Hepatitis A pathophysiology

Revision as of 18:04, 3 February 2012 by Varun Kumar (talk | contribs)
Jump to navigation Jump to search

Hepatitis Main Page

Hepatitis A

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Hepatitis A from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

Ultrasound

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Case Studies

Case #1

Hepatitis A pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hepatitis A pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hepatitis A pathophysiology

CDC on Hepatitis A pathophysiology

Hepatitis A pathophysiology in the news

Blogs on Hepatitis A pathophysiology

Directions to Hospitals Treating Hepatitis A

Risk calculators and risk factors for Hepatitis A pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Is a liver disease caused by the hepatitis A virus (HAV). Hepatitis A can affect anyone. In the United States, hepatitis A can occur in situations ranging from isolated cases of disease to widespread epidemics.

HAV, a 27-nm RNA agent classified as a picornavirus, can produce either asymptomatic or symptomatic infection in humans after an average incubation period of 28 days (range: 15--50 days).

Transmission

The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route but very rarely by blood and blood products. Food-borne outbreaks are not uncommon,[1] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[2] Approximately 40% of all acute viral hepatitis is caused by HAV.[3] Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection. The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform), drying, and temperatures up to 60oC. It can survive for months in fresh and salt water. Common-source (e.g., water, restaurant) outbreaks are typical. Infection is common in children in developing countries, reaching 100% incidence, but following infection there is life-long immunity. HAV can be inactivated by: chlorine treatment (drinking water), formalin (0.35%, 37oC, 72 hours), peracetic acid (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and UV radiation (2 μW/cm2/min).

Pathology

Click on the arrow to view the pathologic findings in viral hepatitis: {{#ev:youtube|_hXvbpSxFZw}}

References

  1. Brundage SC, Fitzpatrick AN (2006). "Hepatitis A". Am Fam Physician. 73 (12): 2162–8. PMID 16848078.
  2. Lees D (2000). "Viruses and bivalve shellfish". Int. J. Food Microbiol. 59 (1–2): 81–116. doi:10.1016/S0168-1605(00)00248-8. PMID 10946842.
  3. Insert footnote text Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). Medical Microbiology," 5th ed., Elsevier Mosby.