Persius/hicric huggingface dataset:
Tirofiban dosage and administration

# Dosage and Administration
Administer intravenously 25 mcg/kg over 3 minutes and then 0.15 mcg/kg/min (or 0.075 mcg/kg/min for patients with serum creatinine 60 mL/min), for up to 18 hours. This is not the regimen that was used in studies that established effectiveness of AGGRASTAT .
The instructions by weight and creatinine clearance are tabulated in Table 1.

## Important Administration Instructions
1.To open the container, first tear off its foil overpouch. The plastic may be somewhat opaque because of moisture absorption during sterilization; the opacity will diminish gradually. Check for leaks by squeezing the inner bag firmly; if any leaks are found or sterility is suspect then the solution should be discarded. Do not use unless the solution is clear and the seal is intact. Suspend the container from its eyelet support, remove the plastic protector from the outlet port, and attach a conventional administration set.
You may administer AGGRASTAT in the same intravenous line asatropine sulfate, dobutamine, dopamine, epinephrine hydrochloride (HCl), famotidine injection, furosemide, idocaine, midazolam HCl, morphine sulfate, nitroglycerin, potassium chloride, and propranolol HCl. Do not administer AGGRASTAT through the same IV line as diazepam.
2.Do not add other drugs or remove solution directly from the bag with a syringe.
3.Do not use plastic containers in series connections; such use can result in air embolism by drawing air from the first container if it is empty of solution.
4.Discard any unused portion left in the bag.
Tooth abscess (patient information)
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# Overview
A tooth abscess is a collection of infected material (pus) resulting from a bacterial infection in the center of a tooth.

# What are the symptoms of Tooth abscess?
The main symptom is a severe toothache. The pain is continuous and may be described as gnawing, sharp, shooting, or throbbing.
Other symptoms may include:
- Bitter taste in the mouth
- Breath odor
- General discomfort, uneasiness, or ill feeling
- Fever
- Pain when chewing
- Sensitivity of the teeth to hot or cold
- Swollen glands of the neck
- Swollen area of the upper or lower jaw -- a very serious symptom

# What causes Tooth abscess?
A tooth abscess is a complication of tooth decay. It may also result from trauma to the tooth, such as when a tooth is broken or chipped. Openings in the tooth enamel allow bacteria to infect the center of the tooth (the pulp). Infection may spread out from the root of the tooth and to the bones supporting the tooth.
Infection results in a collection of pus (dead tissue, live and dead bacteria, white blood cells) and swelling of the tissues within the tooth. This causes a painful toothache. If the pulp of the tooth dies, the toothache may stop, unless an abscess develops. This is especially true if the infection remains active and continues to spread and destroy tissue.

# Diagnosis
The patient will feel pain when the dentist taps the tooth. Biting or closing the mouth tightly also increases the pain. The gums may be swollen and red and may drain thick material.

# When to seek urgent medical care?
Call your dentist if you have a persistent, throbbing toothache.

# Treatment options
The goals of treatment are to cure the infection, save the tooth, and prevent complications.
Antibiotics may be given to fight the infection. Warm salt-water rinses may be soothing. Over-the-counter pain relievers may relieve the toothache and fever.
Do NOT place aspirin directly over the tooth or gums, because this increases irritation of the tissues and can result in mouth ulcers.
A root canal may be recommended in an attempt to save the tooth.
If there is a severe infection, the tooth may be removed or surgery may be needed to drain the abscess. Some people may need to be admitted to the hospital.

# Where to find medical care for Tooth abscess?
Directions to Hospitals Treating Tooth abscess

# What to expect (Outlook/Prognosis)?
Untreated abscesses may get worse and can lead to life-threatening complications.
Prompt treatment usually cures the infection. The tooth can usually be saved in many cases.

# Possible complications
- Loss of the tooth
- Mediastinitis
- Sepsis
- Spread of infection to soft tissue (facial cellulitis, Ludwig's angina)
- Spread of infection to the jaw bone (osteomyelitis of the jaw)
- Spread of infection to other areas of the body resulting in brain abscess, endocarditis, pneumonia, or other complications

# Prevention of Tooth abscess
Prompt treatment of dental caries reduces the risk of tooth abscess. Traumatized teeth should be examined promptly by the dentist.

# Sources
Toxic epidermal necrolysis overview

# Overview
Toxic Epidermal Necrolysis is a life-threatening dermatological condition that is frequently induced by a reaction to medications. It is characterized by the detachment of the top layer of skin (the epidermis) from the lower layers of the skin (the dermis) all over the body. There is broad agreement in the medical literature that TEN can be considered a more severe form of Stevens-Johnson syndrome and debate whether it falls on a spectrum of disease that includes erythema multiforme.

# Historical Perspective

# Classification

# Pathophysiology
Microscopically, TEN causes cell death throughout the epidermis.  Keratinocytes, which are the cells found lower in the dermis,  specialize in holding the skin cells together, undergo necrosis (uncontrolled cell death).

# Causes
Toxic epidermal necrolysis is a rare and usually severe adverse reaction to certain drugs. History of medication use exists in over 95% of patients with TEN. The drugs most often implicated in TEN are antibiotics such as sulfonamides, nonsteroidal anti-inflammatory drugs, allopurinol, antiretroviral drugs, corticosteroids and anticonvulsants such as phenobarbital, phenytoin, carbamazepine, and valproic acid.  The condition might also result from immunizations,  infection with agents such as Mycoplasma pneumoniae or  herpes virus and transplants of bone marrow or organs.

# Differentiating Xyz from Other Diseases

# Epidemiology and Demographics
The incidence is between 0.4 and 1.2 cases per 100,000 each year.

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis
The mortality for toxic epidermal necrolysis is 30-40%.  Loss of the skin leaves patients vulnerable to infections from fungi and bacteria, and can result in septicemia, the leading cause of death in the disease. Death is caused either by infection or by respiratory distress which is either due to pneumonia or damage to the linings of the airway. Microscopic analysis of tissue (especially the degree of dermal mononuclear inflammation and the degree of inflammation in general) can play a role in determining the prognosis of individual cases.

# Diagnosis

## Diagnostic Study of Choice

## History and Symptoms

## Physical Examination

## Laboratory Findings
Sometimes, however, examination of affected tissue under the microscope may be needed to distinguish it between other entities such as staphylococcal scalded skin syndrome. Typical histological criteria of TEN include mild infiltrate of lymphocytes which may obscure the dermoepidermal junction and prominent cell death with basal vacuolar change and individual cell necrosis.

## Electrocardiogram

## X-ray

## Echocardiography and Ultrasound

## CT scan

## MRI

## Other Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Interventions

## Surgery

## Primary Prevention

## Secondary Prevention
Trost asymmetric allylic alkylation
The Trost asymmetric allylic alkylation or Trost AAA or allylic asymmetric substitution is an organic reaction used in asymmetric synthesis.
In the reaction an allylic leaving group in an organic compound is displaced by a nucleophile while at the same time palladium is coordinated to the allyl double bond as a  complex. A typical substrate in this reaction is an allylic compound with a good leaving group such as an acetate group. The reaction was originally developed with a catalyst based on palladium supported the Trost ligand. The nucleophile can be a phenol, a phthalimide or simply water.

# reaction mechanism
Zerovalent palladium is generated in situ from a palladium(II) source and a phosphine ligand such as the Trost ligand. The metal coordinates to the alkene forming a 2 -allyl-Pd0  complex. The next step is oxidative addition in which the leaving group is expelled with inversion of configuration and a 3 -allyl-PdII is created. The nucleophile then adds to the proximus or distal carbon atom of the allyl group regenerating the 2 -allyl-Pd0 complex. The palladium compound detaches from the alkene in the completion of the reaction and can start again in the catalytic cycle. The chirality stored in the ligand is transferred to the final product in one of the complexes formed.

# Scope
An AAA example is the synthesis of an intermediate in the combined total synthesis of galanthamine and morphine with 2.5 mol% Pd2dba3,  7.5 mol% (S,S) Trost ligand, and triethylamine in dichloromethane solvent at room temperature resulting ()-enantiomer of the aryl ether in 64% chemical yield and 77% enantiomeric excess.
Ongoing research is taking place into new asymmetric ligands such as one based on biphenyl and fenchol..

## AAA-Wagner-Meerwein shift
The reaction substrate is also extended to allenes and in a specific ring expansion the AAA reaction is accompanied by a Wagner-Meerwein rearrangement in Scheme 3:
Vaginal cysts (patient information)
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# Overview
A vaginal cyst is a closed sac on or under the vaginal lining that contains fluid or semisolid material.

# What are the symptoms of Vaginal cysts?
Vaginal cysts usually do not cause symptoms, although there may be a soft lump felt in the vaginal wall or protruding from the vagina. Some women with vaginal cysts may have discomfort during sexual intercourse or difficulty inserting tampons.

# What causes Vaginal cysts?
There are several types of vaginal cysts, which can range in size from the size of a pea to that of an orange. Vaginal inclusion cysts are the most common. These may form as a result of trauma sustained by the vaginal walls or following an obstetric or gynecologic procedure, when the lining of the vagina doesn't heal to its normal smoothness.
Gartner's duct cysts develop in the space occupied by the Gartner's duct, usually on the side walls of the vagina. This duct is active during fetal development but ordinarily disappears after birth. In some cases, however, portions of the duct may collect fluid and develop into a vaginal wall cyst later in life.
Benign tumors of the vagina are uncommon and are usually made up of cysts.

# When to seek urgent medical care?
Call your health care provider if a lump is felt inside the vagina or protruding from the vagina.

# Diagnosis
Upon pelvic examination, a mass or bulge of the vaginal wall may be seen or felt by the examiner. A biopsy may be necessary to rule out vaginal cancer, especially if the mass appears to be solid.
If the cyst is located under the bladder or urethra, X-rays may be required to be sure the cyst does not involve these structures.

# Treatment options
The only treatment needed may simply involved routine exams and watching the cysts for growth and other changes.
Surgical excision (removal) may be chosen or possibly required if the cyst is causing symptoms. However, this can sometimes be a very involved surgery and is not recommended unless you are having significant symptoms.

# Where to find medical care for Vaginal cysts?
Directions to Hospitals Treating Vaginal cysts

# What to expect (Outlook/Prognosis)?
The outcome is generally good. Frequently cysts remain small and require no treatment. When surgically removed, the cysts usually do not return.

# Possible complications
There are usually no complications from the cysts themselves. A surgical excision procedure carries a small risk of complications depending on where the cyst is located in relation to other structures.

# Sources
Vesicular acetylcholine transporter
The Vesicular acetylcholine transporter (VAChT) is a neurotransmitter transporter which is responsible for loading acetylcholine (ACh) into secretory organelles in neurons making acetylcholine available for secretion. It is encoded by Solute carrier family 18, member 3 (SLC18A3) gene, located within the first intron of the choline acetyltransferase gene. VAChT is able to transport ACh into vesicles by relying on an exchange between protons (H+) that were previously pumped into the vesicle diffusing out, thus acting as an antiporter. ACh molecules are then carried into the vesicle by the action of exiting protons. Acetylcholine transport utilizes a proton gradient established by a vacuolar ATPase.

# VAChT uptake inhibitors

## Radiolabeled compounds
PET imaging of the VAChT may provide insights into early diagnosis of Alzheimer's disease.
- ()-trans-2-Hydroxy-3-(4-(4-fluorobenzoyl)piperidino)tetralin; racemate: Ki = 2.70 nM for VAChT, 191 nM for 1, and 251 nM for 2
Vitamin D deficiency classification

# Overview
According to the Global Consensus Recommendations on Prevention and Management of Nutritional Rickets and the Institute of Medicine (IOM), vitamin D deficiency is classified into two groups of deficient and Insufficient based on serum 25(OH)D level. It could be further classified as mild, moderate, and severe deficiency. Another classification scheme is based on etiology of vitamin D deficiency which classify it as acquired or inherited.

# Classification
- According to the Global Consensus Recommendations on Prevention and Management of Nutritional Rickets and the Institute of Medicine (IOM), vitamin D deficiency is classified into two groups of deficient and Insufficient based on serum 25(OH) vit D3 level.
- Australian Family Physician classified vitamin D deficiency into three groups based on serum level of 25(OH) vit D.
- Vitamin D deficiency may be classified into two main groups of acquired or inherited based on the etiology.
Weekly EP & ECG rounds at the BIDMC
View more EP & ECG rounds: Weekly EP & ECG rounds at the BIDMC (Archive)

# July 2008
58 year old female admitted to the hospital with shortness of breath for "rule out MI protocol". Cardiac enzymes negative and echo demonstrates normal cardiac structure and function.
Two days following admission: development of chest pain and dyspnea.
This is her ECG on presentation:
This is her ECG on day #2 associated with chest pain and dyspnea:
What is the rhythm and other relevant findings?
- Ventricular Tachycardia
- Atrial fibrillation
- Atrial Flutter
- Acute MI
- 1 and 4
- 2 and 4
The patient had ongoing chest pain and now complained of right flank pain. She was transferred emergently to the cardiac catheterization laboratory where the angiogram demonstrated:
The LAD was treated with thrombectomy and placement of a DES.
Abdominal CT scan confirmed evidence of a right renal infarction. The likely diagnosis was AF related emboli to the LAD and Kidney.
The presumption was that AF had reverted to sinus rhythm prior to the initial day of hospitalization and as atrial mechanical function returned a left atrial appendage clot dislodged.
The cardiac index at the time of PCI was 1.3 and the peak CK reached 11,000.
This is her ECG on presentation:
Why is there RBBB and LAFB and does this require a temporary pacemaker?
This is her telemetry 24 hours after PCI of proximal LAD:
Note the retrograde conduction.
What is the diagnosis and mechanism of this bradyarrhythmia?
- Complete heart block in the AV node
- Complete heart block in the His bundle
- Paroxysmal AV block
Zanamivir dosage and administration

# Dosage and Administration

## Dosing Considerations
- RELENZA is for administration to the respiratory tract by oral inhalation only, using the DISKHALER device provided .
- The 10-mg dose is provided by 2 inhalations (one 5-mg blister per inhalation).*Patients should be instructed in the use of the delivery system. Instructions should include a demonstration whenever possible. If RELENZA is prescribed for children, it should be used only under adult supervision and instruction, and the supervising adult should first be instructed by a healthcare professional .*Patients scheduled to use an inhaled bronchodilator at the same time as RELENZA should use their bronchodilator before taking RELENZA .

## Treatment of Influenza
- The recommended dose of RELENZA for treatment of influenza in adults and pediatric patients aged 7 years and older is 10 mg twice daily (approximately 12 hours apart) for 5 days.
- Two doses should be taken on the first day of treatment whenever possible provided there is at least 2 hours between doses.
- On subsequent days, doses should be about 12 hours apart (e.g., morning and evening) at approximately the same time each day.
- The safety and efficacy of repeated treatment courses have not been studied.

## Prophylaxis of Influenza

### Household Setting
- The recommended dose of RELENZA for prophylaxis of influenza in adults and pediatric patients aged 5 years and older in a household setting is 10 mg once daily for 10 days.
- The dose should be administered at approximately the same time each day.
- There are no data on the effectiveness of prophylaxis with RELENZA in a household setting when initiated more than 1.5 days after the onset of signs or symptoms in the index case.

### Community Outbreaks
- The recommended dose of RELENZA for prophylaxis of influenza in adults and adolescents in a community setting is 10 mg once daily for 28 days.
- The dose should be administered at approximately the same time each day.
- There are no data on the effectiveness of prophylaxis with RELENZA in a community outbreak when initiated more than 5 days after the outbreak was identified in the community.
- The safety and effectiveness of prophylaxis with RELENZA have not been evaluated for longer than 28 days duration.
Zolmitriptan nonclinical toxicology

# Nonclinical Toxicology

### 13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility
Zolmitriptan was administered to mice and rats at doses up to 400 mg/kg/day. Mice were dosed for 85 weeks (males) and 92 weeks (females); rats were dosed for 101 weeks (males) and 86 weeks (females). There was no evidence of drug-induced tumors in mice at plasma exposures (AUC) up to approximately 700 times that in humans at the maximum recommended human dose (MRHD) of 10 mg/day. In rats, there was an increase in the incidence of thyroid follicular cell hyperplasia and thyroid follicular cell adenomas in male rats receiving 400 mg/kg/day. No increase in tumors was observed in rats at 100 mg/kg/day, a dose associated with a plasma AUC approximately 700 times that in humans at the MRHD.
Zolmitriptan was positive in an in vitro bacterial reverse mutation (Ames) assay and in an in vitro chromosomal aberration assay in human lymphocytes. Zolmitriptan was negative in an in vitro mammalian gene cell mutation (CHO/HGPRT) assay and in oral in vivo mouse micronucleus assays in mouse and rat.
Studies of male and female rats administered zolmitriptan prior to and during mating and up to implantation showed no impairment of fertility at oral doses up to 400 mg/kg/day. The plasma exposure (AUC) at this dose was approximately 3000 times that in humans at the MRHD.
21-Hydroxylase Deficiency overview

# Overview
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency (21-OH CAH), in all its forms, accounts for about 95% of diagnosed cases of congenital adrenal hyperplasia, and "CAH" in most contexts refers to 21-hydroxylase deficiency.
- Severe 21-hydroxylase deficiency causes salt-wasting CAH, with life-threatening vomiting and dehydration occurring within the first few weeks of life. Severe 21-hydroxylase deficiency is also the most common cause of ambiguous genitalia due to prenatal virilization of genetically female (XX) infants.
- Moderate 21-hydroxylase deficiency is referred to as simple virilizing CAH; and typically is recognized as causing virilization of prepubertal children.
- Still milder forms of 21-hydroxylase deficiency are referred to as non-classical CAH and can cause androgen effects and infertility in adolescent and adult women.
3-hydroxyisobutyrate dehydrogenase
In enzymology, a 3-hydroxyisobutyrate dehydrogenase (EC 1.1.1.31) also known as -hydroxyisobutyrate dehydrogenase or 3-hydroxyisobutyrate dehydrogenase, mitochondrial (HIBADH) is an enzyme that in humans is encoded by the HIBADH gene.
3-Hydroxyisobutyrate dehydrogenase catalyzes the chemical reaction:
Thus, the two substrates of this enzyme are 3-hydroxy-2-methylpropanoate and NAD+, whereas its 3 products are 2-methyl-3-oxopropanoate, NADH, and H+.
This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is 3-hydroxy-2-methylpropanoate:NAD+ oxidoreductase. This enzyme participates in valine, leucine and isoleucine degradation.

# Function
3-hydroxyisobutyrate dehydrogenase is a tetrameric mitochondrial enzyme that catalyzes the NAD+-dependent, reversible oxidation of 3-hydroxyisobutyrate, an intermediate of valine catabolism, to methylmalonate semialdehyde.

# Structural studies
As of late 2007, 5 structures have been solved for this class of enzymes, with PDB accession codes 1WP4, 2CVZ, 2GF2, 2H78, and 2I9P.
Abacavir dosage and administration

# Dosage and Administration
- A Medication Guide and Warning Card that provide information about recognition of hypersensitivity reactions should be dispensed with each new prescription and refill.
- ZIAGEN may be taken with or without food.

### Adult Patients
The recommended oral dose of ZIAGEN for adults is 600 mg daily, administered as either 300 mg twice daily or 600 mg once daily, in combination with other antiretroviral agents.

### Pediatric Patients
The recommended oral dose of ZIAGEN Oral Solution in HIV-1-infected pediatric patients aged 3 months and older is 8 mg/kg twice daily (up to a maximum of 300 mg twice daily) in combination with other antiretroviral agents.
ZIAGEN is also available as a scored tablet for HIV-1-infected pediatric patients weighing greater than or equal to 14 kg for whom a solid dosage form is appropriate. Before prescribing ZIAGEN Tablets, children should be assessed for the ability to swallow tablets. If a child is unable to reliably swallow ZIAGEN Tablets, the oral solution formulation should be prescribed. The recommended oral dosage of ZIAGEN Tablets for HIV-1-infected pediatric patients is presented in Table 1.

## Dosage Forms and Strengths
ZIAGEN Tablets contain 300 mg of abacavir as abacavir sulfate. The tablets are yellow, biconvex, scored, capsule-shaped, film-coated, and imprinted with GX 623 on both sides.
ZIAGEN Oral Solution contains 20 mg/mL of abacavir as abacavir sulfate. The solution is a clear to opalescent, yellowish, strawberry-banana-flavored liquid.

## Patients With Hepatic Impairment
The recommended dose of ZIAGEN in patients with mild hepatic impairment (Child-Pugh score 5 to 6) is 200 mg twice daily. To enable dose reduction, ZIAGEN Oral Solution (10 mL twice daily) should be used for the treatment of these patients. The safety, efficacy, and pharmacokinetic properties of abacavir have not been established in patients with moderate to severe hepatic impairment; therefore, ZIAGEN is contraindicated in these patients.