Liver Flashcards
Acute viral hepatitis: Changes in hepatocytes (3).
Swollen hepatocytes with rarified and granular cytoplasm.
Apoptotic bodies.
Replacement of lost hepatocytes by small clusters of lymphocytes and macrophages.
Acute hepatitis B: Classic histologic finding.
“Ground glass” hepatocytes.
Chronic viral hepatitis: Definition.
Persistent liver injury with positive viral serology and high serum aminotransferases for more than 6 months.
Chronic viral hepatitis: Location of inflammation.
Portal and periportal regions.
Characteristic features of ___.
A. Chronic hepatitis B.
B. Chronic hepatitis C (3).
A. Ground-glass hepatocytes.
B. Lymphoid aggregates, mild macrovesicular steatosis, damaged interlobular bile ducts.
Epstein-Barr viral hepatitis: Histology (2).
Single-file arrangement in lymphocytes and plasma cells in sinusoids.
Marked regeneration of hepatocytes.
Bacterial abscesses of the liver: Agents (3).
Staphylococcus aureus.
Salmonella typhi.
Treponema pallidum.
Syphilis of the liver: Gross lesions (2).
Gummata.
Hepar lobatum.
Syphilis of the liver: Histopathology.
Gummata are granulomatous abscesses that heal as dense scars.
Echinococcal infection of the liver: Local complication.
Secondary cholangitis.
Malaria of the liver: Histopathology (2).
Hyperplasia of Küpffer cells.
Phagocytosis of ruptured erythrocytes.
Hepatic leishmaniasis: Histopathology (2).
Hyperplasia of Küpffer cells.
Phagocytosis of organisms (Donovan bodies).
Hepatic leishmaniasis: Best special stain.
Giemsa.
Acetaminophen toxicity: Histopathology.
Hepatocellular necrosis in zone 3.
Drugs that cause a pattern mimicking acute viral hepatitis (3).
Antituberculosis drugs.
Anesthetics.
Aspirin (NSAIDs).
Drug that causes cholestasis with loss of bile ducts.
Augmentin (amoxicillin + clavulanic acid).
Drugs that cause the pattern of “vanishing bile ducts” (4).
Chlorpromazine.
Haloperidol.
Amoxicillin.
Flucloxacllin.
Drugs that cause microvesicular steatosis (4).
Valproic acid.
Tetracycline.
Nucleoside analogs.
Aspirin (Reye’s syndrome).
Drugs that cause veno-occlusive disease (2).
Pyrrholizidine alkaloids.
Chemotherapeutic agents.
Drugs that cause a steatohepatitis-like pattern (2).
Amiodarone.
Tamoxifen.
Hypervitaminosis A: Histopathology (2).
Hypertrophy of stellate cells.
Pericellular and perivenular fibrosis.
Histopathologic clues that drugs may be responsible for liver disease (3).
Many eosinophils.
Epithelioid granulomas.
Hepatitis together with cholestasis.
Alcoholic hepatitis: Location of histologic changes.
Zone 3.
Alcoholic hepatitis: Main histologic changes (5).
Steatosis.
Ballooning degeneration.
Lobular inflammatory infiltrates containing neutrophils.
Mallory bodies.
Peri cellular and perivenular (“chicken-wire”) fibrosis.
Alcoholic hepatitis vs. viral hepatitis: Location of inflammation.
Alcoholic: Mostly lobular.
Chronic viral: Mostly portal and periportal.
Ascariasis of the liver: Gross appearance.
Numerous foul-smelling cavities.
Alcoholic hepatitis vs. non-alcoholic steatohepatitis (2).
NASH:
− More glycogen aged nuclei.
− No sclerosing hyaline necrosis.
Non-alcoholic steatohepatitis: Risk factors (4).
Central obesity.
Insulin resistance / diabetes mellitus, type II.
Arterial hypertension.
Hypertriglyceridemia.
Mallory body: Composition.
Cytoskeletal intermediate filaments associated with ubiquitin.
Mallory body: Immunohistochemical stains (2).
p62.
Ubiquitin.
Indian childhood cirrhosis: Histopathology (3).
Mallory bodies.
No steatosis.
Marked overload of copper.
Acute fatty liver of pregnancy: Timing (2).
Onset: Third trimester.
Resolution: Upon delivery.
Acute fatty liver of pregnancy: Clinical presentation (4).
Bleeding.
Vomiting.
Jaundice.
Coma (occasionally).
Acute fatty liver of pregnancy: Histopathology (3).
Microvesicular steatosis.
Cholestasis may be seen.
Possibly much inflammation in the portal tracts.
Acute fatty liver of pregnancy: Pathogenesis.
Defective oxidation of fatty acids in the mitochondria.
Acquired hemochromatosis: Causes (3).
Blood transfusions.
Porphyria cutanea tarda.
Bantu hemosiderosis.
Hereditary hemochromatosis:
− Inheritance.
− Classic clinical triad.
− Autosomal recessive.
− Cirrhosis, skin pigmentation, diabetes mellitus.
Hereditary hemochromatosis: Lethal complication.
Hepatocellular carcinoma.
Hereditary hemochromatosis, early: Histopathology.
Hemosiderin granules in periportal hepatocytes.
Hereditary hemochromatosis, intermediate: Histopathology (3).
Hemosiderin granules in lobular hepatocytes, bile-duct epithelium, Kupffer cells.
Portal inflammation.
Portal and bridging fibrosis.
Hereditary hemochromatosis, late: Histopathology.
Fibrous septa progressing to cirrhosis.
Hepatic iron index: Calculation.
Micromoles of Fe per gram of dry liver ÷ patient’s age.
Hepatic iron index: Values.
Normal: Less than 1.
Homozygotes: Greater than 2.
Heterozygotes: Less than 2.
Hemochromatosis: Pathogenesis in liver.
Iron is directly hepatotoxic.
Ballooned hepatocytes: Immunohistochemistry.
Loss of cytokeratin 8/18.
Steps of metabolism of copper (4).
Absorbed in stomach and duodenum.
Bound to albumin and carried to hepatocytes.
Bound to α₂-globulin to form ceruloplasmin.
Re-secreted into the plasma.
Steps of excretion of copper (3).
Senescent ceruloplasmin is taken up by the hepatocytes, degraded in the lysosomes, and excreted in the bile.
Defective gene in Wilson’s disease:
− Name and location.
− Product.
ATP7B on chromosome 13.
Canalicular transmembrane copper-transporting ATPase.
Wilson’s disease: Laboratory findings (3).
Decreased serum ceruloplasmin.
Increased urinary copper.
Increased hepatic copper.
Wilson’s disease: Ocular finding.
Kayser-Fleischer ring due to deposition of copper in Descemet’s membrane.
Wilson’s disease: Inflammatory changes (2).
Acute hepatitis.
Chronic hepatitis progressing to cirrhosis.
Wilson’s disease: Changes in the hepatocytes (4).
Fatty change.
Focal necrosis.
Glycogenated nuclei.
Mallory bodies.
Wilson’s disease: Special stains (2).
Rhodanine: Copper.
Orcein: Copper-associated protein.
Wilson’s disease: Diagnostic concentration of hepatic copper.
More than 250 μg per gram of dry liver.
Wilson’s disease: Treatment.
D-penicillamine.
Defective gene in α₁-antitrypsin deficiency: Location and function.
Chromosome 14; inhibits neutrophil elastase in the lungs.
α₁-Antitrypsin deficiency: Pathogenesis of liver disease.
Abnormally folded protein gets trapped in the endoplasmic reticulum.
α₁-Antitrypsin deficiency: Variant presentation.
Liver disease without pulmonary emphysema.
α₁-Antitrypsin deficiency: Presentation in neonates.
Hepatitis with cholestatic jaundice.
Eosinophilic globules of α₁-antitrypsin deficiency:
− Location.
− Staining.
Mainly in periportal hepatocytes.
PAS positive, diastase resistant.
α₁-Antitrypsin: Most significant alleles (3).
M: Normal.
Z: Clinically most significant.
S: Reduced concentration of α₁-antitrypsin but no disease.
α₁-Antitrypsin deficiency: Mutation in Z allele.
Glu to Lys.
Autoimmune hepatitis: Antibodies (4).
ANA.
ASMA.
Anti-soluble liver antigen.
Anti-LKM1.
Autoimmune hepatitis: Suggestive histologic findings (2).
Inflammatory infiltrate rich in plasma cells.
Hepatitic rosettes.
Autoimmune hepatitis: Location of inflammatory infiltrate.
Portal, periportal, lobular.
Autoimmune hepatitis: Other histologic findings (3).
Interface hepatitis.
Lobular apoptotic bodies.
Syncytial giant hepatocytes.
Primary biliary cirrhosis: Laboratory findings (3).
Antimitochondrial antibody (directed against subunit E2 of pyruvate dehydrogenase).
Elevated alkaline phosphatase.
Hyperbilirubinemia.
Primary biliary cirrhosis: Stages (4).
I. Florid duct lesion.
II. Ductular reaction.
III. Scarring.
IV. Cirrhosis.
Florid duct lesion of primary biliary cirrhosis: Inflammatory cells.
Granulomas.
Lymphocytes, macrophages, plasma cells, eosinophils.
Ductular reaction of primary biliary cirrhosis: Histologic findings (4).
Small bile ducts: Loss.
Medium-sized bile ducts: Scarring.
Bile ductules in portal tracts: Proliferation.
Periportal inflammation and interface hepatitis.
Scarring stage of primary biliary cirrhosis: Histologic findings (2).
Small and medium-sized bile ducts are replaced by lymphoid aggregates that may contain PAS-positive remnants of basement membrane.
Otherwise little inflammation.
Primary biliary cirrhosis: Treatment.
Liver transplantation.
Primary sclerosing cholangitis: Radiologic finding.
ERCP: Beaded appearance of intrahepatic bile ducts.
Primary sclerosing cholangitis: Association with ulcerative colitis (2).
Present in 70% of patients with PSC.
Only 4% of patients with UC have PSC.
Primary sclerosing cholangitis: Association with carcinoma.
Cholangiocarcinoma occurs in 10% of patients with PSC.
Primary sclerosing cholangitis: Stages.
I: Portal.
II: Periportal.
III: Septal.
IV: Cirrhotic.
Portal stage of primary sclerosing cholangitis: Histologic features (2).
Concentric periductal fibrosis.
Lymphocytic inflammation of portal tracts.
Periportal stage of primary sclerosing cholangitis: Histologic features (3).
Extension of periportal parenchyma.
Interface hepatitis.
Bile-ductular reaction.
Septal stage of primary sclerosing cholangitis: Histologic features (2).
Obliteration of bile ducts.
Bridging fibrosis.
Primary sclerosing cholangitis: Another frequent histologic feature.
Pseudoxanthomatous change due to chronic cholestasis.
Primary sclerosing cholangitis: Histologic mimic.
Secondary sclerosing cholangitis due to obstruction of extrahepatic bile ducts or of large bile ducts.
Primary sclerosing cholangitis: Treatment.
Liver transplantation.
Acute (cellular) rejection of liver transplant: Characteristic histologic triad.
Portal inflammation.
Bile-duct damage.
Endotheliitis.
Acute (cellular) rejection of liver transplant: Composition of inflammatory infiltrates (5).
Lymphocytes, plasmacytoid cells, macrophages, neutrophils, eosinophils.
Chronic (ductopenic) rejection of liver transplant: Histopathology (3).
Loss of interlobular bile ducts.
Aggregates of foam cells in the intima of arteries.
Centrilobular necrosis.
Chronic (ductopenic) rejection of liver transplant: Definitive diagnosis.
At least 50% of at least 20 portal tracts show loss of bile ducts.
Cirrhosis: Histopathology in biliary-type diseases.
Irregular nodules (“jigsaw” pattern).
High-grade dysplastic nodule: Histopathology (2).
Hepatocytes form plates more than two cells thick or pseudoglandular structures.
Cytologic atypia in hepatocytes.
Congenital hepatic fibrosis: Histopathology (2).
Bands of collagen divide liver tissue into geographic areas.
Usually no inflammation or hepatocellular regeneration.
Nodular regenerative hyperplasia: Histopathology.
Diffuse disease consisting of hyperplastic parenchymal nodules without significant fibrosis.
Nodular regenerative hyperplasia: Associations (4).
Myeloproliferative disorders.
Autoimmune diseases.
Chronic venous congestion.
Drugs.
Focal nodular hyperplasia:
− Radiological finding.
− Laboratory finding.
Hypervascularity on arteriography.
Normal tests of liver function.
Focal nodular hyperplasia: Association with oral contraceptives.
No apparent association.
Focal nodular hyperplasia: Classic gross and histologic finding.
Central stellate scar.
Focal nodular hyperplasia: Other histologic features (2).
Presence of all components of the normal liver lobule.
Chronic cholestatic (pseudoxanthomatous) change in hepatocytes next to the fibrous septa.
Focal nodular hyperplasia: What is found in the fibrous septa (3)?
Thick-walled blood vessels, many bile ductules, inflammatory cells.