Persius/hicric huggingface dataset:
Psychotherapy and Counselling Federation of Australia
The Psychotherapy and Counselling Federation of Australia (PACFA) is the umbrella professional body that plays a self-regulating role in the psychotherapy and counselling industry. It represents the interests of more than 3000 practitioners of various forms of psychotherapy and counselling in Australia. It cooperates with 40 related associations to set and meet standards in all states and territories of Australia.

# Goals
- PACFA's vision is to lead the effort to make counselling and psychotherapy widely recognised as a profession.
- PACFA's mission is to be the leading professional body for counselling and psychotherapy and an automatic reference point for anyone seeking information on counselling and psychotherapy in the Australia.
- PACFA's objectives are:
- to promote and provide education and training for counsellors and/or psychotherapists working in either professional or voluntary settings, whether full or part time with a view to raising the standards of counselling and/or psychotherapy for the benefit of the community and in particular for those who are the recipients of counselling and/or psychotherapy.
- to advance the education of the public in the part that counselling and/or psychotherapy can play generally and in particular to meet the needs of those members of society where development and participation in society is impaired by mental, physical or social handicap or disability.

## Government accreditation
The counselling profession in Australia is currently not government regulated so clients are faced with the the task of evaluating qualifications of various counsellors and psychotherapists. PACFA is one of two industry associations that is campaigning for government accreditation of counselling in Australia.
Pulmonary arteriovenous fistula (patient information)

# Overview
Pulmonary arteriovenous fistula is a condition in which an abnormal connection (fistula) develops between an artery and vein in the lungs. As a result, blood passes through the lungs without receiving enough oxygen.

# What are the symptoms of Pulmonary arteriovenous fistula?
Many people have no symptoms. When symptoms occur, they can include:
- Bloody sputum
- Difficulty breathing
- Difficulty exercising
- Nosebleeds
- Shortness of breath with exertion
Other possible symptoms include:
- Blue skin (cyanosis)
- Clubbing of the fingers

# What causes Pulmonary arteriovenous fistula?
Pulmonary arteriovenous fistulas are usually the result of a genetic (inherited) disease that causes the blood vessels of the lung to develop abnormally. Fistulas also can be a complication of liver disease.
Patients with Rendu-Osler-Weber disease (ROWD) -- also called hereditary hemorrhagic telangiectasis (HHT) -- often have abnormal blood vessels in many parts of the body.

# Who is at highest risk?
Patients with Rendu-Osler-Weber disease (ROWD) -- also called hereditary hemorrhagic telangiectasis (HHT) -- often have abnormal blood vessels in many parts of the body, are at highest risk.

# Diagnosis
- Abscesses or infections of the heart valves
- Abnormal blood vessels (telangiectasias) may be seen on the skin or mucus membranes
- Murmur heard when a stethoscope is placed over the abnormal blood vessel
- High red blood cell count
Tests include:
- Arterial blood gas
- Complete blood count (CBC)
- Chest x-ray
- Chest CT scan
- Echocardiogram with bubble study
- Liver function tests
- Perfusion radionuclide lung scan
- Pulmonary arteriogram

# When to seek urgent medical care?
Call your health care provider if you often have nosebleeds or difficulty breathing, especially if you also have a history of HHT.

# Treatment options
A small number of patients who have no symptoms may not need treatment. For most patients with fistulas, the treatment of choice is to block the fistula during an arteriogram (embolization).
Some patients may need surgery to remove the abnormal vessels and nearby lung tissue.
When arteriovenous fistulas are caused by liver disease, the treatment is a liver transplant.

# Where to find medical care for Pulmonary arteriovenous fistula?

# Prevention of Pulmonary arteriovenous fistula
Because this condition is often genetic, prevention is not usually possible.

# What to expect (Outlook/Prognosis)?
The outlook for patients with HHT is not as good as for those without HHT. For patients with HHT, surgery to remove the abnormal vessels usually has a good outcome, and the condition is not likely to return.

# Possible complications
Major complications after treatment for this condition are unusual. Complications may include:
- Bleeding in the lung
- Blood clot that travels from the lungs to the arms, legs, or brain (paradoxical embolism)
- Infection in the brain or heart valve

# Sources
Quantitative insulin sensitivity check index (QUICKI)
The quantitative insulin sensitivity check index (QUICKI) is derived using the inverse of the sum of the logarithms of the fasting insulin and fasting glucose:
This index correlates well with glucose clamp studies (r = 0.78), and is useful for measuring insulin sensitivity (IS), which is the inverse of insulin resistance (IR). It has the advantage of that it can be obtained from a fasting blood sample, and is the preferred method for certain types of clinical research.

# Source
- Katz A, Nambi SS, Mather K, Baron AD, Follmann DA, Sullivan G, Quon MJ. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab. 2000 Jul;85(7):2402-10.PMID: 10902785
Rifampin isoniazid pyrazinamide indications and usage

# Indications And Usage
RIFATER is indicated in the initial phase of the short-course treatment of pulmonary tuberculosis. During this phase, which should last 2 months, RIFATER should be administered on a daily, continuous basis (See Dosage And Administration).
Following the initial phase and treatment with RIFATER, treatment should be continued with rifampin and isoniazid (e.g., RIFAMATE) for at least 4 months. Treatment should be continued for a longer period of time if the patient is still sputum or culture positive, if resistant organisms are present, or if the patient is HIV positive.
In the treatment of tuberculosis, the small number of resistant cells present within large populations of susceptible cells can rapidly become the predominant type. Since resistance can emerge rapidly, susceptibility tests should be performed in the event of persistent positive cultures during the course of treatment. Bacteriologic smears or cultures should be obtained before the start of therapy to confirm the susceptibility of the organism to rifampin, isoniazid, and pyrazinamide and they should be repeated throughout therapy to monitor response to the treatment. If test results show resistance to any of the components of RIFATER and the patient is not responding to therapy, the drug regimen should be modified.
Treponema pallidum hemagglutination assay (TPHA) test

# Overview
The Syphilis TPHA test is a classic, indirect hemagglutination test used for the detection and titration of antibodies against the causative agent of syphilis,Treponema pallidum.
In the test red blood cells (erythrocytes) are sensitized with antigens from T. pallidum. The erythrocytes will then aggregate together to form distinctive patterns on the surface of a microplate wells when exposed to syphilitic serum.
False Positives are common in this test. This is typically caused by antibodies directed against other non-pathogenic or non target treponemas, such as T. pallidum subsp endemicum,  T. pallidum subsp pertenue, and T. carateum. These antibodies can be adsorbed out of the test sample by a variety of methods thereby reducing false positives for syphilis.

# Related chapters
- Syphilis
- Hemagglutination assay
- Hemagglutination
Valganciclovir hydrochloride warnings and precautions

# Warnings and Precautions

## Hematologic Effects
Severe leukopenia, neutropenia, anemia, thrombocytopenia, pancytopenia, bone marrow aplasia, and aplastic anemia have been reported in patients treated with Valcyte or ganciclovir. Valcyte should not be administered if the absolute neutrophil count is less than 500 cells/L, the platelet count is less than 25,000/L, or the hemoglobin is less than 8 g/dL. Valcyte should also be used with caution in patients with pre-existing cytopenias, or who have received or who are receiving myelosuppressive drugs or irradiation. Cytopenia may occur at any time during treatment and may worsen with continued dosing. Cell counts usually begin to recover within 3 to 7 days after discontinuing drug.
Due to the frequency of neutropenia, anemia, and thrombocytopenia in patients receiving Valcyte , complete blood counts with differential and platelet counts should be performed frequently, especially in patients in whom ganciclovir or other nucleoside analogues have previously resulted in leukopenia, or in whom neutrophil counts are less than 1000 cells/L at the beginning of treatment. Increased monitoring for cytopenias may be warranted if therapy with oral ganciclovir is changed to Valcyte, because of increased plasma concentrations of ganciclovir after Valcyte administration .

## Impairment of Fertility
Animal data indicate administration of ganciclovir causes inhibition of spermatogenesis and subsequent infertility. These effects were reversible at lower doses but irreversible at higher doses . In men, Valcyte at the recommended doses may cause temporary or permanent inhibition of spermatogenesis. Animal data also indicate suppression of fertility in females may occur.

## Teratogenesis and Mutagenesis
Animal data indicate ganciclovir is teratogenic and mutagenic. Therefore, Valcyte should be considered to have the potential to cause birth defects and cancers in humans. Women of childbearing potential should be advised to use effective contraception during treatment and for at least 30 days following treatment with Valcyte. Similarly, men should be advised to practice barrier contraception during and for at least 90 days following treatment with Valcyte .

## Carcinogenesis
Animal data indicate that administration of ganciclovir is carcinogenic. Valcyte should therefore be considered a potential carcinogen in humans .

## Acute Renal Failure
Acute renal failure may occur in:
- Elderly patients with or without reduced renal function. Caution should be exercised when administering Valcyte to geriatric patients, and dosage reduction is recommended for those with impaired renal function .
- Patients receiving potential nephrotoxic drugs. Caution should be exercised when administering Valcyte to patients receiving potential nephrotoxic drugs.
- Patients without adequate hydration. Adequate hydration should be maintained for all patients.
Valproic acid capsule/solution nonclinical toxicology

# Nonclinical Toxicology

### 13.1 Carcinogenesis, Mutagenesis, and Impairment of Fertility
Valproate was administered orally to rats and mice at doses of 80 and 170 mg/kg/day (less than the maximum recommended human dose on a mg/m2 basis) for two years. The primary findings were an increase in the incidence of subcutaneous fibrosarcomas in high-dose male rats receiving valproate and a dose-related trend for benign pulmonary adenomas in male mice receiving valproate. The significance of these findings for humans is unknown.
Valproate was not mutagenic in an in vitro bacterial assay (Ames test), did not produce dominant lethal effects in mice, and did not increase chromosome aberration frequency in an in vivo cytogenetic study in rats. Increased frequencies of sister chromatid exchange (SCE) have been reported in a study of epileptic children taking valproate, but this association was not observed in another study conducted in adults. There is some evidence that increased SCE frequencies may be associated with epilepsy. The biological significance of an increase in SCE frequency is not known.
Chronic toxicity studies of valproate in juvenile and adult rats and dogs demonstrated reduced spermatogenesis and testicular atrophy at oral doses of 400 mg/kg/day or greater in rats (approximately equivalent to or greater than the maximum recommended human dose (MRHD) on a mg/m2 basis) and 150 mg/kg/day or greater in dogs (approximately 1.4 times the MRHD or greater on a mg/m2 basis). Fertility studies in rats have shown no effect on fertility at oral doses of valproate up to 350 mg/kg/day (approximately equal to the MRHD on a mg/m2 basis) for 60 days. The effect of valproate on testicular development and on sperm production and fertility in humans is unknown.
Valvular heart disease echocardiography or ultrasound

# 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary

# 2008 and Incorporated 2006 ACC/AHA Guidelines for the Management of Patients with Valvular Heart Disease (DO NOT EDIT) 

## Recommendations for Echocardiography (DO NOT EDIT) 

## Aortic Stenosis Asymptomatic Patient (DO NOT EDIT) 

# Sources
- 2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease
Warfarin over anticoagulation resident survival guide

# Overview
There are several protocols to follow when attempting to correct the effects of over-anticoagulation with warfarin.  Generally, the most important initial step is to stop the warfarin, and to continue to check the INR for its return to therapeutic levels. The additional steps are dependent upon the value of the INR, whether the patient is at a high risk of bleeding, and whether they are actively bleeding. Actively bleeding patients who have a supratherapeutic INR level will require more aggressive measures to prevent complications or death.

# Treatment of Over-anticoagulation of Warfarin

## Supratherapeutic INR Without Bleeding

### INR less than 5
- Decrease dose or hold warfarin.
- Recheck INR in 24 hrs.
- Restart warfarin at a decreased dose when INR is within target therapeutic range.

### INR 5 to 9
- Follow the same steps as above (algorithm of INR less than 5).
- An alternative option is to hold 1-2 doses of warfarin and give vitamin K 2.5 mg PO in high risk patients.
- Patients who have a high risk of bleeding, or who are undergoing surgery, should be given vitamin K 2.5 mg PO or a 5 mg PO.

### INR > 9
- Follow the same steps as above (algorithm of INR 5-9).
- Can repeat Vitamin K in 24 hours if necessary.

## Supratherapeutic INR with Bleeding
- Discontinue warfarin.
- Vitamin K IVPB (IV piggyback) 10 mg in NS 50 ml over 30 minutes.
- FFP or Profilnine SD (Prothrombin complex concentrate) or recombinant factor VII a (Novoseven).
- Check INR 12 hours after Vitamin K.
- Can repeat vitamin K every 12 hours for persistently elevated INR.

# Therapeutic Options

## Vitamin K
- Oral vitamin K tablets are available. The lowest dose is 2.5 mg.
- The oral route preferred over subcutaneous route due to its high efficacy.
- Vitamin K should never be given via intramuscular route or IV push.
- If IV route is necessary it should be IV piggyback.

## Fresh Frozen Plasma
- Dose = 15 ml/kg
- If INR is therapeutic, a dose of 5-8 ml/kg is sufficient.

## Prothrombin Complex Concentrate
- Used in addition to FFP.
- Dose = 25-50 units/kg

## Recombinant Factor VIIa (Novoseven)
- Used in addition to FFP
- Dose = 40 mcg/kg
Accreditation Council for Graduate Medical Education

# Overview
The Accreditation Council for Graduate Medical Education (ACGME) is the body responsible for the accreditation for postgraduate medical training programs (i.e., internships and residencies) for medical doctors in the United States. It is a non-profit private council that evaluates and accredits medical residency and internship programs. The ACGME was founded in 1981 and was preceded by the Liaison Committee for Graduate Medical Education, which was established in 1972.  
Although the ACGME states that it is responsible for post-M.D. training, both M.D.s and D.O.s may apply for residency through the ACGME.

# Footnotes
-  "ACGME". Retrieved 2007-08-18. Text " Accreditation Council for Graduate Medical Education " ignored (help).mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
Nonvalvular cardiovascular device-related infections

# Overview
All implanted cardiac devices can become infected which generally requires removal of the entire device (including pacing leads).

# Pathophysiology
A biofilm forms on the surface of the device and this surface facilitates the attachment of the infectious agent.  Antibiotics are ineffective in treating the infection of a biofilm as there is no blood flow into the biofilm.

# Causes
- Coagulase negative staphylococci: 42%
- Methicillin sensitive staph aureus: 25%
- Gram negative bacilli: 9%
- Culture negative: 7%
- Polymicrobial: 7%
- Other gm + cocci: 4%
- Methicillin resistant staph aureus: 4%
- Fungal: 2%

# Epidemiology and Demographics
There is a rise in the number of cases of CIED infections due to a larger number of devices being implanted, the frequency with which they are being replaced, and the comorbidities of patients in whom the devices are implanted.
- Pacemaker: 0.13% to 19.9%
- Defibrillator: 0% to 3.2%
- LVAD: 25% to 70%
- Ventriculoatrial shunt: 2.4% to 9.4%
- Vascular grafts: 1% to 6%
- Intra-aortic balloon pumps: 5% to 26%
- Arterial closure device: 1.9%
- Vena cava filter: rare
- Coronary artery stents: rare
- Peripheral stent: rare
- PDA, ASD, VSD occlusion device: rare

# Risk Factors
- Revision of a pocket is associated with a 4 to 6 times higher rate of infection.
- Automatic implantable cardiac defibrillators (AICDs) are associated with a higher rate of infection than permanent pacemakers: 8.9/1,000 device years versus 1.0/1,000 device years (p<0.001)
- Hematoma formation
- Warfarin use
- Re-intervention at the pocket site
- Renal failure
- Lack of primary prophylaxis during the initial insertion of the device

# Natural History, Complications, Prognosis
Complications of the device extraction that is necessary in CIED infection include:
- Bleeding
- Tricuspid valve trauma
- Pulmonary embolism
- Myocardial infarction
- Death
Risk factors for complications with device extraction include older age and co-morbidities.

# Diagnosis

## Echocardiography
TEE sensitivity is 95%
TTE sensitivity is <30%

# Treatment
- Complete device extraction including the leads is required.
- The biofilm cannot be treated with antibiotics.
- Antibiotics directed at the pathogen should be administered, but there is no data to guide the route and the duration of treatment.
- There is no data to guide decisions regarding the implantation of a new device.

# Prevention
- Perioperative antibiotic therapy during the initial insertion of the device has been associated with prevention of CIED infection (trial stopped prematurely due to a RR of 0.19, p=0.016).
Abacavir lamivudine zidovudine indications and usage

# Indications And Usage
TRIZIVIR is indicated in combination with other antiretrovirals or alone for the treatment of HIV-1 infection.
Additional important information on the use of TRIZIVIR for treatment of HIV-1 infection:
- TRIZIVIR is one of multiple products containing abacavir. Before starting TRIZIVIR, review medical history for prior exposure to any abacavir-containing product in order to avoid reintroduction in a patient with a history of hypersensitivity to abacavir .
- TRIZIVIR is a fixed-dose combination of 3 nucleoside analogues: abacavir, lamivudine, and zidovudine and is intended only for patients whose regimen would otherwise include these 3 components.
- Limited data exist on the use of TRIZIVIR alone in patients with higher baseline viral load levels (>100,000 copies/mL) .
Short-chain acyl-coenzyme A dehydrogenase deficiency
Short-chain acyl-coenzyme A dehydrogenase deficiency (or "SCADD") is a fatty acid oxidation disorder which affects enzymes required to break down a certain group of fats called short chain fatty acids.

# Diagnosis
Some affected infants will exhibit vomiting, low blood sugar (hypoglycemia), a lack of energy (lethargy), poor feeding, and failure to gain weight and grow at the expected rate (failure to thrive). Other features of this disorder may include poor muscle tone (hypotonia), seizures, developmental delays, and a small head size (microcephaly). The symptoms of short-chain acyl-CoA dehydrogenase deficiency may be triggered by periods of fasting or during illnesses such as viral infections. In some cases, signs and symptoms may not appear until adulthood, when some individuals may develop muscle weakness and wasting. Other people with gene mutations that can cause this disorder may have such mild symptoms that they are never diagnosed.  Many biochemical geneticists consider this to be a biochemical phenotype with a very mild clinical phenotype or no clinical phenotype.

# Genetics
Mutations in the ACADS gene cause short-chain acyl-coenzyme A dehydrogenase deficiency. Mutations in the ACADS gene lead to inadequate levels of an enzyme called short-chain acyl-CoA dehydrogenase. This enzyme is important for the breakdown of short-chain fatty acids. Reduced levels of this enzyme prevent short-chain fatty acids from being further broken down and processed in the mitochondria (the energy-producing centers inside cells). As a result, these short-chain fatty acids are not converted into energy, which can lead to the signs and symptoms of this disorder, such as lethargy and hypoglycemia.
This condition is an autosomal recessive disorder, which means two copies of the faulty gene must be inherited to be afflicted with the disorder. Most often, the parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene, but do not have the disorder. This disorder is thought to affect approximately 1 in 40,000 to 100,000 newborns.
International Classification of Health Interventions

# Overview
The International Classification of Health Interventions (ICHI) is a system of classifying procedure codes being developed by the World Health Organization. It is currently only available as a beta release.
It is designed to replace the "International Classification of Procedures in Medicine" (ICPM), a system that was developed in the 1970s but which never received the same international acceptance as ICD-9. As a result, most nations developed their own incompatible standards for coding procedures and interventions.
It is largely derived from the "Australian Classification of Health Interventions" (ACHI), a portion of the Australian standard ICD-10-AM, which in turn was largely derived from ICD-10 and the United States extension ICD-9-CM.