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16 Flashcards

2
Q

Marked cell enlargement with irregularly clumped cytoplasm showing large, clear spaces.

A

Ballooning degeneration (TOPNOTCH) Robbins Basic Pathology, 8th ed, p633

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3
Q

Multiple tiny fat droplets that do not displace the nucleus which appear in such conditions as alcoholic liver disease, Reye syndrome, and acute fatty liver of pregnancy.

A

Microvesicular steatosis Robbins Basic Pathology, 8th ed, p633

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4
Q

A single large fat droplet that displaces the nucleus seen in alcoholic liver disease or in the livers of obese or diabetic individuals.

A

Macrovesicular steatosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633

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5
Q

Diffuse, foamy, swollen appearance to the hepatocyte caused by retained biliary material.

A

Feathery degeneration(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633

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6
Q

Poorly stained mummified hepatocytes.

A

Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633

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7
Q

Isolated hepatocytes become shrunken, pyknotic, and intensely eosinophilic.

A

Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633

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8
Q

Hepatocyte necrosis is distributed immediately around the central vein, extending into the midzonal area in the setting of ischemia and several drug and toxic reactions.

A

Centrilobular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633

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9
Q

A pattern of nonrhythmic, rapid extension-flexion movements of the head and extremities, best seen when the arms are held in extension with dorsiflexed wrists, seen in patients with hepatic encephalopathy.

A

Asterixis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p635

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10
Q

A diffuse process characterized by bridging fibrous septa, in the form of delicate bands or broad scars around multiple adjacent lobes, and the conversion of normal liver architecture into structurally abnormal nodules, encircled by fibrotic bands. Liver architecture is disrupted.

A

Liver Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p635

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11
Q

Presence of “ground-glass” hepatocytes, a finely granular, eosinophilic cytoplasm and “sanded” nuclei, shown by electron microscopy

A

Hepatitis B infection(TOPNOTCH)Robbins Basic Pathology, 8th ed, p645

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12
Q

Necrotic cells appear to have “dropped out,” with collapse of the sinusoidal collagen reticulin framework where the cells have disappeared; scavenger macrophage aggregates mark sites of dropout.

A

Hepatocyte cytolysis (in viral hepatitis)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647

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13
Q

Hepatocytes shrink, become intensely eosinophilic, and have fragmented nuclei; effector T cells may be present in the immediate vicinity.

A

Hepatocyte apoptosis (in viral hepatitis)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647

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14
Q

The hallmark of serious liver damage.

A

Fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647

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15
Q

May occur as solitary or multiple lesions, ranging from millimeters to massive lesions, many centimeters in diameter. They are generally produced by gram-negative bacteria such as Escherichia coli and Klebsiella sp.

A

Pyogenic (bacterial) hepatic abscesses (TOPNOTCH)Robbins Basic Pathology, 8th ed, p648

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16
Q

Liver is enlarged (4-6kg), soft, yellow and greasy.

A

Hepatic Steatosis (Fatty Liver)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p649

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17
Q

Lipid accumulates to the point of creating large clear macrovesicular globules, compressing and displacing the nucleus to the periphery of the hepatocyte.

A

Hepatic Steatosis (Fatty Liver)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p649

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18
Q

Eosinophilic, cytoplasmic inclusions characteristic of alcoholic hepatitis.

A

Mallory bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650

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19
Q

Almost always accompanied by a brisk sinusoidal and perivenular fibrosis; occasionally periportal fibrosis may predominate.

A

Alcoholic hepatitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650

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20
Q

Liver is yellow-tan, fatty, and enlarged, usually weighing over 2 kg. Over the span of years it is transformed into a brown, shrunken, nonfatty organ, sometimes weighing less than 1 kg.

A

Alcoholic Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650

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21
Q

Pattern of cirrhosis in viral hepatitis.

A

Macronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650

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22
Q

Pattern of cirrhosis in alcoholic hepatitis.

A

Micronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650

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23
Q

The liver may shrink to 500 to 700 gm and become transformed into a limp, red organ covered by a wrinkled, overly large capsule. Necrotic areas have a muddy red, mushy appearance with blotchy bile staining. Complete destruction of hepatocytes in contiguous lobules leaves only a collapsed reticulin framework and preserved portal tracts.

A

Massive hepatic necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p653

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24
Q

Characterized by deposition of hemosiderin in the following organs: liver, pancreas, myocardium, pituitary, adrenal, thyroid and parathyroid glands, joints, and skin; cirrhosis; and pancreatic fibrosis

A

Hereditary hemochromatosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655

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25
Q

Golden-yellow granules in the cytoplasm of periportal hepatocytes, which stain blue with the Prussian blue stain.

A

Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655

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26
Q

Green to brown deposits of copper in Descemet membrane in the limbus of the cornea.

A

Kayser-Fleischer rings (TOPNOTCH)Robbins Basic Pathology, 8th ed, p656

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27
Q

Excessive copper deposition in the liver causing hepatic changes ranging from mild fatty change to massive liver necrosis. In the brain, injury affects the basal ganglia, demonstrating atrophy and cavitation. Kayser-Fleischer rings are characteristic.

A

Wilson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655

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28
Q

Hepatocytes with round to oval cytoplasmic globular inclusions which are strongly positive in a periodic acid-Schiff stain. By electron microscopy they lie within smooth, and sometimes rough, endoplasmic reticulum.

A

Alpha-1 antitrypsin Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th ed, p657

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29
Q

A rare disease characterized by microvesicular fatty change in the liver and encephalopathy. Microscopy of hepatocellular mitochondria reveals pleomorphic enlargement and electron lucency of the matrices, with disruption of cristae and loss of dense bodies.

A

Reye syndrome / “mitochondrial hepatopathies” (TOPNOTCH)Robbins Basic Pathology, 8th ed, p658

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30
Q

A chronic, progressive, and often fatal cholestatic liver disease, characterized by a nonsuppurative destruction of small and medium-sized intrahepatic bile ducts (“florid duct lesion”). On cut surface, the liver is hard, with a finely granular appearance, with extraordinary yellow-green pigmentation.

A

Primary biliary cirrhosis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p659

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31
Q

A chronic cholestatic disorder, characterized by progressive fibrosis and destruction of extrahepatic and large intrahepatic bile ducts. Affected portal tracts show concentric periductal “onion-skin” fibrosis and a modest lymphocytic infiltrate. Progressive atrophy of the bile duct epithelium leads to obliteration of the lumen, leaving behind a solid, cordlike fibrous scar.

A

Primary sclerosing cholangitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p660

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32
Q

Liver is slightly enlarged, tense, and cyanotic, with rounded edges. Microscopically, there is congestion of centrilobular sinusoids. With time, centrilobular hepatocytes become atrophic, resulting in markedly attenuated liver cell cords. Liver fibrosis mostly “centrilobular”.

A

Passive congestion of the liver secondary to right-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p660

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33
Q

Hepatocytes in the central region of the lobule undergo ischemic necrosis. The liver takes on a variegated mottled appearance, reflecting hemorrhage and necrosis in the centrilobular regions, alternating with pale midzonal areas, known traditionally as the “nutmeg” liver.

A

Passive congestion of the liver secondary to left-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p661

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34
Q

A rare condition wherein there is primary dilation of sinusoids, impeding hepatic blood efflux. Associated with exposure to anabolic steroids, OCP’s and danazol.

A

Peliosis hepatis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p661

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35
Q

Results from the thrombosis of two or more major hepatic veins and is characterized by hepatomegaly, weight gain, ascites, and abdominal pain. The liver is swollen, is red-purple, and has a tense capsule. The affected hepatic parenchyma reveals severe centrilobular congestion and necrosis.

A

Budd-Chiari syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p662

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36
Q

Caused by toxic injury to sinusoidal endothelium. Damaged endothelial cells slough off and create emboli that block blood flow. Accompanied by passage of red blood cell into the space of Disse, proliferation of stellate cells, and fibrosis of terminal branches of the hepatic vein.

A

Sinusoidal Obstruction Syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p662

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37
Q

Well-demarcated but poorly encapsulated lesion, consisting of hyperplastic hepatocyte nodules with a central fibrous scar. Appears in noncirrhotic livers and may reach up to many centimeters in diameter. It occurs in response to local vascular injury.

A

Focal nodular hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664

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38
Q

These appear in cirrhotic livers, are larger than surrounding cirrhotic nodules but do not display atypical features. Contains more than one portal tract, have an intact reticulin framework, and do not seem to be precursors of malignant lesions.

A

Macroregenerative nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664

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39
Q

These are lesions larger than 1 mm in diameter that appear in cirrhotic livers. Considered to be precursors of hepatocelluar cancers, are often monoclonal, and may contain chromosome aberrations similar to those present in liver cancers.

A

Dysplastic nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664

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40
Q

May appear grossly as (1) a unifocal, usually massive tumor, (2) a multifocal tumor made of nodules of variable size or (3) a diffusely infiltrative cancer, permeating widely and sometimes involving the entire liver, blending imperceptibly into the cirrhotic liver background.

A

Primary Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p665

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41
Q

A distinctive variant of HCC, which occurs in young male and female adults (20-40 years of age) of equal incidence, no association with cirrhosis or other risk factors. usually consists of a single large, hard “scirrhous” tumor with fibrous bands coursing through it. Composed of well-differentiated polygonal cells growing in nests or cords and separated by parallel lamellae of dense collagen bundles.

A

Fibrolamellar carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p665

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42
Q

Gallbladder stones that are mostly radiolucent, ovoid and firm; can occur singly but most often there are several, with faceted surfaces resulting from apposition to one another. They are pale yellow but w/ increasing proportions of CaCO3, phosphates and bilirubin, they turn gray-white to black and radiopaque.

A

Cholesterol stones (TOPNOTCH)Robbins Basic Pathology, 8th ed, p668

43
Q

May arise anywhere in the biliary tree and are trivially classified as black and as brown. Contain calcium salts of unconjugated bilirubin and lesser amounts of other calcium salts, mucin glycoproteins, and cholesterol.

A

Pigment stones(TOPNOTCH)Robbins Basic Pathology, 8th ed, p668

44
Q

A type of pigment stone found in sterile gallbladder bile, usually small and present in large quantities and crumble easily. 50% to 75% are radiopaque.

A

Black pigment stones (TOPNOTCH)Robbins Basic Pathology, 8th ed, p668

45
Q

A type of pigment stone found in infected intrahepatic or extrahepatic ducts. Tends to be single or few in number and are soft with a greasy, soaplike consistency that results from the presence of retained fatty acid salts released by the action of bacterial phospholipases on biliary lecithins. Contains calcium soaps, and are radiolucent.

A

Brown pigment stones(TOPNOTCH)Robbins Basic Pathology, 8th ed, p668

46
Q

Gallbladder is usually enlarged (twofold to threefold) and tense, and it assumes a bright red or blotchy, violaceous to green-black discoloration, imparted by subserosal hemorrhages. The gallbladder lumen is filled with a cloudy or turbid bile that may contain fibrin, blood, and frank pus.

A

Acute cholecystitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p669

47
Q

Condition wherein the exudate contained in the gallbladder is composed virtually of pure pus.

A

Empyema of the gallbladder(TOPNOTCH)Robbins Basic Pathology, 8th ed, p669

48
Q

Severe cholecystitis wherein the GB is transformed into a green-black necrotic organ.

A

Gangrenous cholecystitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p669

49
Q

The gallbladder may be contracted, of normal size, or enlarged. Presence of stones in the absence of inflammation is diagnostic.

A

Chronic cholecystitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p669

50
Q

Defined as a complete obstruction of bile flow caused by destruction or absence of all or part of the extrahepatic bile ducts.

A

Biliary atresia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p670

51
Q

Appears as a poorly defined area of diffuse thickening and induration of the gallbladder wall that may cover several square centimeters or involve the entire gallbladder, scirrhous and very firm in consistency.

A

Infiltrating pattern of gallbladder carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p671

52
Q

This pattern of GB carcinoma grows into the lumen as an irregular, cauliflower mass, but at the same time it invades the underlying wall.

A

Exophytic pattern of gallbladder carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p671

53
Q

Appear typically with an abundant fibrous stroma (desmoplasia) explaining their firm, gritty consistency Most exhibit clearly defined glandular and tubular structures lined by somewhat anaplastic cuboidal to low columnar epithelial cells. Bile pigment and hyaline inclusions are not found within the cells.

A

Cholangiocarcinomas (TOPNOTCH)Robbins Basic Pathology, 8th ed, p672

54
Q

Morphology: Characterized by fibrosing cholangitis of bile ducts, with a lymphocytic infiltrate, and progressive atrophy of the bile duct epithelium, and obliteration of the lumen

A

Primary Sclerosing Cholangitis(TOPNOTCH)

55
Q

Morphology: Concentric periductal fibrosis or Onion-Skin fibrosis with solid, cordlike fibrous scar.

A

Primary Sclerosing Cholangitis(TOPNOTCH)

56
Q

“Beading” of barium column in radiographs of the intrahepatic and extrahepatic biliary tree

A

Primary Sclerosing Cholangitis(TOPNOTCH)

57
Q

Morphology: Panlobular giant cell transformation of hepatocytes and formation of hepatocyte “rosettes”

A

Neonatal Cholestasis(TOPNOTCH)

58
Q

What is the histological hallmark of irreversible liver damage?

A

Deposition of fibrous tissue(TOPNOTCH)

59
Q

“Ground Glass Hepatocytes” are seen in what type of Viral Hepatitis?

A

Hepatitis B(TOPNOTCH)

60
Q

What type of viral hepatitis frequently show lymphoid aggregates within portal tracts?

A

Hepatitis C(TOPNOTCH)

61
Q

A characteristic feature of this type of viral hepatitis is the high mortality rate among pregnant women, approaching 20%

A

Hepatitis E(TOPNOTCH)

62
Q

A distinctive variant of hepatocellular carcinoma that occurs in young adults and has no association with HBV or cirrhosis risk factors.

A

Fibrolamellar Carcinoma(TOPNOTCH)

63
Q

What is the most common liver tumor of young childhood?

A

Hepatoblastoma(TOPNOTCH)

64
Q

What are the most common benign neoplasm in the liver?

A

Hemangiomas(TOPNOTCH)

65
Q

These benign neoplasms tend to occur in young women who have used oral contraceptives and regress on discontinuance of their use.

A

Liver cell Adenoma(TOPNOTCH)

66
Q

Rokitansky- Aschoff sinuses are structures seen in what organ?

A

Gallbladder(TOPNOTCH)

67
Q

What is the most common congenital anomaly of the gallbladder?

A

Presence of Phrygian Cap (folded fundus)(TOPNOTCH)

68
Q

What is the tetralogy of cholesterol stone formation?

A
  1. Supersaturation of bile with cholesterol2. Gallbladder hypomotility3. Cholesterol nucleation4. Hypersecretion of GB mucus(TOPNOTCH)
69
Q

AKA Strawberry Gallbladder

A

Cholesterolosis(TOPNOTCH)

70
Q

Acute calculous cholecystitis is most commonly precipitated by what condition?

A

Obstruction of the neck or cystic duct by a Gallbladder stone(TOPNOTCH)

71
Q

Morphology: Prominence of Rokitansky-Aschoff sinuses

A

Chronic Cholecystitis(TOPNOTCH)

72
Q

What is the most common cause of cholangitis?

A

Choledocholithiasis(TOPNOTCH)

73
Q

True or False. Gallstones are seen in 60%-90% of Carcinoma of the Gallbladder.

A

True(TOPNOTCH)

74
Q

What is the most common growth pattern of Gallbladder carcinoma? Infiltrating or Exophytic?

A

Infiltrating(TOPNOTCH)

75
Q

These are tumors arising from the part of the common bile duct between the cystic duct junction and the confluence of the right and left hepatic ducts at the liver hilus

A

Klatskin tumors(TOPNOTCH)

76
Q

Morphology: feathery degeneration and focal detergent dissolution of hepatocytes, giving rise to bile lakes filled with cellular debris and pigment

A

Cholestasis(TOPNOTCH)

77
Q

What does unrelieved cholestasis lead to?

A

Portal tract fibrosis(TOPNOTCH)

78
Q

What is the outcome of 85% of Acute Hepatitis infection?

A

Chronic Hepatitis(TOPNOTCH)

79
Q

These inclusions are a characteristic but not specific feature of alcoholic liver disease.

A

Mallory bodies(TOPNOTCH)

80
Q

Morphology: macrovesicular steatosis, involving most regions of the hepatic lobule. The intracytoplasmic fat is seen as clear vacuoles.

A

Alcoholic liver disease(TOPNOTCH)

81
Q

What zone of the liver if particularly vulnerable of ischemic injury and number of drug and toxic reactions?

A

Centrilobular zone(TOPNOTCH)

82
Q

What zone of the liver is particularly affected in eclampsia?

A

Periportal zone(TOPNOTCH)

83
Q

At least how many percent of the liver must be damaged before hepatic failure ensues?

A

at least 80%(TOPNOTCH)

84
Q

What are the 4 major consequences of portal hypertension?

A

Ascites, formation of portosystemic venous shunts, congestive splenomegaly, and hepatic encephalopathy(TOPNOTCH)

85
Q

Ascites becomes clinically detectable at what amount?

A

500 ml(TOPNOTCH)

86
Q

Morphology: portal tract expansion with inflammatory cells and fibrous tissue and interface hepatitis with spillover of inflammation into the adjacent parenchyma. Lymphoid aggregates can also be seen.

A

Chronic Viral Hepatitis C(TOPNOTCH)

87
Q

Morphology: hepatocytes show diffuse granular cytoplasm, so called ground glass hepatocytes

A

Hepatitis B viral infection(TOPNOTCH)

88
Q

Morphology: liver biopsy shows steatosis, multifocal parenchymal inflammation, Mallory hyaline, hepatocyte death, and sinusoidal fibrosis

A

Steatohepatitis or Nonalcoholic Steatohepatitis(TOPNOTCH)

89
Q

In Hemochromatosis, what is the most common site of hemosiderin deposition?

A

Liver(TOPNOTCH)

90
Q

What are the 3 clinical features of Hemochromatosis?

A

Deposition of hemosiderin, cirrhosis, and pancreatic fibrosis(TOPNOTCH)

91
Q

Morphology: characterized by the presence of round to oval cytoplasmic globular inclusions in hepatocytes, which in routine H and E stains are acidophilic and indistinctly demarcated from the surrounding cytoplasm

A

A1 antitrypsin deficiency(TOPNOTCH)

92
Q

Morphology: Panlobular giant cell transformation of hepatocytes and formation of hepatocyte “rosettes”

A

Neonatal Cholestasis(TOPNOTCH)

93
Q

Morphology: characterized by coarse fibrous septae that subdivide the liver in a jigsaw like pattern

A

Secondary biliary cirrhosis(TOPNOTCH)

94
Q

Morphology: florid duct lesion

A

Primary Biliary Cirrhosis(TOPNOTCH)

95
Q

The combination of hypoperfusion and retrograde congestion acts synergistically to generate what type of necrosis in the liver?

A

Centrolobular hemorrhagic necrosis(TOPNOTCH)

96
Q

Morphology: periportal sinusoids contain fibrin deposits with hemorrhage into the space of Disse, leading to periportal hepatocellular coagulative necrosis

A

Pre-Eclampsia/Eclampsia(TOPNOTCH)

97
Q

Type of liver transplant rejection : severe obliterative arteritis of small and larger arterial vessels results in ischemic changes in the liver parenchyma

A

Chronic Rejection(TOPNOTCH)

98
Q

Type of liver transplant rejection: infiltration of a mixed population of inflammatory cells into portal tracts, bile ducts, and hepatocyte injury and endothelitis

A

Acute cellular rejections(TOPNOTCH)

99
Q

What do you call the small tubular channels that are sometimes burried within the gallbladder wall adjacent to the liver?

A

Ducts of Luschka(TOPNOTCH)

100
Q

What is the most common congenital anomaly seen in the Gallbladder?

A

A folded fundus or so called phrygian cap(TOPNOTCH)

101
Q

Gross morphology: the mucosal surface of the gallbladder is studded with minute yellow flecks

A

Strawberry Gallbladder(TOPNOTCH)

102
Q

What type of pigment stones are generally seen in infected intrahepatic or extra hepatic ducts?

A

Brown pigment stones(TOPNOTCH)

103
Q

Gross morphology: GB is shrunken, nodular, and chronically inflamed with foci of necrosis and hemorrhage

A

Xanthogranulomatous cholecystitis(TOPNOTCH)

PM Patho (23 decks)

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