Persius/hicric huggingface dataset:
Child and Adolescent Mental Health Services

# Overview
Child and Adolescent Mental Health Services (CAMHS) is a name for NHS-provided services for children in the mental health arena in the UK. In the UK they are often organised around a  4 Tiers system. Tier 3 services are typically multidisciplinary in nature and the staff come from a range of professional background. There may be a considerable overlap between the skills and competencies of staff working in the specialist services. Tier 4 are highly specialist services for young people. These are typically inpatient units for young people who require admission into hospital, but also include a range of other Tier 4 provision. There are about 90 adolescent units in England and Wales.
The service includes:
- psychiatry
- clinical psychology
- psychiatric nursing
- social worker interface
- psychotherapy
- language development
for the diagnosis and treatment of children and adolescents, generally until school-leaving age. However many services cease at the age of sixteen, whereas the continuing service would be provided by Adult Mental Health at the age of eighteen.
The organisation of CAMHS services in the UK is complex. There is a programme coordinated by National Institute Mental Health England  to look at changing the way the workforce works. This New Ways of working  includes CAMHS. The national Workforce Lead for CAMHS is Barry Nixon and Project Lead for NWW CAMHS is Tim Morris.
Chronic pelvic pain resident survival guide
Synonyms and keywords:

# Overview
Chronic pelvic pain is a symptom, not a diagnosis, and is defined as persistent or recurrent pelvic pain of either men or women for longer than three to six months. It can be classified into two subgroups: specific disease-associated pelvic pain) that there are a pathology to explain the pain such as pelvic inflammatory disease, infections, adnexal pathologies, endometriosis, etc., and chronic pelvic pain syndrome (CPPS), which its diagnosis often based on the history and physical examinations and imaging and laboratory findings are often inconclusive in diagnosing it, and usually, no specific etiology can be found. Ninety-nine percent of all cases of chronic pelvic pain is female. The Pathophysiology of chronic pelvic disease could be related to the somatic structure or viscera pathologies, central sensitization of pain, or both. Treatment of chronic pelvic pain is often complicated and is usually focused on the suspected etiology of the chronic pelvic pain, such as treating a comorbid mood disorder, neuropathy, or uterine dysfunction, which can exacerbate chronic pain.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- Ovarian cyst
- Malignancy
Gender-specific causes classification

## Common Causes
Commonly proposed etiologies of chronic pelvic pain(CCP) include:  
- Endometriosis (very controversial) Deeply Infiltrative Endometriosis may be more important
- Infection or post-infectious neurological hypersensitivity
- Exaggerated bladder, bowel, or uterine pain sensitivity (also known as visceral pain)
- Ovarian cysts, uterine leiomyoma

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of chronic pelvic pain:

# Treatment
Shown below is an algorithm summarizing the treatment of chronic pelvic pain including: Specific disease-associated pelvic pain and CPPS

# Do's
- Managing chronic pelvic pain syndrome requires an interprofessional team of healthcare professionals that includes a physical therapist, psychologist, pharmacist, and several physicians in different specialties. The importance of multi-disciplinary treatment is emphasized by several reviews.
- Depending on the severity of the patient's pain, prescription analgesics may be necessary for adequate analgesia. A pharmacist helps coordinate care and helps aid in patient understanding, including proper usage and side effects.
- A cognitive-behavioral therapist helps in the coping and understanding of a patient's pain.

# Don'ts
- Zafirlukast and prednisone in two low-power placebo-controlled studies failed to show a benefit in prostate pain syndrome.
Cleft Lip and Palate Association of Ireland
The Cleft Lip and Palate Association of Ireland is an Irish-based support group for those born cleft lip and/or palate and their parents. It is a voluntary organisation and a registered charity.
The Association was founded in 1981 and established as a limited company in 1988. It has branches in Dublin, Cork and Galway.

# Aims and Activities
The Association is involved in:-
- Organizing lectures for parents, patients and medical personnel.
- Organizing events and activities for families and patient groups.
- Supporting research into the causes and treatment of cleft lip and palate.
- Providing funds for the purchase of medical equipment.
- Providing information through the provision of a newsletter, information leaflets and its online presence.
- Providing financial support to medical personnel and students in furtherance of their medical knowledge and training.
The Association is also a member of the European Network of Cleft Support Groups.
Clindamycin hydrochloride adverse reactions

# ADVERSE REACTIONS
The following reactions have been reported with the use of clindamycin.
Gastrointestinal: Abdominal pain, pseudomembranous colitis, esophagitis, nausea, vomiting, and diarrhea (see WARNING box). The onset of pseudomembranous colitis symptoms may occur during or after antibacterial treatment (see WARNINGS). Esophageal ulcer.
Hypersensitivity Reactions: Generalized mild to moderate morbilliform-like (maculopapular) skin rashes are the most frequently reported adverse reactions.
Vesiculobullous rashes, as well as urticaria, have been observed during drug therapy. Rare instances of erythema multiforme, some resembling Stevens-Johnson syndrome, and a few cases of anaphylactoid reactions have also been reported. Acute Generalised Exanthematous Pustulosis (AGEP). Toxic epidermal necrolysis.
Skin and Mucous Membranes: Pruritus, vaginitis, and rare instances of exfoliative dermatitis have been reported. (See Hypersensitivity Reactions.)
Liver: Jaundice and abnormalities in liver function tests have been observed during clindamycin therapy.
Renal: Although no direct relationship of clindamycin to renal damage has been established, renal dysfunction as evidenced by azotemia, oliguria, and/or proteinuria has been observed in rare instances.
Hematopoietic: Transient neutropenia (leukopenia) and eosinophilia have been reported. Reports of agranulocytosis and thrombocytopenia have been made. No direct etiologic relationship to concurrent clindamycin therapy could be made in any of the foregoing.
Immune System: Drug reaction with eosinophilia and systemic symptoms (DRESS)
Musculoskeletal: Rare instances of polyarthritis have been reported.
Clindamycin phosphate clinical pharmacology

# CLINICAL PHARMACOLOGY
Although clindamycin phosphate is inactive in vitro, rapid in vivo hydrolysis converts this compound to the antibacterially active clindamycin.
Cross resistance has been demonstrated between clindamycin and lincomycin.
Antagonism has been demonstrated between clindamycin and erythromycin.
Following multiple topical applications of clindamycin phosphate at a concentration equivalent to 10 mg clindamycin per mL in an isopropyl alcohol and water solution, very low levels of clindamycin are present in the serum (03 ng/mL) and less than 0.2% of the dose is recovered in urine as clindamycin.
Clindamycin activity has been demonstrated in comedones from acne patients. The mean concentration of antibiotic activity in extracted comedones after application of CLEOCIN T Topical Solution for 4 weeks was 597 mcg/g of comedonal material (range 01490). Clindamycinin vitro inhibits all Propionibacterium acnes cultures tested (MICs 0.4 mcg/mL). Free fatty acids on the skin surface have been decreased from approximately 14% to 2% following application of clindamycin.
Colistimethate sodium clinical pharmacology

# Clinical Pharmacology
Typical serum and urine levels following a single 150 mg dose of Coly-Mycin M Parenteral IM or IV in normal adult subjects are shown in Figure 1.
Higher serum levels were obtained at 10 minutes following IV administration. Serum concentration declined with a half-life of 23 hours following either intravenous or intramuscular administration in adults and in the pediatric population, including premature infants.
Average urine levels ranged from about 270 mcg/mL at 2 hours to about 15 mcg/mL at 8 hours after intravenous administration and from 200 to about 25 mcg/mL during a similar period following intramuscular administration.
Colistimethate sodium indications and usage

# Indications and Usage
Coly-Mycin M Parenteral is indicated for the treatment of acute or chronic infections due to sensitive strains of certain gram-negative bacilli. It is particularly indicated when the infection is caused by sensitive strains of Pseudomonas aeruginosa. This antibiotic is not indicated for infections due to Proteus or Neisseria. Coly-Mycin M Parenteral has proven clinically effective in treatment of infections due to the following gram-negative organisms: Enterobacter aerogenes, Escherichia coli, Klebsiella pneumoniae and Pseudomonas aeruginosa.
Coly-Mycin M Parenteral may be used to initiate therapy in serious infections that are suspected to be due to gram-negative organisms and in the treatment of infections due to susceptible gram-negative pathogenic bacilli.
To reduce the development of drug-resistant bacteria and maintain the effectiveness of Coly-Mycin M and other antibacterial drugs, Coly-Mycin M should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible 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.
Compartment syndrome historical perspective

# Overview
Like the most of medical conditions, the CS has an interesting historical perspective form the first descriptions to the categorized sign and symptoms and diagnostic systems .

# Historical Respective
In 1872, Richard von Volkmann described the consequences of unchecked rising intracompartmental pressures in a publication which nowdays is known as the  Volkmann contracture.
In 1912, Wilson described the initial case of exertional compartment syndrome.
In 1926, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction.
In 1956, Mavor  reported a case of chronic compartment syndrome.
In 1941, Bywaters and Beall reported the effect of crush injury while working with victims of the London Blitz and revealed mechanisms and consequences of compartment syndrome.
In 1970, the importance of measuring intracompartmental pressures became apparent.
In 1979, Owen et al described the use of the wick catheter for pressure measurement and then documented high compartmental pressures in various circumstances.
Congenital amegakaryocytic thrombocytopenia

# Overview
Congenital amegakaryocytic thrombocytopenia (CAMT) is a rare inherited disorder.

# Historical Perspective

# Classification

# Pathophysiology

# Causes
The cause for this disorder appears to be a mutation in the gene for the TPO receptor, c-mpl, despite high levels of serum TPO. In addition, there may be abnormalities with the central nervous system including the cerebrum and cerebellum which could cause symptoms.

# Differentiating Congenital amegakaryocytic thrombocytopenia from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History
The primary manifestations are thrombocytopenia and megakaryocytopenia, or low numbers of platelets and megakaryocytes. There is an absence of megakaryocytes in the bone marrow with no associated physical abnormalities.

## Complications

## Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy
The primary treatment for CAMT is bone marrow transplantation.
Bone Marrow/Stem Cell Transplant is the only thing that ultimately cures this genetic disease. Frequent platelet transfusions are required to ensure that platelet levels do not fall to dangerous levels, although this is not always the case. It is known for patients to continue to create very small numbers of platelets over time.

## Surgery

## Prevention
Demadex tablet/adult indications and dosage

# FDA-Labeled Indications and Dosage (Adult)
Chronic renal failure - Edema: The usual initial dose of DEMADEX is 20 mg of once-daily oral DEMADEX. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.
Congestive heart failure - Edema: The usual initial dose of DEMADEX is 10 mg or 20 mg of once-daily oral DEMADEX. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.
Hepatic disease - Edema: The usual initial dose is 5 mg or 10 mg of once-daily oral DEMADEX, administered together with an aldosterone antagonist or a potassium-sparing diuretic. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 40 mg have not been adequately studied.
Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials.
Hypertension: The usual initial dose is 5 mg once daily. If the 5 mg dose does not provide adequate reduction in blood pressure within 4 to 6 weeks, the dose may be increased to 10 mg once daily. If the response to 10 mg is insufficient, an additional antihypertensive agent should be added to the treatment regimen.

# Off-Label Use and Dosage (Adult)
Drug-induced nonautoimmune hemolytic anemia

# Overview
Drug-induced nonautoimmune hemolytic anaemia is a form of hemolytic anaemia.
Non-immune drug induced hemolysis can occur via oxidative mechanisms.  This is particularly likely to occur when there is an enzyme deficiency in the antioxidant defence system of the red blood cells.  An example is where antimalarial oxidant drugs like primaquine damage red blood cells in Glucose-6-phosphate dehydrogenase deficiency in which the red blood cells are more susceptible to oxidative stress due to reduced NADPH production consequent to the enzyme deficiency.
Some drugs cause RBC (red blood cell) lysis even in normal individuals. These include dapsone and sulfasalazine.
Non-immune drug-induced hemolysis can also arise from drug-induced damage to cell volume control mechanisms; for example drugs can directly or indirectly impair regulatory volume decrease mechanisms, which become activated during hypotonic RBC swelling to return the cell to a normal volume. The consequence of the drugs actions are irreversible cell swelling and lysis (e.g. ouabain at very high doses).
Shortness of breath resident survival guide

# Overview
Dyspnea is a symptom, it must generally be distinguished from signs that clinicians typically invoke as evidence of respiratory distress, such as tachypnea, use of accessory muscles, and intercostal retractions.
Respiratory discomfort may arise from many clinical conditions, but also may be a manifestation of poor cardiovascular fitness in our increasingly sedentary population. Diagnosis and treatment of the underlying cause of dyspnea is the preferred and most direct approach to improve this symptom, but there are many patients for whom the cause is unclear or for whom dyspnea persists despite optimal treatment.

# Definitions
- Dyspnea
- Tachypnea
- Bradypnea
- Hyperpnea
- Hyperventilation
- Dyspnea on exertion
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Platypnea
- Trepopnea

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Life-threatening causes of the upper airway
- Aspiration foreign body
- Angioedema
- Anaphylaxis
- Infections of the pharynx and neck
- Airway trauma
- Life-threatening pulmonary causes
- Pulmonary embolism
- COPD
- Asthma
- Pneumothorax and pneumomediastinum
- Pneumonia
- Adult Respiratory Distress Syndrome
- Chest trauma
- Pulmonary hemorrhage
- Life-threatening cardiac causes
- Acute coronary syndrome
- Acute decompensated heart failure
- Flash pulmonary edema
- High output failure
- Cardiomyopathy
- Cardiac arrhythmia
- Valvular dysfunction
- Cardiac tamponade
- Life-threatening neurologic causes
- Stroke
- Neuromuscular disease
- Life-threatening toxic and metabolic causes
- Poisoning
- Salicylate poisoning
- Carbon monoxide poisoning
- Toxin related metabolic acidosis
- Diabetic ketoacidosis
- Sepsis
- Anemia
- Acute chest syndrome- in patients with sickle cell disease

## Miscellaneous Causes
- Lung cancer
- Pleural effusion
- Intraabdominal infection
- Ascites
- Pregnancy
- Morbid obesity
- Hyperventilation and anxiety

# FIRE: Focused Initial Rapid Evaluation
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.

# Complete Diagnostic Approach and Treatment
A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention
Echo in transposition of the great arteries

# Transposition of the Great Arteries
Echocardiogram done in TGA to evaluate:
- atrioventricular connections
- atrial morphology: determined by venous return and atrial appendage morphology
- ventricular morphology:
determined by presence of moderator band (right ventricle), trabeculi, valvular morphology, etc.
seen best in subcostal, parasternal short axis and apical 4 chamber views
- determined by presence of moderator band (right ventricle), trabeculi, valvular morphology, etc.
- seen best in subcostal, parasternal short axis and apical 4 chamber views
- presence of outflow obstruction
Though transthoracic echo can provide valuable information, in adults a transesophageal echo (TEE) is usually necessary.  Typically, MRI is performed as well.
Consists of two basic types:
- D-TGA
- L-TGA otherwise known as congenitally-corrected TGA

## D-TGA
Image obtained from: 

## L-TGA (congenitally-corrected TGA)
Echo series of ccTGA:
LA-RV RA-LV connections
RV-aorta LV-PA connections
For more information please go to Transposition of the great vessels.
Endonuclease/Exonuclease/phosphatase family
Endonuclease/Exonuclease/phosphatase family  is a structural domain found in the large family of proteins including magnesium dependent endonucleases and many phosphatases involved in intracellular signaling .

# Examples
- AP endonuclease proteins EC 4.2.99.18,
- DNase I proteins EC 3.1.21.1,
- Synaptojanin, an inositol-1,4,5-trisphosphate phosphatase EC 3.1.3.56
- Sphingomyelinase EC 3.1.4.12 and Nocturnin O35710.

# Subfamilies
- Inositol polyphosphate related phosphatase InterPro: IPR000300

# Human proteins containing this domain
2'-PDE;    2-PDE;     ANGEL1;    ANGEL2;    APEX1;     APEX2;     CCRN4L;    CNOT6;
CNOT6L;    DNASE1;    DNASE1L1;  DNASE1L2;  DNASE1L3;  INPP5A;    INPP5B;    INPP5D;
INPP5E;    INPPL1;    KIAA1706;  OCRL;      PIB5PA;    SKIP;      SMPD2;     SMPD3;
SYNJ1;     SYNJ2;     TTRAP;

# Notes
-  Dlaki M (2000). "Functionally unrelated signalling proteins contain a fold similar to Mg2+-dependent endonucleases". Trends Biochem. Sci. 25 (6): 272273. PMID 10838565..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}
Ezetimibe/Simvastatin indications and usage

# Indications and Usage
Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate.

## Primary hyperlipidemia
VYTORIN is indicated for the reduction of elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and non-high-density lipoprotein cholesterol (non-HDL-C), and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary (heterozygous familial and non-familial) hyperlipidemia or mixed hyperlipidemia.

## Homozygous Familial Hypercholesterolemia (HoFH)
VYTORIN is indicated for the reduction of elevated total-C and LDL-C in patients with homozygous familial hypercholesterolemia, as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable.

## Limitations of Use
No incremental benefit of VYTORIN on cardiovascular morbidity and mortality over and above that demonstrated for simvastatin has been established.
VYTORIN has not been studied in Fredrickson type I, III, IV, and V dyslipidemias.