Persius/hicric huggingface dataset:
Penicillin G procaine indications and usage

# Indications and Usage
To reduce the development of drug-resistant bacteria and maintain the effectiveness of Bicillin C-R and other antibacterial drugs, Bicillin C-R should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria. 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.
This drug is indicated in the treatment of moderately severe infections due to penicillin-G-susceptible microorganisms that are susceptible to serum levels common to this particular dosage form. Therapy should be guided by bacteriological studies (including susceptibility testing) and by clinical response.
Bicillin C-R is indicated in the treatment of the following in adults and pediatric patients:
Moderately severe to severe infections of the upper-respiratory tract, scarlet fever, erysipelas, and skin and soft-tissue infections due to susceptible streptococci.
NOTE: Streptococci in Groups A, C, G, H, L, and M are very sensitive to penicillin G. Other groups, including Group D (enterococci), are resistant. Penicillin G sodium or potassium is recommended for streptococcal infections with bacteremia.
Moderately severe pneumonia and otitis media due to susceptible Streptococcus pneumoniae.
NOTE: Severe pneumonia, empyema, bacteremia, pericarditis, meningitis, peritonitis, and arthritis of pneumococcal etiology are better treated with penicillin G sodium or potassium during the acute stage.
When high, sustained serum levels are required, penicillin G sodium or potassium, either IM or IV, should be used. This drug should not be used in the treatment of venereal diseases, including syphilis, gonorrhea, yaws, bejel, and pinta.
Perinatal infection resident survival guide
Synonyms and keywords: Neonatal infection; TORCH infection

# Overview
Most of the perinatal infections in the neonate are bacterial. These infections may be acquired from the mother prior to or at birth or from environmental sources. Premature babies are prone to perinatal infections. Neonates, especially those born prematurely have very limited ability to express symptoms, so, even minor deviations from normal behaviour should suggest bacterial disease. Chronic congenital and perinatal infections are usually asymptomatic in mother and neonate and may remain latent or sub-clinically active in host tissue for prolonged time.It may cause insidious injury to the central nervous and perceptual systems. When noticeable, these infections almost invariably cause mental or perceptual handicaps or both. Cytomegalovirus is the most common cause of congenital infections and the fetal effects of primary maternal infection during gestation can be devastating.Perinatal infection occurring in the 1st few days to 14 days occurs due to contact with the pathogens present in the cervico-vaginal canal during delivery. causes are Escherichia coli, Group B beta haemolytic Streptococci,Gonococci, Listeria monocytogenes ,Bacteroides species, Candida albicans, Cytomegalo virus,Herpes Simplex Virus Type-2.The mortality and morbidity associated with either acute or chronic infections is quite high. So, appropriate diagnosis and treatment is required and should be aggressive.

# Causes
Perinatal infection occurring in the 1st few days to 14 days occurs due to contact with the pathogens present in the cervico-vaginal canal during delivery.
causes are
- Escherichia coli
- Group B beta haemolytic Streptococci
- Gonococci
- Listeria monocytogenes
- Bacteroides species
- Candida albicans
- Cytomegalo virus
- Herpes Simplex Virus Type-2
Perinatal infections that occurs late, usually 3 to 6 weeks after birth are caused by environmental pathogens.
Causes are
- Klebsiella
- Aerobacter
- Proteus species
- Staphylococcus aureus
- Haemophilus influenzae
- Pseudomonas aeruginosa
- Coxsackie B virus
- Candida albicans
- Echovirus
- Influenza virus
- Parainfluenzae virus
- Respiratory syncytial virus
Several vertically transmitted infections are included in the TORCH complex:
- T  toxoplasmosis from Toxoplasma gondii
- O  other infections (see below)
- R  rubella
- C  cytomegalovirus
- H  herpes simplex virus-2 or neonatal herpes simplex
Other infections include:
- Parvovirus B19
- Coxsackievirus
- Chickenpox (caused by varicella zoster virus)
- Chlamydia infection
- HIV
- Human T-lymphotropic virus
- Syphilis
- Zika fever, caused by Zika virus, can cause microcephaly and other brain defects in the child.
- Hepatitis B

# Diagnosis

# Treatment

# Do's
- The content in this section is in bullet points.

# Don'ts
- The content in this section is in bullet points.
Perturbation of biological system (Biology)
Perturbation or perturb may refer to any of numerous concepts in several fields:
- Perturbation theory, mathematical methods that give approximate solutions to problems that cannot be solved exactly
- Perturbation (geology), changes in the nature of alluvial deposits over time
- Perturbation (astronomy), alterations to an object's orbit caused by gravitational interactions with other bodies
- Perturbation theory (quantum mechanics), a set of approximation schemes directly related to mathematical perturbation for describing a complicated quantum system in terms of a simpler one
- Perturbation (biology), an alteration of the function of a biological system, induced by external or internal mechanisms
- Perturbation (economic), an alteration of the function of an economic system, induced by external or internal mechanisms
- Perturbation (machine learning), making changes in the dataset to (re)learn a classifier (used in bagging and boosting).
Pharmacotherapy in patients undergoing CABG

# 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization (Please do not edit). Pharmacotherapy in patients undergoing CABG

## Insulin Infusion and Other Measures to Reduce Sternal Wound Infection in Patients Undergoing CABG

##  Antiplatelet Therapy in Patients Undergoing CABG

## Beta Blockers and Amiodarone in Patients Undergoing CABG

# 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization (Please do not edit). Pharmacotherapy in patients after CABG

## Antiplatelet Therapy in Patients After CABG

## Beta Blockers for the Prevention of Atrial Fibrillation After CABG
Pineocytoma echocardiography and ultrasound

# Overview
There are no echocardiography/ultrasound findings associated with .
OR
Echocardiography/ultrasound may be helpful in the diagnosis of . Findings on an echocardiography/ultrasound suggestive of/diagnostic of  include , , and .
OR
There are no echocardiography/ultrasound  findings associated with . However, an echocardiography/ultrasound  may be helpful in the diagnosis of complications of , which include , , and .

# Echocardiography/Ultrasound
There are no echocardiography/ultrasound findings associated with .
OR
Echocardiography/ultrasound may be helpful in the diagnosis of . Findings on an echocardiography/ultrasound suggestive of/diagnostic of  include:
OR
There are no echocardiography/ultrasound findings associated with . However, an echocardiography/ultrasound  may be helpful in the diagnosis of complications of , which include:
Piperacillin tazobactam sodium how supplied

# How Supplied/Storage And Handling
ZOSYN (piperacillin and tazobactam) for Injection are supplied as single-dose vials and pharmacy bulk vials in the following sizes:
Each ZOSYN 2.25 g vial provides piperacillin sodium equivalent to 2 grams of piperacillin and tazobactam sodium equivalent to 0.25 g of tazobactam. Each vial contains 5.58 mEq (128 mg) of sodium. Supplied 10 per boxNDC 0206-8852-16
Each ZOSYN 3.375 g vial provides piperacillin sodium equivalent to 3 grams of piperacillin and tazobactam sodium equivalent to 0.375 g of tazobactam. Each vial contains 8.38 mEq (192 mg) of sodium. Supplied 10 per boxNDC 0206-8854-16
Each ZOSYN 4.5 g vial provides piperacillin sodium equivalent to 4 grams of piperacillin and tazobactam sodium equivalent to 0.5 g of tazobactam. Each vial contains 11.17 mEq (256 mg) of sodium. Supplied 10 per boxNDC 0206-8855-16
Each ZOSYN 40.5 g pharmacy bulk vial provides piperacillin sodium equivalent to 36 grams of piperacillin and tazobactam sodium equivalent to 4.5 grams of tazobactam. Each pharmacy bulk vial contains 100.4 mEq (2,304 mg) of sodium. NDC 0206-8859-10.
ZOSYN for Injection vials should be stored at controlled room temperature (20C to 25C ) prior to reconstitution.
ZOSYN (piperacillin and tazobactam) Injection in Galaxy Containers are supplied as a frozen, iso-osmotic, sterile, nonpyrogenic solution in single dose plastic containers as follows:
2.25 g (piperacillin sodium equivalent to 2 g piperacillin/tazobactam sodium equivalent to 0.25 g tazobactam) in 50 mL. Each container has 5.58 mEq (128 mg) of sodium. Supplied 24/boxNDC 0206-8860-02
3.375 g (piperacillin sodium equivalent to 3 g piperacillin/tazobactam sodium equivalent to 0.375 g tazobactam) in 50 mL. Each container has 8.38 mEq (192 mg) of sodium. Supplied 24/boxNDC 0206-8861-02
4.5 g (piperacillin sodium equivalent to 4 g piperacillin/tazobactam sodium equivalent to 0.5 g tazobactam) in 100 mL. Each container has 11.17 mEq (256 mg) of sodium. Supplied 12/boxNDC 0206-8862-02
ZOSYN Injection in Galaxy Containers should be stored at or below -20C (-4F).
Renal vein thrombosis (patient information)
For the WikiDoc page for this topic, click here

# Overview
Renal vein thrombosis is a blood clot that develops in the vein that drains blood from the kidney.

# What are the symptoms of Renal vein thrombosis?
- Blood clot to the lung
- Bloody urine
- Decreased urine output
- Flank pain or low back pain

# What causes Renal vein thrombosis?
Renal vein thrombosis is an uncommon disorder that may be caused by:
- Abdominal aortic aneurysm
- Clotting disorders
- Dehydration (mostly in infants)
- Estrogen use
- Nephrotic syndrome
- Pregnancy
- Scar formation with pressure on the renal vein
- Trauma (to the back or abdomen)
- Tumor
In adults, the most common cause is nephrotic syndrome. In infants, the most common cause is dehydration.

# Who is at highest risk?
Its a relatively less common disease but any of the above mentioned condition can predispose risk for renal vein thrombosis.

# When to seek urgent medical care?
Call your health care provider if you have symptoms of renal vein thrombosis.
If you have experienced renal vein thrombosis, call your health care provider if you develop decreased urine output, difficulty breathing, or other new symptoms.

# Diagnosis
An examination may not reveal the specific problem, but may indicate nephrotic syndrome or other causes of renal vein thrombosis.
- Abdominal CT scan
- Abdominal MRI
- Abdominal ultrasound
- Duplex Doppler exam of the renal veins
- Urinalysis may show protein in the urine or red blood cells in the urine
- X-ray of the kidney veins (venography)

# Treatment options
The treatment is focused on preventing new clot formations and reducing the risk of the clot traveling to other locations in the body (embolization).
You may get medications that prevent blood clotting (anticoagulants) to stop new clots from forming. Your doctor may recommend bedrest or limited activity for a brief period.
If severe acute renal failure develops, you may need dialysis, but it should be temporary.

# Where to find medical care for Renal vein thrombosis?
Directions to Hospitals Treating Renal vein thrombosis

# What to expect (Outlook/Prognosis)?
Renal vein thrombosis usually gets better over time without permanently injuring the kidneys.

# Possible complications
- Acute renal failure (especially if thrombosis occurs in a dehydrated child)
- Blood clot moves to the lungs (pulmonary embolism)
- Formation of new blood clots

# Prevention
There is no specific prevention for renal vein thrombosis in most people. Keeping enough fluids in the body to avoid dehydration may help reduce its risk.
In people who have had a kidney transplant, aspirin is sometimes used to prevent renal vein thrombosis. In people with certain chronic kidney diseases, blood thinners such as warfarin may be recommended.
Rifampin isoniazid pyrazinamide description

# Description
RIFATER (rifampin/isoniazid/pyrazinamide USP) tablets are combination tablets containing 120 mg rifampin, 50 mg isoniazid, and 300 mg pyrazinamide for use in antibacterial therapy. The tablets also contain as inactive ingredients: povidone, carboxymethylcellulose sodium, calcium stearate, sodium lauryl sulfate, sucrose, talc, acacia, titanium dioxide, kaolin, magnesium carbonate, colloidal silicon dioxide, dried aluminum hydroxide gel, ferric oxide, black iron oxide, carnauba wax, white beeswax, colophony, hard paraffin, lecithin, shellac, and propylene glycol. The RIFATER triple therapy combination was developed for dosing convenience.

## Rifampin
Rifampin is a semisynthetic antibiotic derivative of rifamycin SV. Rifampin is a red-brown crystalline powder very slightly soluble in water at neutral pH, freely soluble in chloroform, soluble in ethyl acetate and methanol. Its molecular weight is 822.95 and its chemical formula is C43H58N4O12. The chemical name for rifampin is either:
3--methyl]-rifamycin;
-r
5,6,9,17,19,21-hexahydroxy-23methoxy-2,4,12,16,18,20,22 heptamethyl-8--2,7-(epoxypentadecatrienimino)naphthofuran-1,11(2H)-dione 21-acetate.
Its structural formula is:

## Isoniazid
Isoniazid is the hydrazide of isonicotinic acid. It is a colorless or white crystalline powder or white crystals. It is odorless and slowly affected by exposure to air and light. It is freely soluble in water, sparingly soluble in alcohol and slightly soluble in chloroform and in ether. Its molecular weight is 137.14 and its chemical formula is C6H7N3O.
The chemical name for isoniazid is 4-pyridinecarboxylic acid, hydrazide and its structural formula is:

## Pyrazinamide
Pyrazinamide, the pyrazine analogue of nicotinamide, is a white, crystalline powder, stable at room temperature, and sparingly soluble in water. The chemical name for pyrazinamide is pyrazinecarboxamide and its molecular weight is 123.11. Its chemical formula is C5H5N3O and its structural formula is:
ST Elevation Myocardial Infarction Template

# Classification
Acute myocardial infarction is a type of acute coronary syndrome, which is most frequently (but not always) a manifestation of coronary artery disease. The acute coronary syndromes include ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).
Depending on the location of the obstruction in the coronary circulation, different zones of the heart can become injured. Using the anatomical terms of location, one can describe anterior, inferior, lateral, apical and septal infarctions (and combinations, such as anteroinferior, anterolateral, and so on).  For example, an occlusion of the left anterior descending coronary artery will result in an anterior wall myocardial infarct.
Another distinction is whether a MI is subendocardial, affecting only the inner third to one half of the heart muscle, or transmural, damaging (almost) the entire wall of the heart. The inner part of the heart muscle is more vulnerable to oxygen shortage, because the coronary arteries run inward from the epicardium to the endocardium, and because the blood flow through the heart muscle is hindered by the heart contraction.
The phrases transmural and subendocardial infarction used to be considered synonymous with Q-wave and non-Q-wave myocardial infarction respectively, based on the presence or absence of Q waves on the ECG. It has since been shown that there is no clear correlation between the presence of Q waves with a transmural infarction and the absence of Q waves with a subendocardial infarction, but Q waves are associated with larger infarctions, while the lack of Q waves is associated with smaller infarctions. The presence or absence of Q-waves also has clinical importance, with improved outcomes associated with a lack of Q waves.
The phrase "massive heart attack" is not a recognized medical term.
Sandbox:Otitis externa history and symptoms

# Overview
Symptoms for all forms of otitis externa are primarily pain, itching, and swelling of the ear canal. Symptoms of chronic, recurrent otitis externa include lack of earwax and buildup of dead skin causing narrowing of the ear canal. Symptoms of malignant necrotizing otitis externa include severe ear pain, facial paralysis, difficulty opening mouth, and difficulty swallowing. History of allergies, aquatic-based occupations, or exposure to sources of immunocompromise, including chemotherapy and diabetes mellitus should be considered in otitis externa patients.

# History
- History of allergies should be considered for dermatitis caused otitis externa.
- History of an occupation involving swimming, scuba-diving, or surfing should be considered.
- Sources of immunocompromise in a patient history should be considered for malignant otitis externa:
Chemotherapy
Diabetes mellitus
- Chemotherapy
- Diabetes mellitus

# Symptoms
Symptoms of acute otitis externa include the following:
- Ear pain
- Itching of the ear canal
- Swelling of the ear canal
- Redness of the ear canal
- Pressure inside the ear
- Discharge
- Pain in the jaw when in motion
- Partial hearing loss
- Swollen lymph nodes
- Scaley skin in the ear canal
Symptoms of chronic, recurrent otitis externa include the following:
- Persistent itching of the ear
- Lack of earwax
- Buildup of dead skin causing narrowing of the ear canal
Symptoms of malignant necrotizing otitis externa include the following:
- Severe ear pain
- Facial paralysis
- Difficulty opening mouth
- Difficulty swallowing
Sandbox:Otitis externa physical examination

# Overview
Physical examination of the ear canal will reveal findings indicative of acute, chronic, and malignant necrotizing otitis externa. For acute otitis externa, the patient can appear ill if the cause is infectious and is accompanied by fever. Patients with chronic otitis externa are usually well-appearing. Malignant necrotizing otitis externa patients are usually ill-appearing due to the accompanying fever and facial palsies.

# Physical Examination

## HEENT and Neck
- The following physical exam findings in the ear canal are indicative of otitis externa:
Erythema and edema.
Tenderness of the tragus and auricle.
Cellulitis of the auricle and ear canal.
Otorrhea
Granulation tissue
Stenosis of the ear canal.
Buildup of mycotic debris.
Lack of cerumen.
- Erythema and edema.
- Tenderness of the tragus and auricle.
- Cellulitis of the auricle and ear canal.
- Otorrhea
- Granulation tissue
- Stenosis of the ear canal.
- Buildup of mycotic debris.
- Lack of cerumen.
- In the neck, lymphadenitis may be present in acute otitis externa.
- In malignant necrotizing otitis externa, the patient may present signs of trismus and partial facial palsy.

## Appearance of the Patient
- For acute otitis externa, the patient can appear ill if the cause is infectious and is accompanied by fever.
- Patients with chronic otitis externa are usually well-appearing.
- Malignant necrotizing otitis externa patients are usually ill-appearing due to the accompanying fever and facial palsies.

# Key Examples of Otitis Externa Physical Findings
- A severe case of acute otitis externa.  Note the narrowing of the external auditory channel, the prominent amounts of exudate and swelling of the auricle. Case presented by James Heilman, MD.
- A mild case of otitis externa. Case presented by Klaus D. Peter.
Sterol regulatory element-binding protein 1
Sterol regulatory element-binding transcription factor 1 (SREBF1) also known as sterol regulatory element-binding protein 1 (SREBP-1) is a protein that in humans is encoded by the SREBF1 gene.
This gene is located within the Smith-Magenis syndrome region on chromosome 17. Two transcript variants encoding different isoforms have been found for this gene.  The isoforms are SREBP-1a and -1c (ADD-1).

# Function
The proteins encoded by this gene are transcription factors that bind to a sequence in the promoter of different genes, called sterol regulatory element-1 (SRE1).  This element is a decamer flanking the LDL receptor gene and other genes involved in, for instance, sterol biosynthesis. The protein is synthesized as a precursor that is attached to the nuclear membrane and endoplasmic reticulum. Following cleavage, the mature protein translocates to the nucleus and activates transcription by binding to the SRE1. Sterols inhibit the cleavage of the precursor, and the mature nuclear form is rapidly catabolized, thereby reducing transcription. The protein is a member of the basic helix-loop-helix-leucine zipper (bHLH-Zip) transcription factor family.
SREBP-1c regulates genes required for glucose metabolism and fatty acid and lipid production and its expression is regulated by insulin.   Insulin-stimulated SBREP-1c increases glycolysis by activation of glucokinase enzyme, and increases lipogenesis (conversion of carbohydrates into fatty acids).
SREBP-1a regulates genes related to lipid and cholesterol production and its activity is regulated by sterol levels in the cell.

# Interactions
SREBF1 has been shown to interact with:
- CREB-binding protein,
- DAX1
- LMNA, and
- TWIST2.
- BHLHE40
- BHLHE41
Sterol regulatory element-binding protein 2
Sterol regulatory element-binding protein 2 (SREBP-2) also known as sterol regulatory element binding transcription factor 2 (SREBF2) is a protein that in humans is encoded by the SREBF2 gene.

# Function
This gene encodes a ubiquitously expressed transcription factor that controls cholesterol homeostasis by stimulating transcription of sterol-regulated genes. The encoded protein contains a basic helix-loop-helix leucine zipper (bHLH-Zip) domain.
Various single nucleotide polymorphisms (SNPs) of the SREBF2 have been identified and some of them are found to be associated with higher risk of knee osteoarthritis. 

# Interactions
SREBF2 has been shown to interact with INSIG1 and CREB-binding protein.
Streptococcus pneumoniae infection overview

# Overview
Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic diplococcus bacterium and a member of the genus Streptococcus. A significant human pathogen, S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century and is the subject of many humoral immunity studies.
Despite the name, the organism causes many types of infection other than pneumonia, including acute sinusitis, otitis media, meningitis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.
S. pneumoniae is the most common cause of bacterial meningitis in adults and children, and is one of the top two isolates found in otitis media. Pneumococcal pneumonia is more common in the very young and the very old.
S. pneumoniae can be differentiated from Streptococcus viridans, which is also alpha hemolytic, using an optochin test, as S. pneumoniae is optochin sensitive. The encapsulated, gram-positive coccoid bacteria have a distinctive morphology on gram stain, the so-called, "lancet shape." It has a polysaccharide capsule that acts as a virulence factor for the organism; 91 different capsular types are known, and these types differ in virulence, prevalence, and extent of drug resistance.