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Definition & causative organisms • Infections of the liver caused by a group of viruses having an affinity for the liver • Infection of the hepatocytes produces necrosis and inflammation of the liver • Hepatitis virus A,B,C,D,E (G -no acute or chronic illness)….. • EBV,CMV, yellow fever, HSV etc. • Part of systemic infection
Epidimiology • >500 million people infected • >350 million chronic carriers of HBV • 200 million infected with HCV • Highest HBV carrier rate in Africa, Asia,W Pacific • Carrier rates 0.3 (US)-20(SE Asia)%
Clinico pathological outcomes of hepatitis • Acute asymptomatic infection with recovery: serologic evidence only • Acute symptomatic hepatitis with recovery: anicteric or icteric • Chronic hepatitis: without or with progression to cirrhosis • Fulminant hepatitis: with massive to submassive hepatic necrosis • Diagnosis of aetiology by serology,history etc
Hepatitis virus • A,E : Oro fecal transmission • Acute phase and fulminant hepatitis • No chronic phase • B,C,D: parenteral transmission • Acute, chronic, carrier phase • Predisposes to HCC
Hepatitis A • Hepatovirus RNA virus • Replication in hepatocyte (few in enterocyte) • Oro fecal transmission,2-6 wks incubation • No carrier state or chronic course • Ig G Anti HAV + → immunity • Fulminant liver failure rare ----0.1% • Worse outcome if superimposed on chronic hepatitis C,D or alcoholic • Vaccine + .
Pathogenesis • Immunologic reaction to virally infected hepatocytes.
Biochemical changes in viral hepatitis • Necrosis of hepatocytes, release of enzymes ALT ↑↑, AST ↑↑ • S. biliribin ↑↑ 10 days-1 month –conjugated (disruption of bile canaliculi & interference with excertion) • Alk phosphatase ↑ (interference with excertion) • ↓ protein production ↑ prothrombin time
Morphology of acute hepatitis • Gross • Early stage • Enlarged tender liver • Later stage • smaller greenish focal depressions due to areas of collapse may be seen
Ballooning degeneration Apoptosis (councilman bodies), Necrosis > zone 3 spotty,bridging,panacinar Inflammatory infiltrate Periportal,perihepatocytic Interface hepatitis Cholestasis Healing with mitotic activity in hepatocytes Lobular disarray hypertrophy and pigment in kupffer cells Microscopy of acute hepatitis
Fulminant hepatitis • Entire/part of liver involved • Liver shrinks,limp,wrinkled capsule • Microscopy: destruction of hepatocytes in contiguous lobules, collapsed reticulin framework,preserved portal tracts • Regeneration +/- fibrosis • C/F jaundice,encephalopathy etc
Hepatitis B • Hepadnaviridae, complete virion (Dane particle) • Parenteral transmission IV ,blood , body fluids, saliva, breast milk, semen, transplacental. • 4-26 weeks incubation period • HBV vaccination recombinant HbsAg or its immunogenic epitopes, lifelong immunity • Immunization in infancy
DNA partly double stranded • Core protein (HBcAg) • Lipo protein coat bearing Envelope glycoprotein (HBsAg) (Australia antigen Baruch S Blumberg in the serum of an aborigine) • DNA polymerase • HBx necessary for virus replication
Pathogenesis of hepatitis B • Proliferative phase: Episomal form produces complete viral particles (Infectivity) • Target viral antigens(HBsAg,HBcAg )expressed on the surface in association with HLA class I • Cytotoxic T lymphocytes directed against multiple HBV epitopes kill infected hepatocytes • Antiviral Antibodies appear → infectivity ends, hepatitis ends • Replication continues → carrier with chronic hepatitis Integrative phase: Integrated into the DNA (chronic hepatitis, HCC)