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Exam review. GIT and Liver, Gall bladder. Liver. Hepatitis Circulatory diseases. Hepatitis. Interpretation of HBV serology. Delta virus infection. Acute Hepatitis Liver cell swelling, feathery degeneration. Ground glass Hepatocytes and sanded nuclei and apoptosis (HBV).
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Exam review GIT and Liver, Gall bladder
Liver Hepatitis Circulatory diseases
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 ) • General features • Bridging necrosis and fibrosis • Lymphoid aggregates • 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
Budd-Chiari syndrome Def: acute thrombotic occlusion of the hepatic vein. Etiology; • Polycythemia Vera • Myeloproliferative disorder (CML) • Use of OC pill, HCC. • 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
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