XVI - The Liver, Gallbladder and Biliary Tree Flashcards
1
Q
Marked cell enlargement with irregularly clumped cytoplasm showing large, clear space
A
Ballooning degeneration (TOPNOTCH) Robbins Basic Pathology, 8th ed,. 633
2
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, p. 633
3
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, p. 633
4
Q
Diffuse, foamy, swollen appearance to the hepatocyte caused by retained biliary material.
A
Feathery degeneration(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 633
5
Q
Poorly stained mummified hepatocytes
A
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 633
6
Q
Isolated hepatocytes become shrunken, pyknotic, and intensely eosinophilic.
A
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 633
7
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, p. 633
8
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, p. 635
9
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, p. 635
10
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, p. 645
11
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, p. 647
12
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, p. 647
13
Q
The hallmark of serious liver damage
A
Fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 647
14
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, p. 648
15
Q
Liver is enlarged, soft, yellow and greasy. 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, p. 649
16
Q
Eosinophilic, cytoplasmic inclusions characteristic of alcoholic hepatitis.
A
Mallory bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 650
17
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, p. 650
18
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, p. 650
19
Q
Pattern of cirrhosis in viral hepatitis.
A
Macronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 650
20
Q
Pattern of cirrhosis in alcoholic hepatitis.
A
Micronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 650
21
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, p. 653
22
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, p. 655
23
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, p. 656
24
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, p. 655
25
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.
Alpha-1 antitrypsin Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 657
26
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.
Reye syndrome / "mitochondrial hepatopathies" (TOPNOTCH)Robbins Basic Pathology, 8th ed, p658
27
A chronic, progressive, and often fatal cholestatic liver disease, characterized by a nonsuppurative destruction of small and medium-sized intrahepatic bile ducts florid duct leesion. On cut surface, the liver is hard, with a finely granular appearance, with extraordinary yellow-green pigmentation.
Primary biliary cirrhosis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 659
28
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.
Primary sclerosing cholangitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 660
29
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".
Passive congestion of the liver secondary to right-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 660
30
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.
Passive congestion of the liver secondary to left-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 661
31
A rare condition wherein there is primary dilation of sinusoids, impeding hepatic blood efflux. Associated with exposure to anabolic steroids, OCP's and danazol.
Peliosis hepatis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 661
32
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.
Budd-Chiari syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 662
33
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.
Sinusoidal Obstruction Syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 662
34
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.
Focal nodular hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 664
35
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.
Macroregenerative nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 664
36
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.
Dysplastic nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 664
37
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.
Primary Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 665
38
A distinctive variant of HCC, which occurs in adults (
Fibrolamellar carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th ed, p. 873
39
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.
Cholesterol stones (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 668
40
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.
Pigment stones(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 668
41
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.
Black pigment stones (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 668
42
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.
Brown pigment stones(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 668
43
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.
Acute cholecystitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 669
44
Condition wherein the exudate contained in the gallbladder is composed virtually of pure pus.
Empyema of the gallbladder(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 669
45
Severe cholecystitis wherein the GB is transformed into a green-black necrotic organ.
Gangrenous cholecystitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 669
46
The gallbladder may be contracted, of normal size, or enlarged. Presence of stones in the absence of inflammation is diagnostic.
Chronic cholecystitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 669
47
Defined as a complete obstruction of bile flow caused by destruction or absence of all or part of the extrahepatic bile ducts.
Biliary atresia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 670
48
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.
Infiltrating pattern of gallbladder carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 671
49
This pattern of GB carcinoma grows into the lumen as an irregular, cauliflower mass, but at the same time it invades the underlying wall.
Exophytic pattern of gallbladder carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 671
50
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.
Cholangiocarcinomas (TOPNOTCH)Robbins Basic Pathology, 8th ed, p. 672
51
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
Primary Sclerosing Cholangitis(TOPNOTCH)
52
Morphology: Concentric periductal fibrosis or Onion-Skin fibrosis with solid, cordlike fibrous scar.
Primary Sclerosing Cholangitis(TOPNOTCH)
53
Morphology: Panlobular giant cell transformation of hepatocytes and formation of hepatocyte "rosettes"
Neonatal Cholestasis(TOPNOTCH)
54
What is the histological hallmark of irreversible liver damage?
Deposition of fibrous tissue(TOPNOTCH)
55
"Ground Glass Hepatocytes" are seen in what type of Viral Hepatitis?
Hepatitis B(TOPNOTCH)
56
What type of viral hepatitis frequently show lymphoid aggregates within portal tracts?
Hepatitis C(TOPNOTCH)
57
What is the most common liver tumor of young childhood?
Hepatoblastoma(TOPNOTCH)
58
What are the most common benign neoplasm in the liver?
Hemangiomas(TOPNOTCH)
59
These benign neoplasms tend to occur in young women who have used oral contraceptives and regress on discontinuance of their use.
Liver cell Adenoma(TOPNOTCH)
60
Rokitansky- Aschoff sinuses are structures seen in what organ?
Gallbladder(TOPNOTCH)
61
What is the most common congenital anomaly of the gallbladder?
Presence of Phrygian Cap (folded fundus)(TOPNOTCH)
62
What is the tetralogy of cholesterol stone formation?
1. Supersaturation of bile with cholesterol2. Gallbladder hypomotility3. Cholesterol nucleation4. Hypersecretion of GB mucus(TOPNOTCH)
63
AKA Strawberry Gallbladder
Cholesterolosis(TOPNOTCH)
64
Acute calculous cholecystitis is most commonly precipitated by what condition?
Obstruction of the neck or cystic duct by a Gallbladder stone(TOPNOTCH)
65
Morphology: Prominence of Rokitansky-Aschoff sinuses
Chronic Cholecystitis(TOPNOTCH)
66
What is the most common cause of cholangitis?
Choledocholithiasis(TOPNOTCH)
67
True or False. Gallstones are seen in 60%-90% of Carcinoma of the Gallbladder.
True(TOPNOTCH)
68
What is the most common growth pattern of Gallbladder carcinoma? Infiltrating or Exophytic?
Infiltrating(TOPNOTCH)
69
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
Klatskin tumors(TOPNOTCH)
70
Morphology: feathery degeneration and focal detergent dissolution of hepatocytes, giving rise to bile lakes filled with cellular debris and pigment
Cholestasis(TOPNOTCH)
71
What does unrelieved cholestasis lead to?
Portal tract fibrosis(TOPNOTCH)
72
What is the outcome of 85% of Acute Hepatitis infection?
Chronic Hepatitis(TOPNOTCH)
73
These inclusions are a characteristic but not specific feature of alcoholic liver disease.
Mallory bodies(TOPNOTCH)
74
Morphology: macrovesicular steatosis, involving most regions of the hepatic lobule. The intracytoplasmic fat is seen as clear vacuoles.
Alcoholic liver disease(TOPNOTCH)
75
What zone of the liver if particularly vulnerable of ischemic injury and number of drug and toxic reactions?
Centrilobular zone(TOPNOTCH)
76
What zone of the liver is particularly affected in eclampsia?
Periportal zone(TOPNOTCH)
77
At least how many percent of the liver must be damaged before hepatic failure ensues?
at least 80%(TOPNOTCH)
78
What are the 4 major consequences of portal hypertension?
Ascites, formation of portosystemic venous shunts, congestive splenomegaly, and hepatic encephalopathy(TOPNOTCH)
79
Ascites becomes clinically detectable at what amount?
500 ml(TOPNOTCH)
80
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.
Chronic Viral Hepatitis C(TOPNOTCH)
81
Morphology: liver biopsy shows steatosis, multifocal parenchymal inflammation, Mallory hyaline, hepatocyte death, and sinusoidal fibrosi
Steatohepatitis or Nonalcoholic Steatohepatitis(TOPNOTCH)
82
In Hemochromatosis, what is the most common site of hemosiderin deposition?
Liver(TOPNOTCH)
83
What are the 3 clinical features of Hemochromatosis?
Deposition of hemosiderin, cirrhosis, and pancreatic fibrosis(TOPNOTCH)
84
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
A1 antitrypsin deficiency(TOPNOTCH)
85
Morphology: characterized by coarse fibrous septae that subdivide the liver in a jigsaw like pattern
Secondary biliary cirrhosis(TOPNOTCH)
86
Morphology: florid duct lesion
Primary Biliary Cirrhosis(TOPNOTCH)
87
The combination of hypoperfusion and retrograde congestion acts synergistically to generate what type of necrosis in the liver?
Centrolobular hemorrhagic necrosis(TOPNOTCH)
88
Morphology: periportal sinusoids contain fibrin deposits with hemorrhage into the space of Disse, leading to periportal hepatocellular coagulative necrosis
Pre-Eclampsia/Eclampsia(TOPNOTCH)
89
Type of liver transplant rejection : severe obliterative arteritis of small and larger arterial vessels results in ischemic changes in the liver parenchyma
Chronic Rejection(TOPNOTCH)
90
Type of liver transplant rejection: infiltration of a mixed population of inflammatory cells into portal tracts, bile ducts, and hepatocyte injury and endothelitis
Acute cellular rejections(TOPNOTCH)
91
What do you call the small tubular channels that are sometimes burried within the gallbladder wall adjacent to the liver?
Ducts of Luschka(TOPNOTCH)
92
What is the most common congenital anomaly seen in the Gallbladder?
A folded fundus or so called phrygian cap(TOPNOTCH)
93
Gross morphology: the mucosal surface of the gallbladder is studded with minute yellow flecks
Strawberry Gallbladder(TOPNOTCH)
94
What type of pigment stones are generally seen in infected intrahepatic or extra hepatic ducts?
Brown pigment stones(TOPNOTCH)
95
Gross morphology: GB is shrunken, nodular, and chronically inflamed with foci of necrosis and hemorrhage
Xanthogranulomatous cholecystitis(TOPNOTCH)
96
Hallmarks of HCV infection
Persistent infection and chronic hepatitis (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th ed., p. 834
97
Defining histologic feature of chronic viral hepatitis
Mononuclear portal infiltration (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 837
98
Diagnostic hallmark of Hepatitis B; these are cells with ER swollen by HBsAg
Ground-glass hepatocytes(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 837
99
Characteristic feature of alcoholic hepatitis which present as clumped, amorphous, eosinophilic material in ballooned hepatocytes. May also be present in Wilson disease and in chronic biliary tract disease.
Mallory-Denk bodies (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 843
100
Deeply eosinophilic staining apoptotic hepatocytes seen in acute and chronic hepatitis.
Acidophilic bodies (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 823
101
The principal cell type involve in scar deposition in the liver
Hepatic stellate cell(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 823
102
Associated with encephalopathy and coagulopathy that occurs within 26 weeks of initial liver injury in the absence of pre-existing liver disease, caused by massive hepatic necrosis
Acute liver failure(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 825
103
Most common intrahepatic cause of portal hypertension
Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 828
104
Most frequent mode of transmission of HBV in high prevalence regions
Transmission during childbirth(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 832
105
Most frequent mode of transmission of HBV in low prevalence regions
Unprotected sex and IV drug abuse(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 832
106
Serologic marker detected during window period of HBV infection
IgM anti-HBc antibody(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 833
107
Best predictor of chronicity of HBV infection
Age at the time of infection(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 833
108
Most common risk factor for HCV infection
IV drug abuse(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 834
109
Type of viral hepatitis associated with metabolic syndrome
Hepatitis C virus infection (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 835
110
Type of viral hepatitis implicated in the high mortality rate among pregnant women
Hepatitis E Virus infection(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 835
111
Main inflammatory cells in both acute and chronic viral hepatitis
T cells(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 839
112
Type of autoimmune hepatitis most often seen in middle-aged women and is most characteristically associated with antinuclear and anti-smooth muscle antibodies
Type 1 autoimmune hepatitis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 840
113
Type of autoimmune hepatitis most often seen in children or teenager and is associated with anti-liver kidney microsomal autoantibodies
Type 2 autoimmune hepatitis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 840
114
Predominant cells and characteristic component of inflammatory infiltrate in biopsy specimens showing autoimmune hepatitis
Plasma cells(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 840
115
Most common hepatotoxin causing acute liver failure
Acetaminophen(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 841
116
Most common hepatotoxin causing chronic liver disease
Alcohol(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 841
117
Characterized by hepatocyte swelling and necrosis, Mallory-Denk bodies, neutrophilic reaction, fibrosis, perisinosoidal scar in the space of Disse of the centrilobilar region
Alcohol Hepatitis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 843
118
Micronodular cirrhosis described for end-stage alcoholic liver disease due o long-term alochol use
Laennec cirrhosis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 843
119
Volume threshold for the developmet of alcoholic liver disease
80gm/day of alcohol(TOPNOTCH)Robbins Basic Pathology, 9th ed. P. 845
120
Most common site of hemosiderin deposition
Liver(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 848
121
An autosomal disorder caused by mutation of ATP7B gene resulting in impaired copper excretion into bile and failure to incorporate copper into ceruloplasmin
Wilson Disease(TOPNOTCH)Robbins Basic Pathology, 9th ed, p. 849
122
Presents with movement disorders (tremor, chorea, tremor),rigid dystonia, psychiatric symptoms, hemolytic anemia, green to brown deposits in Descemet membrane in the limbus
Wilson Disease(TOPNOTCH)Robbins Basic Pathology, 9th ed, p. 849
123
Most sensitive and accurate test for Wilson disease
Increase in hepatic copper content(TOPNOTCH)Robbins Basic Pathology, 9th ed, p. 850
124
Most specific screening test for Wilson Disease
Increased urinary excretion of copper copper content(TOPNOTCH)Robbins Basic Pathology, 9th ed, p. 850
125
Most characteristic laboratory finding in primary biliary cirrhosis
Antimitochondrial antibodies(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 858
126
Mechanism of physiologic jaundice of the newborn
Impaired bilirubin conjugation(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 853
127
Hereditary unconjugated hyperbilirubinemia caused by severe UGT1A1 deficiency and is fatal around the time of birth
Crigler-Najjar syndrome type 1(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 853
128
An autosomal recessive disorder caused by impaired biliary excretion of bilirubin glucoronides due to mutation in canalicular multidrug resistance protein 2(MRP2)
Dubin-Johnson syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 854
129
Most common cause of bile duct obstruction in adults
Extrahepatic cholelithiasis(gallstones)(TOPNOTCH)Robbins Basic Pathology,9th ed., p. 854
130
Histologic hallmark: influx of periductular neutrophils directly into the bile duct epithelium and lumen
Ascending cholangitis(TOPNOTCH)Robbins Basic Pathology,9th ed., p. 854
131
Most common form of cholestasis of sepsis wherein bile plugs within predominantly centrilobular canaliculi
Canalicular cholestasis(TOPNOTCH)Robbins Basic Pathology,9th ed., p. 855
132
Disorder of intrahepatic gallstone formation leading to repeated bouts of ascending cholangitis; has pigmented calcium bilirubinate stones in distended intrahepatic bile ducts
Hepatolithiasis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 856
133
Presents with neonatal cholestasis, normal birthweight and postnatal weight gain, initially normal stools change to acholic stools.
Biliary atresia(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 857
134
Morphology: Inflammation and fibrosing stricture of the hepatic or common bile ducts; cirrhosis develops within 3-6 mos of birth if uncorrected
Biliary atresia(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 857
135
Florid duct lesion by liver biopsy, elevated alkaline phosphatase and gamma-glutamyltransferase, hypercholesterolemia,
Primary biliary cirrhosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. P. 858
136
Presents with characteristic beading on radiographs of intrahepatic and extrahepatic biliary tree; strong association with IBD particularly ulcerative colitis
Primary biliary cirrhosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. P. 861
137
Presents most often in children before age 10 as jaundice, recurrent abdominal pain, symptoms that are typical of biliary colic; caused by congenital dilations of CBD
Choledochal cyst(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 861
138
Presents with liver enlargement, pain, and ascites due to obstruction of two or more hepatic veins.
Budd-Chiari syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 863
139
Most important premalignant lesions for cholangiocarcinoma
Biliary intraepithelial neoplasias(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 874
140
Most common malignancy of the extrahepatic biliary tract
Carcinoma of the gallbladder(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 879
141
Most important risk factor for gallbladder cancer
Gallstones(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 879
142
Atrophic, chronically obstructed, often dilated gallbladder, containing clear secretions
Hydrops of the gallbladder(TOPNOTCH)
143
Patients with chronic hemolytic anemias, severe ileal dysfunction or bypass, and bacterial contamination of the biliary tree are at risk for developing what kind of gallbladder stones?
Pigment stones(TOPNOTCH)
144
In severe form of this condition, patient presents with micronodular cirrhosis, diabetes mellitus, and abnormal skin pigmentation.
Hemochromatosis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 847
145
A 28 year old man with a history of IV drug abuse develops jaundice and malaise. Which of the following liver biopsy findings particularly suggests a hepatitis C infection? (A) ballooning degeneration of hepatocytes (B) ground glass appearance of hepatocyte cytoplasm, with "sanded" nuclei (C) bile duct proliferation and lymphoid aggregate formation (D) tangled skeins of pink cytoplasmic inclusions in degenerating hepatocytes, with neutrophilic infiltrates
bile duct proliferation and lymphoid aggregate formation (TOPNOTCH)Robbins Basic Pathology, 8th ed, p646-647
146
A 25 year old medical intern draws blood from a chronic hepatitis B patient sustains a needlestick injury. He forgets to consult the infection control unit, and develops jaundice 2 months later. A biopsy of his liver will show (A) hemosiderin-laden periportal hepatocytes ((B) ground glass appearance of hepatocyte cytoplasm, with "sanded" nuclei (C) bile duct proliferation and lymphoid aggregate formation (D) tangled skeins of pink cytoplasmic inclusions in degenerating hepatocytes, with neutrophilic infiltrates
ground glass appearance of hepatocyte cytoplasm, and "sanded" nuclei (TOPNOTCH)Robbins Basic Pathology, 8th ed, p646-647
147
A 45 year old male during a drinking spree gets into a fight, and is stabbed. A medicolegal autopsy is performed. Given his chronic alcoholism, his liver will likely show (A) hemosiderin-laden periportal hepatocytes (B) ground glass appearance of hepatocyte cytoplasm, with "sanded" nuclei (C) bile duct proliferation and lymphoid aggregate formation (D) tangled skeins of pink cytoplasmic inclusions in degenerating hepatocytes, with neutrophilic infiltrates
tangled skeins of pink cytoplasmic inclusions in degenerating hepatocytes (Mallory bodies), with neutrophilic infiltrates (TOPNOTCH)Robbins Basic Pathology, 8th ed, p 649-650
148
Which of the following is most likely to have nonalcoholic fatty liver disease? (A) 28 year old overweight man with dyslipidemia and family history of Type 2 DM (B) 14 year old student with alpha thalassemia with history of multiple blood transfusions since childhood (C) 33 year old teacher on his 1st month of taking anti-Koch's medication (D) 44 year old architect with a 30 pack year smoking history
28 year old overweight man with dyslipidemia and family history of Type 2 DM (insulin resistance) (TOPNOTCH)Robbins Basic Pathology, 8th ed, p 654
149
A 40 year old man with beta thalassemia and long history of blood transfusions dies of congestive heart failure. At autopsy, his liver, heart, and pancreas appear dark brown. Histologic examination of his liver shows hepatocytes with golden brown cytoplasmic granules. These granules will stain with (A) prussian blue (B) rhodanine (C) periodic acid schiff (D) hematoxylin
Prussian blue (iron stain)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p 654-655
150
Patients with hemochromatosis have a 200-fold higher risk of developing which malignancy compared to the normal population?
hepatocellular carcinoma (TOPNOTCH)Robbins Basic Pathology, 8th ed, p 656
151
A 30 year old male with inflammatory bowel disease develops jaundice. On hepatic ultrasound, there are strictures and beading of the large bile ducts, and pruning of the small bile ducts. A liver biopsy showed portal tracts with concentric periductal onion-skin fibrosis, and a modest lymphocytic infiltrate. In five years, he has a 10 to 15% chance of developing (A) colorectal carcinoma (B) hepatocellular carcinoma (C) cholangiocarcinoma (D) hepatic lymphoma
cholangiocarcinoma (primary sclerosisng cholangitis) (TOPNOTCH)Robbins Basic Pathology, 8th ed, p 659
152
In which of the following conditions is Budd-Chiari syndrome most likely? (A) Christmas disease (B) von Willebrand disease (C) Factor VIII deficiency (D) pregnancy
pregnancy (TOPNOTCH)Robbins Basic Pathology, 8th ed, p 662
153
Which of the following is a risk factor for the development of cholangiocarcinoma? (A) primary sclerosing cholangitis (B) exposure to the radiologic agent Thorotrast (C) infection with Clonorchis (D) all of the above
all of the above (TOPNOTCH)Robbins Basic Pathology, 8th ed, p 671
