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Anatomic pathology > Liver > Flashcards

Liver Flashcards

0
Q

Acute viral hepatitis: Changes in hepatocytes (3).

A

Swollen hepatocytes with rarified and granular cytoplasm.

Apoptotic bodies.

Replacement of lost hepatocytes by small clusters of lymphocytes and macrophages.

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1
Q

Acute viral hepatitis: Type and location of inflammation.

A

Mainly lymphocytic; zone 3.

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2
Q

Acute hepatitis B: Classic histologic finding.

A

“Ground glass” hepatocytes.

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3
Q

Chronic viral hepatitis: Definition.

A

Persistent liver injury with positive viral serology and high serum aminotransferases for more than 6 months.

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4
Q

Chronic viral hepatitis: Location of inflammation.

A

Portal and periportal regions.

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5
Q

Characteristic features of ___.

A. Chronic hepatitis B.
B. Chronic hepatitis C (3).

A

A. Ground-glass hepatocytes.

B. Lymphoid aggregates, mild macrovesicular steatosis, damaged interlobular bile ducts.

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6
Q

Epstein-Barr viral hepatitis: Histology (2).

A

Single-file arrangement in lymphocytes and plasma cells in sinusoids.

Marked regeneration of hepatocytes.

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7
Q

Bacterial abscesses of the liver: Agents (3).

A

Staphylococcus aureus.

Salmonella typhi.

Treponema pallidum.

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8
Q

Syphilis of the liver: Gross lesions (2).

A

Gummata.

Hepar lobatum.

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9
Q

Syphilis of the liver: Histopathology.

A

Gummata are granulomatous abscesses that heal as dense scars.

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10
Q

Echinococcal infection of the liver: Local complication.

A

Secondary cholangitis.

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11
Q

Malaria of the liver: Histopathology (2).

A

Hyperplasia of Küpffer cells.

Phagocytosis of ruptured erythrocytes.

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12
Q

Hepatic leishmaniasis: Histopathology (2).

A

Hyperplasia of Küpffer cells.

Phagocytosis of organisms (Donovan bodies).

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13
Q

Hepatic leishmaniasis: Best special stain.

A

Giemsa.

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14
Q

Acetaminophen toxicity: Histopathology.

A

Hepatocellular necrosis in zone 3.

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15
Q

Drugs that cause a pattern mimicking acute viral hepatitis (3).

A

Antituberculosis drugs.

Anesthetics.

Aspirin (NSAIDs).

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16
Q

Drug that causes cholestasis with loss of bile ducts.

A

Augmentin (amoxicillin + clavulanic acid).

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17
Q

Drugs that cause the pattern of “vanishing bile ducts” (4).

A

Chlorpromazine.

Haloperidol.

Amoxicillin.

Flucloxacllin.

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18
Q

Drugs that cause microvesicular steatosis (4).

A

Valproic acid.

Tetracycline.

Nucleoside analogs.

Aspirin (Reye’s syndrome).

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19
Q

Drugs that cause veno-occlusive disease (2).

A

Pyrrholizidine alkaloids.

Chemotherapeutic agents.

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20
Q

Drugs that cause a steatohepatitis-like pattern (2).

A

Amiodarone.

Tamoxifen.

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21
Q

Hypervitaminosis A: Histopathology (2).

A

Hypertrophy of stellate cells.

Pericellular and perivenular fibrosis.

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22
Q

Histopathologic clues that drugs may be responsible for liver disease (3).

A

Many eosinophils.

Epithelioid granulomas.

Hepatitis together with cholestasis.

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23
Q

Alcoholic hepatitis: Location of histologic changes.

A

Zone 3.

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24
Q

Alcoholic hepatitis: Main histologic changes (5).

A

Steatosis.

Ballooning degeneration.

Lobular inflammatory infiltrates containing neutrophils.

Mallory bodies.

Peri cellular and perivenular (“chicken-wire”) fibrosis.

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25
Q

Alcoholic hepatitis vs. viral hepatitis: Location of inflammation.

A

Alcoholic: Mostly lobular.

Chronic viral: Mostly portal and periportal.

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26
Q

Ascariasis of the liver: Gross appearance.

A

Numerous foul-smelling cavities.

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27
Q

Alcoholic hepatitis vs. non-alcoholic steatohepatitis (2).

A

NASH:

− More glycogen aged nuclei.
− No sclerosing hyaline necrosis.

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28
Q

Non-alcoholic steatohepatitis: Risk factors (4).

A

Central obesity.

Insulin resistance / diabetes mellitus, type II.

Arterial hypertension.

Hypertriglyceridemia.

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29
Q

Mallory body: Composition.

A

Cytoskeletal intermediate filaments associated with ubiquitin.

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30
Q

Mallory body: Immunohistochemical stains (2).

A

p62.

Ubiquitin.

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31
Q

Indian childhood cirrhosis: Histopathology (3).

A

Mallory bodies.

No steatosis.

Marked overload of copper.

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32
Q

Acute fatty liver of pregnancy: Timing (2).

A

Onset: Third trimester.

Resolution: Upon delivery.

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33
Q

Acute fatty liver of pregnancy: Clinical presentation (4).

A

Bleeding.

Vomiting.

Jaundice.

Coma (occasionally).

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34
Q

Acute fatty liver of pregnancy: Histopathology (3).

A

Microvesicular steatosis.

Cholestasis may be seen.

Possibly much inflammation in the portal tracts.

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35
Q

Acute fatty liver of pregnancy: Pathogenesis.

A

Defective oxidation of fatty acids in the mitochondria.

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36
Q

Acquired hemochromatosis: Causes (3).

A

Blood transfusions.

Porphyria cutanea tarda.

Bantu hemosiderosis.

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37
Q

Hereditary hemochromatosis:

− Inheritance.
− Classic clinical triad.

A

− Autosomal recessive.

− Cirrhosis, skin pigmentation, diabetes mellitus.

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38
Q

Hereditary hemochromatosis: Lethal complication.

A

Hepatocellular carcinoma.

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39
Q

Hereditary hemochromatosis, early: Histopathology.

A

Hemosiderin granules in periportal hepatocytes.

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40
Q

Hereditary hemochromatosis, intermediate: Histopathology (3).

A

Hemosiderin granules in lobular hepatocytes, bile-duct epithelium, Kupffer cells.

Portal inflammation.

Portal and bridging fibrosis.

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41
Q

Hereditary hemochromatosis, late: Histopathology.

A

Fibrous septa progressing to cirrhosis.

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42
Q

Hepatic iron index: Calculation.

A

Micromoles of Fe per gram of dry liver ÷ patient’s age.

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43
Q

Hepatic iron index: Values.

A

Normal: Less than 1.

Homozygotes: Greater than 2.

Heterozygotes: Less than 2.

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44
Q

Hemochromatosis: Pathogenesis in liver.

A

Iron is directly hepatotoxic.

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45
Q

Ballooned hepatocytes: Immunohistochemistry.

A

Loss of cytokeratin 8/18.

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46
Q

Steps of metabolism of copper (4).

A

Absorbed in stomach and duodenum.

Bound to albumin and carried to hepatocytes.

Bound to α₂-globulin to form ceruloplasmin.

Re-secreted into the plasma.

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47
Q

Steps of excretion of copper (3).

A

Senescent ceruloplasmin is taken up by the hepatocytes, degraded in the lysosomes, and excreted in the bile.

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48
Q

Defective gene in Wilson’s disease:

− Name and location.
− Product.

A

ATP7B on chromosome 13.

Canalicular transmembrane copper-transporting ATPase.

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49
Q

Wilson’s disease: Laboratory findings (3).

A

Decreased serum ceruloplasmin.

Increased urinary copper.

Increased hepatic copper.

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50
Q

Wilson’s disease: Ocular finding.

A

Kayser-Fleischer ring due to deposition of copper in Descemet’s membrane.

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51
Q

Wilson’s disease: Inflammatory changes (2).

A

Acute hepatitis.

Chronic hepatitis progressing to cirrhosis.

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52
Q

Wilson’s disease: Changes in the hepatocytes (4).

A

Fatty change.

Focal necrosis.

Glycogenated nuclei.

Mallory bodies.

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53
Q

Wilson’s disease: Special stains (2).

A

Rhodanine: Copper.

Orcein: Copper-associated protein.

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54
Q

Wilson’s disease: Diagnostic concentration of hepatic copper.

A

More than 250 μg per gram of dry liver.

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55
Q

Wilson’s disease: Treatment.

A

D-penicillamine.

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56
Q

Defective gene in α₁-antitrypsin deficiency: Location and function.

A

Chromosome 14; inhibits neutrophil elastase in the lungs.

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57
Q

α₁-Antitrypsin deficiency: Pathogenesis of liver disease.

A

Abnormally folded protein gets trapped in the endoplasmic reticulum.

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58
Q

α₁-Antitrypsin deficiency: Variant presentation.

A

Liver disease without pulmonary emphysema.

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59
Q

α₁-Antitrypsin deficiency: Presentation in neonates.

A

Hepatitis with cholestatic jaundice.

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60
Q

Eosinophilic globules of α₁-antitrypsin deficiency:

− Location.
− Staining.

A

Mainly in periportal hepatocytes.

PAS positive, diastase resistant.

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61
Q

α₁-Antitrypsin: Most significant alleles (3).

A

M: Normal.

Z: Clinically most significant.

S: Reduced concentration of α₁-antitrypsin but no disease.

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62
Q

α₁-Antitrypsin deficiency: Mutation in Z allele.

A

Glu to Lys.

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63
Q

Autoimmune hepatitis: Antibodies (4).

A

ANA.

ASMA.

Anti-soluble liver antigen.

Anti-LKM1.

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64
Q

Autoimmune hepatitis: Suggestive histologic findings (2).

A

Inflammatory infiltrate rich in plasma cells.

Hepatitic rosettes.

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65
Q

Autoimmune hepatitis: Location of inflammatory infiltrate.

A

Portal, periportal, lobular.

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66
Q

Autoimmune hepatitis: Other histologic findings (3).

A

Interface hepatitis.

Lobular apoptotic bodies.

Syncytial giant hepatocytes.

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67
Q

Primary biliary cirrhosis: Laboratory findings (3).

A

Antimitochondrial antibody (directed against subunit E2 of pyruvate dehydrogenase).

Elevated alkaline phosphatase.

Hyperbilirubinemia.

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68
Q

Primary biliary cirrhosis: Stages (4).

A

I. Florid duct lesion.

II. Ductular reaction.

III. Scarring.

IV. Cirrhosis.

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69
Q

Florid duct lesion of primary biliary cirrhosis: Inflammatory cells.

A

Granulomas.

Lymphocytes, macrophages, plasma cells, eosinophils.

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70
Q

Ductular reaction of primary biliary cirrhosis: Histologic findings (4).

A

Small bile ducts: Loss.

Medium-sized bile ducts: Scarring.

Bile ductules in portal tracts: Proliferation.

Periportal inflammation and interface hepatitis.

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71
Q

Scarring stage of primary biliary cirrhosis: Histologic findings (2).

A

Small and medium-sized bile ducts are replaced by lymphoid aggregates that may contain PAS-positive remnants of basement membrane.

Otherwise little inflammation.

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72
Q

Primary biliary cirrhosis: Treatment.

A

Liver transplantation.

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73
Q

Primary sclerosing cholangitis: Radiologic finding.

A

ERCP: Beaded appearance of intrahepatic bile ducts.

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74
Q

Primary sclerosing cholangitis: Association with ulcerative colitis (2).

A

Present in 70% of patients with PSC.

Only 4% of patients with UC have PSC.

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75
Q

Primary sclerosing cholangitis: Association with carcinoma.

A

Cholangiocarcinoma occurs in 10% of patients with PSC.

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76
Q

Primary sclerosing cholangitis: Stages.

A

I: Portal.

II: Periportal.

III: Septal.

IV: Cirrhotic.

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77
Q

Portal stage of primary sclerosing cholangitis: Histologic features (2).

A

Concentric periductal fibrosis.

Lymphocytic inflammation of portal tracts.

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78
Q

Periportal stage of primary sclerosing cholangitis: Histologic features (3).

A

Extension of periportal parenchyma.

Interface hepatitis.

Bile-ductular reaction.

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79
Q

Septal stage of primary sclerosing cholangitis: Histologic features (2).

A

Obliteration of bile ducts.

Bridging fibrosis.

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80
Q

Primary sclerosing cholangitis: Another frequent histologic feature.

A

Pseudoxanthomatous change due to chronic cholestasis.

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81
Q

Primary sclerosing cholangitis: Histologic mimic.

A

Secondary sclerosing cholangitis due to obstruction of extrahepatic bile ducts or of large bile ducts.

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82
Q

Primary sclerosing cholangitis: Treatment.

A

Liver transplantation.

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83
Q

Acute (cellular) rejection of liver transplant: Characteristic histologic triad.

A

Portal inflammation.

Bile-duct damage.

Endotheliitis.

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84
Q

Acute (cellular) rejection of liver transplant: Composition of inflammatory infiltrates (5).

A

Lymphocytes, plasmacytoid cells, macrophages, neutrophils, eosinophils.

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85
Q

Chronic (ductopenic) rejection of liver transplant: Histopathology (3).

A

Loss of interlobular bile ducts.

Aggregates of foam cells in the intima of arteries.

Centrilobular necrosis.

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86
Q

Chronic (ductopenic) rejection of liver transplant: Definitive diagnosis.

A

At least 50% of at least 20 portal tracts show loss of bile ducts.

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87
Q

Cirrhosis: Histopathology in biliary-type diseases.

A

Irregular nodules (“jigsaw” pattern).

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88
Q

High-grade dysplastic nodule: Histopathology (2).

A

Hepatocytes form plates more than two cells thick or pseudoglandular structures.

Cytologic atypia in hepatocytes.

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89
Q

Congenital hepatic fibrosis: Histopathology (2).

A

Bands of collagen divide liver tissue into geographic areas.

Usually no inflammation or hepatocellular regeneration.

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90
Q

Nodular regenerative hyperplasia: Histopathology.

A

Diffuse disease consisting of hyperplastic parenchymal nodules without significant fibrosis.

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91
Q

Nodular regenerative hyperplasia: Associations (4).

A

Myeloproliferative disorders.

Autoimmune diseases.

Chronic venous congestion.

Drugs.

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92
Q

Focal nodular hyperplasia:

− Radiological finding.
− Laboratory finding.

A

Hypervascularity on arteriography.

Normal tests of liver function.

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93
Q

Focal nodular hyperplasia: Association with oral contraceptives.

A

No apparent association.

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94
Q

Focal nodular hyperplasia: Classic gross and histologic finding.

A

Central stellate scar.

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95
Q

Focal nodular hyperplasia: Other histologic features (2).

A

Presence of all components of the normal liver lobule.

Chronic cholestatic (pseudoxanthomatous) change in hepatocytes next to the fibrous septa.

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96
Q

Focal nodular hyperplasia: What is found in the fibrous septa (3)?

A

Thick-walled blood vessels, many bile ductules, inflammatory cells.

97
Q

Focal nodular hyperplasia: Immunohistochemistry.

A

Glutamine synthetase:

− Stains clusters of hepatocytes in a geographic pattern.
− Shows perivenular staining in the adjacent liver tissue.

98
Q

Hepatic adenoma: Risk factors (3).

A

Oral contraceptives.

Obesity.

Ethanol.

99
Q

Hepatic adenoma: Complications (2).

A

Rupture.

Progression to hepatocellular carcinoma.

100
Q

Hepatic adenoma: Definition of adenomatosis.

A

More than 10 adenomas.

101
Q

Hepatic adenoma: Possible changes within hepatocytes (3).

A

Glycogen-rich cytoplasm.

Fatty change.

Intracellular bile.

102
Q

Hepatic adenoma: Architectural features (3).

A

No portal tracts.

Arteries without their veins.

No thickened hepatocellular plates; no pseudoglandular structures.

103
Q

Immunohistochemistry of hepatic adenoma: Stains common to all types (4).

A

HepPar-1, arginase-1, glypican-3.

Glutamine synthetase in perivenular pattern.

104
Q

Immunohistochemistry of hepatic adenoma: Stains used in classifying (4).

A

LFABP (liver fatty-acid-binding protein).

Glutamine synthetase.

β-Catenin.

SAA/CRP.

105
Q

Immunohistochemistry of hepatic adenoma: HNF-1α-mutated type.

A

Negative for all stains (absence of staining for LFABP is abnormal).

106
Q

Immunohistochemistry of hepatic adenoma: β-Catenin-activated type.

A

Staining for all except SAA/CRP.

107
Q

Immunohistochemistry of hepatic adenoma: Inflammatory type.

A

Staining for LFABP and for SAA/CRP.

108
Q

Immunohistochemistry of hepatic adenoma: Unclassified type.

A

Staining for LFABP only.

109
Q

Hepatic adenoma: Association with cirrhosis (2).

A

Absent by definition.

An adenoma-like lesion in the setting of cirrhosis is called low-grade dysplasia (macroregenerative nodule).

110
Q

Hepatocellular carcinoma: In how many is serum AFP elevated?

A

In about 60-80%.

111
Q

Hepatocellular carcinoma: Diagnostic level of serum AFP.

A

More than 100 times normal (in the absence of a germ-cell tumor).

112
Q

Hepatocellular carcinoma: Associated protein of hepatitis B virus.

A

The product of the gene Hbx.

113
Q

Hepatocellular carcinoma: Most strongly associated type of hepatic adenoma.

A

The β-catenin-activated type.

114
Q

Hepatocellular carcinoma: Appearance of trabecular pattern.

A

Hepatocytic cords are more than 3 cells thick and are lined y flat endothelial cells but lack Kupffer cells.

115
Q

Hepatocellular carcinoma: Appearance of the acinar pattern.

A

Degeneration of solid trabecula results in pseudoglandular spaces filled with colloid-like matter or bile.

116
Q

Hepatocellular carcinoma: Least common pattern.

A

The solid pattern.

117
Q

Hepatocellular carcinoma: Possible nuclear features (4).

A

Vesicular nuclei.

Eosinophilic inclusions.

Bizarre shape.

Prominent nucleoli.

118
Q

Hepatocellular carcinoma, fibrolamellar variant: Appearance of hepatocytes (3).

A

Abundant oncocytic-appearing cytoplasm.

Cytoplasmic pale bodies.

Prominent nucleoli.

119
Q

Hepatocellular carcinoma, fibrolamellar variant: Immunohistochemistry.

A

Malignant cells are positive for CD68.

120
Q

Hepatocellular carcinoma, fibrolamellar variant: Association with cirrhosis.

A

The tumor occurs in the absence of cirrhosis and other liver disease.

121
Q

Hepatocellular carcinoma: Utility of stain for AFP.

A

Highly specific but positive in less than 25% of cases.

122
Q

HepPar-1:

A. Biological function.
B. Cells that stain positively.

A

A. Mitochondrial enzyme of the urea cycle.

B. Hepatocytes, metaplastic and neoplastic intestinal.

123
Q

Patterns of staining for markers of HCC:

A. TTF-1.
B. CK8/18.
C. Glutamine synthetase.

A

A. Cytoplasmic.

B. Sub-plasmalemmal.

C. Diffuse.

124
Q

Immunohistochemical stains for HCC:

A. CK19.
B. EMA.
C. CD34.

A

A. Positivity predicts poor outcome.

B. Usually negative.

C. May stain sinusoids (abnormal).

125
Q

Immunohistochemical staining of hepatocellular carcinoma for CEA:

A. Patterns.
B. Markers that give a similar pattern (4).

A

A. Polyclonal CEA highlights canaliculi; monoclonal CEA is negative.

B. CD10, multidrug-resistant p-glycoprotein, and (occasionally) villin mark the canaliculi.

126
Q

Other immunohistochemical markers for HCC (3).

A

Arginase.

Glypican-3.

CK7.

127
Q

High-grade dysplasia in cirrhosis: Histologic distinction from HCC (2).

A

High-grade dysplasia:

− Cords are generally no more than 3 cells thick.
− Portal elements are retained.

128
Q

High-grade dysplasia in cirrhosis: Immunohistochemistry (2).

A

Staining for Ki-67 and TGF-α is intermediate between that of cirrhosis and that of HCC.

129
Q

Cholangiocarcinoma: Positive stains (5).

A

CEA, mucicarmine, EMA.

CK19, CK8/18.

130
Q

Hepatoblastoma:

A. How many are associated with a syndrome?
B. Examples of syndromes (2).

A

A. About one third.

B. Beckwith-Wiedemann syndrome; FAP.

131
Q

Hepatoblastoma: Possible clinical presentation.

A

Virilization, infrequently with sexual precocity in boys.

132
Q

Hepatoblastoma: Laboratory findings (2).

A

Elevated serum AFP (frequent) or hCG (infrequent).

133
Q

Hepatoblastoma: Main histologic types.

A

Epithelial.

Mixed epithelial and mesenchymal.

134
Q

Hepatoblastoma, epithelial type: Components.

A

Fetal and embryonal.

135
Q

Hepatoblastoma, epithelial type: Appearance of fetal component.

A

Large cells with clear or granular cytoplasm and a single nucleolus.

Extramedullary hematopoiesis sometimes.

136
Q

Hepatoblastoma, epithelial type: Appearance of embryonal component.

A

Smaller, elongated cells with hyperchromatic nuclei and scant cytoplasm.

Solid pattern.

137
Q

Hepatoblastoma, epithelial type: Variants (2).

A

Anaplastic small-cell variant resembles neuroblastoma.

Macrotrabecular variant resembles HCC.

138
Q

Hepatoblastoma, epithelial-mesenchymal type: Histology.

A

Mixture of fetal component, embryonal component, and mesenchymal component consisting of osteoid, cartilage, or undifferentiated spindle cells.

139
Q

Hepatoblastoma, epithelial-mesenchymal type: Immunohistochemical staining of the osteoid.

A

Positive for keratin.

140
Q

Hepatoblastoma: Positive “non-hepatocellular” immunohistochemical markers (4).

A

Often: NSE, S-100, chromogranin.

Variable: Bcl-2.

141
Q

Cytogenetic abnormalities in hepatoblastoma:

A. Overall (3).
B. In Beckwith-Wiedemann syndrome.

A

A. +2q, +20, +X.

B. Loss of heterozygosity at 11p15.

142
Q

Immunohistochemical distinction of hepatoblastoma from

A. Wilms’ tumor.
B. Neuroblastoma.

A

A. Wilms’ tumor: Positive for WT-1.

B. Neuroblastoma lacks keratin; neuroendocrine markers are not helpful.

143
Q

Hepatoblastoma: Clinical predictors of poor outcome (3).

A

Age less than 1 year.

Large size.

Involvement of vital structures.

144
Q

Hepatoblastoma: Pathological predictors of poor outcome (2).

A

Predominance of anaplastic small-cell or macrotrabecular pattern.

Aneuploidy.

145
Q

Bile-duct hamartoma:

A. Synonym.
B. Embryology.
C. Associations (2).

A

A. Von Meyenburg’s complex.

B. Malformation of ductal plate.

C. Polycystic disease of liver or of kidney.

146
Q

Bile-duct hamartoma: Gross pathology.

A

Scattered small white nodules, mimicking metastatic tumor.

147
Q

Bile-duct hamartoma: Histopathology.

A

Variably dilated, sometimes bile-filled ductal structures in a hyalinized stroma.

148
Q

Mesenchymal hamartoma: Gross pathology.

A

Usually solitary, unlike bile-duct hamartoma.

149
Q

Mesenchymal hamartoma: Histopathology (3).

A

Myxoid stroma.

Islands of hepatocytes.

Bile rarely present within the ducts.

150
Q

Peribiliary-gland hamartoma: Synonym.

A

Bile-duct adenoma.

151
Q

Peribiliary-gland hamartoma: Architectural features (3).

A

Closely packed tubules with a single epithelial layer.

Fibrous stroma that may be cellular or hyalinized.

No connection with interlobular bile ducts.

152
Q

Peribiliary-gland hamartoma: Contents (2).

A

Lumens: No bile.

Lining cells may contain mucin.

153
Q

Mucinous cystic neoplasm of the liver:

A. Epidemiology.
B. Other locations (2).

A

A. Found almost exclusively in women.

B. Extrahepatic biliary tree, gallbladder.

154
Q

Mucinous cystic neoplasm: Gross pathology (2).

A

Forms lobules of variable size.

No connection with the biliary tree.

156
Q

Mucinous cystic neoplasm of the liver: Lining cells (2).

A

Columnar but may become flatter or form papillae.

Intestinal metaplasia with goblet cells may occur.

157
Q

Mucinous cystic neoplasm of the liver: Stroma.

A

Ovarian-like.

158
Q

Mucinous cystic neoplasm of the liver: Grading of dysplasia.

A

Adenoma: Low-grade dysplasia.

Borderline: Intermediate-grade dysplasia.

Carcinoma in situ: High-grade dysplasia.

159
Q

Mucinous cystadenocarcinoma of the liver:

A. Origin.
B. Signs of malignancy (3).

A

A. Most arise from a non-malignant mucinous cystic neoplasm.

B. Nuclear atypia, epithelial stratification, invasion.

160
Q

Intraductal papillary neoplasm of the bile duct: Gross pathology (2).

A

Dilated bile ducts containing papillary excrescences.

May spread throughout the biliary tree, even to the gallbladder.

161
Q

Intraductal papillary neoplasm of the bile duct: Lining cells (3).

A

May mimic biliary epithelial cells.

May show gastric or intestinal metaplasia.

May produce mucin.

162
Q

Intraductal papillary neoplasm of the bile duct: Grading of dysplasia.

A

Same as for mucinous cystic neoplasm.

163
Q

Cholangiocarcinoma: Types.

A

Intrahepatic.

Extrahepatic.

Hilar (Klatskin’s) tumor: Generally considered extrahepatic.

164
Q

Cholangiocarcinoma: Possible precursors lesions (4).

A

Biliary hyperplasia.

Biliary dysplasia.

Intraductal papillary neoplasm of the bile ducts.

Mucinous cystic neoplasm.

165
Q

Cholangiocarcinoma: Laboratory findings (2).

A

Elevated serum CEA.

Normal serum AFP.

166
Q

Cholangiocarcinoma: Presentation (3).

A

Intrahepatic: Abdominal pain, weight loss.

Extrahepatic: Jaundice, ascites, large mass.

Hilar: Jaundice, small mass.

167
Q

Cholangiocarcinoma: Gross pathology (3).

A

Intrahepatic: Infiltrating gray-white, scirrhous mass.

Extrahepatic: Deep invasion into wall of bile duct.

Hilar: Large, green liver; collapsed gallbladder.

168
Q

Cholangiocarcinoma: Cytologic clues to malignancy (3).

A

Heterogeneity of cells within the same gland.

Increased N:C ratio.

Large nucleoli.

169
Q

Cholangiocarcinoma: Architectural clues to malignancy (2).

A

Marked desmoplasia.

Spread within sinusoids and along bile ducts and nerves.

170
Q

Cholangiocarcinoma: Pertinently infrequent histologic features (2).

A

Necrosis.

Vascular invasion.

171
Q

Cholangiocarcinoma: Keratin stains.

A

Positive for CK19 and CK7.

172
Q

Cholangiocarcinoma: Mutated genes (3).

A

C-Ras.

β-Catenin: Underexpressed

COX-2: Overexpressed.

173
Q

Cholangiocarcinoma: Most helpful feature on frozen section.

A

Perineural invasion.

174
Q

Cholangiocarcinoma: Diagnostic pitfall.

A

Confusion with the periluminal sacculi of Beale (small acini normally found within the walls of extrahepatic bile ducts).

175
Q

Carcinoma of the gallbladder: Geography.

A

Most common in Latin American countries.

176
Q

Carcinoma of the gallbladder: Associated cancer syndrome.

A

Familial adenomatous polyposis / Gardner’s syndrome.

177
Q

Carcinoma of the gallbladder: Laboratory finding.

A

Elevated alkaline phosphatase.

178
Q

Carcinoma of the gallbladder: Growth patterns by gross pathology (2).

A

Diffuse.

Polypoid or papillary.

179
Q

Carcinoma of the gallbladder: Pitfall of gross pathology.

A

Diffuse pattern may be confused with cholecystitis, especially when there is much fibrosis.

180
Q

Carcinoma of the gallbladder: Pitfall of microscopic pathology.

A

Mistaking carcinoma in situ in Rokitansky-Aschoff sinuses for invasive carcinoma.

181
Q

Carcinoma of the gallbladder: Epithelial changes frequently found near invasive carcinoma (4).

A

Hyperplasia.

Metaplasia: Gastric or intestinal.

Dysplasia.

Carcinoma in situ.

182
Q

Carcinoma of the gallbladder: Histopathlogic clues to malignancy (2).

A

Cytologic atypia.

Concentric desmoplasia.

*By contrast, the glands are typically well formed.

183
Q

Carcinoma of the gallbladder: Spread (2).

A

Follows nerves.

Spreads to regional lymph nodes.

184
Q

Carcinoma of the gallbladder: Less common types (5).

A

High-grade endocrine (small-cell).

Low-grade endocrine.

Squamous.

Adenosquamous.

Sarcomatoid.

185
Q

Carcinoma of the gallbladder: Keratins.

A

CK19, CK7,

More likely than cholangiocarcinoma to express CK20.

186
Q

Carcinoma of the gallbladder: Immunohistochemical pitfall.

A

May express AFP.

187
Q

Carcinoma of the gallbladder: Mutation.

A

Overexpression of TP53.

188
Q

Carcinoma of the gallbladder: Most important prognostic indicator.

A

Stage.

189
Q

Metastasis to the liver: Typical gross pathology (3).

A

Well-circumscribed.

Hyperemic rim.

Single or multiple.

190
Q

Metastasis to the liver: Mimics of benign disease (3).

A

Metastases from the breast, prostate, or stomach can form punctuate lesions that mimic cirrhosis.

191
Q

Metastasis to the liver: Gross appearance of colonic metastases.

A

Multiple, large, umbilicated nodules on the surface.

192
Q

Source of hepatic metastasis suggested by this immunohistochemical profile:

+: CK20, villin (brush border), CDX2 (uniform).
−: CK7.

A

Lower intestinal tract.

193
Q

Immunohistochemical profile suggestive of metastasis from the upper gastrointestinal / pancreaticobiliary tract (3,2).

A

+: CK7, villin (brush border), CK17 or CK19.

v: CK20, CDX2.

194
Q

Immunohistochemical profile suggestive of metastasis from the lung (4,3).

A

+: CK7, TTF-1, napsin, surfactant A.

−: CK20, villin, CDX2.

195
Q

Immunohistochemical profile suggestive of metastasis from urothelium (5,1).

A

+: CK7, CK20, HMW-CK, p63, GATA-3.

-: CDX2.

196
Q

Immunohistochemical profile suggestive of metastasis of conventional renal-cell carcinoma (4,2).

A

+: CD10, EMA, PAX2, PAX8.

-: CK7, CK20.

197
Q

Immunohistochemical profile suggestive of metastasis from the prostate gland (2,4).

A

+: PSA, prostatic alkaline phosphatase.

-: CK7, CK20, HMW-CK, p63.

198
Q

Immunohistochemical profile suggestive of metastasis from the thyroid gland (4,1).

A

+: TTF-1, thyroglobulin, PAX2, PAX8.

-: Surfactant A.

199
Q

Immunohistochemical profile suggestive of metastasis from the breast (5).

A

+: GCDFP-15, mammaglobin, S-100, ER, PR.

200
Q

Immunohistochemical profile suggestive of metastasis from a salivary ductal carcinoma (3,1).

A

+: GCDFP-15, S-100, AR.

-: ER.

201
Q

Immunohistochemical profile suggestive of metastasis from a non-mucinous müllerian tumor (6,1).

A

+: CK7, p53, CA125, WT-1, PAX8, ER.

-: CEA.

202
Q

Immunohistochemical profile suggestive of metastasis from a mucinous müllerian tumor (1,3).

A

Similar to that of an intestinal tumor.

-: CA125, WT-1, PAX8.

203
Q

Causes of peliosis hepatis:

A. Drugs (4).
B. Pathogen.

A

A. Anabolic steroids, danazol, oral contraceptives, thiopurines.

B. Bartonella henselae.

204
Q

Histopathology of peliosis hepatis: Common features (2).

A

Blood lakes surrounded by hepatocytes but without lining cells.

Disrupted sinusoids.

205
Q

Histopathology of peliosis hepatis: Bartonella-associated cases.

A

Myxoid perisinusoidal stroma containing clumps of granular matter.

206
Q

Peliosis hepatis: Helpful stains (2).

A

Reticulin: Disrupted sinusoids.

Warthin-Starry: Bartonellids.

207
Q

Hemangioma: Types (2).

A

Capillary.

Cavernous.

208
Q

Hemangioma: Variable histologic finding.

A

Thrombosis.

209
Q

Infantile hemangioendothelioma: Epidemiology (2).

A

Mostly diagnosed in the first year of life.

Mostly in males.

210
Q

Infantile hemangioendothelioma: Lethal complications (2).

A

Arteriovenous shunt leading to high-output heart failure.

Rupture.

211
Q

Infantile hemangioendothelioma: Treatment.

A

Excision, unless multiple.

Vascular ligation.

Embolization.

212
Q

Infantile hemangioendothelioma: Distinctive gross feature.

A

Central scar.

213
Q

Infantile hemangioendothelioma: Histopathology (2).

A

Center: Necrosis, calcification, few vessels.

Periphery: Proliferation of capillary-like vessels with plump, focally epithelioid endothelial cells and occasional mitotic figures.

214
Q

Epithelioid hemangioendothelioma: Epidemiology (3).

A

Middle age; females.

215
Q

Epithelioid hemangioendothelioma: Radiography.

A

Calcifications.

216
Q

Epithelioid hemangioendothelioma: Treatment.

A

Liver transplantation often necessary due to multifocality.

Recurrence in 40% of cases.

217
Q

Epithelioid hemangioendothelioma: Gross pathology.

A

Central scar.

218
Q

Epithelioid hemangioendothelioma: Histopathology (3).

A

Poorly defined vascular channels lined by atypical epithelioid tumor cells.

Sparing of sinusoids.

Myxoid or sclerotic stroma.

219
Q

Epithelioid hemangioendothelioma: Possibly helpful cytologic feature.

A

Intracytoplasmic vacuoles.

220
Q

Intraductal papillary neoplasm of the bile duct: Prognosis.

A

Frequently complicated by recurrence.

221
Q

Epithelioid hemangioendothelioma: Immunohistochemistry (3).

A

+: Vascular markers, (occasionally) LMW-CK.

-: Villin.

222
Q

Epithelioid hemangioendothelioma: Electron microscopy.

A

Weibel-Palade bodies.

223
Q

Synchronous extrahepatic epithelioid hemangioendothelioma:

A. Incidence.
B. Organs (4).

A

A. Occurs in 30% of cases.

B. Spleen, lymph nodes, lungs, bones.

224
Q

Angiosarcoma: Epidemiology (2).

A

Sixth and seventh decades; males.

225
Q

Angiosarcoma: Chemical risk factors (4).

A

Thorium dioxide.

Vinyl chloride.

Arsenic.

Anabolic steroids.

226
Q

Angiosarcoma: Growth patterns (4).

A

Growth along sinusoids.

Cavernous structures lined by pseudopapillae.

Solid nests.

Individual malignant cells.

227
Q

Angiosarcoma: Immunohistochemistry (2).

A

Vascular markers may be relatively weak.

Keratin may be positive in epithelioid variant.

228
Q

Mesenchymal hamartoma: Epidemiology (2).

A

First 2 years of life; mostly in males.

229
Q

Mesenchymal hamartoma: Associations (3).

A

Polycystic disease.

Congenital hepatic fibrosis.

Bile-duct hamartoma.

230
Q

Mesenchymal hamartoma: Gross pathology (3).

A

Solitary, smooth, spherical.

Fluctuant and made up of solid and cystic areas.

Can be very large (>1 kg).

231
Q

Mesenchymal hamartoma: Appearance on low power.

A

Resembles fibroadenoma.

232
Q

Mesenchymal hamartoma: Histopathology (5).

A

Loose, edematous, myxoid stroma containing

− Fluid-filled cysts.
− Dilated lymphatics and blood vessels.
− Disorganized bile ducts.
− Scattered hepatocellular nodules.

233
Q

Mesenchymal hamartoma: Possible additional histopathologic finding.

A

Extramedullary hematopoiesis.

234
Q

Mesenchymal hamartoma: Putative origin.

A

Connective tissue of portal tracts.

235
Q

Angiosarcoma: Mutation.

A

Point mutations in K-Ras-2 (in cases associated with vinyl chloride).

236
Q

Embryonal sarcoma: Laboratory finding.

A

Normal AFP.

237
Q

Embryonal sarcoma: Epidemiology.

A

Prepubertal children, especially at ages 5-10.

238
Q

Embryonal sarcoma: Cytologic feature.

A

Intracytoplasmic eosinophilic globules that are positive for PAS-D and α₁-antitrypsin.

239
Q

Embryonal sarcoma: Histopathology (3).

A

Mesenchymal only, albeit with benign entrapped bile ducts.

Phenotypically diverse malignant cells.

Extensive necrosis.

240
Q

Embryonal sarcoma: Prognosis.

A

Poor.

241
Q

Embryonal sarcoma: Gross pathology (3).

A

Large, solid and cystic, fibrous pseudocapsule.

Anatomic pathology (17 decks)

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