Persius/hicric huggingface dataset:
Comprehensive metabolic panel

# Overview
The comprehensive metabolic panel (CMP; CPT code 80053) is a standard suite of 14 blood tests which serves as an initial broad screening tool for physicians.  Because it is often ordered as a routine part of an annual physical examination or check up, over time the CMP provides an important baseline of a patient's basic physiology.  Any changes or abnormal results, and in particular combinations of abnormal results, thus provides important initial data for differential diagnosis, in which case more specialized tests may be indicated.  In and of itself, however, the CMP provides an important if gross check on the status of kidney function, liver function, and electrolyte and fluid balance.
In addition to being used at routine physicals of healthy patients, the CMP is routinely administered to monitor the status of a patient with a chronic disease, such as diabetes mellitus or hypertension.

# Testing
Typically, the patient fasts for ten or twelve hours before the blood is drawn for the test. The following tests are then performed:

## General tests
These tests help screen for a wide variety of problems. The glucose test in particular helps screen for diabetes mellitus and pre-diabetes.
- Oral glucose tolerance test (OGTT or GTT)
- Calcium

## Protein tests
Tests of protein levels in the blood help screen for both kidney and liver disorders.
- Human serum albumin
- Serum total protein (TP)

## Electrolytes
Electrolyte levels and the balance among them are tightly regulated by the body. Both individual values and ratios among the values are significant; abnormalities among either can indicate problems such as an electrolyte disturbance, acid-base imbalance, or kidney dysfunction.
- Sodium
- Potassium
- Carbon dioxide (CO2)
- Chloride

## Kidney function assessment
- Blood urea nitrogen (BUN)
- Creatinine

## Liver function assessment
- Alkaline phosphatase (ALP)
- Alanine aminotransferase (ALT or SGPT)
- Aspartate aminotransferase (AST or SGOT)
- Bilirubin
Computational learning theory

# Overview
In theoretical computer science, computational learning theory or computational learning problem is a mathematical field related to the analysis of machine learning algorithms. It is traditionally referred to as the grammatical inference problem.
Machine learning algorithms take a training set, form hypotheses or models, and make predictions about the future. Because the training set is finite and the future is uncertain, learning theory usually does not yield absolute guarantees of performance of the algorithms. Instead, probabilistic bounds on the performance of machine learning algorithms are quite common.
In addition to performance bounds, computational learning theorists study the time complexity and feasibility of learning. In computational learning theory, a computation is considered feasible if it can be done in polynomial time. There are two kinds of time complexity results:
- Positive results --- Showing that a certain class of functions is learnable in polynomial time.
- Negative results - Showing that certain classes cannot be learned in polynomial time.
Negative results are proven only by assumption. The assumptions that are common in negative results are:
- Computational complexity - P = NP
- Cryptographic - One-way functions exist.
There are several different approaches to computational learning theory, which are often mathematically incompatible. This incompatibility arises from using different inference principles: principles which tell you how to generalize from limited data. The incompatibility also arises from differing definitions of probability (see frequency probability, Bayesian probability). The different approaches include:
- Probably approximately correct learning (PAC learning), proposed by Leslie Valiant;
- VC theory, proposed by Vladimir Vapnik;
- Bayesian inference, arising from work first done by Thomas Bayes.
- Algorithmic learning theory, from the work of E. M. Gold.
Computational learning theory has led to practical algorithms. For example, PAC theory inspired boosting, VC theory led to support vector machines, and Bayesian inference led to belief networks (by Judea Pearl).
See also:
- information theory
Cortical spreading depression

# Overview
Cortical spreading depression is a wave of electrophysiological hyperactivity followed by a wave of inhibition, usually in the visual cortex.

# Terminology
Neuroscientists use the term cortical spreading depression to represent at least one of the following cortical processes:
- The spreading of a self-propagating wave of cellular depolarization in the cerebral cortex.
- The spreading of a wave of ischemia passing through an area of cortex.
- The spreading of a wave of vasoconstriction following vasodilation and prolonged sustained vasoconstriction of contiguous cortical arterioles.
The scintillating scotoma of migraine in humans may be related to the neurophysiologic phenomenon termed the spreading depression of Leao.
The spreading depression wave progresses across the cortex at approximately 25 mm/minute.
Increased extracellular potassium ion concentration and excitatory glutamate contribute to the initiation and propagation of cortical spreading depression, which is the underlying cause of migraine aura.
Chronic daily administration of migraine prophylactic drugs (topiramate, valproate, propranolol, amitriptyline, and methysergide) dose-dependently suppressed frequency of CSD induced by continuous cortical application of 1 M KCl solution. However lamotrigine (a drug with specific anti-aura action, but no efficacy in migraine in general) has a marked suppressive effect which correlates with its rather selective action on the migraine aura. Valproate and riboflavin were shown to have no effect on the triggering of cortical spreading depression though they are effective in migraine without aura. Taken together, these results are compatible with a causal role of cortical spreading depression in migraine with aura, but not in migraine without aura.

# See Also
- Transient ischemic attack
- Scintillating scotoma
- Migraine

# Notes
-  Dodick DW & Gargus JJ (August 2008). "Why migraines strike". Scientific American.
-  Brennan KC et al. (2007) "Distinct vascular conduction with cortical spreading depression." J Neurophysiol. 2007 Jun;97(6):4143-51. Epub 2007 Feb 28.
-  Leao AAP (1944). "Spreading depression of activity in the cerebral cortex". J Neurophysiol 7, 359-390.
-  Porooshani H, Porooshani GH, Gannon L, & Kyle GM (2004). "Speed of progression of migrainous visual aura measured by sequential field assessment". Neuro-Ophthalmology 28(2), 101-105.
-  Richter and Lehmenkuhler (2008)
-  Ayata et al. (2006) "Suppression of cortical spreading depression in migraine prophylaxis." Ann Neurol. 2006 Apr;59(4):652-61.
-  Bogdanov et al. (2011) "Migraine preventive drugs differentially affect cortical spreading depression in rat." Neurobiol Dis. 2011 Feb;41(2):430-5. doi: 10.1016/j.nbd.2010.10.014. Epub 2010 Oct 23.
Cost Effectiveness of Therapy
To go to the main page, click here.

# Introduction to the  Page
- The page name should be "(Disease name) cost-effectiveness of therapy", with only the first letter of the title capitalized.
- Goal: To provide a brief description of the cost-effectiveness of therapy for the disease you are describing.
- As with all microchapter pages linking to the main page, at the top of the edit box put {{CMG}}, your name template, and the microchapter navigation template you created at the beginning.
- Remember to create links within Wikidoc by placing ] around key words which you want to link to other pages. Make sure you makes your links as specific as possible. For example if a sentence contained the phrase anterior spinal artery syndrome, the link should be to anterior spinal artery syndrome not anterior or artery or syndrome.  For more information on how to create links click here.
- Remember to follow the same format and capitalization of letters  as outlined in the template below.

# Overview
- The overview section should include the disease name in the first sentence.
- The goal is to summarize the remainder of the page in several sentences. This section can be the same as the cost-effectiveness segment on the overview page.
- To see an example of an overview section on a cost effectiveness page, click here.

# Cost-Effectiveness of Therapy
- Describe in detail the cost-effectivenes of each therapy that you have outlined for the disease that you are describing.
- For an example of the prevention segment in the prevention page, click here.

# Template
Given the morbidity and mortality associated with __________, and the low cost of safe and effective treatment with ________________, current pharmacotherapy to treat _______ is relatively cost-effective.

# Example
Given the morbidity and mortality associated with Anthrax infection, and the low cost of safe and effective antibiotics, current pharmacotherapy to treat anthrax is relatively cost-effective.
Countercurrent multiplication
The term countercurrent multiplication refers to the process underlying the process of urine concentration, that is, the production of hyperosmolar urine by the mammalian kidney.
The ability to concentrate urine is also present in birds, but involves another mechanism which is not comparable.

# Physiological principles
The term dervies from the form and function of Henle's loop, which consists of two parallel limbs of renal tubulus running in opposite directions, separated by the interstital space of the renal medulla.
- Water flows from the tubular fluid of the descending limb of Henle's loop into the medullary space.
- The ascending limb is impermeable to water, but here NaCl is actively reabsorbed into the medullary space, effectively diluting the tubular fluid. This constitutes the single effect of the countercurrent multiplication process.
- Reabsorbtion of salt from the ascending loop creates an osmotic force drawing water from the descending limb into the hyperosmolar medullar space, further concentrating tubular fluid.
- The countercurrent flow within the descending and ascending limb thus increases, or multiplies the osmotic gradient between tubular fluid and interstitial space.
Cryotherapy (chamber therapy)
Cryotherapy (Cryogenic chamber therapy) is a treatment whereby the patient is placed in a cryogenic chamber for a short duration, i.e. no more than three minutes, which is comparable to ice swimming, and if used properly, will not destroy tissue. The term "cryotherapy" comes from the Greek cryo () meaning cold and the word therapy () meaning cure.
The chamber is cooled, typically with liquid nitrogen, to a temperature of 110 C. The patient is protected from acute frostbite with socks, gloves and mouth and ear protection, but in addition to that, wears nothing but a bathing suit. The patients spends a few minutes in the chamber. During treatment the average skin temperature drops 12 C, while the coldest skin temperature can be 5 C. The core body temperature remains unchanged during the treatment, while after it, it may drop slightly. Curiously enough, some patients compare the feeling to sauna at +110 C. Release of endorphines occurs, resulting in analgesia (immediate pain relief).
Patients report that the experience is invigorating and improves a variety of conditions. These include symptoms of psychological stress, insomnia, rheumatism, muscle and joint pain, fibromyalgia, itching, and psoriasis. The immediate effect of skin cooling and analgesia lasts for 5 minutes, but the release of endorphines can have a lasting effect, where the pains and signs of inflammation as found in blood tests remain suppressed for weeks. The effects of extreme cold and endorphine release are scientifically studied.
Dapsone clinical pharmacology

# Clinical Pharmacology

## Actions
The mechanism of action in Dermatitis herpetiformis has not been established. By the kinetic method in mice, Dapsone is bactericidal as well as bacteriostatic against Mycobacterium leprae.

## Absorption and Excretion
Dapsone, when given orally, is rapidly and almost completely absorbed. About 85 percent of the daily intake is recoverable from the urine mainly in the form of water-soluble metabolites. Excretion of the drug is slow and a constant blood level can be maintained with the usual dosage.

## Blood Level
Detected a few minutes after ingestion, the drug reaches peak concentration in 4-8 hours. Daily administration for at least eight days is necessary to achieve a plateau level. With doses of 200 mg daily, this level averaged 2.3 g/ml with a range of 0.1-7.0 g/ml. The half-life in the plasma in different individuals varies from ten hours to fifty hours and averages twenty-eight hours. Repeat tests in the same individual are constant. Daily administration (50 - 100 mg) in leprosy patients will provide blood levels in excess of the usual minimum inhibitory concentration even for patients with a short Dapsone half-life.
Gamma-glutamyl transpeptidase
Synonyms or Keywords: GGT; GGTP; gamma-GT; gamma-glutamyl transferase

# Overview
Gamma-glutamyl transferase (GGT or GGTP, or Gamma-GT) (EC 2.3.2.2) is primarily a liver enzyme.

# Function
It is involved in the transfer of amino acids across the cellular membrane. It is also involved in glutathione metabolism by transferring the glutamyl moiety to a variety of acceptor molecules including water, certain L-amino acids and peptides. Leaving the cysteine product to preserve intracellular homeostasis of oxidative stress. 

# Location
GGT is found on the cell surface on all cells, with particularly high concentrations in the liver, bile ducts, and kidney.
The enzyme is also present in other tissues, such as the epididymis.

# Clinical significance
Its level in the blood may be tested for, as an elevated level may indicate an abnormality in the liver, though this can be caused by a number of conditions including:
- congestive heart failure
- cholestasis (congestion of the bile ducts)
- cirrhosis of the liver
- Restricted blood flow to the liver
- restricted venous outflow from liver like Budd-Chiari syndrome
- Necrosis of the liver
- Liver tumors
- hepatitis
- hepatotoxic drugs
Its levels are increased in chronic and acute alcohol abuse.

# Differential Diagnosis
In alphabetical order.  

## Increased
- Alcohol
- Brain tumor
- Ceftazidime
- Cholestasis
- Chronic inflammatory bowel disease
- Cirrhosis
- Congestive heart failure, particularly right sided heart failure, or "shock liver"
- Cytomegalovirus infections
- Diabetes Mellitus
- Disorders of the lipid metabolism
- Fatty liver
- Hepatic necrosis
- Hepatitis
- Hepatocellular carcinoma
- Hepatotoxic drugs
- Hyperthyroidism
- Infectious mononucleosis (Epstein-Barr Virus)
- Inflammation
- Jaundice
- Myocardial Infarction
- Nephritis
- Obesity
- Pancreatic cancer
- Pancreatitis
- Pneumonia
- Porphyria
- Portal vein thrombosis
- Prostate cancer
- Ritonavir
- Restricted blood flow to the liver
- Restricted venous outflow from liver like Budd-Chiari syndrome
- Right ventricular failure causing hepatic congestion, also known as "shock liver"
Vesicular and bullous lesions

# Overview
To avoid missing serious causes, Vesicular and Bullous lesions must be approached systemically.
Primarily, the decision as to whether lesions are focal or diffuse is made, lesion history is taken, system review, and a focused physical exam. Non obvious lesions should be referred to a dermatologist.

# Differential Diagnosis
In alphabetical order.  

## Localized
- Allergic contact Dermatitis
- Bullous impetigo
- Bites from various insects
- Burns
- Diabetics
- may develop bollous on the legs
- Dyshidrotic eczema (pompholyx)
- Friction blisters
- Herpes Zoster
- Herpes Simplex Viruses
- Shingles

## Diffuse
- Blistering diseases
- bullous pemphigoid
- pemphigus vulgaris
- porphyria cutanea tarda
- Polymorphous light eruption
- Stevens-Johnson Syndrome
- Toxic epidermal necrolysis (TEN)
- Varicella

## Other
Skin biopsy if PCT, pemphigus, and pemphigoid is seen

# Laboratory Findings
- Obtain HSV-2 culture if suspect.
- IgM & IgG antibodies will also contain HSV-2

# Diagnostic Findings
Image courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- Skin: Tinea Pedis, Vesicular; Vesiculobullous Diseases
- Skin: Dyshidrosis, Vesicular; Vesiculobullous Diseases
- Skin: Scabies, Vesicular; Vesiculobullous Diseases
- Skin: Erythema Multiforme, Vesicular; Vesiculobullous Diseases
- Skin: Erythema Multiforme, Vesicular; Vesiculobullous Diseases
- Skin: Pityriasis Lichenoides, Vesicular; Vesiculobullous Diseases

# Treatment

## Acute Pharmacotherapies
HSV-1, HSV-2, HZV
- acyclovir
- famciclovir
Bullous impetigo
- topical mupirocin
- systemic antibiotics
- erythromycin
- cephalexin
Pemphigus
- Systemic immunosuppressants
- prednisone
- cyclosporin
- azathioprine

## Chronic Pharmacotherapies
SJS/TEN
- discontiue offending drug
- IVIG
- Systemic steroids
Dyshidrotic eczema
- high potency topical steroid
- heavy emollients
Delavirdine adverse reactions

# Adverse Reactions
The safety of RESCRIPTOR Tablets alone and in combination with other therapies has been studied in approximately 6,000 patients receiving RESCRIPTOR. The majority of adverse events were of mild or moderate (i.e., ACTG Grade 1 or 2) intensity. The most frequently reported drug-related adverse event (i.e., events considered by the investigator to be related to the blinded study medication or events with an unknown or missing causal relationship to the blinded medication) among patients receiving RESCRIPTOR was skin rash.
a. Includes events reported regardless of causality.
b. ACTG Toxicity Grading System; includes events reported as rash, maculopapular rash, and urticaria.
Adverse events of moderate to severe intensity reported by at least 5% of evaluable patients in any treatment group in the pivotal trials, which includes patients receiving RESCRIPTOR in combination with zidovudine and/or lamivudine in Study 21 Part II for up to 98 weeks and in combination with zidovudine and either lamivudine, didanosine, or zalcitabine in Study 13C for up to 72 weeks are summarized in Table 9.
a Evaluable patients in Study 21 Part II were those who received at least 1 dose of study medication and returned for at least 1 clinic study visit. Evaluable patients in Study 13C were those who received at least 1 dose of study medication.

## Other Adverse Events in Phase II/III Studies
Other adverse events that occurred in patients receiving RESCRIPTOR (in combination treatment) in all Phase II and III studies, considered possibly related to treatment, and of at least ACTG Grade 2 in intensity are listed below by body system.

### Body as a Whole

### Cardiovascular System

### Digestive System

### Hemic and Lymphatic System

### Metabolic and Nutritional Disorders

### Musculoskeletal System

### Nervous System

### Respiratory System

### Skin and Appendages

### Special Senses

### Urogenital System

## Postmarketing Experience
Adverse event terms reported from postmarketing surveillance that were not reported in the Phase II and III trials are presented below.
Digestive System: Hepatic failure.
Hemic and Lymphatic System: Hemolytic anemia.
Musculoskeletal System: Rhabdomyolysis.
Urogenital System: Acute kidney failure.
Laboratory Abnormalities
Marked laboratory abnormalities observed in at least 2% of patients during Studies 21 Part II and 13C are summarized in Table 10. Marked laboratory abnormalities are defined as any Grade 3 or 4 abnormality found in patients at any time during study.
Delayed onset muscle soreness
Synonyms and keywords: DOMS

# Overview
Delayed Onset Muscle Soreness (DOMS) is the pain or discomfort often felt 24 to 72 hours after exercising and subsides generally within 2 to 3 days. Once thought to be caused by lactic acid buildup, a more recent theory is that it is caused by tiny tears in the muscle fibers caused by eccentric contraction, or unaccustomed training levels. Since lactic acid disperses fairly rapidly, it could not explain pain experienced days after exercise.
Although the precise cause is still unknown, the type of muscle contraction seems to be a key factor in the development of DOMS. Exercises that involve many eccentric contractions, such as downhill running, will result in the most severe DOMS. This has been shown to be the result of more muscle cell damage than is seen with typical concentric contractions, in which a muscle successfully shortens during contraction against a load.
Some research claims that DOMS is not caused by the pain from damaged muscle cells, but from the reinforcement process. The muscle responds to training by reinforcing itself up to and above its previous strength by adding new sarcomeresthe segments in the muscle fibrils. This reinforcement process causes the cells to swell and put pressure on nerves and arteries, causing DOMS.

# Training with DOMS
DOMS typically causes stiffness, swelling, strength loss and pain. Continued exertion of sore muscles can cause further swelling and pain, and lengthen the period of muscular soreness. There is some scientific evidence that further traininga so-called second bouthas no negative effect on the reinforcement process. Training in a state of constant soreness would be uncomfortable, although one may be able to adapt to it. The relationship between muscular soreness, the rest required and hypertrophy is a contentious topic in bodybuilding. Claims that perpetual muscular soreness assures muscle growth are opposed by reports of stagnation through overtraining.
Stretching before and after exercising have been suggested as ways of reducing DOMS, as has warming up before exercise, cooling down after, and gently warming the area, though there is also evidence that the effect of stretching on muscle soreness is negligible.
Diarrheal shellfish poisoning

# Overview
Diarrhetic shellfish poisoning (DSP) is one of the four recognised symptom types of shellfish poisoning, the others being paralytic shellfish poisoning, neurotoxic shellfish poisoning and amnesic shellfish poisoning.
As the name suggests, this syndrome manifests itself as diarrhea, although nausea, vomiting and cramps are all common too.
DSP and its symptoms usually set in within about half an hour of ingesting infected shellfish, and last for about one day. The causative poison is okadaic acid which inhibits intestinal cellular phosphorylation. This causes the cells to become very permeable to water and causes profuse diarrhoea with risk of dehydration. As no life-threatening symptoms generally emerge from this, no fatalities from DSP have ever been recorded.