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BLOCK POSTING 2 > HEPATOBILIARY > Flashcards

HEPATOBILIARY Flashcards

1
Q

Front

A

Back

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2
Q

What are centrilobular and periportal hepatocytes?

A

Centrilobular hepatocytes are near the terminal hepatic vein, while periportal hepatocytes are near the portal tract.

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3
Q

What is the significance of dividing the liver lobule into zones?

A

Each zone has different metabolic activities and susceptibilities to hepatic injury.

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4
Q

What is biliary atresia?

A

A developmental anomaly or inflammatory destruction of bile ducts, leading to cholestatic jaundice and ESLD in children.

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5
Q

What are the clinical features of biliary atresia?

A

Cholestatic jaundice at 1 week of life, enlarged dark green liver, and absence of bile.

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6
Q

What are the features of choledochal cyst?

A

Cystic dilatation of the biliary tree; may involve fibrosis and risk of cholangiocarcinoma.

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7
Q

What is neonatal jaundice?

A

Transient unconjugated hyperbilirubinemia in newborns due to immature conjugation machinery.

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8
Q

What are the types of jaundice based on bilirubin?

A

Unconjugated (e.g., hemolysis, low UGT) and conjugated (e.g., biliary obstruction, Dubin-Johnson syndrome).

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9
Q

What is Crigler-Najjar syndrome?

A

A hereditary condition with severe (type 1) or mild (type 2) UGT deficiency, leading to unconjugated hyperbilirubinemia.

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10
Q

What is Dubin-Johnson syndrome?

A

An AR disorder with defective canalicular bilirubin transport, causing conjugated hyperbilirubinemia and dark liver.

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11
Q

What causes viral hepatitis?

A

Hepatitis viruses A, B, C, D, and E; other viruses like EBV, CMV, and yellow fever.

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12
Q

What are the stages of HBV serology?

A

Acute (HBsAg, HBeAg, anti-HBc IgM), Window (anti-HBc IgM), Resolved (anti-HBc IgG, anti-HBs), Chronic (HBsAg > 6 months).

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13
Q

What is fulminant hepatic failure?

A

Acute liver failure with encephalopathy, seen in severe cases of viral hepatitis (e.g., HAV, HBV, HEV).

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14
Q

What is the risk of chronicity in hepatitis B and C?

A

HBV: 20% chronic; HCV: 75-85% chronic, with cirrhosis in 10-15% within 20 years.

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15
Q

What is the pathogenesis of HBV?

A

HBV targets hepatocytes, with immune-mediated destruction by cytotoxic lymphocytes reacting to HBsAg and HBeAg.

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16
Q

What is Wilson disease?

A

An AR defect in ATP7B gene causing copper accumulation in hepatocytes, leading to cirrhosis, neurological symptoms, and Kayser-Fleischer rings.

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17
Q

What is hemochromatosis?

A

Excessive iron deposition due to HFE gene mutations, causing cirrhosis, diabetes, bronze skin, and increased HCC risk.

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18
Q

What are the clinical features of cirrhosis?

A

Portal hypertension, hepatic encephalopathy, jaundice, hypoalbuminemia, coagulopathy, and ascites.

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19
Q

What is alcoholic liver disease?

A

Hepatic damage from alcohol, ranging from fatty liver (reversible) to alcoholic hepatitis (AST > ALT) to cirrhosis.

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20
Q

What is non-alcoholic fatty liver disease (NAFLD)?

A

Fatty liver, hepatitis, or cirrhosis without alcohol exposure, commonly associated with obesity.

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21
Q

What is the treatment for Wilson disease?

A

D-penicillamine, which chelates copper.

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22
Q

What is the treatment for hemochromatosis?

A

Phlebotomy to reduce iron overload.

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23
Q

What are Kayser-Fleischer rings?

A

Copper deposits in the cornea seen in Wilson disease.

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24
Q

What are the complications of biliary obstruction?

A

Pruritus, pale stool, dark urine, fat malabsorption, and vitamin deficiencies.

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25
Q

What is the role of stellate cells in cirrhosis?

A

They produce TGF-β, leading to fibrosis in liver damage.

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26
Q

What is the classic triad of hemochromatosis?

A

Cirrhosis, diabetes mellitus, and bronze skin.

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27
Q

Front

A

Back

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28
Q

What are centrilobular and periportal hepatocytes?

A

Centrilobular hepatocytes are near the terminal hepatic vein, while periportal hepatocytes are near the portal tract.

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29
Q

What is biliary atresia?

A

A developmental anomaly causing cholestatic jaundice and ESLD in children due to inflammatory destruction of bile ducts.

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30
Q

What are the clinical features of biliary atresia?

A

Cholestatic jaundice within 1 week of life, enlarged dark green liver, and bile duct fibrosis.

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31
Q

What are the microscopic features of intrahepatic biliary atresia?

A

Few bile ducts, cholestasis, periportal inflammation, and late-stage cirrhosis.

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32
Q

What is a choledochal cyst?

A

Cystic dilatation of the biliary tree, which may lead to fibrosis and cholangiocarcinoma.

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33
Q

What is Caroli disease?

A

Dilation of large intrahepatic bile ducts with complications like cholangitis, sepsis, and cholelithiasis.

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34
Q

What is Alagille syndrome?

A

An autosomal dominant disorder due to JAG1 and Notch2 mutations causing reduced bile ducts.

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35
Q

What causes jaundice?

A

Retention of bilirubin due to increased production, hepatocyte dysfunction, or bile flow obstruction.

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36
Q

What is neonatal jaundice?

A

Transient unconjugated hyperbilirubinemia in newborns due to immature bilirubin metabolism.

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37
Q

What are the classifications of jaundice?

A

Predominantly unconjugated (e.g., hemolysis, low UGT) or conjugated (e.g., biliary obstruction, Dubin-Johnson syndrome).

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38
Q

What is Crigler-Najjar syndrome?

A

A hereditary condition with severe (type 1) or mild (type 2) UGT deficiency causing unconjugated hyperbilirubinemia.

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39
Q

What is Dubin-Johnson syndrome?

A

An autosomal recessive disorder with defective bilirubin transport, causing conjugated hyperbilirubinemia and dark liver.

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40
Q

What is viral hepatitis?

A

Inflammation of the liver caused by hepatitis viruses (A, B, C, D, E) or other infections (e.g., CMV, EBV).

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41
Q

What is fulminant hepatic failure?

A

Acute liver failure with encephalopathy, often fatal, seen in severe viral hepatitis cases.

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42
Q

What are the chronic risks of hepatitis B and C?

A

HBV: Chronic in 20%, HCC risk. HCV: Chronic in 75-85%, cirrhosis in 10-15% within 20 years.

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43
Q

What is HAV’s mode of transmission?

A

Fecal-oral, often from contaminated water or food, with no chronic state.

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44
Q

What is HBV’s mode of transmission?

A

Parenteral, including childbirth, unprotected sex, and IV drug use.

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45
Q

What is the significance of HBsAg in HBV?

A

Indicates active infection and blood infectivity.

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46
Q

What is HCV’s progression risk?

A

Chronic disease in most cases, with high risk of cirrhosis and need for liver transplantation.

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47
Q

What is unique about HDV?

A

It only co-infects with HBV, leading to more severe disease, including cirrhosis and liver cancer.

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48
Q

What is the mode of transmission of HEV?

A

Fecal-oral, especially in developing countries; severe in pregnant women.

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49
Q

What are Kayser-Fleischer rings?

A

Copper deposits in the cornea, seen in Wilson disease.

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50
Q

What is Wilson disease?

A

An autosomal recessive disorder of copper metabolism causing cirrhosis, neurological symptoms, and corneal rings.

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51
Q

What are the features of hemochromatosis?

A

Iron overload causing cirrhosis, diabetes, bronze skin, and increased HCC risk.

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52
Q

What is alcoholic hepatitis?

A

Liver inflammation from alcohol, characterized by Mallory bodies, AST > ALT, and hepatocyte damage.

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53
Q

What are the complications of cirrhosis?

A

Portal hypertension, ascites, hepatic encephalopathy, jaundice, and coagulopathy.

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54
Q

What are the treatments for Wilson disease and hemochromatosis?

A

Wilson disease: D-penicillamine. Hemochromatosis: Phlebotomy.

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55
Q

Front

A

Back

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56
Q

What is primary biliary cirrhosis (PBC)?

A

An autoimmune granulomatous destruction of intrahepatic bile ducts, commonly in women around age 40.

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57
Q

What is primary biliary cirrhosis associated with?

A

Other autoimmune diseases; antimitochondrial antibodies are present.

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58
Q

What are the clinical features of primary biliary cirrhosis?

A

Obstructive jaundice with cirrhosis as a late complication.

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59
Q

What is primary sclerosing cholangitis (PSC)?

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts.

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60
Q

What is the characteristic histological feature of PSC?

A

Periductal fibrosis with an ‘onion-skin’ appearance.

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61
Q

What imaging findings are associated with PSC?

A

Dilated, uninvolved bile ducts causing a ‘beaded’ appearance on contrast imaging.

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62
Q

What conditions are associated with PSC?

A

Ulcerative colitis; p-ANCA is often positive.

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63
Q

What are the complications of PSC?

A

Cirrhosis and increased risk of cholangiocarcinoma.

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64
Q

What is Reye syndrome?

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin.

65
Q

What causes Reye syndrome?

A

Likely mitochondrial damage to hepatocytes caused by aspirin use.

66
Q

What are the clinical features of Reye syndrome?

A

Hypoglycemia, elevated liver enzymes, vomiting, and potential progression to coma and death.

67
Q

What is hepatic adenoma?

A

A benign tumor of hepatocytes, often associated with oral contraceptive use.

68
Q

What are the complications of hepatic adenoma?

A

Risk of rupture and intraperitoneal bleeding, especially during pregnancy.

69
Q

What is hepatocellular carcinoma (HCC)?

A

A malignant tumor of hepatocytes.

70
Q

What are the risk factors for HCC?

A

Chronic hepatitis (HBV, HCV), cirrhosis (alcohol, NAFLD, hemochromatosis, Wilson disease, A1AT deficiency), and aflatoxins.

71
Q

What is Budd-Chiari syndrome?

A

Liver infarction secondary to hepatic vein obstruction, presenting with painful hepatomegaly and ascites.

72
Q

What are the clinical challenges of diagnosing HCC?

A

Symptoms are often masked by underlying cirrhosis, leading to late detection.

73
Q

What is the serum tumor marker for HCC?

A

Alpha-fetoprotein (AFP).

74
Q

What is more common than primary liver tumors?

A

Metastasis to the liver, most commonly from colon, pancreas, lung, and breast cancers.

75
Q

What is a common presentation of liver metastasis?

A

Multiple liver nodules with hepatomegaly and a nodular free edge.

76
Q

Front

A

Back

77
Q

What is primary biliary cirrhosis (PBC)?

A

An autoimmune granulomatous destruction of intrahepatic bile ducts, commonly in women around age 40.

78
Q

What is primary biliary cirrhosis associated with?

A

Other autoimmune diseases; antimitochondrial antibodies are present.

79
Q

What are the clinical features of primary biliary cirrhosis?

A

Obstructive jaundice with cirrhosis as a late complication.

80
Q

What is primary sclerosing cholangitis (PSC)?

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts.

81
Q

What is the characteristic histological feature of PSC?

A

Periductal fibrosis with an ‘onion-skin’ appearance.

82
Q

What imaging findings are associated with PSC?

A

Dilated, uninvolved bile ducts causing a ‘beaded’ appearance on contrast imaging.

83
Q

What conditions are associated with PSC?

A

Ulcerative colitis; p-ANCA is often positive.

84
Q

What are the complications of PSC?

A

Cirrhosis and increased risk of cholangiocarcinoma.

85
Q

What is Reye syndrome?

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin.

86
Q

What causes Reye syndrome?

A

Likely mitochondrial damage to hepatocytes caused by aspirin use.

87
Q

What are the clinical features of Reye syndrome?

A

Hypoglycemia, elevated liver enzymes, vomiting, and potential progression to coma and death.

88
Q

What is hepatic adenoma?

A

A benign tumor of hepatocytes, often associated with oral contraceptive use.

89
Q

What are the complications of hepatic adenoma?

A

Risk of rupture and intraperitoneal bleeding, especially during pregnancy.

90
Q

What is hepatocellular carcinoma (HCC)?

A

A malignant tumor of hepatocytes.

91
Q

What are the risk factors for HCC?

A

Chronic hepatitis (HBV, HCV), cirrhosis (alcohol, NAFLD, hemochromatosis, Wilson disease, A1AT deficiency), and aflatoxins.

92
Q

What is Budd-Chiari syndrome?

A

Liver infarction secondary to hepatic vein obstruction, presenting with painful hepatomegaly and ascites.

93
Q

What are the clinical challenges of diagnosing HCC?

A

Symptoms are often masked by underlying cirrhosis, leading to late detection.

94
Q

What is the serum tumor marker for HCC?

A

Alpha-fetoprotein (AFP).

95
Q

What is more common than primary liver tumors?

A

Metastasis to the liver, most commonly from colon, pancreas, lung, and breast cancers.

96
Q

What is a common presentation of liver metastasis?

A

Multiple liver nodules with hepatomegaly and a nodular free edge.

97
Q

Front

A

Back

98
Q

What is cirrhosis?

A

Diffuse liver injury with transformation into regenerative nodules surrounded by fibrous bands, associated with chronic liver disease.

99
Q

What are the main causes of cirrhosis?

A

Chronic hepatitis B, chronic hepatitis C, non-alcoholic fatty liver disease (NAFLD), and alcoholic liver disease.

100
Q

What is the pathogenesis of cirrhosis?

A

Hepatocyte injury leads to necrosis/apoptosis, activation of stellate cells into fibrogenic myofibroblasts, and formation of fibrous septae.

101
Q

What are ductular reactions in cirrhosis?

A

Stem cell-mediated duct-like structures seen in chronic liver disease and cirrhosis.

102
Q

What is the morphology of cirrhosis?

A

Diffuse nodular transformation of the liver with regenerative nodules surrounded by fibrous bands.

103
Q

What are the types of primary liver tumors?

A

Hepatocellular carcinoma (HCC), cholangiocarcinomas, hepatoblastoma, and angiosarcoma.

104
Q

What is the most common primary liver tumor?

A

Hepatocellular carcinoma (HCC).

105
Q

What are the risk factors for hepatocellular carcinoma?

A

Chronic hepatitis B and C, cirrhosis, alcohol, aflatoxins, and metabolic disorders like hemochromatosis.

106
Q

What are the most common genetic mutations in HCC?

A

Gain-of-function mutations in beta-catenin and loss-of-function mutations in p53.

107
Q

What is the morphology of HCC?

A

Can appear as unifocal masses, multifocal nodules, or diffusely infiltrative cancer.

108
Q

What is cholelithiasis?

A

The presence of gallstones, often associated with the ‘4Fs’: fat, female, fertile, and forty.

109
Q

What are the types of gallstones?

A

Pure (cholesterol, pigment, calcium carbonate), mixed, and combined gallstones.

110
Q

What is the pathogenesis of cholesterol gallstones?

A

Supersaturation of bile with cholesterol, gallbladder stasis, and mucus hypersecretion leading to crystal aggregation.

111
Q

What causes pigment stones?

A

High unconjugated bilirubin in bile due to hemolysis or biliary infections, forming calcium bilirubinate salts.

112
Q

What are the characteristics of cholesterol stones?

A

Yellow, radiolucent stones found in the gallbladder, sometimes with calcium carbonate making them radiopaque.

113
Q

What is the difference between black and brown pigment stones?

A

Black stones form in sterile bile, while brown stones form in infected intrahepatic or extrahepatic bile ducts.

114
Q

What are common benign gallbladder tumors?

A

Adenomyoma (most common), adenoma, lipoma, fibroma, and hemangioma.

115
Q

What is the most common malignant gallbladder tumor?

A

Adenocarcinoma, accounting for 90% of malignant cases.

116
Q

What is the pathogenesis of pigment gallstones?

A

Increased unconjugated bilirubin in bile leads to calcium bilirubinate precipitates, forming black or brown stones.

117
Q

What is the role of aflatoxins in HCC?

A

Aflatoxins induce TP53 mutations, increasing the risk of hepatocellular carcinoma.

118
Q

Front

A

Back

119
Q

What is the cause of jaundice in paravascular hemolysis or ineffective erythropoiesis?

A

High levels of unconjugated bilirubin (UCB) overwhelm the liver’s conjugating ability.

120
Q

What are the laboratory findings in paravascular hemolysis or ineffective erythropoiesis?

A

Increased UCB and dark urine due to increased urine urobilinogen (UCB is not water soluble).

121
Q

What is the risk associated with paravascular hemolysis?

A

Increased risk for pigmented bilirubin gallstones.

122
Q

What causes physiologic jaundice of the newborn?

A

Transiently low UGT activity in the newborn liver.

123
Q

What are the clinical features of physiologic jaundice of the newborn?

A

Increased UCB, risk of kernicterus (UCB deposits in basal ganglia), neurological deficits, and death.

124
Q

What is the treatment for physiologic jaundice of the newborn?

A

Phototherapy, which makes UCB water-soluble.

125
Q

What is Gilbert syndrome?

A

An autosomal recessive condition with mildly low UGT activity, causing increased UCB.

126
Q

When does jaundice occur in Gilbert syndrome?

A

During periods of stress (e.g., severe infection); otherwise, it is not clinically significant.

127
Q

What is Crigler-Najjar syndrome?

A

An autosomal recessive disorder with an absence of UGT, leading to severe UCB elevation.

128
Q

What are the clinical features of Crigler-Najjar syndrome?

A

Kernicterus, which is usually fatal.

129
Q

What is Dubin-Johnson syndrome?

A

An autosomal recessive disorder with a deficiency in bilirubin canalicular transport protein, causing increased conjugated bilirubin (CB).

130
Q

What is a characteristic feature of Dubin-Johnson syndrome?

A

Darkly pigmented liver, but it is otherwise not clinically significant.

131
Q

What is Rotor syndrome?

A

Similar to Dubin-Johnson syndrome but lacks liver discoloration.

132
Q

What causes obstructive jaundice?

A

Biliary tract obstruction due to gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, or liver flukes (e.g., Clonorchis sinensis).

133
Q

What are the laboratory findings in obstructive jaundice?

A

Increased CB, decreased urine urobilinogen, and increased alkaline phosphatase.

134
Q

What are the clinical features of obstructive jaundice?

A

Dark urine (bilirubinuria), pale stools, pruritus (due to increased plasma bile acids), hypercholesterolemia with xanthomas, and steatorrhea.

135
Q

What causes jaundice in viral hepatitis?

A

Inflammation disrupting hepatocytes and small bile ductules.

136
Q

What are the laboratory findings in viral hepatitis?

A

Increased CB and UCB.

137
Q

What are the clinical features of viral hepatitis?

A

Dark urine due to increased urine bilirubin, with normal or decreased urine urobilinogen.

138
Q

Front

A

Back

139
Q

What is the transmission route for Hepatitis A (HAV) and Hepatitis E (HEV)?

A

Fecal-oral transmission.

140
Q

What are common sources of HAV and HEV infection?

A

HAV: Travelers; HEV: Contaminated water or undercooked seafood.

141
Q

Do HAV and HEV cause chronic hepatitis?

A

No, they only cause acute hepatitis.

142
Q

What serologic markers indicate active HAV or HEV infection?

A

Anti-virus IgM indicates active infection.

143
Q

What does the presence of Anti-HAV IgG indicate?

A

Prior infection or immunization (available for HAV only).

144
Q

What is HEV infection in pregnancy associated with?

A

Fulminant hepatitis (liver failure with massive necrosis).

145
Q

What is the transmission route for Hepatitis B (HBV)?

A

Parenteral (e.g., childbirth, unprotected intercourse, intravenous drug abuse).

146
Q

What is the chronicity rate of HBV infection?

A

Chronic disease occurs in 20% of cases.

147
Q

What is the transmission route for Hepatitis C (HCV)?

A

Parenteral (e.g., intravenous drug abuse, unprotected intercourse, needle stick).

148
Q

What is the risk of transfusion-related HCV infection?

A

Almost nonexistent due to blood supply screening.

149
Q

What is the chronicity rate of HCV infection?

A

Chronic disease occurs in most cases.

150
Q

What test confirms HCV infection?

A

HCV-RNA test.

151
Q

What indicates recovery from HCV?

A

Decreased HCV-RNA levels.

152
Q

What is required for Hepatitis D (HDV) infection?

A

HBV infection is necessary for HDV replication.

153
Q

Which is more severe: HDV superinfection or coinfection?

A

Superinfection upon existing HBV is more severe.

154
Q

What is the first serologic marker to rise in acute HBV infection?

A

HBsAg.

155
Q

What indicates active replication and infectivity in HBV?

A

HBeAg or HBV-DNA presence.

156
Q

What serologic markers are present in the window phase of HBV?

A

Anti-HBc IgM.

157
Q

What serologic markers are present in resolved HBV infection?

A

Anti-HBc IgG and Anti-HBs IgG (protective).

158
Q

What defines chronic HBV infection?

A

HBsAg persistence for more than 6 months.

159
Q

What serologic marker is seen in individuals vaccinated against HBV?

A

Anti-HBs IgG (protective).

BLOCK POSTING 2 (11 decks)

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