Exam review GIT and Liver, Gall bladder

Liver Hepatitis Circulatory diseases

Hepatitis

Hepatitis A infection (infectious hepatitis) : RNA virus Spread: Fecal-oral route. C/F: Never develop a carrier, chronic state, Hepatocellular carcinoma. C/F: Mild disease, quick recovery, Acute disease: Positive for IgM antibody to hepatitis A virus (antigen). Incidence: Sporadic outbreaks in restaurants. In places with poor hygiene. Common in children Adults are often seropositive

Hepatitis B infection (DNA virus) Spread: Parenterally and by intimate contact through mucosal surfaces. Vertical transmission is common. Carrier state is common, Less chance of Chronic hepatitis, cirrhosis. Increased chance of Developing Hepatocellular carcinoma. Carrier: Positive HBsAg even after 6 months, with normal health but can transmit infection.

Interpretation of HBV serology Acute phaseCarrier phase Chronic HBsAg +IgM Anti- HBs. HBsAg + > 6 months No surface antigen* HBcAg +IgM Anti- HBc IgG Anti-HBc > 6 months IgG Anti-HBc > 6 months DNA polymerase/ HBV DNA HBV DNA

Hepatitis C infection (non-A, non-B hepatitis) RNA virus Spread : Parenterally and via contact-associated mechanisms. Vertical transmission is NOT common. C/F : More chance of Chronic hepatitis cirrhosis and Hepatocellular carcinoma. Acute disease: Positive for IgM antibody to hepatitis C virus antigen. Chronic disease: Positive for IgG antibody to hepatitis C virus (antigen). Fatty change seen. Incidence: It is seen most commonly in the homosexual community, intravenous drug users, and patients who have received multiple blood transfusions.

Delta virus infection RNA virus that is replication defective : cause infection when encapsulated by HBsAg Co-infection : Positive for IgM antibody to hepatitis D virus antigen and IgM antibody to HBc antigen. Super infection: Positive for IgM antibody to hepatitis D virus antigen and HBsAg. Incidence: common in drug addict and hemophiliac Clinical features: Fulminant hepatitis common with this infection, cirrhosis.

Acute Hepatitis Liver cell swelling, feathery degeneration

Ground glass Hepatocytes and sanded nuclei and apoptosis (HBV).

Chronic hepatitis Symptomatic, biochemical and/or serological evidence of relapsing hepatic disease for more than 6 months. Etiology: HCV ( commonest ) A. General features A. Bridging necrosis and fibrosis B. Lymphoid aggregates C. Piecemeal necrosis= interface hepatitis

Circulatory disorders of liver These are the disease due to circulatory disturbances Disturbance of circulation within the liver: Cirrhosis, sinusoidal dilatation, veno occlusive disease. Disturbance of circulation Out side the liver : Shock, RHF, hepatic artery thrombosis (cause infarct), portal vein thrombosis, hepatic vein thrombosis.

Disease Sinusoidal dilation (aka)= Peliosis hepatis –Etiology : Anabolic steroid, danazol, OC pill –Peliotic lesions usually disappear after cessation of drug treatment. Nutmeg liver/ centrilobular necrosis/ cardiac cirrhosis –Etiology : Right sided heart failure/shock

Nutmeg liver and centrilobular necrosis

Budd-Chiari syndrome Def: acute thrombotic occlusion of the hepatic vein. Etiology; 1. Polycythemia Vera 2. Myeloproliferative disorder (CML) 3. Use of OC pill, HCC. 4. Deficiencies in antithrombin, protein S, or protein C, or mutations of factor V Clinical: Tender hepatomegaly, some features of PHT, liver enzyme elevation. Diagnostic procedure: venogram

Veno occlusive diseases (VOD) Etiology : Immediate week after bone marrow transplantation with immunosuppressant therapy. Pathogenesis : Fibrosis of Small hepatic vein radicles. Clinical: tender hepatomegaly, ascites, weight gain, and jaundice

Liver infarct Cause: –thrombosis or compression of an intrahepatic branch of the hepatic artery by embolism, neoplasia,sepsis.

Portal Vein Obstruction and Thrombosis Insidious and well tolerated Morphology: Well demarcated area of red- blue discoloration (infarct of Zahn), no necrosis only atrophy. Ascites and other manifestations of portal hypertension

Drug and toxin induces liver disease Type of Hepatobiliary damage Drug or toxin Micro vesicular fatty change Tetracycline, ethanol Macro vesicular fatty change Ethanol, Methotrexate and diabetes mellitus Centrilobular necrosisAcetaminophen, halothane.

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