Path Liver Tbl 3

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Chronic hepatitis attributed to Tcell mediated autoimmunity (cytotoxic t cells and t cell production of IFN gamma)

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Autoimmune hepatitis

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What can triggered Autoimmune hepatitis?

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viral infections or drugs or it may be a component of other autoimmune disorders like RA , sjogren syndrome or ulcerative colitis

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The main morphological characteristic of Autoimmune hepatitis is

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clusters of periportal plasma cells

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Who gets more Autoimmune hepatitis?

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Females with elevated IgG levels but no serum markers of viral infection

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Type 2 Autoimmune hepatitis

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Autoantibodies against liver kidney microsome 1 and liver cytosol antigens

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Type 1Autoimmune hepatitis

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Autoantibodies against nuclear, smooth muscle, actin and soluble liver antigen/liver pancreas antigens. Associated with HLA-DR3 haplotype

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Patients with symptoms of Autoimmune hepatitis by the time of diagnosis show

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substantial liver destruction and scarring. Immunosuprresion is the course of tx with transplant for end stage disease

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prime cause of fulminant hepatitis in the US with an incidence of about 14 to 40 / 100,000 patients

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Drug (or Toxin) Induced Liver Injury (DILI)

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Drug (or Toxin) Induced Liver Injury (DILI) Susceptibility is influenced by

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1) Direct toxicity to hepatocytes or biliary epithelial cells causing necrosis, apoptosis or disruption of cell function; 2) hepatic conversion of xenobiotic to an active toxin; or 3) immune mediated injury with the drug or its metabolite serving as a hapten converting a cellular protein to an immunogen; are the mechanisms of liver injury.

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Leading cause of drug induced acute liver failure

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acetaminophen

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What is reye syndrome

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children taking aspirin develop mitochondrial dysfunction characterized by massive microvesicular steatosis.

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Examples of predictable drug reactions are toxicities from

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acetaminophen, Amanita phalloides, or carbon tetrachloride

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Unpredictable or idiosyncratic drug reactions are host dependent, specifically influenced by

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the rate of metabolism & the intensity of the immune response of the host. Adults are more susceptible than children.

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examples of idiosyncratic drug reaction

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Slow metabolism resulting in cholestatic liver injury associated with chlorpromazine and fatal immune injury following multiple exposures to halothane

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Isoniazids, NSAIDs & anti-seizure medications cause

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idiosyncratic reactions

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The evolution of idiosyncratic drug reaction is usually subacute & characterized by

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high bilirubin levels

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There are 3 distinctive forms of Alcoholic Liver Disease (ALD)

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1.) hepatic steatosis; 2) alcoholic hepatitis; 3) cirrhosis

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Hepatomegaly with mild elevations of serum bilirubin and alkaline phosphatase. Fat liver with microvesicular lipid droplets within hepatocytes. No fibrosis

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Hepatic steatosis. It is reversible

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Acute manifestation after heavy drinking. It can be minimal to fulminant hepatic failure with malaise, anorexia and hepatomegaly. High bilirubin and alkaline phosphatase. Liver fibrosis, hepatocyte necrosis, mallory bodies (intracellular eosinophilic aggregates) and inflamation

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Alcoholic hepatitis. Progresses to cirrhosis

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Alcoholic cirrhosis

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Classic cirrhosis presentation. Liver transforms from fatty to brown shrunken not fatty. Causes of death are hepatic coma, massive gastrointestinal hemorrhage, intercurrent infection, hepatocellular carcinoma.

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Non alcoholic fatty liver diseases present hepatic steatosis in the absence of heavy alcohol consumption. These diseases are

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Metabolic diseases like Non alcoholic fatty liver disease, hemochromatosis, wilson disease, alpha 1 antitrypsin deficiency, neonatal cholestasis

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Metabolic diseases rising in incidence due to

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obesity,

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Asymptomatic steatosis, but there can be fatigue, malaise and upper right quadrant pain, discomfort. High serum transaminase levels. Hepatocytes show fat vacuoles with no inflammation or with inflammation. Fibrosis

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Nonalcoholic fatty liver disease

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Nonalcoholic fatty liver disease is associated with

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metabolic syndrome of dyslipidemia, hyperinsulinemia and ROS generation.

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Infant with jaundice, dark urine, light stools and hepatomegaly. Hepatocyte death and lobular disarray, hepatocyte giant cell formation, prominent cholestasis, portal tract inflammation and extramedullary hematopoiesis.

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Neonatal cholestasis. The major cause is biliary atresia and alpha 1 AT. Important to distinguish since biliary atresia requires surgery

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Pruritus, jaundice, malaise, dark urine, light stools and hepatosmegaly. Conjugated hyperbilirubinemia, increased serum alkaline phosphatase, bile acid, cholesterol.

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Secondary billary cirrhosis

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Before secondarybillary cirrhosis develops what pathologic findings are observed?

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Prominent bile stasis in bile ducts, bile ducturlar proliferation with surrounding neutrophils, portal tract edema.

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Pruritus, jaundice, malaise, dark urine, light stools and hepatosmegaly. Conjugated hyperbilirubinemia, increased serum alkaline phosphatase, bile acid, cholesterol. ELEvated IGM autoantibodies (automitochondrial antibodies)

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Primary biliary cirrhosis. More prevalent in women

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Before primary billary cirrhosis develops what pathologic findings are observed?

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dense lymphocytic infiltrate in portal tracts with granulomatous destruction of bile ducts

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What causes secondary biliary cirrhosis?

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Extrahepatic bile duct obstruction, biliary atresia, gallstones, strictures, carcinoma of pancreatic head

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What causes primary biliary cirrhosis?

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Possibly autoimmune

Front 32

ruritus, jaundice, malaise, dark urine, light stools and hepatosmegaly. Conjugated hyperbilirubinemia, increased serum alkaline phosphatase, bile acid, cholesterol. ELEvated IGM autoantibodies (automitochondrial antibodies) and HYPERGAMMAGLOBULINEMIA

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Primary sclerosing cholangitis. More prevalent in females

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Before primary sclerosing cholangitis develops what pathologic findings are observed?

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periductal portal tracts fibrosis, segmental stenosis of extrahepatic and intrahepatic bile ducts.

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what causes primary sclerosing cholangitis

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Unknown possible autoimmune. Mostly associated with inflammatory bowel disease.