Persius/hicric huggingface dataset:
Complications and prognosis

# Overview
The prognosis of the patient depends on a number of donor and recipient factors. If left untreated, patients develop acute graft rejection. Common complications of cardiac transplant include acute graft rejection, graft failure, infections, Cardiac allograft vasculopathy (CAV), malignancies, and late graft rejection.

# Complications and Causes of Death after Transplantation
The following table outlines the common causes of death in post-cardiac transplant patients 

# Prognosis
- Depending on the various factors of the donor and recipient at the time of transplant, the prognosis may vary.
- Prognosis is generally regarded as good. The 1-year survival is 84.5% and 5-year survival is 72.5%. 
- Post-transplant survival has improved over time.
- The median survival after adult heart transplants performed between 2002 and 2009 is 12.5 years, which extends to 14.8 years among 1-year survivors. 
The following are the factors determining prognosis-

## Donor factors
Both the following factors are associated with an increased one-year mortality rate in the recipient.
- Advanced donor age 
- Prolonged ischemia time

## Recipient factors
- Use of total artificial heart as a bridge to transplant or a need for end-organ support in the form of mechanical ventilation or dialysis- associated with the greatest one-year mortality
- Best prognosis is seen if the indication for transplant is ischemic and nonischemic cardiomyopathy 
- Patients with a history of congenital heart disease, restrictive cardiomyopathy, and those undergoing retransplantation have a worse prognosis.
- Younger recipients (below age 55) have an advantage
- Pre-transplant serum creatinine and total bilirubin are linearly related to survival.
Some other risk factors are:
- Use of Amiodarone pretransplantation  
- Hypertension
- Hypercholesterolemia  
- Diabetes
- Renal insufficiency
- Use of specific immunosuppressive regimen
- Elevated body mass index
- Tobacco use
- Obesity
- Early post-transplant complications
- Prior cardiac surgery
- Transplantation of a female heart into a male or female recipient.
Preauricular sinus and cyst

# Overview
A preauricular sinus or cyst (also known as a "Congenital auricular fistula," "Congenital preauricular fistula," "Ear pit":782, and "Preauricular cyst"
) is a common congenital malformation characterized by a nodule, dent or dimple located anywhere adjacent to the external ear. They are inherited features and usually appear on one side, but may be bilateral in 25-50% of cases. Preauricular sinuses and cysts result from developmental defects of the first and second branchial arches. Occasionally a preauricular sinus or a cyst can become infected. This and other congenital ear malformations are associated with renal anomalies.
Most preauricular sinuses are asymptomatic and remain untreated unless they become infected too often. Preauricular cysts are treated with surgery which, because of their close proximity to the facial nerve should be left to an experienced surgeon, such as an otolaryngologist - head and neck surgeon.
In rare cases they may be associated with branchio-oto-renal syndrome.

# Diagnosis

## Physical Examination

### Skin
- Congenital auricular fistula. Adapted from Dermatology Atlas.
- Congenital auricular fistula. Adapted from Dermatology Atlas.
Constant visual observation

# Overview
Constant visual observation, often abbreviated to "constant visual", is a term used in various mental health services, prisons and special schools to describe the status of a prisoner or patient who poses a threat to himself or a third party, and must therefore be kept under constant observation.
There are essentially two levels of constant visual observations. The highest level, employed only for those patients who are considered to be extremely high risk to either themselves or a third party, involves a care worker remaining within arms reach of the service user at all times. The second level involves only maintaining a constant watch on a patient, sometimes from a distance.
Constant visual observations have been criticised by many service user groups.
Constitutional bradygenesis
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# Overview
Related Key Words and Synonyms:

# Epidemiology and Demographics

# Risk Factors

# Screening

# Pathophysiology & Etiology

# Molecular Biology

# Genetics

# Natural History

# Diagnosis

## Differential Diagnosis

## History and Symptoms

## Physical Examination

### Appearance of the Patient

### Vital Signs

### Skin

### Eyes

### Ear Nose and Throat

### Heart

### Lungs

### Abdomen

### Extremities

### Neurologic

### Other

## Laboratory Findings

### Electrolyte and Biomarker Studies

### Electrocardiogram

### Chest X Ray

### MRI and CT

### Echocardiography or Ultrasound

### Other Imaging Findings

## Other Diagnostic Studies

# Risk Stratification and Prognosis

# Treatment

## Pharmacotherapy

### Acute Pharmacotherapies

### Chronic Pharmacotherapies

## Surgery and Device Based Therapy

### Indications for Surgery

### Pre-Operative Assessment

### Post-Operative Management

### Transplantation

## Primary Prevention

## Secondary Prevention

## Cost-Effectiveness of Therapy

## Future or Investigational Therapies

# "The Way I Like To Do It ..." Tips and Tricks From Clinicians Around The World

## Suggested Revisions to the Current Guidelines
Watson's water hammer pulse
Synonyms and keywords: Corrigan's pulse, collapsing pulse, cannonball pulse, hyperkinetic pulse

# Overview
Watson's water hammer pulse is the medical sign which describes a pulse that is bounding and forceful, as if it were the hitting of a water hammer that was causing the pulse.  This is associated with increased stroke volume of the left ventricle and decrease in the peripheral resistance leading to the widened pulse pressure of aortic regurgitation.  Also, the carotid pulsations seen in aortic regurgitation is known as Corrigan's pulse.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.  There are no known life threatening causes of Watson's water hammer pulse that would result in death or permanent disability if not treated within 24 hours.

## Common Causes
- Aortic regurgitation
- Fever
- Pregnancy

## Causes by Organ System

## Causes in Alphabetical Order

# Physical Examination
To feel a water hammer pulse with the patient reclining, the examiner raises the patient's arm vertically upwards. The examiner grasps the muscular part of the patient's forearm. A waterhammer pulse is felt as a tapping impulse which is transmitted through the bulk of the muscles. This happens because the blood that is pumped to the arm during systole is emptied very quickly due to the gravity effect on the raised arm. This results in the artery emptying back into the heart during diastole, therefore causing a palpable pulse.
This is commonly found when a patient has a leaking prosthetic aortic valve.

# Videos
Video demonstrating Corrigan's sign (rapid upstroke and collapse of the carotid artery pulse)

# Related Chapters
- Aortic Insufficiency Physical Examination
- Blood hammer
Cost-effectiveness analysis

# Overview
Cost-effectiveness analysis (CEA) is a form of economic analysis that compares the relative expenditure (costs) and outcomes (effects) of two or more courses of action.

# CEA in pharmacoeconomics
In the context of pharmacoeconomics, the cost-effectiveness of a therapeutic or preventive intervention is the ratio of the cost of the intervention to a relevant measure of its effect. Cost refers to the resource expended for the intervention, usually measured in monetary terms such as dollars or pounds. The measure of effects depends on the intervention being considered. Examples include the number of people cured of a disease, the mm Hg reduction in diastolic blood pressure and the number of symptom-free days experienced by a patient. The selection of the appropriate effect measure should be based on clinical judgment in the context of the intervention being considered.
A special case of CEA is cost-utility analysis, where the effects are measured in terms of years of full health lived, using a measure such as quality-adjusted life years or disability-adjusted life years.
Cost-effectiveness is typically expressed as an incremental cost-effectiveness ratio (ICER),  the ratio of change in costs to the change in effects.
A complete compilation of cost-utility analyses in the peer reviewed medical literature is available at the CEA Registry Website

# CEA in environmental economics
In environmental terms, "cost-effective measures" allude to various (mostly industrial) attempts to prevent environmental degradation as written in principle 15 of the Rio declaration of the Earth Summit conference 1992.
Proportional hazards models

# Overview
Proportional hazards models are a sub-class of survival models in statistics.
For the purposes of this article, consider survival models to consist of two parts: the underlying hazard function, describing how hazard (risk) changes over time, and the effect parameters, describing how hazard relates to other factors - such as the choice of treatment, in a typical medical example.  The proportional hazards assumption is the assumption that effect parameters multiply hazard: for example, if taking drug X halves your hazard at time 0, it also halves your hazard at time 1, or time 0.5, or time t for any value of t.  The effect parameter(s) estimated by any proportional hazards model can be reported as hazard ratios.
Sir David Cox observed that if the proportional hazards assumption holds (or, is assumed to hold) then it is possible to estimate the effect parameter(s) without any consideration of the hazard function.  This approach to survival data is called application of the Cox proportional hazards model, sometimes abbreviated to Cox model or to proportional hazards model.
Other proportional hazards models exist.  Another approach to survival data is to assume that the proportional hazards assumption holds, but in addition to assume that the hazard function follows a known form.  For example, assuming the hazard function to be the Weibull hazard function gives the Weibull proportional hazards model (in which the survival times follow a Weibull distribution).

## Note on terminology
The generic term parametric proportional hazards models can be used to describe proportional hazards models in which the hazard function is specified.  The Cox proportional hazards model is sometimes called a semi-parametric model by contrast.
Some authors (e.g. Bender, Augustin and Blettner, Statistics in Medicine 2005) use the term Cox proportional hazards model even when specifying the underlying hazard function, to acknowledge the debt of the entire field to David Cox.
The term Cox regression model (omitting proportional hazards) is sometimes used to describe the extension of the Cox model to include time-dependent factors.  However, this usage is potentially ambiguous since the Cox proportional hazards model can itself be described as a regression model.

# Relationship to Poisson models
There is a relationship between proportional hazards models and Poisson regression models which is sometimes used to fit approximate proportional hazards models in software for Poisson regression.  The usual reason for doing this is that calculation is much quicker.  This was more important in the days of slower computers but can still be useful for particularly large data sets or complex problems.  Authors giving the mathematical details include Laird and Olivier (Journal of the American Statistical Association, 1981), who remark
"Note that we do not assume  is true, but simply use it as a device for deriving the likelihood."
Craniometaphyseal dysplasia

# Overview
Craniometaphyseal Dysplasia Autosomal Dominant is a disorder is a rare skeletal disorder that results from a heterozygous mutation in human homologous of progress in ankylosis gene (ANKH). Abnormal bone overgrowth occurs from the beginning of a child's life as well as throughout their lifetime resulting in the narrowing of the cranial formania.This leads to cranial nerve and facial features compression. In addition, this disorder is located on the 5p chomsome.

# Causes
The mutation in ANKH gene causes a decrease in the to transport pyrophosphate out of cells. Pyrophosphate regulates bone formation by preventing mineralization. The ANKH gene provides instructions for making a protein present in the bones. Only one mutated ANKH gene can cause autosomal dominant Craniometahyseal Dysplasia.

## Inheritance
This autosomal dominant disorder is inherited in and autosomal dominant manner and  is caused by a pathogenic variant in ANKH. If one parent has this disorder then there is fifty percent chance of them having a child with the disorder as well. Yet it can also be a single occurrence in a family also known as de novo. Through time the disorder can seem to go away on its own due to it becoming less noticeable as the child grows. People who are affected by this disorder are young children and infants.

# Effects
This disorder can lead to blindness. Some effects it has on the body are:
- facial palsy
- deafness
- paranasal bossing
- wide set eyes
- delay teething
- thickening of bones in the skull
- sclerosis of alveolar bone
- abnormal growth

# Diagnosis
Craniometaphyseal Dysplasia Autosomal Dominant is diagnosed based on clinical and radiographic findings that include hyperostosis. Some things such as cranial base sclerosis and nasal sinuses obstruction can be seen during the beginning of the child's life. In radiographic findings the most common thing that will be found is the narrowing of foramen magnum and the widening of long bones. Once spotted treatment is soon suggested to prevent further compression of the foramen magnum and disabling conditions.

# Treatment
The only treatment for this disorder is surgery, Craniofacial Surgery. The surgery would reduce the compression of cranial nerves and spinal cord. However, bone regrowth is common since the surgical procedure can be technically difficult. Genetic counseling is offered to the families of the people with this disorder. There they will learn about the causes and effects of the disease as well as treatment.
Lateral corticospinal tract

# Overview
The lateral corticospinal tract (also called the crossed pyramidal tract or lateral cerebrospinal fasciculus) is the largest part of the corticospinal tract. It extends throughout the entire length of the medulla spinalis, and on transverse section appears as an oval area in front of the posterior column and medial to the posterior spinocerebellar tract.
Its fibres arise from cells in the motor area of the cerebral hemisphere of the opposite side.
They pass downward in company with those of the anterior corticospinal tract through the same side of the brain as that from which they originate, but they cross to the opposite side in the medulla oblongata and descend in the lateral funiculus of the medulla spinalis.
The lateral corticospinal tract moves limbs and digits.
Hypersensitivity vasculitis
Synonyms and keywords: Hypersensitivity angiitis, leukocytoclastic vasculitis, LCV, leucocytoclastic venulitis, small-vessel vasculitis, cutaneous leukocytoclastic angiitis

# Overview
Hypersensitivity vasculitis is inflammation of the vessel wall which is usually due to a hypersensitivity reaction to a known drug, auto-antigens or infectious agents such as bacteria.

# Pathophysiology
Immune complexes lodge in the vessel wall, attracting polymorphonuclear leukocytes who in turn release tissue-degrading substances leading to an inflammatory process.  This disorder may affect the skin only, but sometimes affect nerves, the kidneys, joints and the heart. Renal involvement is common.

# Causes

## Causes by Organ System

## Causes in Alphabetical Order

# Diagnosis

# History
A detailed history should be obtained regarding medications and potential exposure to infectious agents.

# Physical Examination

## Skin
- Palpable, normally painful, petechiae or purpura (skin vasculitis).
- The lesions normally arise in crops, with common localizations being the forearms and legs.
- Necrosis of skin tissue can yield lesions with black or brown centres.

# Laboratory Studies
The following studies are routinely obtained:
- Hepatitis serologies
- Antinuclear antibodies
- Rheumatoid factor
- Cryoglobulins

# Skin Biopsy
Skin biopsy of the lesions reveal inflammation of the small vessels, termed leukocytoclastic vasculitis, which is most prominent in postcapillary venules.

# Diagnostic Criteria
At least 3 out of 5 criteria yields a sensitivity of 71% and a specificity of 84%:
- Age over 16 years
- Use of possible triggering drug in relation to symptoms
- Palpable painful purpura (the three P's)
- Maculopapular rash
- Skin biopsy showing neutrophil infiltration around vessels

# Treatment
The most important part of the treatment is to eliminate the cause of the vasculitis, if at all possible. Antihistamines prove helpful to some patients. If the vasculitis is damaging organ systems such as the kidneys, immunosuppressive agents are indicated.
DIC resident survival guide

# Overview
Disseminated intravascular coagulation, is a pathological process in the body where the blood starts to coagulate throughout the whole body.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
Disseminated intravascular coagulation in itself is a life-threatening condition and must be treated as such irrespective of the cause.

## Common Causes
- Abruptio placentae
- Amniotic fluid embolism
- Aortic aneurysm
- Drugs (e.g. Amphetamines)
- Eclampsia
- Giant hemangioma
- HELLP syndrome
- Hemolytic transfusion reaction
- Malignancy (especially APL)
- Sepsis
- Severe allergic reaction
- Transplant rejection
- Trauma (e.g. Fat embolism, head injury)
- Venomous snake

# Management
Below is an algorithm showing the initial approach to DIC.

## Treatment
The goal of treatment of DIC is the treatment of the underlying disorder.  Shown below is an algorithm for the general treatment of DIC.

# Do's
- The transfusion of platelets should be considered for those patients actively bleeding or at an increased risk of bleeding with a platelet count of less than 50,000 microliter.
- Fibrinogen level should be kept at a level greater than 100mg/dl
- Therapy with heparin used generally for patients with low grade DIC having predominantly thrombotic episodes such as acral ischemia and thrombophlebitis.

# Dont's
- Do not transfuse platelets or plasma based primarily on laboratory results but should generally be for patients who are bleeding.
- Don't give recombinant human activated protein C to patients with increased risk of bleeding.
- Don't give recombinant human activated protein C to patients with platelet counts < 30,000 microliter.
- Avoid the intravenous bolus injection of heparin of 50,000-10,000 units.
DNA replication factor CDT1
CDT1 (Chromatin licensing and DNA replication factor 1) is a protein that in humans is encoded by the CDT1 gene. It is a licensing factor that functions to limit DNA from replicating more than once per cell cycle.

# Role in pre-replication complexes
The protein encoded by this gene is a key licensing factor in the assembly of pre-replication complexes (pre-RC), which occurs during the G1 phase of the cell cycle. In the assembly of pre-RCs, origin recognition complexes (ORC1-6) recognize and bind to DNA replication origins. CDT1, along with the protein CDC6, are then recruited to the forming pre-RC, followed by minichromosome maintenance complexes (MCM2-7).
The activity of CDT1 during the cell cycle is tightly regulated during the S phase by the protein geminin, which inhibits its, and by SCFSKP2, which ubiquinates the protein to tag it for proteasomal degradation. This regulation is important in preventing relicensing, thus ensuring that DNA is only replicated once per cell cycle.

# Orthologs
CDT1 belongs to a family of replication proteins conserved from yeast to humans. Examples of orthologs in other species include:
- S. pombe  CDT1 (CDC10-dependent transcript 1)
- Drosophila melanogaster  'double parked' or Dup
- Xenopus laevis - CDT1

# Interactions
DNA replication factor CDT1 has been shown to interact with SKP2. Cdt1 is recruited by the origin recognition complex in origin licensing. Null-mutations for CDT1 are lethal in yeast; the spores undergo mitosis without DNA replication. The overexpression of CDT1 causes rereplication in H. sapiens, which activates the CHK1 pathway, preventing entry into mitosis.
Drug susceptibility testing

# Overview
Drug Susceptibility Testing (DST) determines the ability of several anti-tuberculosis drugs to inhibit the growth of Mycobacterium tuberculosis complex (MTBC).  DST is very important to assess the correct drug regimen for patients with tuberculosis.

# Drug Susceptibility Testing
Drug susceptibility testing is a difficult procedure to standardize, and proficiency in performing these tests requires an understanding of many elements, including:
- Origin of drug resistance and the criteria for resistance
- Potency and stability of drugs during laboratory manipulation
- Antimycobacterial activity of drugs when incorporated into different media
- Reading, interpretation, and reporting of results
The CDC Laboratory Branch uses an indirect proportion method for testing M. tuberculosis complex mycobacteria to 12 drugs at 35C on Middlebrook 7H10 agar. The test requires 1 month to complete. Growth on the control medium is compared to the growth on the drug-containing medium to determine susceptibility or resistance. When performed properly, this method allows a quantitation of the proportion of mutants resistant to a drug and can detect the 1% proportion of drug- resistant mutants above which therapeutic failure is likely.
M. tuberculosis complex are tested by this method with the following drugs:
- Isoniazid
- Rifampin
- Ethambutol
- Ciprofloxacin
- Ofloxacin
- Streptomycin
- Kanamycin
- Capreomycin
- Amikacin
- Rifabutin
- Ethionamide
- Para-aminosalicylic acid (PAS)
In addition, pyrazinamide is tested by the MGIT 960 method (Becton Dickinson).