Persius/hicric huggingface dataset:
Low back pain overview

# Overview
Low back pain is a common musculoskeletal disorder which affects the lumbar segment of the spine. It can be either acute, subacute or chronic in its clinical presentation. Typically, the symptoms of low back pain do show significant improvement within two to three months from its onset. In a significant number of individuals, low back pain tends to be recurrent in nature with a waxing and waning quality to it. In a small proportion of sufferers this condition can become chronic. Population studies show that back pain affects most adults at some stage in their life and accounts for more sick leave and disability than any other single medical condition.
An acute lower back injury may be caused by a traumatic event, like a car accident or a fall. It occurs suddenly and its victims will usually be able to pinpoint exactly when it happened. In acute cases, the structures damaged will more than likely be soft tissue like muscles, ligaments and tendons. These tissues can account for chronic low back pain as well. With a serious accident, or when osteoporosis or other causes of weakened vertebral bones is present, vertebral fractures in the lumbar spine may also occur. At the lowest end of the spine, some patients may have tailbone pain (also called coccyx pain or coccydynia). Others may have pain from their sacroiliac joint at the bottom of the lumbar spine, called sacroiliac joint dysfunction.
Chronic lower back pain usually has a more insidious onset, occurring over a long period of time. Physical causes may include soft tissue injury or pathology as previously described, nerve root irritation radiculopathy, osteoarthritis, rheumatoid arthritis, degeneration of the discs between the vertebrae, spinal disc herniation, vertebral fracture (such as from osteoporosis), or rarely, a tumor (including cancer) or infection. Psychological or emotional issues can also have a profound impact upon low back pain.

# Natural History, Complications and Prognosis
Many people will feel better within 1 week after the start of acute low back pain. After another 4-6 weeks, the back pain will likely be completely gone.
Mycobacterium kansasii
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# Overview
Mycobacterium kansasii

# Description
Gram-positive, nonmotile, moderately long to long and acid-fast rods.
Colony characteristics
- Smooth to rough colonies after 7 or more days of incubation.
- Colonies grown in dark are nonpigmented, when grown in light or when young colonies are exposed briefly to light, colonies become brilliant yellow (photochromogenic).
- If grown in a lighted incubator, most strains form dark red crystals of -carotene on the surface and inside of colony.
Physiology
- Growth on Middlebrook 7H10 agar at 37C within 7 days or more.
- Resistant to isoniazid.
- Susceptible to ethambutol.
Differential characteristics
- Closely related to the non-pathogenic, also slowly growing, nonpigmented M. gastri.
- Both species share an identical 16S rDNA but differentiation is possible by differences in the ITS and hsp65 sequences
- A commercial hybridisation assay (AccuProbe) to identify M. kansasii exists.

# Pathogenesis
- Chronic human pulmonary disease resembling tuberculosis (involvement of the upper lobe).
- Extrapulmonary infections, (cervical lymphadenitis in children, cutaneous and soft tissues infections and musculoskeletal system involvement), are uncommon.
- Rarely causes disseminated disease except in patients with severely impaired cellular immunity (patients with organ transplants or AIDS).
- Normally considered not to be contagious from person to person.
- Natural sources of infections unclear. Tap water is believed to be the major reservoir associated with human disease.
- Biosafety level 2

# Type Strain
- First and most frequently isolated from human pulmonary secretions and lesions.
Strain ATCC 12478 = CIP 104589 = DSM 44162 = JCM 6379 = NCTC 13024.

# Treatment

## Antimicrobial regimen
- 1. pulmonary disease 
- Preferred regimen: Rifampin 10 mg/kg/day (maximum, 600 mg) AND Ethambutol 15 mg/kg/ day AND Isoniazid 5 mg/kg/day (maximum 300 mg) AND Pyridoxine 50 mg/day
- NOTE: Treatment duration for M. kansasii lung disease should include 12 months of negative sputum cultures
- 2. Rifampin-resistant M. kansasii disease
- Preferred regimen: Use three-drug regimen include Clarithromycin OR Azithromycin OR Moxifloxacin OR Ethambutol OR Sulfamethoxazole OR Streptomycin
- 3. Disseminated M. kansasii disease
- Preferred regimen: The treatment regimen for disseminated disease should be the same as for pulmonary disease
Mean arterial pressure

# Overview
The mean arterial pressure (MAP) is a term used in medicine to describe a notional average blood pressure in an individual. It is defined as the average arterial pressure during a single cardiac cycle.

# Calculation
MAP = (CO  x SVR) + CVP, where
- CO is cardiac output
- SVR is systemic vascular resistance
- CVP is central venous pressure
CVP is usually small enough to be neglected in this formula.

# Estimation
At normal resting heart rates MAP can be approximated using the more easily measured systolic and diastolic pressures, SP and DP:
-r
-r equivalently
where PP is the pulse pressure, SP-DP
At high heart rates MAP is more closely approximated by the arithmetic mean of systolic and diastolic pressures because of the change in shape of the arterial pressure pulse.

# Clinical significance
MAP is considered to be the perfusion pressure seen by organs in the body.
It is believed that a MAP of greater than 60 mmHg is enough to sustain the organs of the average person under most conditions.
If the MAP falls significantly below this number for an appreciable time, the end organ will not get enough blood flow, and will become ischemic.
MR severity assessment

# Colour flow mapping
- Size of flow recruitment is noted
- Jet base width at the valve level
- Intra atrial jet area if it is a central jet
- Jet direction is usually away from a prolapsing leaflet and behind a restricted leaflet

# Continuous wave doppler
- Shape and density of signal - In severe Mitral regurgitation, the flow is dense and triangular
- If as dense as forward flow, it is severe.

# Pulse wave doppler(PW)
- PW in apical-4-chamber view
- E wave more than 1.2m/s indicates severe MR
- Even minor mitral stenosis or hyperdynamic circulation can increase E wave
- If A-wave dominant, severe MR is virtually ruled out.

# vena contracta
- vena contracta is the narrowest region of regurgitant jet (usually just below the valve in LA)
- >0.7 cm - severe MR

# Pulmonary Venous Flow
- usually forward throughout cycle
- systolic dominant
- as MR worsens, there is a blunting of systolic flow
- If severe MR - systolic flow reversal.

# Regurgitant volume
- Mitral regurgitant volume = Mitral inflow volume - LV outflow volume
- Regurtitant volume - 50% severe

# PISA (Proximal isovelocity surface area)
The radius of Proximal isovelocity surface area or flow convergence zone which is a 3-dimensional surface area proximal to a narrowed orifice at which all the blood velocities are equal, can be used to calculate the severity of mitral regurgitation. The principle is that if the mitral regurgitation is mild, only the blood nearer to the valve orifice accelerates towards the atrium while in severe regurgitation, blood farther away from the valve moves back.

## PISA radius
A simple method to determine severity of mitral regurgitation is to measure the PISA radius. Regurgitation is mild if radius is 1 cm.

## Regurgitant flow (instantaneous)
The instantaneous regurgitant flow can be calculated from the PISA radius and can be used to assess the severity of mitral regurgitation.
Regurgitant flow  = 2 - r2 - Valiasing

# Effective regurgitant orifice area (EROA)
Effective regurgitant orifice area can be calculated using the instantaneous regurgitant flow. 
The formula can be derived from the following:
Valiasing - 2r2 = Vmax - EROA
hence:
- EROA = PISA (2r2) - Valiasing / Vmax
Mild = 0-20 cm2, moderate = 20 - 40 cm2, severe = >40 cm2
Regurgitant volume can be calculated from this.
- Regurgitant volume = Effective regurgitant orifice area - Vtime integrale

# Diastolic Mitral Regurgitation Secondary to Severe Aortic Stenosis
- Diastolic mitral regurgitation due to severe aortic stenosis
- Diastolic mitral regurgitation due to severe aortic stenosis
- Diastolic mitral regurgitation due to severe aortic stenosis
- 424719160215823743&hl=en
- -1316686479831791521&hl=en
Machado-Joseph disease
Machado-Joseph disease is a type of spinocerebellar ataxia caused by a mutation in the ATXN3 gene.
It causes ophthalmoplegia and mixed sensory and cerebellar ataxia
It is also known as Spinocerebellar ataxia type 3.
It was first identified in 1972.
Machado-Joseph Disease is a rare, inherited disease that causes lack of muscle control.  Chromosome 14 is where the gene that is responsible for MJD is located.
Based on DNA studies, MJD is the most widespread, autosomal dominant inherited form of ataxia in the world.

# Symptoms
Symptoms of MJD are spasticity, difficulty with speech and swallowing, weakness in arms and legs, clumsiness, frequent urination and involuntary eye movements.  Symptoms can being in early adolescence and they get worse over time.  There is no cure for Machado-Joseph Disease, however, there are treatments available for some symptoms.  For example, spasticity can be reduced with Antispasmodic drugs, such as baclofen.  Eventually, MJD leads to paralysis however, intellectual functions usually remain the same.

# Prognosis
Life expectancy ranges with people who have the disease.  A normal life expectancy is expected in patients with a mild form of MJD.  Those with severe forms of MJD are expected to live only to their mid-thirties.  The cause of death of those who die early is often aspiration pneumonia.

# Pathophysiology
MJD has lengthy irregular repetition of the DNA genetic code located within a gene on chromosome 14q.  The code "CAG" is repeated and produces a mutated protein called ataxin-3.  In affected cells, this protein piles up and assembles intranuclear inclusion bodies.
These insoluble spheres are located in the nucleus of the cell.  These spheres conflict with the normal activity of the nucleus and induce the cell to degenerate and die.

# Classification
The types of MJD are characterized by the onset and age and range of symptoms.
- Type I is distinguished by arrival between the ages of 10 and 30 years of age.  It usually has fast development and severe rigidity and dystonia.
- Type II typically begins between 20 and 50 years of age.  It has an intermediate progression and causes symptoms that include spasticity, exaggerated reflex responses and spastic gait.
- Type III MJD has a slow progression.  Symptoms include muscle twitching, tingling, cramps, unpleasant sensations such as numbness, pain in the feet, hands and limbs and muscle atrophy.  Patients typically have an onset between the ages of 40 and 70.  Nearly all patients experience a decline in their vision such as blurred vision, double vision, inability to control eye movements, and loss of capability to distinguish color.  Some patients also experience Parkinsons-like symptoms.

# Diagnosis
MJD can be diagnosed by recognizing the symptoms of the disease and by taking a family history.  Physicians ask patients questions about the kind of symptoms relatives with the disease had, the progression and harshness of symptoms, and the ages of onset in family members.  The best diagnosis of MJD can be made only with a genetic test.
Malabsorption overview

# Overview
Malabsorption is a state arising from an abnormality in digestion or absorption of food nutrients across the gastrointestinal (GI) tract.
Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition and variety of anemias.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Malabsorption overview from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

### Abdominal X Ray
Barium follow through is useful in delineating small intestinal anatomy. Barium enema may be undertaken to see colonic or ileal lesions.

### CT
CT abdomen is useful in ruling out structural abnormalities, and it is done as part of the pancreatic protocol when visualizing the pancreas.

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
MalloryWeiss syndrome

# Overview
MalloryWeiss syndrome or gastro-esophageal laceration syndrome refers to bleeding from a laceration in the mucosa at the junction of the stomach and esophagus. This is usually caused by severe vomiting because of alcoholism or bulemia, but can be caused by any conditions which causes violent vomiting and retching such as food poisoning. The syndrome presents with painful hematemesis. The laceration is sometimes referred to as a Mallory-Weiss tear.

# Causes
It is often associated with alcoholism and eating disorders and there is some evidence that presence of a hiatal hernia is a predisposing condition. Forceful vomiting causes tear of the mucosa at the junction.
NSAID abuse is also a rare association. The tear involves mucosa and submucosa but not the muscular layer (contrast to Boerhaave syndrome which involves all the layers). The mean age is more than 60 and 80% are men.
Hyperemesis gravidarum, which is severe morning sickness associated with vomiting and retching in pregnancy, is also a known cause of Mallory-Weiss tear.

# Presentation
MalloryWeiss syndrome often presents as an episode of vomiting up blood (hematemesis) after violent retching or vomiting, but may also be noticed as old blood in the stool (melena), and a history of retching may be absent.
In most cases, the bleeding stops spontaneously after 2448 hours, but endoscopic or surgical treatment is sometimes required and rarely the condition is fatal. There won't be any abdominal pain.

# Diagnosis
Definitive diagnosis is by endoscopy.

# Treatment
Treatment is usually supportive as persistent bleeding is uncommon. However cauterization or injection of epinephrine to stop the bleeding may be undertaken during the index endoscopy procedure. Very rarely embolization of the arteries supplying the region may be required to stop the bleeding.  If all other methods fail, high gastrostomy can be used to ligate the bleeding vessel. It is to be noted that the tube will not be able to stop bleeding as here the bleeding is arterial and the pressure in the balloon is not sufficient to overcome the arterial pressure.

# History
The condition was first described in 1929 by G. Kenneth Mallory and Soma Weiss in 15 alcoholic patients.
Mandibular first molar
The mandibular first molar (also known as 6 yr molar) is the tooth located distally (away from the midline of the face) from both the mandibular second premolars of the mouth but mesial (toward the midline of the face) from both mandibular second molars. It is located on the mandibular (lower) arch of the mouth, and generally opposes the maxillary (upper) first molars and the maxillary 2nd premolar in normal class I occlusion.  The function of this molar is similar to that of all molars in regard to grinding being the principal action during mastication, commonly known as chewing. There are usually five well-developed cusps on mandibular first molars: two on the buccal (side nearest the cheek), two palatal (side nearest the palate), and one distal.  There are great differences between the deciduous (baby) mandibular molars and those of the permanent mandibular molars, even though their function are similar. It is important to note that the permanent mandibular molars are not considered to have any teeth that precede it. Despite being named molars, the deciduous molars are followed by permanent premolars.
In the universal system of notation, the deciduous mandibular first molars are designated by a letter written in uppercase. The right deciduous mandibular first molar is known as "S", and the left one is known as "L". The international notation has a different system of notation. Thus, the right deciduous mandibular first molar is known as "84", and the left one is known as "74".
In the universal system of notation, the permanent mandibular first molars are designated by a number. The right permanent mandibular first molar is known as "30", and the left one is known as "19". The Palmer notation uses a number in conjunction with a symbol designating in which quadrant the tooth is found. For this tooth, the left and right first molars would have the same number, "6", but the right one would have the symbol, "", over it, while the left one would have, "". The international notation has a different numbering system than the previous two, and the right permanent mandibular first molar is known as "46", and the left one is known as "36".
Mature cystic teratoma

# Overview
Mature cystic teratomas are cystic tumors composed of well-differentiated derivations from at least two of the three germ cell layers (ectoderm, mesoderm, and endoderm). They affect a younger age group (mean patient age, 30 years) than epithelial ovarian neoplasms. Mature cystic teratoma is the most common germ cell neoplasm and, in some series, the most common ovarian neoplasm. The tumors are bilateral in about 10% of cases. Most mature cystic teratomas are asymptomatic. Complications include rupture, malignant degeneration, or (most commonly) ovarian torsion.

# Imaging Findings
- Most mature cystic teratomas can be diagnosed at US.
- The most common manifestation is a cystic lesion with a densely echogenic tubercle (Rokitansky nodule) projecting into the cyst lumen.
- The second manifestation is a diffusely or partially echogenic mass with the echogenic area usually demonstrating sound attenuation owing to sebaceous material and hair within the cyst cavity.
- The third manifestation consists of multiple thin, echogenic bands caused by hair in the cyst cavity.
- The diagnosis of mature cystic teratoma at CT and MR imaging is fairly straightforward because these modalities are more sensitive for fat than US.
Patient #1: US and MR images demonstrate a large dermoid
- T1
- T1
- T2
- T2
- T2
- T1 fat sat
- T1 fat sat post contrast
- T1 fat sat post contrast
Patient #2: CT images demonstrate left ovarian mature cystic teratoma
Mefloquine description

# Description
Mefloquine Hydrochloride Tablets USP are an antimalarial agent available as 250 mg tablets of mefloquine hydrochloride (equivalent to 228 mg of the free base) for oral administration.
Mefloquine Hydrochloride USP is a 4-quinolinemethanol derivative with the specific chemical name of (R*, S*)-()--2-piperidinyl-2,8-bis (trifluoromethyl)-4-quinolinemethanol hydrochloride. It is a 2-aryl substituted chemical structural analog of quinine. The drug is a white to almost white crystalline compound, slightly soluble in water. The structural formula is as follows:a
The inactive ingredients are colloidal silicon dioxide, corn starch, crospovidone, lactose monohydrate, magnesium stearate, microcrystalline cellulose, pregelatinized starch, poloxamer and talc.
Melancholic depression

# Overview
Melancholic Depression, or 'depression with melancholic features'  is a subtype of depression characterized by the inability to find pleasure in positive things combined with physical agitation, insomnia, or decreased appetite.  Roughly 10% of people with depression suffer from Melancholic Depression.

# Diagnostic criteria (DSM-IV-TR)
The DSM-IV-TR, a widely used manual for diagnosing mental disorders, defines Depression with Melancholic Features as a subtype of depression characterized by:
- At least one of the following:
Loss of pleasure in all or almost all, activities
Lack of mood reactivity to usually pleasurable stimuli (can't feel much better, even when something good happens)
- Loss of pleasure in all or almost all, activities
- Lack of mood reactivity to usually pleasurable stimuli (can't feel much better, even when something good happens)
- At least three of the following:
Distinct quality of depressed mood (i.e., the depressed mood is experienced as distinctly different from the kind of feeling experienced after the death of a loved one)
Depression is regularly worse in the morning
Early morning awakening (at least 2 hours before usual time of awakening)
Marked psychomotor retardation or agitation
Significant anorexia or weight loss
Excessive or inappropriate guilt
- Distinct quality of depressed mood (i.e., the depressed mood is experienced as distinctly different from the kind of feeling experienced after the death of a loved one)
- Depression is regularly worse in the morning
- Early morning awakening (at least 2 hours before usual time of awakening)
- Marked psychomotor retardation or agitation
- Significant anorexia or weight loss
- Excessive or inappropriate guilt
Metabolic intermediate

# Overview
Metabolic intermediates refers to molecules which are the precursors or metabolites of biologically significant molecules.
Although these intermediates are of relatively less direct importance to cellular function, they can play important roles both in the allosteric regulation of enzymes.
Some can be useful in measuring rates of metabolic processes (for example, Dopac or 3-aminoisobutyrate).
Methylmalonic acidemia

# Overview
Methylmalonic acidemia (MMA, also known as "methylmalonic aciduria") is an inborn error of intermediary metabolism that may present in the early neonatal period with progressive encephalopathy and death due to a secondary hyperammonemia.
Methylmalonic acidemia does not always result in death, if it is diagnosed at an early age.

# Historical Perspective

# Classification

## Types
- Online Mendelian Inheritance in Man (OMIM) 251100 - cblA type
- Online Mendelian Inheritance in Man (OMIM) 251110 - cblB type
- Online Mendelian Inheritance in Man (OMIM) 277400 - cblC type
- Online Mendelian Inheritance in Man (OMIM) 277410 - cblD type
- Online Mendelian Inheritance in Man (OMIM) 277380 - cblF type
- Online Mendelian Inheritance in Man (OMIM) 606169 - cblH type
- Online Mendelian Inheritance in Man (OMIM) 251000 - mut type
Cobalmin (vitamin B12) is also needed for the conversion of methylmalonyl-CoA to Succinyl-CoA.  Mutations leading to defects in cobalmin or in its transport frequently result in the development of acidemia.  The numerous pat

# Pathophysiology

# Causes
Methylmalonic acidemia is an inherited disorder in which the body is unable to process certain proteins and fats (lipids) properly. Methylmalonic acidemia is a disorder of amino acid metabolism, involving a defect in the conversion of methylmalonyl-coenzyme A (CoA) to succinyl-CoA by methylmalonyl-CoA mutase.

# Differentiating Methylmalonic acidemia 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