemia, familial combined hyperlipidemia and familial hypertriglyceridemia.  Acquired (secondary) hyperlipoproteinemia often mimic primary forms of hyperlipoproteinemia and common causes include the use of drugs (diuretics, beta blockers and estrogens); endocrine disorders (diabetes mellitus, hypothyroidism); metabolic disorders and renal causes such as renal failure.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Acute renal failure

## Common Causes

## Causes Based on Major Lipoprotein Detected in Blood Laboratory Test

### High Chylomicron Causes

### High Chylomicron Remnant Causes

### High HDL Causes

### High IDL Causes
- Apolipoprotein E deficiency
- Chronic renal failure 
- Decreased hepatic triglyceride lipase
- Diabetes mellitus type 2 
- Diabetic nephropathy
- Familial alphalipoprotein deficiency
- Glycogen storage disease type 1a
- Hyperparathyroidism 
- Hypocalcemia 
- Reaven X syndrome

### High LDL Causes

### High VLDL Causes

### High Total Cholesterol Causes

### High Triglyceride Causes

## Combined List of Causes in Alphabetical Order
Hyperpolarization (biology)
Hyperpolarization is any change in a cell's membrane potential that makes it more polarized. That is, hyperpolarization is an increase in the absolute value of a cell's membrane potential. Thus, any change of membrane voltage in which the membrane potential moves farther from zero, in either a positive or negative direction, is a hyperpolarization.

# Examples
1. During the undershoot period after an action potential, the membrane potential is more negative than when the cell is in the "resting state". In the figure to the right, this undershoot is from approximately 3 to 4 milliseconds (ms) on the graph. The undershoot is the time when the membrane potential is hyperpolarized relative to the resting potential.
2. During the rising phase of an action potential, the membrane potential changes from negative to positive. In the figure, the rising phase is from approximately 1 to 2 milliseconds on the graph. During the rising phase, once the membrane potential becomes positive, the membrane potential continues to hyperpolarize until the peak of the action potential is reached at about +40 millivolts.
In both examples 1 and 2 (above), the hyperpolarization of a biological cell means an increase in the trans-membrane voltage; the membrane charge is more polarized.  Thus, hyperpolarizations can be changes in membrane potential that are either in the positive or the negative direction.
In the scientific vernacular however, "hyperpolarization" (and its opposite, "depolarization") are sometimes used in a different way than described above.  See the article depolarization for its technical definition and how it is used in descriptions of membrane potential changes. See the next section (below) for hyperpolarization.

# Vernacular usage
For the description of action potentials, "hyperpolarization" has taken on an informal, technically incorrect meaning. In this scientific vernacular, hyperpolarization is often used to describe a change in membrane potential that makes it more negative (less positive). However, during the falling phase of the action potential (approximately from 2 to 3 milliseconds in the figure) the membrane potential first becomes less positive after the peak of the action potential and approaches zero. Membrane potential changes from +40 to 0 are technically depolarization of the membrane, not hyperpolarization. Despite it being technically incorrect, text books sometimes use "hyperpolarization" to describe membrane potential changes in the direction from positive to negative such as the entire falling phase of the action potential.
Hyperprolactinemia overview
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# Overview
Hyperprolactinaemia (BrE) or hyperprolactinemia (AmE) is the presence of abnormally high levels of prolactin in the blood. Normal levels are less than 580 mIU/L for women, and less than 450 mIU/L for men.
The hormone prolactin is downregulated by dopamine and is upregulated by estrogen.  A falsely high measurement may occur due to the presence of the biologically inactive macroprolactin in the serum. This can show up as high prolactin in some types of tests, but is asymptomatic.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Hyperprolactinermia from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Interferon- release assays
Synonyms and keywords: Interferon gamma release assay, IGRA, IGRAs

# Overview
Interferon- release assays are medical tests used in the diagnosis of some infectious diseases, especially tuberculosis.  Interferon- release assays rely on the fact that T-lymphocytes will release interferon- when exposed to specific antigens.  These tests are mostly developed for the field of tuberculosis diagnosis, but in theory, may be used in the diagnosis of other diseases which rely on cell-mediated immunity, e.g. cytomegalovirus and leishmaniasis.  For example, in patients with cutaneous adverse drug reactions, challenge of peripheral blood lymphocytes with the drug causing the reaction produced a positive test result for half of the drugs tested.
There are currently two interferon- release assays available for the diagnosis of tuberculosis:
- QuantiFERON-TB Gold (licensed in US, Europe and Japan); and
- T-SPOT.TB, a form of ELISPOT (licensed in Europe).
The former test quantitates the amount of gamma interferon produced in response to the ESAT-6 and CFP-10 antigens from Mycobacterium tuberculosis, which are distinguishable from those present in BCG and most other non-tuberculous mycobacteria.  The latter test determines the total number of individual effector T cells expressing gamma interferon.
The indications for the test are still disputed.  It has been evaluated for the diagnosis of latent tuberculosis in HIV patients (who frequently have a negative Mantoux test).
IMPROVE bleeding risk score

# Overview
The IMPROVE bleeding risk score estimates the risk of bleeding among acutely ill hospitalized patients.

# IMPROVE Bleeding Risk Score
The IMPROVE bleeding risk score estimates the risk of bleeding among acutely ill hospitalized patients.

# IMPROVE Bleeding Risk Score Calculator

# Interpretation
The IMPROVE risk score for bleeding can be interpreted as such:
- Score 7: Increased risk of bleeding
- Score <7: Not increased risk of bleeding
Indinavir adverse reactions

# Adverse Reactions
- Clinical Trials in Adults
Nephrolithiasis/urolithiasis, including flank pain with or without hematuria (including microscopic hematuria), has been reported in approximately 12.4% (301/2429; range across individual trials: 4.7% to 34.4%) of patients receiving CRIXIVAN at the recommended dose in clinical trials with a median follow-up of 47 weeks (range: 1 day to 242 weeks; 2238 patient-years follow-up). The cumulative frequency of nephrolithiasis events increases with duration of exposure to CRIXIVAN; however, the risk over time remains relatively constant. Of the patients treated with CRIXIVAN who developed nephrolithiasis/urolithiasis in clinical trials during the double-blind phase, 2.8% (7/246) were reported to develop hydronephrosis and 4.5% (11/246) underwent stent placement. Following the acute episode, 4.9% (12/246) of patients discontinued therapy. (See WARNINGS and DOSAGE AND ADMINISTRATION, Nephrolithiasis/Urolithiasis.)
Asymptomatic hyperbilirubinemia (total bilirubin 2.5 mg/dL), reported predominantly as elevated indirect bilirubin, has occurred in approximately 14% of patients treated with CRIXIVAN. In <1% this was associated with elevations in ALT or AST.
Hyperbilirubinemia and nephrolithiasis/urolithiasis occurred more frequently at doses exceeding 2.4 g/day compared to doses 2.4 g/day.
- Post-Marketing Experience
Body As A Whole: redistribution/accumulation of body fat (see PRECAUTIONS, Fat Redistribution).
Cardiovascular System: cardiovascular disorders including myocardial infarction and angina pectoris; cerebrovascular disorder.
Digestive System:  liver function abnormalities; hepatitis including reports of hepatic failure (see WARNINGS); pancreatitis; jaundice; abdominal distention; dyspepsia.
Hematologic: increased spontaneous bleeding in patients with hemophilia (see PRECAUTIONS); acute hemolytic anemia (see WARNINGS).
Endocrine/Metabolic: new onset diabetes mellitus, exacerbation of pre-existing diabetes mellitus, hyperglycemia (see WARNINGS).
Hypersensitivity:  anaphylactoid reactions; urticaria; vasculitis.
Musculoskeletal System:  arthralgia.
Nervous System/Psychiatric: oral paresthesia; depression.
Skin and Skin Appendage:  rash including erythema multiforme and Stevens-Johnson syndrome; hyperpigmentation; alopecia; ingrown toenails and/or paronychia; pruritus.
Urogenital System:  nephrolithiasis/urolithiasis, in some cases resulting in renal insufficiency or acute renal failure, pyelonephritis with or without bacteremia (see WARNINGS); interstitial nephritis sometimes with indinavir crystal deposits; in some patients, the interstitial nephritis did not resolve following discontinuation of CRIXIVAN; renal insufficiency; renal failure; leukocyturia (see PRECAUTIONS), crystalluria; dysuria.
- Laboratory Abnormalities
Increased serum triglycerides; increased serum cholesterol.
Inferior hypogastric plexus
The inferior hypogastric plexus (pelvic plexus in some texts) is a plexus of nerves that supplies the viscera of the pelvic cavity.
The inferior hypogastric plexus is a paired structure, with each situated on the side of the rectum in the male, and at the sides of the rectum and vagina in the female.

# Sources
Contributions to the plexus include:
- a continuation of the hypogastric plexus on either side, in the form of the hypogastric nerve.
- sacral splanchnic nerves, which emerge from the sympathetic trunk.
- pelvic splanchnic nerves (from the second, third, and fourth sacral nerves) also contribute, parasympathetic efferent fibers to the plexus.
At the points of junction of these nerves small ganglia are found.

# Course
From these plexuses numerous branches are distributed to the viscera of the pelvis.
They accompany the branches of the internal iliac artery.
It is the source for the middle rectal plexus, vesical plexus, prostatic plexus, and uterovaginal plexus.

# Additional images