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Hepatitis. Dr. Meg- angela Christi M. Amores. Hepatitis. Inflammation of the liver Acute Viral Hepatitis Toxic and Drug-induced Hepatitis Chronic Hepatitis. Acute Viral Hepatitis. Almost all cases of acute viral hepatitis are caused by one of five viral agents: hepatitis A virus (HAV)
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Hepatitis Dr. Meg-angela Christi M. Amores
Hepatitis • Inflammation of the liver • Acute Viral Hepatitis • Toxic and Drug-induced Hepatitis • Chronic Hepatitis
Acute Viral Hepatitis • Almost all cases of acute viral hepatitis are caused by one of five viral agents: • hepatitis A virus (HAV) • hepatitis B virus (HBV) • hepatitis C virus (HCV) • HBV-associated delta agent or hepatitis D virus (HDV) • hepatitis E virus (HEV)
Hepatitis A • Non-enveloped RNA virus • in the hepatovirus genus of the picornavirus family • Inactivation of viral activity can be achieved by boiling for 1 min, by contact with formaldehyde and chlorine, or by ultraviolet irradiation
Hepatitis A • incubation period of ~4 weeks • replication is limited to the liver • viral shedding in feces, viremia, and infectivity diminish rapidly once jaundice becomes apparent
Hepatitis A • diagnosis of hepatitis A is made during acute illness by demonstrating anti-HAV of the IgMclass • After acute illness, anti-HAV of the IgGclass remains detectable indefinitely • patients with serum anti-HAV are immune to reinfection
Hepatitis A • transmitted almost exclusively by the fecal-oral route • Person-to-person spread of HAV is enhanced by poor personal hygiene and overcrowding • contaminated food, water, milk, frozen raspberries and strawberries, green onions and shellfish • Declining incidence in developed countries
Hepatitis B • DNA virus • hepadnaviruses (hepatotropic DNA viruses) • Mode of transmission: • Percutaneous inoculation • intimate (especially sexual) contact and perinatal transmission • Oral ingestion - potential but inefficient route of exposure
Hepatitis C • Linear, single stranded RNA Virus • genus Hepacivirus in the family Flaviviridae • Cell-mediated immune responses and elaboration by T cells of antiviral cytokines contribute to the containment of infection and pathogenesis of liver injury associated with hepatitis C
Hepatitis C • Mode of transmission: • Percutaneous inoculation • Transfusions • other percutaneous routes, such as injection drug use • occupational exposure to blood • studies have failed to identify sexual transmission • chances of sexual and perinatal transmission have been estimated to be ~5%
Symptoms and Signs • occurs after an incubation period that varies • incubation periods for: • hepatitis A range from 15–45 days • hepatitis B and D from 30–180 days • hepatitis C from 15–160 days • hepatitis E from 14–60 days
Symptoms and Signs • Prodromal Phase • symptoms: systemic, variable • anorexia, nausea and vomiting, fatigue, malaise, arthralgias, myalgias, headache, photophobia, pharyngitis, cough, and coryza may precede the onset of jaundice by 1–2 weeks • low-grade fever between 38° and 39°Cmore often present in hepatitis A and E than in hepatitis B or C • Dark urine and clay-colored stools 1-5 days before jaundice appears
Symptoms and signs • clinical JAUNDICE phase • liver becomes enlarged and tender • right upper quadrant pain and discomfort
jaundice • Yellow coloration of skin, sclera, palms • visible in the sclera or skin when the serum bilirubin value is >43 mol/L (2.5 mg/dL) • Bilirubin levels >340 mol/L (20 mg/dL) extending and persisting late into the course of viral hepatitis – severe disease
Symptoms and Signs • Recovery phase • constitutional symptoms disappear • some liver enlargement and abnormalities in liver biochemical tests are still evident • Complete clinical and biochemical recovery is to be expected 1–2 months after all cases of hepatitis A and E and 3–4 months after the onset of jaundice in three-quarters of uncomplicated, self-limited cases of hepatitis B and C
Lab Features • serum aminotransferasesaspartateaminotransferase (AST) and ALT (previously designated SGOT and SGPT) • variable increase during the prodromal phase • does not correlate well with the degree of liver cell damage • Peak levels at time of clinical jaundice • High bilirubin levels • Serologic tests
Treatment • antiviral therapy – not recommended in all cases of Hep B – due to complete recovery • acute hepatitis C, recovery is rare, progression to chronic hepatitis is the rule • interferon monotherapy • 24-week course (beginning within 2–3 months after onset) of the best regimen identified for the treatment of chronic hepatitis C
Treatment • most cases of typical acute viral hepatitis, specific treatment generally is not necessary • patients will feel better with restricted physical activity • high-calorie diet is desirable • Intravenous feeding when necessary
Prevention • Hep A: • gloves should be worn when the bedpans or fecal material of patients • Hep B and C: • blood precautions, i.e., avoiding direct, ungloved hand contact with blood and other body fluids • hand washing • Vaccination: Hep A, Hep B
Prognosis • all previously healthy patients with hepatitis A recover completely • hepatitis B, 95–99% of previously healthy adults have a favorable course and recover completely • advanced age and with serious underlying medical disorders may have a prolonged course • prolonged PT, low serum albumin level, hypoglycemia, and very high serum bilirubin values suggest severe hepatocellular disease