Alcoholic and Infectious Liver Diseases MCQs

Mallory hyaline are tangled skeins of intermediate filaments such as keratin 8 and keratin 18 that are partially degraded and ubiquitinated Reference: Robin's basic pathology 10 th edition, 842

Because of the low fidelity of the HCV RNA polymerase, the viral genome is inherently unstable, giving rise to new genetic variants at a high pace. This has led to the appearance of six major HCV genotypes worldwide, each with one or more "subspecies." Infections in most individuals are due to a virus of a single genotype, but new genetic variants are generated in the host as long as viral replication persists. As a result, each patient usually comes to be infected with a population of divergent but closely related HCV variants known as quasi species. Reference: Robbins Basic Pathology, 10 th ed, Pg-646

The individual has laboratory evidence of liver damage, with elevated AST, ALT, GGT, and alkaline phosphatase. The AST: ALT ratio is around 6:1, which is most characteristic of an alcoholic hepatitis. Reference: Robbins Basic Pathology, 10 th ed, Pg-652

The condition reflects Jaundice with Hyperbilirubinemia. Bilirubin is the normal non-iron containing pigment present in the bile. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10 th ed Pg: 52-53

Explanation: In acute hepatitis B, biopsy findings typically include ballooning degeneration, focal necrosis, and confluent necrosis in severe cases. Ground-glass hepatocytes, however, are absent in acute infection and instead signify chronic HBV infection. Explanation of other options: Ballooning change (Option A): Seen in acute hepatitis as hepatocyte swelling and degeneration. Focal or spotty necrosis (Option C): Common in acute HBV, involving scattered apoptotic hepatocytes. Confluent necrosis (Option D): Seen in severe acute hepatitis with widespread cell death. Key Takeaways: Acute HBV is marked by hepatocyte ballooning and necrosis, without ground-glass cells. Ground-glass hepatocytes are pathognomonic for chronic HBV infection. Serology differentiates acute from chronic HBV.

Budd-Chiari syndrome is due to thrombosis of the hepatic veins or inferior vena cava. Risk factors include pregnancy, use of oral contraceptives, Factor V Leiden, and other coagulation disorders. Patients can develop ascites due to the acute increased pressure in the portal system. Reference: Robbins Basic Pathology, 10 th ed, Pg-667

HBeAg, HBV DNA, and HBV DNA polymerase are detectable in the serum soon after HBsAg and signify active viral replication. (a & b) Microscopically, there is a portal and lobular inflammatory infiltrate comprised predominantly of lymphocytes and variably admixed with plasma cells and eosinophils. (c) In chronic hepatitis B, the swollen endoplasmic reticulum of hepatocytes are swollen and filled with HBsAg, leading to a "ground-glass" appearance. (d) The hepatocyte injury may result in necrosis or apoptosis. Necrosis of groups of hepatocytes (i.e., confluent necrosis) may be seen in severe cases and can progress to necrosis of the entire lobule (i.e., panlobular or panacinar necrosis) or connect vascular structures (i.e., bridging necrosis). Reference: Robbins 10th Ed, pg 837

The morphologic findings in alcoholic hepatitis include the following: (a) Ballooned hepatocytes. These are injured, swollen hepatocytes with cleared-out cytoplasm and cytoskeletal damage, which when extensive, results in formation of Mallory hyaline. (b) Lobular lymphocytic infiltrates are common, and portal lymphocytic infiltrates also may occur. (c) Perivenular/pericellular fibrosis. Steatohepatitis is often accompanied by fibrosis. Reference: Robbins 10th Ed, pg 844