Persius/hicric huggingface dataset:
Calcium channel blockers overdose

# Overview
Calcium channel blockers are a class of medication used to treat high blood pressure.
Calcium channel blocker  overdose occurs when someone accidentally or intentionally takes more than the normal or recommended amount of this medication.

# Prognosis
Taking too much of this medication can be extremely dangerous. Death can occur, especially with verapamil. If your low heart rate and blood pressure can be corrected survival is likley. Survival depends on how much and what type of this medication you take along with how quickly you seek medical treatment.

# Diagnosis

## Symptoms
- Confusion
- Constipation
- Dizziness
- Drowsiness
- Irregular heartbeat
- Nausea
- Slow heartbeat
- Slurred speech
- Shortness of breath
- Weakness

## Electrocardiogram
EKG findings in calcium channel blocker overdose include:
- Sinus bradycardia
- 2nd and 3rd degree heart block
- Sinus arrest with nodal escape rhythms
- Accelerated atrioventricular node conduction
- Asystole

# Treatment
- Early treatment with high insulin/glucose to treat severe calcium channel blocker overdose.
- Airway protection to prevent vomiting and aspiration.
- Activated charcoal
- Breathing tube (artificial respiration)
- Fluids through a vein (by IV)
- Laxative
- Medications to increase heart rate and blood pressure, and help reverse poisoning
- Tube through the nose into the stomach to wash out the stomach (gastric lavage)
Carnitine palmitoyltransferase II
Carnitine O-palmitoyltransferase 2, mitochondrial is an enzyme that in humans is encoded by the CPT2 gene.

# Function
Carnitine palmitoyltransferase II precursor (CPT2) is a mitochondrial membrane protein which is transported to the mitochondrial inner membrane. CPT2 together with carnitine palmitoyltransferase I oxidizes long-chain fatty acids in the mitochondria. Defects in this gene are associated with mitochondrial long-chain fatty-acid (LCFA) oxidation disorders and carnitine palmitoyltransferase II deficiency.

# Model organisms
Model organisms have been used in the study of CPT2 function. A conditional knockout mouse line called Cpt2tm1b(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed:  - In-depth immunological phenotyping
Caspofungin indications and usage

# Indications and Usage
CANCIDAS is indicated in adults and pediatric patients (3 months and older) for:
- Empirical therapy for presumed fungal infections in febrile, neutropenic patients
- Treatment of candidemia and the following Candida infections: intra-abdominal abscesses, peritonitis and pleural space infections. CANCIDAS has not been studied in endocarditis, osteomyelitis, and meningitis due to Candida.
- Treatment of esophageal candidiasis
- Treatment of invasive aspergillosis in patients who are refractory to or intolerant of other therapies (e.g., amphotericin B, lipid formulations of amphotericin B, itraconazole). CANCIDAS has not been studied as initial therapy for invasive aspergillosis.
Cassia Stocco dos Santos syndrome

# Overview
Cassia Stocco dos Santos syndrome is autosomal recessive disease with characteristic features of anophthalmia, megalocornea, cardiopathy and skeletal anomalies with the age of onset of infancy and neonates and the prevalence rate of <1 / 1 000 000.

# Pathophysiology
Cassia Stocco dos Santos syndrome is inherited as an autosomal recessive disease.

# Diagnosis

## Symptoms
Cassia Stocco dos Santos syndrome is characterised by anophthalmia, megalocornea, cardiopathy and skeletal anomalies.
Cefamandole clinical pharmacology

# Clinical Pharmacology
After intramuscular administration of a 500-mg dose of cefamandol (cefamandole) to normal volunteers, the mean peak serum concentration was 13 g/mL. After a 1-g dose, the mean peak concentration was 25 g/mL. These peaks occurred at 30 to 120 minutes. Following intravenous doses of 1, 2, and 3 g, serum concentrations were 139, 240, and 533 mcg/mL respectively at 10 minutes. These concentrations declined to 0.8, 2.2, and 2.9 mcg/mL at 4 hours. Intravenous administration of 4-g doses every 6 hours produced no evidence of accumulation in the serum. The half-life after an intravenous dose is 32 minutes; after intramuscular administration, the half-life is 60 minutes.
Sixty-five percent to 85% of cefamandol (cefamandole) is excreted by the kidneys over an 8-hour period, resulting in high urinary concentrations. Following intramuscular doses of 500 mg and 1 g, urinary concentrations averaged 254 and 1,357 mcg/mL respectively. Intravenous doses of 1 and 2 g produced urinary levels averaging 750 and 1,380 mcg/mL respectively. Probenecid slows tubular excretion and doubles the peak serum level and the duration of measurable serum concentrations.
The antibiotic reaches therapeutic levels in pleural and joint fluids and in bile and bone.
Cefixime warnings and precautions

# Warnings and Precautions

### Hypersensitivity Reactions
Anaphylactic/anaphylactoid reactions (including shock and fatalities) have been reported with the use of cefixime.
Before therapy with Suprax is instituted, careful inquiry should be made to determine whether the patient has had previous hypersensitivity reactions to cephalosporins, penicillins, or other drugs. If this product is to be given to penicillin-sensitive patients, caution should be exercised because cross hypersensitivity among beta-lactam antibiotics has been clearly documented and may occur in up to 10% of patients with a history of penicillin allergy. If an allergic reaction to Suprax occurs, discontinue the drug.

### Clostridium difficile-Associated Diarrhea
Clostridium difficile associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including Suprax, and may range in severity from mild diarrhea to fatal colitis. Treatment with antibacterial agents alters the normal flora of the colon leading to overgrowth of C. difficile.
C. difficile produces toxins A and B which contribute to the development of CDAD. Hypertoxin producing isolates of C. difficile cause increased morbidity and mortality, as these infections can be refractory to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea following antibiotic use. Careful medical history is necessary since CDAD has been reported to occur over two months after the administration of antibacterial agents.
If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued. Appropriate fluid and electrolyte management, protein supplementation, antibiotic treatment of C. difficile, and surgical evaluation should be instituted as clinically indicated.

### Dose Adjustment in Renal Impairment
The dose of Suprax should be adjusted in patients with renal impairment as well as those undergoing continuous ambulatory peritoneal dialysis (CAPD) and hemodialysis (HD). Patients on dialysis should be monitored carefully .

### Coagulation Effects
Cephalosporins, including Suprax, may be associated with a fall in prothrombin activity. Those at risk include patients with renal or hepatic impairment, or poor nutritional state, as well as patients receiving a protracted course of antimicrobial therapy, and patients previously stabilized on anticoagulant therapy. Prothrombin time should be monitored in patients at risk and exogenous vitamin K administered as indicated.

### Development of Drug-Resistant Bacteria
Prescribing Suprax (cefixime) in the absence of a proven or strongly suspected bacterial infection is unlikely to provide benefit to the patient and increases the risk of the development of drug-resistant bacteria.
Ceftaroline indications and usage
Teflaro (ceftaroline fosamil) is indicated for the treatment of patients with the following infections caused by susceptible isolates of the designated microorganisms.
1. Acute Bacterial Skin and Skin Structure Infections
Teflaro is indicated for the treatment of acute bacterial skin and skin structure infections (ABSSSI) caused by susceptible isolates of the following Gram-positive and Gram-negative microorganisms:Staphylococcus aureus(including methicillin-susceptible and -resistant isolates),Streptococcus pyogenes,Streptococcus agalactiae,Escherichia coli,Klebsiella pneumoniae, and Klebsiella oxytoca.
2. Community-Acquired Bacterial Pneumonia
Teflaro is indicated for the treatment of community-acquired bacterial pneumonia (CABP) caused by susceptible isolates of the following Gram-positive and Gram-negative microorganisms:Streptococcus pneumoniae(including cases with concurrent bacteremia),Staphylococcus aureus(methicillin-susceptible isolates only),Haemophilus influenzae, Klebsiella pneumoniae, Klebsiella oxytoca,andEscherichia coli.

# Usage
To reduce the development of drug-resistant bacteria and maintain the effectiveness of Teflaro and other antibacterial drugs, Teflaro should be used to treat only ABSSSI or CABP that are proven or strongly suspected to be caused by susceptible bacteria. Appropriate specimens for microbiological examination should be obtained in order to isolate and identify the causative pathogens and to determine their susceptibility to ceftaroline. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Ceftazidime clinical pharmacology
After IV administration of 500 mg and 1 g doses of ceftazidime over 5 minutes to normal adult male volunteers, mean peak serum concentrations of 45 and 90 mcg/mL, respectively, were achieved. After IV infusion of 500 mg, 1 g, and 2 g doses of ceftazidime over 20 to 30 minutes to normal adult male volunteers, mean peak serum concentrations of 42, 69, and 170 mcg/mL, respectively, were achieved. The average serum concentrations following IV infusion of 500 mg, 1 g, and 2 g doses to these volunteers over an 8-hour interval are given in Table 1.
The absorption and elimination of ceftazidime were directly proportional to the size of the dose. The half-life following IV administration was approximately 1.9 hours. Less than 10% of ceftazidime was protein bound. The degree of protein binding was independent of concentration. There was no evidence of accumulation of ceftazidime in the serum in individuals with normal renal function following multiple IV doses of 1 and 2 g every 8 hours for 10 days.
The presence of hepatic dysfunction had no effect on the pharmacokinetics of ceftazidime in individuals administered 2 g intravenously every 8 hours for 5 days. Therefore, a dosage adjustment from the normal recommended dosage is not required for patients with hepatic dysfunction, provided renal function is not impaired.
Approximately 80% to 90% of an IV dose of ceftazidime is excreted unchanged by the kidneys over a 24-hour period. After the IV administration of single 500 mg or 1 g doses, approximately 50% of the dose appeared in the urine in the first 2 hours. An additional 20% was excreted between 2 and 4 hours after dosing, and approximately another 12% of the dose appeared in the urine between 4 and 8 hours later. The elimination of ceftazidime by the kidneys resulted in high therapeutic concentrations in the urine.
The mean renal clearance of ceftazidime was approximately 100 mL/min. The calculated plasma clearance of approximately 115 mL/min indicated nearly complete elimination of ceftazidime by the renal route. Administration of probenecid before dosing had no effect on the elimination kinetics of ceftazidime. This suggested that ceftazidime is eliminated by glomerular filtration and is not actively secreted by renal tubular mechanisms.
Since ceftazidime is eliminated almost solely by the kidneys, its serum half-life is significantly prolonged in patients with impaired renal function. Consequently, dosage adjustments in such patients as described in the DOSAGE AND ADMINISTRATION     section are suggested.
Therapeutic concentrations of ceftazidime are achieved in the following body tissues and fluids.
Ceftizoxime clinical pharmacology

# Clinical Pharmacology
Following IV administration of 1, 2, and 3 gram doses of Cefizox to normal volunteers, the following serum levels were obtained.
A serum halflife of approximately 1.7 hours was observed after IV administration.
Cefizox is 30% protein bound.
Cefizox is not metabolized, and is excreted virtually unchanged by the kidneys in 24 hours. This provides a high urinary concentration. Concentrations greater than 6000 g/mL have been achieved in the urine by 2 hours after a 1 gram dose of Cefizox intravenously. Probenecid slows tubular secretion and produces even higher serum levels, increasing the duration of measurable serum concentrations.
Cefizox achieves therapeutic levels in various body fluids, e.g., cerebrospinal fluid (in patients with inflamed meninges), bile, surgical wound fluid, pleural fluid, aqueous humor, ascitic fluid, peritoneal fluid, prostatic fluid and saliva, and in the following body tissues: heart, gallbladder, bone, biliary, peritoneal, prostatic, and uterine.
In clinical experience to date, no disulfiramlike reactions have been reported with Cefizox.
Ceftriaxone clinical pharmacology
Average plasma concentrations of ceftriaxone following a single 30 minute intravenous (IV) infusion of a 0.5, 1 or 2 gm dose in healthy subjects are presented in Table 1.
Multiple IV doses ranging from 0.5 to 2 gm at 12 to 24 hour intervals resulted in 15% to 36% accumulation of ceftriaxone above single dose values.
Ceftriaxone concentrations in urine are shown in Table 2.
Thirty-three percent to 67% of a ceftriaxone dose was excreted in the urine as unchanged drug and the remainder was secreted in the bile and ultimately found in the feces as microbiologically inactive compounds. After a 1 gm IV dose, average concentrations of ceftriaxone, determined from 1 to 3 hours after dosing, were 581 mcg/mL in the gallbladder bile, 788 mcg/mL in the common duct bile, 898 mcg/mL in the cystic duct bile, 78.2 mcg/gm in the gallbladder wall and 62.1 mcg/mL in the concurrent plasma.
Over a 0.15 to 3 gm dose range in healthy adult subjects, the values of elimination half-life ranged from 5.8 to 8.7 hours; apparent volume of distribution from 5.78 to 13.5 L; plasma clearance from 0.58 to 1.45 L/hour; and renal clearance from 0.32 to 0.73 L/hour. Ceftriaxone is reversibly bound to human plasma proteins, and the binding decreased from a value of 95% bound at plasma concentrations of <25 mcg/mL to a value of 85% bound at 300 mcg/mL. Ceftriaxone crosses the blood placenta barrier.
The average values of maximum plasma concentration, elimination half-life, plasma clearance and volume of distribution after a 50 mg/kg IV dose and after a 75 mg/kg IV dose in pediatric patients suffering from bacterial meningitis are shown in Table 3. Ceftriaxone penetrated the inflamed meninges of infants and pediatric patients; CSF concentrations after a 50 mg/kg IV dose and after a 75 mg/kg IV dose are also shown in Table 3.
Compared to that in healthy adult subjects, the pharmacokinetics of ceftriaxone were only minimally altered in elderly subjects and in patients with renal impairment or hepatic dysfunction (Table 4); therefore, dosage adjustments are not necessary for these patients with ceftriaxone dosages up to 2 gm per day. Ceftriaxone was not removed to any significant extent from the plasma by hemodialysis; in six of 26 dialysis patients, the elimination rate of ceftriaxone was markedly reduced.
The elimination of ceftriaxone is not altered when ceftriaxone for injection is co-administered with probenecid.
Interaction with Calcium: Two in vitro studies, one using adult plasma and the other neonatal plasma from umbilical cord blood have been carried out to assess interaction of ceftriaxone and calcium. Ceftriaxone concentrations up to 1 mM (in excess of concentrations achieved in vivo following administration of 2 grams ceftriaxone infused over 30 minutes) were used in combination with calcium concentrations up to 12 mM (48 mg/dL). Recovery of ceftriaxone from plasma was reduced with calcium concentrations of 6 mM (24 mg/dL) or higher in adult plasma or 4 mM (16 mg/dL) or higher in neonatal plasma. This may be reflective of ceftriaxone-calcium precipitation.
Cerivastatin detailed information

# Overview
In pharmacology, cerivastatin (Baycol, Lipobay) is a synthetic member of the class of statins, used to lower cholesterol and prevent cardiovascular disease. It was withdrawn from the market in 2001 because of the high rate of serious side-effects.
Cerivastatin was marketed by the pharmaceutical company Bayer A.G. in the late 1990s as a new synthetic statin, to compete with Pfizer's highly successful Lipitor.
During post-marketing surveillance, 52 deaths were reported in patients using cerivastatin, mainly from rhabdomyolysis and its resultant renal failure. Risks were higher in patients using fibrates (mainly gemfibrozil/Lopid) and in patients using the high (0.8 mg/day) dose of cerivastatin. Another 385 nonfatal cases of rhabdomyolysis were reported. This put the risk of this (rare) complication at 5-10 times that of the other statins.
In 2001, Bayer announced the voluntary withdrawal of the drug from the market.

# Important Note
On August 8, 2001 the U.S. Food and Drug Administration (FDA) announced that Bayer Pharmaceutical Division voluntarily withdrew Baycol from the U.S. market, due to reports of fatal Rhabdomyolysis, a severe adverse reaction from this cholesterol-lowering (lipid-lowering) product. The FDA agrees with and supports this decision. All patients taking Baycol should contact their healthcare providers to discuss alternative treatments.
Chloroquine phosphate description

# Description
Chloroquine Phosphate, USP, is a 4-aminoquinoline compound for oral administration. It is a white, odorless, bitter tasting, crystalline substance, freely soluble in water.
Chloroquine Phosphate Tablets are an antimalarial and amebicidal drug.
Each tablet, for oral administration, contains 250 mg chloroquine phosphate (equivalent to 150 mg base) or 500 mg chloroquine phosphate (equivalent to 300 mg base).
Inactive ingredients 250 mg: Calcium Stearate, Colloidal Silicon Dioxide, Dibasic Calcium Phosphate, Microcrystalline Cellulose, and Talc.
Inactive ingredients 500 mg: Colloidal Silicon Dioxide, Corn Starch, Lactose Monohydrate, Magnesium Stearate, Microcrystalline Cellulose, Polyvinylpyrrolidone, Sodium Starch Glycolate, and Titanium Dioxide. Film Coating and Polishing Solution contains: D&C Red #27 Aluminum Lake, D&C Yellow #10 Aluminum Lake, FD&C Blue #1 Aluminum Lake, Hypromellose, Polyethylene Glycol, Polysorbate 80 and Titanium Dioxide.
Chemically, it is 7-chloro-4-amino] quinoline phosphate (1:2) and has the following structural formula:
Chronic fatigue syndrome overview

# Overview
Chronic fatigue syndrome (CFS) is one of several names given to a poorly understood, variably debilitating disorder of uncertain causation. CFS is thought, based on a 1999 study, to affect approximately 4 per 1,000 adults in the United States.
Other names for this syndrome are:
- Myalgic Encephalomyelitis
- Systemic Exertion Intolerance Disease. Proposed by the Institute of Medicine in 2015.
For unknown reasons, CFS occurs more often in women than men, and in people in their 40s and 50s. The illness is estimated to be less prevalent among children and adolescents, but studies are contradictory as to the degree.
CFS often manifests with widespread myalgia and arthralgia, cognitive difficulties, chronic mental and physical exhaustion, often severe, and other characteristic symptoms in a previously healthy and active person. Despite promising avenues of research, there remains no assay or pathological finding which is widely accepted to be diagnostic of CFS. It remains a diagnosis of exclusion based largely on patient history and symptomatic criteria, although a number of tests can aid diagnosis. Whereas there is agreement on the genuine threat to health, happiness, and productivity posed by CFS, various physicians' groups, researchers, and patient activists champion very different nomenclature, diagnostic criteria, etiologic hypotheses, and treatments, resulting in controversy about nearly all aspects of the disorder. Even the term chronic fatigue syndrome is controversial because a large part of the patient community believes the name trivializes the illness.
Chronic fatigue syndrome is not the same as "chronic fatigue". Fatigue is a common symptom in many illnesses, but CFS is a multi-systemic disease and is relatively rare by comparison. Definitions (other than the 1991 UK Oxford criteria) require a number of features, the most common being severe mental and physical exhaustion which is "unrelieved by rest" (1994 Fukuda definition), and may be worsened by even trivial exertion (a mandatory diagnostic criterion according to some systems). Most diagnostic criteria require that symptoms must be present for at least six months, and all state the symptoms must not be caused by other medical conditions. CFS patients may report many symptoms which are not included in all diagnostic criteria, including muscle weakness, cognitive dysfunction, hypersensitivity, orthostatic intolerance, digestive disturbances, depression, poor immune response, and cardiac and respiratory problems. It is unclear if these symptoms represent co-morbid conditions or are produced by an underlying etiology of CFS. Some cases improve over time, and treatments (though none are universally accepted) bring a degree of improvement to many others, though full resolution may be only 5-10% according to the United States Centers for Disease Control and Prevention (CDC).
Chronic functional abdominal pain

# Overview
Chronic functional abdominal pain (CFAP) is the ongoing presence of abdominal pain for which there is no known medical explanation.  It is quite similar to, but less common than, irritable bowel syndrome (IBS), and many of the same treatments for IBS can also be of benefit to those with CFAP.  The fundamental difference between IBS and CFAP is that in CFAP, unlike in IBS, there is no change in bowel habits such as constipation or diarrhea.  Bowel dysfunction is a necessary diagnostic criteria of IBS.

# Pathophysiology
CFAP is characterized by chronic pain, with no physical explanation or findings (no structural, infectious, or mechanical causes can be found).  It is theorized that CFAP is a disorder of the nervous system where normal nerve impulses are amplified "like a stereo system turned up too loud" resulting in pain.  This visceral hypersensitivity may be a stand-alone cause of CFAP, or CFAP may result from the same type of brain-gut nervous system disorder that underlies IBS.  As with IBS, low doses of antidepressants have been found useful in controlling the pain of CFAP.

# Causes

## Common Causes
- Gynecologic etiologies
Dysmenorrhea
Endometriosis
Mullerian abnormalities
Pelvic inflammatory disease
Ovarian abnormalities
- Dysmenorrhea
- Endometriosis
- Mullerian abnormalities
- Pelvic inflammatory disease
- Ovarian abnormalities
- Abdominal etiologies

# Treatment

## Medical Therapy
Non-pharmaceutical approaches to CFAP also overlap with treatments for irritable bowel syndrome. This includes enteric coated peppermint oil capsules, which act as anti-spasmodics to relax the gut and also have pain-killing properties due to the methyl salicylate that naturally occurs in peppermint.  Gut-directed hypnotherapy or self-hypnosis can also mitigate the hyperreactive nervous system of CFAP, and help alleviate abdominal pain.