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HEPATITIS

HEPATITIS. Dr. FERDA ÖZKAN. Objectives and Aim. To learn the types of inflammatory diseases of liver To learn the inflammatory changes in liver. I nflammatory diseases. Viral Hepatitis Autoimmune Hepatitis Fulminant Hepatitis Postnecrotic Cirrhosis Liver Abscesses .

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HEPATITIS

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  1. HEPATITIS Dr. FERDA ÖZKAN

  2. Objectives and Aim • To learn the types of inflammatory diseases of liver • To learn the inflammatory changes in liver

  3. Inflammatory diseases • Viral Hepatitis • Autoimmune Hepatitis • Fulminant Hepatitis • Postnecrotic Cirrhosis • Liver Abscesses. • Secondary infections: • miliary tuberculosis, • malaria, • staphylococcal bacteremia, • the salmonellosis, • candida, • amebiasis.

  4. Viral Hepatitis • Viral Hepatitis: • Specific – Hepatitis A, B, C, D, E, & others • Systemic - CMV, EBV, yellow fever.

  5. Infection of the liver caused by a small group of viruses having a particular affinity for the liver. • However, the anatomic pathology is generally similar. • Systemic viral infections • (1) Infectious mononucleosis (Epstein-Barr virus), which may cause a mild hepatitis during the acute phase; • (2) Cytomegalovirus, particularly in the newborn or immunosuppressed patient; • (3) Yellow fever, which has been a major and serious cause of hepatitis in tropical countries.

  6. Patterns of Viral Hepatitis • Carrier state / Asymptomatic phase • Acute hepatitis • Chronic Hepatitis • Chronic Persistent Hepatitis (CPH) • Chronic Active Hepatitis (CAH) • Fulminant hepatitis • Cirrhosis

  7. Acute viral hepatitis Widespread liver cell injury • cell swelling ("hydropic change"; "cloudy swelling"; "ballooning degeneration") • necrosis & lysis (individually or in small groupsdue to the viruses or to antibodies) • apoptosis (individual liver cells as eosinophilic Councilman bodies)

  8. hypertrophy/hyperplasia of Kupffer cells • inflammatory cells (mostly lymphocytes, macrophages) in the portal areas, and some among the hepatocytes, • portal inflammation and cholestasis • hepatocyte regeneration (purple cells with big nuclei; during the recovery phase).

  9. Patterns of Liver Damage • Porto-portal Bridging fibrosis • Porto-central fibrosis • Apoptotic body • Piece meal necrosis • Centrilobulary necrosis

  10. Trichrome stain demonstrates the collapse of the liver parenchyma with viral hepatitis. The blue-staining areas are the connective tissue of many portal tracts that have collapsed together

  11. 1. Carrier state: • (a) without clinically apparent disease • (b) with chronic hepatitis • 2. Asymptomatic infection: • serologic evidence only • 3. Acute hepatitis: • (a) anicteric • (b) icteric. • 4. Chronic hepatitis: • without or with progression to cirrhosis. • 5. Fulminant hepatitis: • submassive to massive hepatic necrosis.

  12. Councilman body

  13. Viral hepatitis. A large pink cell undergoing "ballooning degeneration" is seen below the right arrow.

  14. Hepatitis A ("infectious hepatitis“; HAV) • Usually self-limited, • RNA enterovirus (picornavirus), • is transmitted by the fecal-oral route,poor sanitation. • Hepatitis A very seldom becomes chronic or leads directly to cirrhosis. • There is probably no carrier state. • At worst, the disease might be a trigger for autoimmune chronic hepatitis, but the virus won't stay around.

  15. Hepatitis B Virus(HBV), serum hepatitis • World's most serious DNA-virus-related health problem • millionsof carriers, • Route: • blood transfusions, • shared needles • hospital(cuts, needle sticks) • sex • bugs • vertical transmission (mother-to-child).

  16. HBV can produce (1) acute hepatitis, (2) chronic nonprogressive hepatitis, (3) progressive chronic disease ending in cirrhosis, (4) fulminant hepatitis with massive liver necrosis, (5) an asymptomatic carrier state with or without progressive disease, (6) hepatocellular carcinoma.

  17. Carrying hepatitis B (with or without ongoing liver disease) is an important cause of : • hepatocellular carcinoma • immune complex, type III immune injury problems • cryoglobulinemia • polyarteritis nodosa of hepatitis B

  18. Symptoms begin • when T-cells are activated with HBsAg and HBc • start killing the hepatocytes • Histopathologists find T-cytotoxic cells where the hepatocytes are dying. • The only surviving liver cells are the ones that won't continue making viruses, and these replenish the liver.

  19. Hepatitis C Virus(non-A, non-B hepatitis) • Route: • intravenous drug abusers (50 to 90%) • blood transfusion (55 to 85%) • hemodialysis (8 to 24%) • Hospitals & dental clinics(cuts, needle sticks) • vertical transmission (mother-to-child) • Patients with unexplained cirrhosis and hepatocellular carcinoma have anti-HCV prevalence rates exceeding 50% • In contrast to HBV, HCV has a high rate of progression to chronic disease and eventual cirrhosis, exceeding 70%

  20. Hallmarks: • persistent infection, • chronic hepatitis, • cirrhosis.

  21. Chronic hepatitis graded by the degree of activity (necrosis and inflammation) and staged by the degree of fibrosis. necrosis and inflammation are prominent, and there is some steatosis

  22. Viral hepatitis C which is at a high stage with extensive fibrosis and progression to macronodular cirrhosis, as evidenced by the large regenerative nodule at the center right.

  23. Hepatitis D(HDV; hepatitis delta virus) • Common in homosexual men and iv drug-abusers. • 1.Acute coinfection: occurs following exposure to serum containing both HDV and HBV. • 2. Superinfection of a chronic carrier: HBV with a new inoculum of HDV. • The carrier may have been previously “healthy” or may have had underlying chronic hepatitis.

  24. Chronic Viral Hepatitis 1.Chronic persistent hepatitis: inflammation is confined to the portal tracts. 2.Chronic active hepatitis:portal tract inflammation spills into the parenchyma and surrounds regions of necrotic hepatocytes. 3.Chronic lobular hepatitis: persistent inflammation is confined to the lobule.

  25. Chronic Viral Hepatitis : as a complication • HAV: • Extremely rare. • HBV: • more than 90% of infected neonates • 5% of infected adults • one-fourth progress to cirrhosis. • HCV: • more than 50% of infected patients • half progress to cirrhosis. • HDV: • most frequent outcome of HDV superinfection.

  26. Viral Hepatitis: Microbiology

  27. The morphology of chronic hepatitis • ranges from exceedingly mild to severe, to eventual cirrhosis. Mildest form (inflammatory infiltrate is limited to portal tracts): • lymphocytes, • macrophages, • occasional plasma cells, • occasional rare neutrophil or eosinophil • liver architecture is usually well preserved but may exhibit vestiges of acute disease.

  28. Progressive form • Piecemeal necrosis, • the chronic inflammatory infiltrate spills out from portal tracts into adjacent parenchyma, • necrosis of hepatocytes • lobular inflammation with focal necrosis of hepatocytes. • Continued loss of hepatocytes results in • fibrous septum formation, • accompanied by hepatocyte regeneration, • cirrhosis.

  29. Autoimmune (lupoid)Hepatitis • without chronic virus infectionbut with evidence of immune injury • chronic hepatitis  cirrhosis • most common autoantibodies against smooth muscle. • Usually features a lot more plasma cells than does viral chronic hepatitis.

  30. Female predominance (70%), particularly young and perimenopausal women. • The absence of viral serologic markers. • Elevated serum IgG levels. • High serum titers of autoantibodies in 80% of cases: • anti-smooth muscle (SMA), • antinuclear (ANA), • antimitochondrial (AMA), • anti-liver and kidney microsome (LKM) antibodies.

  31. Fulminant Hepatitis • Hepatic insufficiency  progresses from onset of symptoms to hepatic encephalopathy (within 2 to 3 weeks), • Drug or chemical toxicity (25 to 30%): • acetaminophen (in suicidal doses), • isoniazid, • antidepressants (particularly monoamine oxidase inhibitors), • halothane, • methyldopa, • mycotoxins(Amanita phalloides).

  32. Fulminant hepatic failure may present with • jaundice, • encephalopathy, • fetor hepaticus, • coagulopathy and bleedinginstability, • cardiovascular instability, • renal failure, • adult respiratory distress syndrome, • electrolyte and acid-base disturbances, • sepsis.

  33. Hepatic failure within 2-3 weeks. • Reactivation of chronic or acute hepatitis • Massive necrosis, shrinkage, wrinkled • Collapsed reticulin network • Only portal tracts visible • Little or massive inflammation – time • More than a week – regenerative activity • Cholestasis (blotchy green bile staining) • Complete recovery – or - cirrhosis.

  34. Histologically • Necrosis • destroying the central and midzonal regions and sparing the periportal area of the lobule. • Complete destruction of contiguous lobules • There may be surprisingly little inflammatory reaction • except possibly for an increase in lymphocytes, macrophages, • occasional neutrophils within the portal tracts.

  35. Survivors: • secondary regeneration of hepatocytes (primitive ductules) • Kupffer cellproliferation(laden with lipofuscin and cellular debris) • nodular masses of liver cells • broad bands of scar tissue • postnecrotic cirrhosis.

  36. Postnecrotic Cirrhosis • Irregularly sized nodules (some several centimeters in diameter) • separated by variable but mostly broad scars. • Common causes: • Previous viral infection • Hepatotoxin: • phosphorus • carbon tetrachloride • mushroom poisoning • Drugs: • acetaminophen, • oxyphenisatin, • alpha-methyldopa.

  37. Liver Abscess • The organisms reach the liver via • (1) the portal vein, • (2) arterial supply, • (3) ascending infection in the biliary tract (ascending cholangitis), • (4) direct invasion of the liver from a nearby source, • (5) a penetrating injury.

  38. Most abscesses are pyogenic, • The majority of hepatic abscesses used to result from portal spread of intra-abdominal infections: • appendicitis, • diverticulitis, • colitis. • Others: • amebic, • echinococcal, • helminthic.

  39. Biliary abscesses: • usually multiple, • purulent material in adjacent bile ducts. • Pyogenic hepatic abscesses: • Solitary or multiple lesions, • Solitary abscess:direct extension and trauma usually cause a solitary large abscess, • Multiple small abscesses: bacteremic spread through the arterial or portal system tends to produce from millimeters to massive lesions many centimeters in diameter.

  40. Complications • Sepsis & Pyemia • Rupture • Rupture thoracic cavity: • empyema • lung abscess. • Rupture of subcapsular liver abscesses: • peritonitis • localized peritoneal abscesses.

  41. Drug-Induced and Toxin-Induced Liver Disease • Liver the major drug-metabolizing and drug-detoxifying organ  subject to potential damage. • Injury may result from • (1) direct toxicity; • (2) hepatic conversion of a xenobiotic to an active toxin; • (3) via immune mechanisms, • usually when the drug or a metabolite acts as a hapten to convert a cellular protein into an immunogen.

  42. The injury may be immediate or take weeks to months to develop, presenting only after severe liver damage has developed. • The injury may take the form of hepatocyte necrosis, cholestasis, or insidious onset of liver dysfunction. • Drug-induced chronic hepatitis is clinically and histologically indistinguishable from chronic viral hepatitis. • Exposure to a toxin or therapeutic agent should be included in the differential diagnosis of any form of liver disease.

  43. Drugs: Acetaminophen (paracetamol, "Tylenol") overdose Acetaminophen + alcohol Stimulants: Cocaine,Ecstasy & Amphetamine Isoniazid Methyldopa Arsenic (as for syphilis therapy) Chemicals: Carbon tetrachloride Chloroform Phosphorus Nature: Mushrooms Amanita phalloides (the death angel)

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