Persius/hicric huggingface dataset:
Recurrent pyogenic cholangitis
Contributors:  Cafer Zorkun M.D., PhD.

# Overview
Recurrent pyogenic cholangitis (a.k.a. cholangiohepatitis) is a condition that most commonly affects humans of East Asian origins. It is characterized by recurrent bouts of cholangitis in association with intrahepatic pigment stones and intrahepatic biliary obstruction. 

# Pathogenesis
In recurrent pyogenic cholangitis the gallstones found within the biliary system are calcium bilirubinate stones or pigmented calcium stones. Calcium bilirubinate stones are prevalent in Asia and very rare in Europe and the United States.
In addition to the presence of these friable concretions of various shapes and sizes within the biliary tree, the bile is often muddy in consistency and contains numerous fine particles of calcium bilirubinate. This differs greatly from cholesterol stones, which are common in Europe and the United States. Pure cholesterol stones contain >96% cholesterol whereas mixed cholesterol stones contain 71.3% cholesterol. The formation of calcium bilirubinate stones in RPC has been attributed to the high incidence of infection with Escherichia coli in the bile. In man, the majority of bilirubin is excreted in the bile as bilirubin glucuronide.

# Symptoms
Recurrent pyogenic cholangitis is characterized by recurrent attacks of abdominal pain, fever, and jaundice caused by intrahepatic ductal strictures and calculi.

# Diagnostic Findings
- Centrally dilated bile ducts with peripheral tapering.
- Biliary duct stones.

## Patient #1: MR images from a patient with recurrent pyogenic cholangitis
Images courtesy of RadsWiki

## Patient #2
Images courtesy of RadsWiki
Resident survival guide topics

# Overview
This section shows the list of topics available for the resident survival guide project and how to select a topic.  You can also update the status of your chosen topic here by entering the authorship details so that your work is not overlapped by the work of other editors.

# Select a Topic
- Select a topic from the list of resident survival guide topics shown below.
- The topics that are completed or have been worked on by wikidoc scholars are highlighted in blue.
- The topics in black are still available for scholars on campus or remote collaborators to work on.

# List of All Topics

## Cardiology

## Pulmonology

## Gastroenterology

## Nephrology

## Hematology-Oncology

## Infectious Diseases

## Endocrinology

## Rheumatology and Immunology:

## Immunology:

## Neurology:

## Miscellaneous

## Primary care

## Toxicology
Rifampin isoniazid description

# Description
RIFAMATE is a combination capsule containing 300 mg rifampin and 150 mg isoniazid. The capsules also contain as inactive ingredients: colloidal silicon dioxide, FD&C Blue No. 1, FD&C Red No. 40, gelatin, magnesium stearate, sodium starch glycolate, and titanium dioxide.
Rifampin is a semisynthetic antibiotic derivative of rifamycin B. The chemical name for rifampin is 3-(4-methyl-1-piperazinyliminomethyl) rifamycin SV.
Isoniazid is the hydrazide of isonicotinic acid. It exists as colorless or white crystals or as a white, crystalline powder that is water soluble, odorless, and slowly affected by exposure to air and light.
Robert A. Phillips (scientist)

# Overview
Dr. Robert A. Phillips PhD is a Canadian scientist, with a long-term interest in cancer research, and special interests in blood cell development and in retinoblastoma, an inherited eye tumour in children. His expertise has spanned the breadth of disciplines including radiation biology, cellular and molecular biology, immunology and molecular genetics.
He has been a tireless ambassador for cancer research and cancer control throughout a career that has spanned more than 3 decades. He is a key member of a band of veteran scientists, also including John Evans, the founding dean of faculty of health sciences at McMaster University and former president of the University of Toronto and Cal Stiller, an organ transplant expert and entrepreneur, who pushed for years for the creation of the Ontario Institute for Cancer Research (OICR), an independent, not-for-profit corporation established in December 2005, and funded by the Government of Ontario through the Ministry of Research and Innovation.
He has been a member of various Boards of Directors, including the Canadian Cancer Society, the Canadian Network for Vaccines and Immunotherapeutics (CANVAC), the Canadian Prostate Cancer Research Foundation, and Partners in Research.

# Career
Dr. Phillips  received his B.A. in chemistry and zoology from Carleton College in Northfield, Minnesota, and his Ph.D. in molecular biology from Washington University in St. Louis, Missouri.
In 1965, he moved to Toronto to do postdoctoral work with Dr. James Till at the Ontario Cancer Institute/Princess Margaret Hospital. He had an independent research career there until 1986.
He was also a faculty member in the Department of Medical Biophysics at the University of Toronto and was Chair of that Department from 1981 to 1986.
In 1986, Dr. Phillips moved his research group to the Hospital for Sick Children where he became Director of the Division of Immunology and Cancer Research.
In 1996, Dr. Phillips gave up laboratory research to become the Executive Director of the National Cancer Institute of Canada (NCIC). At NCIC, he was instrumental in widening the scope of cancer research that was funded and bringing together different organizations under common mandates.
In 1997, Dr. Phillips was one of the initial members of the Board of Directors of the Canadian Foundation for Innovation (CFI).
In January 2002, Dr. Phillips became the founding president and CEO of the Ontario Cancer Research Network, a non-profit organization established to speed up the development and testing of promising new cancer therapies.
As of 2007, Dr. Phillips is the Chief Operating Officer of the Ontario Institute for Cancer Research, which merged with the Ontario Cancer Research Network in late 2005.

# Honours
- 2003, awarded the R. M. Taylor Medal and Award of the National Cancer Institute of Canada and the Canadian Cancer Society.
Serum-ascites albumin gradient

# Overview
The serum-ascites albumin gradient (SAAG) helps determine the cause of ascites. SAAG = albumin concentration of serum - albumin concentration of ascitic fluid
The SAAG is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive etiology.
Important causes of high SAAG ascites  (> 11 gm/L) include cirrhosis of the liver, Budd Chiari syndrome and heart failure.
Sandbox:differential diagnosis

# Overview
-  must be differentiated from other diseases that cause , , and , such as , , and .
-  must be differentiated from , , and .

# Differentiating X from other Diseases
-  must be differentiated from other diseases that cause , , and , such as , , and .
-  must be differentiated from , , and .
- As  manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype.  must be differentiated from other diseases that cause , such as  and . In contrast,  must be differentiated from other diseases that cause , such as  and .

## Preferred Table

## Use if the above table can not be made
Sandbox:historical perspective

# Overview

# Historical Perspective

## Discovery
-  was first discovered by , a , in /during/following .
- The association between  and  was made in/during .
- In ,  was the first to discover the association between  and the development of .
- In ,  mutations were first implicated in the pathogenesis of .

# Outbreaks
- There have been several outbreaks of , which are summarized below:

# Landmark Events in the Development of Treatment Strategies
- In ,  was developed by  to treat/diagnose .

# Impact on Cultural History

# Famous Cases
- The following are a few famous cases of disease name:
Saphenous Vein Graft Pathology
Images  courtesy of Professor Peter Anderson DVM PhD and published with  permission  PEIR, University of Alabama at Birmingham, Department of  Pathology
- Saphenous vein coronary bypass graft: Gross, natural  color, external view of heart with thrombosed veins
- Saphenous vein coronary bypass graft: Thrombosis,  Acute: Gross, fixed tissue but well shown cross sections of bypass graft  and anastomotic site with thrombosis. 61 yo male, with and acute  infarct treated with streptokinase and two days later had bypass. Died 5  days post op. Two veins are thrombosed
- Myocardial Infarct Acute Reflow Type: Gross, fixed tissue but  good color. A very enlarged heart with moderate LV dilation and high  anterior wall hemorrhagic infarct. Initially treated with streptokinase  and two days later had saphenous vein grafts. Both grafts are  thrombosed. He died after 5 days
Images  courtesy of Professor Peter Anderson DVM PhD and published with  permission  PEIR, University of Alabama at Birmingham, Department of  Pathology
Satellite Tobacco Mosaic Virus
The Satellite Tobacco Mosaic Virus or Tobacco mosaic satellivirus  was first reported in Nicotiana glauca from southern California, U.S.A. by Valverde and Dodds. Its genome consists of linear single-stranded RNA. (1986)
"Satellite Tobacco Mosaic Virus is a small, icosahedral plant virus which worsens the symptoms of infection by Tobacco Mosaic Virus (TMV). Satellite viruses are some of the smallest possible reproducing units in nature; they achieve this by relying on both the host cell and a host virus (in this case, TMV) for the machinery necessary for them to reproduce. The entire STMV particle consists of 60 identical copies of a single protein that make up the viral capsid (coating), and a 1063-nucleotide single-stranded RNA genome which codes for the capsid and one other protein of unknown function." 
"Klaus Schulten at the University of Illinois, Urbana, and his colleagues built a computer model of the satellite tobacco mosaic virus, a tiny spherical package of RNA.  Running on a machine at the National Center for Supercomputing Applications, Urbana, the program calculated how each of the million or so atoms in the virus and a surrounding drop of salt water was interacting with almost every other atom every femtosecond, or millionth of a billionth of a second.  The fleeting simulation, published in this month's Structure, reveals that although the virus looks symmetrical it pulses in and out asymmetrically, as if it were breathing." 

# Sources
-  Plant Viruses Online
-  Molecular Dynamics of STMV Beckman Institute for Advanced Science and Technology // National Institutes of Health  // National Science Foundation  // Physics, Computer Science, and Biophysics at the University of Illinois
-  Supercomputer builds a virus at Nature magazine
Seronegative spondyloarthritis

# Overview
Seronegative spondyloarthritis (SpA) are a group of chronic inflammatory arththropathies which are inter-related to each other. "Seronegative" refers to the fact that autoimmune antibodies are not found in these diseases. SpA primarily affects axial skeleton but may also have peripheral as well as extra-articular involvement. Individuals affected with seronegative SpA are generally genetically predisposed to have positive major histocompatibility complex (MHC) class I molecule HLA-B27. As the diseases feature overlap, it is difficult to make a precise diagnosis; hence, the diseases are monitored and treated on the basis of clinical presentation. Common clinical manifestations includes sacroiliitis, peripheral arthritis, and enthesitis. Extra-articular involvement depends on the disease such as skin manifestations for psoriatic arthritis, gastrointestinal tract manifestations for enteropathy associated arthritis, and ocular and genitourinary manifestations for reactive arthritis.

# Classification

# Classification Criteria

## ASAS classification criteria for axial spondyloarthritis (axial SpA)
The Assessment of SpondyloArthritis International Society classification criteria for axial spondyloarthritis (axial SpA) include:
- Patient with back pain  3 months and age of onset <45 years should fulfill either of the two criteria:
Sacroiliitis on imaging- plus  1 feature of SpA
HLA-B27 plus  2 feature of SpA
- Sacroiliitis on imaging- plus  1 feature of SpA
- HLA-B27 plus  2 feature of SpA
- Active (acute) inflammation on MRI highly suggestive of sacroiliitis associated with SpA
- Definite radiographic sacroillitis accorging to modified New York criteria
- Inflammatroy back pain
- Arthritis
- Enthesitis (heel)
- Uveitis
- Dactylitis
- Psoriasis
- Crohn's disease or ulcerative colitis
- Good response to NSAIDs
- Family history for SpA
- HLA-B27
- Elevated CRP

## ASAS classification criteria for peripheral spondyloarthritis
- The Assessment of SpondyloArthritis International Society classification criteria for peripheral spondyloarthritis (peripheral SpA) include:
- Psoriasis
- Inflammatory bowel disease
- Preceding infection
- HLA-B27
- Uveitis
- Sacroiliitis on imaging (radiograph or MRI)
- Arthritis
- Enthesitis
- Dactylitis
- Inflammatory back pain in the past
- Positive family history of SpA

# Differential Diagnosis
Key:+ : Infrequently present, ++ : Frequently present, +++ : Always present, - : Absent
Simian hemorrhagic fever virus
Simian hemorrhagic fever virus or Simian haemorrhagic fever virus or SHFV, is a highly pathogenic virus in monkeys.  It is a positive-stranded RNA virus classified in the family Arteriviridae.

# Hosts
Patas are believed to be the natural host for the virus since about 50% of wild patas monkeys have antibodies for the virus, while antibodies are much less prevalent in other simian species such as vervets and baboons. In macaques, however, infection with this virus can result in acute severe disease with high mortality.

# Symptoms
Asymptomatic infection of the virus can occur in patas monkeys, vervet monkeys, and baboons, although it is observed primarily in patas monkeys.  Infection has a rapid onset with animals developing a high fever, facial edema, cyanosis, anorexia, melena, and may begin to hemorrhage at the cutaneous, subcutaneous, and retrobulbar levels. Thrombocytopenia will develop soon after. Death usually occurs within 10-15 days after symptoms appear .
Spinal Muscular Atrophy Type 2
Spinal Muscular Atrophy Type 2 (also known as "spinal muscular atropy type II") is an autosomal recessive disease and is a form of spinal muscular atrophy (SMA).

# Symptoms
Children with spinal muscular atrophy type 2 manifest less severe weakness than children with Werdnig-Hoffman disease. Symptoms are usually noticed later in life, usually between the age of 6 to 18 months. The clinical features are similar to those found in children with Type 1; in fact, there are many children for whom the characterization of Type 1 (Werdnig-Hoffman) or Type 2 SMA becomes a "best guess". Children with Type 2 SMA usually achieve the ability to sit independently, however, they almost never achieve the ability to walk or stand without support.

# Prognosis
Some children with SMA Type 2 have a relatively static course and remain free of life threatening complications such as pneumonia. Other children, have progressive weakness of their swallowing and respiratory muscles. Many youngsters with SMA Type 2 develop curvature of the spine (Kyphoscoliosis) and other orthopedic problems. Skillful management by a team of physical therapists and orthopedic surgeons is usually needed to manage these problems.

# See Also
- Motor neurone disease
- Spinal Muscular Atrophy
- Kugelberg-Welander disease
- Werdnig-Hoffman disease

# Source
- Fight SMA Spinal Muscular Atrophy Guidebook
Stent thrombosis complications

# Overview
Stent thrombosis(ST) is associated with a mortality rate of 25%.

# Complications
- Recurrence of stent thrombosis
- Myocardial infarction secondary to stent thrombosis has worse prognosis compared to those who develop MI secondary to thrombus else where in the arteries. Stent thrombosis induced MI have higher incidence of in-hospital major cardiovascular and cerebrovascular adverse events including higher death rates.
- Death occurs in approximately 25% of patients.

## Recurrence of Stent Thrombosis
- Incidence of recurrent stent thrombosis has been reported as high as 12% at 6-months.
- 1 year recurrence rate of 4.6% was reported in patients with DES.
- The Dutch stent thrombosis registry reported a 3 year recurrence rate of stent thombosis of 20.1%.

## Myocardial Infarction / Death
- A sub-analysis of TRITON-TIMI 38 study showed that stent thrombosis was associated with death or myocardial infarction in 89% (186/210) of patients. In follow up studies after stent thrombosis, recurrent stent thrombosis has also been noticed, especially during the following six months.
- Van Werkum et al studied the long term outcome after definite stent thrombosis (ST). 431 patients with definite stent thrombosis were enrolled in this multicenter registry. The primary end point was the composite of cardiac death and definite recurrent ST. The primary end point occurred in 111 patients after a median follow-up of 27.1 months. Clinical outcome was not affected by the type of previously implanted stent (drug-eluting stent or bare-metal stent) or the category of ST (early versus late). Authors concluded that the long-term clinical outcome after a first definite ST is unfavorable, with a high mortality and recurrence rate. Diabetes mellitus, left ventricular ejection fraction < 45%, long total stent length, complex coronary lesions, TIMI flow grade < 3 after percutaneous coronary intervention, and implantation of an additional coronary stent during the emergent percutaneous coronary intervention for the ST were associated with this unfavorable outcome.
- A pooled analysis of multicenter coronary stent clinical trials showed that in patients with angiographic stent thrombosis the incidence of death or myocardial infarction was 64.4% at the time of stent thrombosis and had a 6-month mortality rate of 8.9%.
- One year mortality rate was 16% and stent thrombosis recurrence was 4.6% in a multicenter study in Spain.
- The mortality rate was 31% and MI was seen in 83% of patients with stent thrombosis at 4 years follow-up in a pooled analysis.
- In a study to investigate the efficacy and outcome of emergency percutaneous coronary interventions (PCI) in patients with stent thrombosis, 6 month major adverse clinical events were comprised of death (11%), reinfarction (16%), and recurrent stent thrombosis (12%).
Streptomycin adverse reactions

# Adverse Reactions
The following reactions are common: vestibular ototoxicity (nausea, vomiting, and vertigo); paresthesia of face; rash; fever; urticaria; angioneurotic edema; and eosinophilia.
The following reactions are less frequent: cochlear ototoxicity (deafness); exfoliative dermatitis; anaphylaxis; azotemia; leucopenia; thrombocytopenia; pancytopenia; hemolytic anemia; muscular weakness; and amblyopia.
Vestibular dysfunction resulting from the parenteral administration of streptomycin is cumulatively related to the total daily dose. When 1.8 to 2 g/day are given, symptoms are likely to develop in the large percentage of patients - especially in the elderly or patients with impaired renal function - within four weeks. Therefore, it is recommended that caloric and audiometric tests be done prior to, during, and following intensive therapy with streptomycin in order to facilitate detection of any vestibular dysfunction and/or impairment of hearing which may occur.
Vestibular symptoms generally appear early and usually are reversible with early detection and cessation of streptomycin administration. Two to three months after stopping the drug, gross vestibular symptoms usually disappear, except from the relative inability to walk in total darkness or on very rough terrain.
Although streptomycin is the least nephrotoxic of the aminoglycosides, nephrotoxicity does occur rarely.
Clinical judgment as to termination of therapy must be exercised when side effects occur.
Stroke resident survival guide
Synonyms and Keywords: stroke management, stroke workup, stroke approach, approach to stroke, stroke treatment

# Overview
Stroke is used to describe pathological conditions caused by brain ischemia or hemorrhage.  According to the American Heart Association/American Stroke Association (July, 2013),  it is defined as a neurological deficit attributed to an acute focal injury of the central nervous system (CNS) by a vascular cause, including cerebral infarction, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). Therefore, by definition, trauma has to be ruled out before stroke can be diagnosed in a patient with a focal neurological deficit.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- All strokes can potentialy lead to death or permanent disability within 24 hours if left untreated.

## Common Causes
- Aneurysms
- Atrial fibrillation
- Eclampsia
- Infective endocarditis
- Myocardial infarction
- Pulmonary embolism
- Arteriovenous malformations
- Atherosclerosis
- Atrial fibrillation
- Embolism
- Hypertension
- Subarachnoid hemorrhage
- Thrombosis
- Transient ischemic attack
- Traumatic brain injury
- Warfarin

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of stroke according to the American Academy of Neurology guidelines:

## Initial Evaluation

# Treatment
The management of stroke will greatly depend on the type of stroke (if it is either hemorrhagic or ischemic).
- To view the specific treatment of hemorrhagic stroke click here.
- To view the specific treatment of ischemic stroke click here.

# Do's
- Perform tertiary preventive measure to decrease subsecuent episodes, such as using statins and anticoagulants, controling glucose levels and blood pressure.

# Don'ts
- Do not lower blood pressure in hypertensive patients with ischemic stroke when below
Sulfadiazine adverse reactions

# Adverse Reactions
Blood Dyscrasias
Agranulocytosis, aplastic anemia, thrombocytopenia, leukopenia, hemolytic anemia, purpura, hypoprothrombinemia and methemoglobinemia.
Allergic Reactions
Erythema multiforme (Stevens-Johnson syndrome), generalized skin eruptions, epidermal necrolysis, urticaria, serum sickness, pruritus, exfoliative dermatitis, anaphylactoid reactions, periorbital edema, conjunctival and scleral injection, photosensitization, arthralgia, allergic myocarditis, drug fever and chills.
Gastrointestinal Reactions
Nausea, emesis, abdominal pains, hepatitis, diarrhea, anorexia, pancreatitis and stomatitis.
C.N.S. Reactions
Headache, peripheral neuritis, mental depression, convulsions, ataxia, hallucinations, tinnitus, vertigo and insomnia.
Renal
Crystalluria, stone formation, toxic nephrosis with oliguria and anuria; periarteritis nodosa and lupus erythematosus phenomenon have been noted.
Miscellaneous Reactions
The sulfonamides bear certain chemical similarities to some goitrogens, diuretics (acetazolamide and the thiazides) and oral hypoglycemic agents. Goiter production, diuresis, and hypoglycemia have occurred rarely in patients receiving sulfonamides. Cross-sensitivity may exist with these agents.