Persius/hicric huggingface dataset:
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Quinine Sulfate microbiology

# Microbiology

## Mechanism of Action
Quinine inhibits nucleic acid synthesis, protein synthesis, and glycolysis in Plasmodium falciparum and can bind with hemazoin in parasitized erythrocytes. However, the precise mechanism of the antimalarial activity of quinine sulfate is not completely understood.

## Activity In Vitro and In Vivo
Quinine sulfate acts primarily on the blood schizont form of P. falciparum. It is not gametocidal and has little effect on the sporozoite or pre-erythrocytic forms.

## Drug Resistance
Strains of P. falciparum with decreased susceptibility to quinine can be selected in vivo. P. falciparum malaria that is clinically resistant to quinine has been reported in some areas of South America, Southeast Asia, and Bangladesh.
Retinoic acid receptor alpha
Retinoic acid receptor alpha (RAR-), also known as NR1B1 (nuclear receptor subfamily 1, group B, member 1) is a nuclear receptor that in humans is encoded by the RARA gene.

# Function
Retinoid signaling is transduced by 2 families of nuclear receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), which form RXR/RAR heterodimers. In the absence of ligand, DNA-bound RXR/RARA represses transcription by recruiting the corepressors NCOR1, SMRT (NCOR2), and histone deacetylase. When ligand binds to the complex, it induces a conformational change allowing the recruitment of coactivators, histone acetyltransferases, and the basic transcription machinery.

# Clinical significance
Translocations that always involve rearrangement of the RARA gene are a cardinal feature of acute promyelocytic leukemia (APL; MIM 612376). The most frequent translocation is t(15,17)(q21;q22), which fuses the RARA gene with the PML gene.

# Interactions
Retinoic acid receptor alpha has been shown to interact with:
- BAG1,
- CLOCK,
- CCND3,
- NCOA6,
- NCOR1,
- NCOR2,
- NPAS2,
- NRIP1,
- NR0B2,
- NR4A2,
- PML
- RXRA.
- Src,
- TADA3L, and
- ZBTB16.
RNA dependent RNA polymerase

# Overview
RNA dependent RNA polymerase, or RDRP, is an enzyme that catalyzes the replication of RNA from an RNA template. In contrast to a typical RNA polymerase, which uses DNA as a template, RDRP is, as its name suggests, dependent on RNA.
Viral RDRPs were discovered in the early 1960s from studies on mengovirus and polio virus when it was observed that these viruses were not sensitive to actinomycin D, a drug that inhibits cellular DNA directed RNA synthesis.This lack of sensitivity suggested that there was a virus specific enzyme that could copy RNA from an RNA template and not from a DNA template.
The most famous example of RDRP is the polio virus.  The virus is made up of RNA which enters the cell through receptor-mediated endocytosis. From there, the RNA is able to act as a template for complementary RNA synthesis, immediately. The complementary strand is then, itself, able to act as a template for the production of new viral genomes which are further packaged and released from the cell ready to infect more host cells. The advantage of this method of replication is that there is no DNA stage, replication is quick and easy. The disadvantage is that there is no 'back-up' DNA copy.
Many RDRPS are associated tightly with the membranes and are therefore difficult to study. The best known RDRPs are polioviral 3Dpol, vesicular stomatitis virus L, and hepatitis C virus NS5b protein.
Ramsay Hunt syndrome type II

# Overview
Ramsay Hunt syndrome (RHS) type 2, is a disorder that is caused by the reactivation of pre-existing herpes zoster virus in a nerve cell bundle (the geniculate ganglion). The neurons in this ganglion are responsible for the movements of facial muscles, the touch sensation of a part of ear and ear canal, the taste function of the frontal two-thirds of the tongue, and the moisturization of the eyes and the mouth. The syndrome specifically refers to the combination of this entity with weakness of the muscles activated by the facial nerve. In isolation the latter entity would be called Bell's Palsy.

# Pathophysiology
RHS type 2 is essentially shingles of the geniculate ganglion. Briefly, the herpes zoster virus, which causes chicken pox, lies dormant in various nerve cells in the body, where it is kept in check by the patient's immune system. Given the opportunity, for example during an illness that suppresses the immune system, the virus is reactivated and travels to the end of the nerve cell, where it causes the symptoms described above.

# Disease States to Differentiate Ramsay Hunt from
Like shingles, however, lack of lesions does not definitely exclude the existence of a herpes infection.  The virus can be detected, even before the eruption of vesicles, from the skin of the ear.

# Differential diagnosis
ABBREVIATIONS
VZV= Varicella zoster virus, MRI= Magnetic resonance imaging, ESR= Erythrocyte sedimentation rate, EEG= Electroencephalogram, CSF= Cerebrospinal fluid, GPe= Globus pallidus externa, ICHD=  International Classification of Headache Disorders

# Diagnosis

## Symptoms
- Pain in the ear (otalgia)
- Taste loss in the front two-thirds of the tongue
- Dry mouth
- Dry eyes
- Tinnitus. Since the vestibulocochlear nerve is in proximity to the geniculate ganglion, it may also be affected, and patients may also suffer from tinnitus, hearing loss, and vertigo.

## Physical Examination

### HEENT
- Acute facial nerve paralysis
- Vesicles in the ear canal, the tongue, and/or hard palate

# Treatment
The largest study on the treatment of RHS type 2 has shown that complete recovery can be achieved in 75% of patients if treatment with prednisone and acyclovir is  started within the first 3 days of onset of symptoms. Chances of complete recovery decrease as treatment is delayed. Studies have shown that half of all patients whose  treatment was delayed had complete loss of response to facial nerve stimulation. Treatment apparently has no effect on the recovery of hearing loss.
Red eye history and symptoms
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# Symptoms
There are three main danger symptoms in a red eye: reduced visual acuity, severe ocular pain, and photophobia (light sensitivity).

## Blurry vision
Blurry vision often indicates serious ocular disease.
If the blurriness improves with blinking, it suggests ocular surface discharge of some variety.

## Severe pain
Those suffering from conjunctivitis may report mild irritation or scratchiness, but never extreme pain.
Severe pain is an indicator of keratitis, corneal ulceration, iridocyclitis, or acute glaucoma.

## Photophobia
Photophobia, or fear of light, is usually an indication of iritis.

## Colored halos
Colored halos are an indication of corneal edema, and are a warning that acute glaucoma may be present.
Red eye physical examination

# Physical Examination

## Eye
Some signs and symptoms of red eye represent warnings that the underlying cause is serious and requires immediate attention.
The person conducting a thorough eye examination should be attentive to the warning signs and symptoms during the eye exam.
There are six danger signs: conjunctival injection, ciliary flush (circumcorneal injection), corneal edema or opacities, corneal staining, abnormal pupil size, and abnormal intraocular pressure.

### Visual Acuity
Reduced visual acuity is indicative of serious ocular disease, such as corneal inflammation, iridocyclitis, and glaucoma, and never occurs in simple conjunctivitis without concurrent corneal involvement.

### Ciliary Flush
Ciliary flush is usually present in eyes with corneal inflammation, iridocyclitis or acute glaucoma, though not simple conjunctivitis.
A ciliary flush is a ring of red or violet around the cornea of the eye.

### Corneal Opacification
Corneal opacities always indicate that a serious disease process is in progress.
Opacification may be detected using an ophthalmoscope or, in more obvious cases, with a pen light.
These opacities may be keratic, haze-like (usually from corneal edema), or they may be localized such as with ulcerated corneas or those affected by keratitis.

### Corneal Epithelial Disruption
Corneal epithelial disruptions may be detected with fluorescein staining of the eye, and careful observation with cobalt-blue light.
Corneal epithelial disruptions would stain green, which represents some injury of the corneal epithelium.
These types of disruptions may be due to corneal inflammations or physical trauma to the cornea.

### Pupillary Abnormalities
An eye with iridocyclitis would have one pupil that is smaller than the other, which is caused by a reflex muscle spasm of the iris sphincter muscle.
As is the general rule, conjunctivitis does not affect the pupils.
With acute angle-closure glaucoma, the pupil would be partially dilated and oval.

### Shallow Anterior Chamber Depth
Shallow anterior chamber depth usually indicates some problem.
If the eye is red, anterior chamber depth may indicate acute glaucoma, which requires immediate attention.

### Abnormal Intraocular Pressure
Intraocular pressure should be measured as part of the routine eye examination.
It is usually affected only by iridocyclitis or acute-closure glaucoma, but not by relatively benign conditions.
In iritis and traumatic perforating ocular injuries, pressure is usually low.

### Proptosis
Proptosis, or forward displacement of the globe, may be caused by an infection of the orbit, or a cavernous sinus disease.
Most commonly, chronic proptosis is caused by thyroid diseases such as Graves disease.
Respiratory disease overview

# Overview
Respiratory disease is an umbrella term for diseases of the lung, pleural cavity, bronchial tubes, trachea, upper respiratory tract and of the nerves and muscles of breathing. Respiratory diseases range from mild and self-limiting such as the common cold to life-threatening such as bacterial pneumonia or pulmonary embolism.
Respiratory disease is responsible for over 10% of hospitalizations and over 16% of deaths in Canada. The study of respiratory disease is known as pulmonology. A doctor who specializes in respiratory disease is known as a pulmonologist, a chest medicine specialist, a respiratory medicine specialist, a respirologist or a thoracic medicine specialist.

# Classification
Respiratory diseases can be classified as either obstructive (i.e. conditions which impede the rate of flow into and out of the lungs, for example asthma) or restrictive (i.e. conditions which cause a reduction in the functional volume of the lungs, for example pulmonary fibrosis).
Respiratory disease can be further classified as either upper or lower respiratory tract (most commonly used in the context of infectious respiratory disease), parenchymal and vascular lung diseases.

# Epidemiology and Demographics
In the US, people suffer 1 billion colds per year. One in seven people in the UK is affected by some form of chronic lung disease, most commonly chronic obstructive pulmonary disease and asthma.
Respiratory sinus arrhythmia
Synonyms and keywords: RSA

# Overview
Respiratory sinus arrhythmia (RSA) refers to the normal slowing down of heart rate during expiration (breathing out) and speeding up of heart rate during inspiration.  Heart rate is normally controlled by centers in the medulla oblongata.  One of these centers, the nucleus ambiguus, increases parasympathetic nervous system input to the heart via the vagus nerve.  The vagus nerve decreases heart rate by decreasing the rate of SA node firing.  Upon expiration, the cells in the nucleus ambiguus are activated and heart rate is slowed down.  In contrast, inspiration triggers inhibitory signals to the nucleus accumbens and consequently the vagus nerve remains unstimulated.

# Causes

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

## Common Causes
- Normal variation in vagal tone

## Causes by Organ System

## Causes in Alphabetical Order
- Anidulafungin
- Atherosclerosis
- Congestive heart failure
- Digitalis
- Guanfacine
- Hypertension
- Hypercapnia
- Morphine
- Myocardial infarction
- Normal variation in vagal tone
- Obesity

# Diagnosis

## Electrocardiogram
- EKG of a patient with acute inferior myocardial infarction shows sinus bradycardia (59 bpm) and respiratory sinus arrhythmia (please note to rhythm line at the bottom). QRS=104 msec, PR=172 msec
On an electrocardiogram (EKG), RSA is seen as subtle changes in the R-R interval (time between two of the distinctive, large, upward "R" spikes on an electrocardiogram) synchronized with respiration. The R-R interval on an EKG is shortened during inspiration and prolonged during expiration. Meditation and relaxed breathing techniques can temporarily alter RSA.
Salter-Harris classification

# Overview
Injuries leading to the bone fracture affecting the epiphyseal plate, or physis, are important and common in orthopedic medicine and the cause diagnostic and treatment challenges for orthopaedic surgeons. The related incidence rate of these fracture among pedicatric population is 15-20%.

# Historical Perspective 
In 1863, Foucher JT was the first person who described the injuries affecting the epiphyseal plate.
In 1895, Poland J, classified the injuries affecting the epiphyseal plat into the four types.
In 1936 , Aitken AP, defined the specific differences of different types of physes based on their differences in: structure, location, weightbearing status, and susceptibility to injury.
In 1963, two Canadian orthopaedic surgeons, Robert B. Salter (19242010) and W. Robert Harris (19222005), introduced a physeal fracture classification system according to the anatomy, fracture pattern, and prognosis of bone fracture.
Then, various researchers and physicians tried to expanded the original work of Salter and Harris in order to make it to be to be more comprehensive:
In 1968, Rang M, added a different sixth type of physeal injuries describing the caused damage to the perichondral ring due to the direct open injuries to the affected bone.
In 1981, Ogden JA, described nine types of injuries such as injuries affecting the developing bones other growth mechanisms.

# Salter-Harris classification
Sandbox:Hypercholesterolemia
For patient information on hypercholesterolemia click here
For patient information on coronary risk profile click here
Synonyms and keywords: cholesterol guidelines, NCEP guidelines, ATP guidelines, high cholesterol, hyperlipidemia

# Overview

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Hypercholesterolemia from other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications and Prognosis

# Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

# Treatment
Medical Therapy | Surgery | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

# Case Studies
Case #1
Sandbox:Infectious Balanitis
Synonyms and keywords:Candida balanitis, Candidal balanitis, Infectious balanoposthitis

# Overview
Balanitis is inflammation of glans penis, whenever balanitis involves foreskin and perpuce, it is termed as balanoposthitis. Studies have showed that Balanitis commonly occurs around 10% of the patient population visiting the STD clinc, with infectious etiology responsible for around 50% of the cases. Risk factors for balanitis include Diabetes, Immunocompromised, Age>40 yrs,tight foreskin, sub-optimal hygienic maintenance, Multiple sexual partners, and Uncircumcised penis. Orgnaism could be part of the normal flora or transmitted by sexually, or autoinoculation, or via direct contact. Patients may be asymptomatic or present with pruritic, or painful lesions in the genital region. Specific infectious balanitis etiology is diagnosed based on clinical presentation supported with laboratory findings. Infectious balanitis is usually treated with antimicrobials. Prognosis is usually good with treatment. Safe sex practices and maintaining proper penile hygiene are helpful in preventing Infective balanitis.

# Historical Perspective
Balanitis is an ancient disease,The term Balanitis is derived from a Greek term balanos or acorn

# Classification
There is no established classification system for Infectious Balanitis.

# Pathophysiology
Pathophysiology of Infectious balanitis varies from pathogen to pathogen:

# Causes
Causes of Infectious balanitis include:

# Epidemiology and Demographics

### Epidemiology
There are no comprehensive studies, studying the incidence and prevalence in general population. Studies have showed that Balanitis commonly occurs around 10% of the patient population visiting the STD clinc, with infectious etiology responsible for around 50% of the cases.
Candida being the most common cause responsible for 30-35% of cases.

### Demographics

# Screening
There is no established screening guidelines for Infectious Balanitis

# Natural History, Complications, and Prognosis

## Natural history
If left untreated, Infection balanitis may result in complications.

## Complications
Complication of Infectious balanitis include:
- Pain
- Erosions
- Fissures
- Phimosis
- Paraphimosis
- Painful erection
- Reduced urinary flow
- Urinary retention

## Prognosis
Prognosis is good with treatment.

# Diagnosis

### History and symptoms
Patients may be asymptomatic or present with pruritic, or painful lesions in the genital region.

### Laboratory findings

# Treatment

# Prevention

## Primary Prevention
Primary prevention of Infectious balanitis include:
Safe sex practices.
Maintaining proper penile hygiene.

## Secondary prevention
There ares no specific secondary preventive measures for Infective balanitis.
Sandbox:secondary prevention

# Overview
- There are no established measures for the secondary prevention of .
OR
- Effective measures for the secondary prevention of  include , , and .

# Secondary Prevention
- There are no established measures for the secondary prevention of .
OR
- Effective measures for the secondary prevention of  include:
Saquinavir contraindications

# Contraindications
QT interval prolongation and torsades de pointes have been reported rarely with INVIRASE/ritonavir use. Do not use in patients with congenital long QT syndrome, those with refractory hypokalemia or hypomagnesemia, and in combination with drugs that both increase saquinavir plasma concentrations and prolong the QT interval .
INVIRASE is contraindicated in patients with complete atrioventricular (AV) block without implanted pacemakers, or patients who are at high risk of complete AV block .
INVIRASE is contraindicated in patients with clinically significant hypersensitivity (e.g., anaphylactic reaction, Stevens-Johnson syndrome) to saquinavir, saquinavir mesylate, or any of its ingredients.
INVIRASE when administered with ritonavir is contraindicated in patients with severe hepatic impairment.
Coadministration of INVIRASE/ritonavir is contraindicated with drugs that are CYP3A substrates for which increased plasma levels may result in serious or life-threatening reactions. These drugs and potentially related adverse events are listed in Table 1.
Saquinavir drug interactions

# Drug Interactions
Drug interaction studies have been completed with both INVIRASE and saquinavir soft gel capsules. Observations from drug interaction studies with saquinavir soft gel capsules may not be predictive for INVIRASE/ritonavir. Because ritonavir is coadministered with INVIRASE, prescribers should also refer to the prescribing information for ritonavir regarding drug interactions associated with this agent.

## Potential for INVIRASE to Affect Other Drugs
The combination INVIRASE/ritonavir is a potent inhibitor of CYP3A and may significantly increase the exposure of drugs primarily metabolized by CYP3A. Drugs that are contraindicated specifically due to the observed or expected magnitude of interaction and potential for serious or life-threatening adverse events are listed in Table 1 . Coadministration with other CYP3A substrates may require a dose adjustment or additional monitoring (see Table 3).

## Potential for Other Drugs to Affect INVIRASE
The metabolism of saquinavir is mediated primarily by CYP3A. Additionally, saquinavir is a substrate for P-glycoprotein (P-gp). Therefore, drugs that affect CYP3A and/or P-gp may modify the pharmacokinetics of saquinavir. Coadministration with drugs that are potent inducers of CYP3A (e.g., phenobarbital, phenytoin, carbamazepine) may result in decreased plasma concentrations of saquinavir and reduced therapeutic effect.

## Established and Other Potentially Significant Drug Interactions
Based on the finding of dose-dependent prolongations of QT and PR intervals in healthy volunteers receiving INVIRASE/ritonavir, additive effects on QT and/or PR interval prolongation may occur with certain members of the following drug classes: antiarrhythmics class IA or class III, neuroleptics, antidepressive agents, PDE5 inhibitors (when used for pulmonary arterial hypertension), antimicrobials, antihistaminics and others. This effect might lead to an increased risk of ventricular arrhythmias, notably torsades de pointes. Therefore, concurrent administration of these agents with INVIRASE/ritonavir is contraindicated .
Table 3 provides a listing of established or potentially clinically significant drug interactions. Alteration in dose or avoidance of the combination may be recommended depending on the interaction