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Path 18

front 1

Hepatitis ___: This is typically an acute, short-term infection spread through contaminated food or water that does not lead to chronic liver disease.

back 1

A

front 2

Hepatitis ___: It is transmitted through infected blood, sexual contact, or from mother to child during birth and can transition from an acute illness into a lifelong chronic infection (but rarely)

back 2

B

front 3

Hepatitis ___: Primarily spread through blood-to-blood contact (often via shared needles), this type is notorious for being a "silent" infection that becomes chronic in the majority of cases.

back 3

C

front 4

Hepatitis ___: This unique "satellite" virus can only infect people who already have Hepatitis B, as it requires the B virus to replicate.

back 4

D

front 5

Hepatitis ___: Similar to Type A, it is usually spread via the fecal-oral route through tainted water and is generally acute, though it poses a significant risk to pregnant women.

back 5

E

front 6

A patient is developing jaundice from rising bilirubin levels. Which finding is most likely to appear first on physical exam?
A. Diffuse yellowing of trunk skin
B. Yellow discoloration of sclera
C. Orange discoloration of palms
D. Pale conjunctiva without icterus

back 6

B. Yellow discoloration of sclera

front 7

A patient has chronic hemolysis with increased bilirubin production that exceeds the liver’s conjugating capacity. Which condition best explains this mechanism?
A. Extravascular hemolysis causing jaundice
B. Rotor syndrome causing black liver
C. Obstructive jaundice from gallstones
D. Viral hepatitis with duct inflammation

back 7

A. Extravascular hemolysis causing jaundice

front 8

A patient with anemia develops jaundice and is noted to have a higher risk of pigmented bilirubin gallstones. Which underlying process best fits this presentation?
A. Extrahepatic bile duct obstruction
B. Increased bilirubin production from hemolysis
C. Impaired canalicular bilirubin transport
D. Hepatocyte inflammation from hepatitis

back 8

B. Increased bilirubin production from hemolysis

this is Extravascular hemolysis causing jaundice

front 9

A jaundiced patient has dark urine, but the bilirubin responsible for the jaundice itself is not present in the urine because it is not water soluble. What most likely explains the dark urine?
A. Bilirubinuria from obstructive disease
B. Increased urinary urobilinogen excretion
C. Hematuria from renal pigment injury
D. Excess ketones from fasting state

back 9

B. Increased urinary urobilinogen excretion

front 10

A newborn develops jaundice shortly after birth because the liver temporarily has low activity of UGT needed for bilirubin conjugation. What is the most likely diagnosis?
A. Gilbert syndrome
B. Crigler-Najjar syndrome
C. Physiologic jaundice of the newborn
D. Dubin-Johnson syndrome

back 10

C. Physiologic jaundice of the newborn

front 11

A neonate with severe jaundice is at risk for bilirubin deposition in the basal ganglia, causing permanent neurologic injury. Which complication is this?
A. Kernicterus
B. Hepatic encephalopathy
C. Wilson degeneration
D. Subdural hematoma

back 11

A. Kernicterus

Physiologic jaundice of the newborn

front 12

A newborn with jaundice is treated with light exposure that converts UCB into a more water-soluble form. Which treatment was used?
A. Exchange transfusion
B. Phototherapy
C. Ursodiol therapy
D. Iron chelation

back 12

B. Phototherapy

Physiologic jaundice of the newborn

front 13

A healthy young adult has intermittent jaundice only during periods of physiologic stress, such as severe infection. The disorder is otherwise not clinically significant. Which diagnosis is most likely?
A. Crigler-Najjar syndrome
B. Gilbert syndrome
C. Biliary tract obstruction
D. Viral hepatitis

back 13

B. Gilbert syndrome

front 14

A patient has an inherited disorder caused by mildly decreased UGT activity and is otherwise asymptomatic except during stress. What is the inheritance pattern of this condition?
A. X-linked dominant
B. Autosomal dominant
C. Mitochondrial
D. Autosomal recessive

back 14

D. Autosomal recessive

this is Gilbert syndrome

front 15

An infant has a complete absence of UGT1A1 activity and rapidly develops severe neurologic injury from bilirubin deposition. Which syndrome is most likely?
A. Rotor syndrome
B. Crigler-Najjar syndrome
C. Gilbert syndrome
D. Physiologic newborn jaundice

back 15

B. Crigler-Najjar syndrome

front 16

A child has profound jaundice due to complete failure of bilirubin conjugation and develops kernicterus. What is the usual prognosis without effective intervention?
A. Usually self-limited
B. Usually benign
C. Usually fatal
D. Usually relapsing-remitting

back 16

C. Usually fatal

front 17

A patient has an inherited defect in the canalicular transport protein (MRP2) that normally moves bilirubin into bile. Which diagnosis is most likely?
A. Dubin-Johnson syndrome
B. Gilbert syndrome
C. Viral hepatitis
D. Extravascular hemolysis

back 17

A. Dubin-Johnson syndrome

front 18

A patient with chronic jaundice is found incidentally to have a darkly pigmented liver, but is otherwise largely asymptomatic. Which syndrome best fits this picture?
A. Rotor syndrome
B. Dubin-Johnson syndrome
C. Crigler-Najjar syndrome
D. Physiologic neonatal jaundice

back 18

A. Dubin-Johnson syndrome

front 19

A patient has a disorder very similar to Dubin-Johnson syndrome but lacks liver discoloration. Which diagnosis is this comparison describing?
A. Gilbert syndrome
B. Rotor syndrome
C. Viral hepatitis
D. Biliary atresia

back 19

B. Rotor syndrome

front 20

A patient presents with jaundice, intense itching, pale stools, and dark urine. Which mechanism best explains this presentation?
A. Hemolysis overwhelming conjugation
B. Impaired bilirubin uptake into spleen
C. Obstruction of bile flow to intestine
D. Decreased albumin production alone

back 20

C. Obstruction of bile flow to intestine

Biliary tract obstruction

front 21

A patient with jaundice is also found to have xanthomas and pruritus due to retained bile acids. Which disease process most strongly fits this constellation?
A. Viral hepatitis
B. Biliary tract obstruction
C. Gilbert syndrome
D. Crigler-Najjar syndrome

back 21

B. Biliary tract obstruction

front 22

A patient with obstructive jaundice develops greasy stools and deficiency of fat-soluble vitamins. What is the most direct explanation?
A. Failure of bile delivery impairs fat absorption
B. Renal loss of vitamins causes deficiency
C. Pancreatic insulin deficiency limits uptake
D. Splenic sequestration reduces lipid transport

back 22

A. Failure of bile delivery impairs fat absorption

Biliary tract obstruction

front 23

A patient with jaundice is found to have a biliary obstruction. Which underlying cause is specifically associated with this disorder?
A. Severe UGT deficiency
B. Defective canalicular transporter
C. Clonorchis sinensis infestation
D. Basal ganglia bilirubin deposition

back 23

C. Clonorchis sinensis infestation

Biliary tract obstruction

front 24

A patient develops jaundice in the setting of pancreatic carcinoma compressing the biliary tree. Which broader category does this belong to?
A. Obstructive jaundice
B. Hemolytic jaundice
C. Neonatal jaundice
D. Hereditary conjugation defect

back 24

A. Obstructive jaundice

front 25

A patient with liver inflammation develops jaundice because both hepatocytes and small bile ductules are disrupted. Which diagnosis best fits this mechanism?
A. Dubin-Johnson syndrome
B. Viral hepatitis
C. Gilbert syndrome
D. Extravascular hemolysis

back 25

B. Viral hepatitis

front 26

A patient with jaundice has dark urine, but the mechanism is increased urinary bilirubin rather than increased urinary urobilinogen. Which diagnosis best fits that distinction?
A. Extravascular hemolysis
B. Physiologic newborn jaundice
C. Viral hepatitis
D. Gilbert syndrome

back 26

C. Viral hepatitis

front 27

what two are only increased in Conjucated Bilirubin?

back 27

dubin-johnson

biliary tract obstruction

front 28

what is this?

back 28

cirrhosis

front 29

A male patient with chronic liver disease develops gynecomastia, spider angiomata, and palmar erythema. What is the most likely cause of these findings?
A. Increased androgen production from adrenal glands
B. Decreased hepatic metabolism of circulating estrogen
C. Excess bile acid deposition in the skin

back 29

B. Decreased hepatic metabolism of circulating estrogen

front 30

A patient with liver failure develops jaundice. Which mechanism best explains this presentation?
A. Increased conjugation of bilirubin in hepatocytes
B. Enhanced renal excretion of bilirubin
C. Decreased metabolism of unconjugated bilirubin

back 30

C. Decreased metabolism of unconjugated bilirubin

front 31

A patient with cirrhosis presents with confusion and a flapping tremor of the hands. Which underlying mechanism best explains these neurologic findings?
A. Accumulation of ammonia due to impaired detoxification
B. Increased bilirubin deposition in peripheral nerves
C. Decreased glucose uptake by neurons

back 31

A. Accumulation of ammonia due to impaired detoxification

front 32

rmbr that the liver does protein synthesis and clotting factor synthesis, so messed up liver would lead to

back 32

less protein/albumin

bleeding

front 33

is pt or ptt used to monitor cirrhosis liver destruction

back 33

pt

similar to warfarin

front 34

alcohol-related liver disease: damage to hepatic ______ due to consumption of alc

back 34

parenchyma

front 35

______ ______

back 35

fatty liver

front 36

A patient presents with acute liver injury after a weekend of heavy binge drinking. The hepatocyte damage is primarily mediated by accumulation of which toxic metabolite?
A. Acetaldehyde
B. Acetone
C. Lactate
D. Pyruvate

back 36

A. Acetaldehyde

front 37

A patient with alcoholic hepatitis develops liver injury due to a toxic intermediate formed during ethanol metabolism. Which step in ethanol metabolism produces this harmful compound?
A. Conversion of ethanol to acetaldehyde
B. Conversion of acetaldehyde to acetate
C. Conversion of acetate to acetyl-CoA
D. Conversion of NADH to NAD⁺

back 37

A. Conversion of ethanol to acetaldehyde

front 38

A patient with a history of heavy alcohol use presents with right upper quadrant pain and hepatomegaly. Laboratory studies show elevated transaminases with AST significantly higher than ALT. What is the most likely explanation for this enzyme pattern?
A. Preferential mitochondrial injury increasing AST release
B. Increased cytosolic enzyme release favoring ALT
C. Selective inhibition of AST synthesis in hepatocytes
D. Enhanced renal clearance of ALT from circulation

back 38

A. Preferential mitochondrial injury increasing AST release

front 39

A patient with obesity and no history of alcohol use is found to have elevated liver enzymes on routine testing. Further evaluation excludes viral, toxic, and other known causes of liver injury. Which diagnosis best fits a disorder that can range from simple fatty change to hepatitis and eventually cirrhosis?
A. Alcoholic hepatitis
B. Nonalcoholic fatty liver disease
C. Dubin-Johnson syndrome
D. Acute viral hepatitis

back 39

B. Nonalcoholic fatty liver disease

front 40

An obese patient with chronically elevated transaminases undergoes evaluation for liver disease. He denies alcohol use, and workup for other known hepatic insults is negative. Which laboratory pattern would most support the suspected diagnosis?
A. AST greater than ALT
B. AST equal to ALT
C. ALT greater than AST
D. Isolated alkaline phosphatase elevation

back 40

C. ALT greater than AST

front 41

A 52-year-old man presents with fatigue, joint pain, and mild hepatomegaly. Labs show elevated liver enzymes. Over time, he develops diabetes and restrictive cardiomyopathy. Liver biopsy shows iron deposition within hepatocytes. Which mechanism best explains the cellular injury leading to this patient’s organ dysfunction?
A. Direct inhibition of mitochondrial DNA replication by iron
B. Free radical formation causing lipid membrane damage
C. Immune-mediated cytotoxic T-cell destruction of hepatocytes
D. Impaired bilirubin conjugation leading to cholestasis

back 41

B. Free radical formation causing lipid membrane damage

hemochromatosis

front 42

primary or secondary hemochromatosis?

damage to the HFE gene, most commonly C282Y

back 42

primary

front 43

primary or secondary hemochromatosis?

complications of transfusions

back 43

hemochromatosis

front 44

back 44

hemochromatosis

front 45

back 45

hemochromatosis

front 46

A patient is diagnosed with an inherited disorder affecting copper handling in hepatocytes. The mutation disrupts an ATP-dependent transport process. Which immediate consequence most directly results from this defect?
A. Failure to transport copper into bile
B. Increased renal excretion of copper
C. Enhanced incorporation of copper into ceruloplasmin
D. Increased intestinal absorption of copper

back 46

A. Failure to transport copper into bile

front 47

A patient with an autosomal recessive defect in the ATP7B gene has impaired copper metabolism. Which combination of abnormalities best reflects the primary defect in hepatocyte function?
A. Increased copper secretion into bile and plasma
B. Decreased copper incorporation into ceruloplasmin
C. Increased binding of copper to albumin
D. Enhanced copper storage in lysosomes only

back 47

B. Decreased copper incorporation into ceruloplasmin

front 48

A patient with a copper metabolism disorder develops progressive liver dysfunction and later presents with confusion and movement abnormalities. Which additional finding would most strongly support the same underlying disease process?
A. Kayser-Fleischer rings in the cornea
B. Elevated alkaline phosphatase only
C. Isolated increase in LDL cholesterol
D. Decreased pancreatic enzyme secretion

back 48

A. Kayser-Fleischer rings in the cornea

front 49

Best initial treatment for Wilson disease:
A. Oral zinc alone
B. IV iron chelation
C. Copper chelators (penicillamine, trientine)
D. Eliminate dietary fructose

back 49

C. Copper chelators (penicillamine, trientine)

front 50

Typical diagnostic profile in Wilson disease:
A. ↑Ceruloplasmin, ↓urine copper
B. ↓Ceruloplasmin, ↑urine copper
C. Normal ceruloplasmin, normal urine Cu
D. ↓Ceruloplasmin, ↓liver copper

back 50

B. ↓Ceruloplasmin, ↑urine copper

front 51

Hereditary hemochromatosis is mainly a disorder of:
A. Excessive iron storage
B. Excessive copper storage
C. Defective zinc export
D. Defective manganese uptake

back 51

B. Excessive copper storage

front 52

The commonest HH mutation:
A. Frameshift in HFE promoter
B. Missense in ATP7B gene
C. Deletion of SLC39A4 exon
D. Tyr→Cys missense in HFE

back 52

A. Frameshift in HFE promoter

front 53

HFE normally binds the transferrin receptor to help induce:
A. Ceruloplasmin
B. Ferritin
C. Hepcidin
D. Albumin

back 53

C. Hepcidin

front 54

In HH, decreased hepcidin leads to:
A. Increased free iron
B. Decreased intestinal iron
C. Severe hypoferritinemia
D. Increased iron in urine

back 54

A. Increased free iron

front 55

HH is usually inherited as:
A. X-linked recessive
B. Autosomal dominant
C. Mitochondrial
D. Autosomal recessive

back 55

D. Autosomal recessive

front 56

A middle-aged patient presents with fatigue and pruritus. Liver biopsy shows lymphocytic and granulomatous destruction of small intrahepatic bile ducts (florid duct lesion). Which mechanism best explains the underlying pathogenesis of this condition?
A. T cell–mediated autoimmune destruction of bile ducts
B. Direct toxic injury to hepatocytes from bile acids
C. Obstruction of extrahepatic bile ducts by stones
D. Increased bilirubin production from hemolysis

back 56

A. T cell–mediated autoimmune destruction of bile ducts

Primary biliary cholangitis

front 57

A patient with chronic cholestatic liver disease undergoes biopsy showing bile duct destruction and hepatocytes with feathery degeneration. What is the most direct cause of this hepatocyte change?
A. Accumulation of bile components within hepatocytes
B. Excess iron deposition causing oxidative damage
C. Viral-mediated cytotoxic injury to hepatocytes
D. Increased glycogen storage within liver cells

back 57

A. Accumulation of bile components within hepatocytes

front 58

A patient with inflammatory bowel disease develops progressive cholestasis. Which additional finding would most strongly support a diagnosis of primary sclerosing cholangitis?
A. Association with HLA alleles and autoantibodies
B. Isolated hepatocyte necrosis without duct involvement
C. Increased iron deposition within hepatocytes
D. Accumulation of copper due to transport defect

back 58

A. Association with HLA alleles and autoantibodies

front 59

A patient with chronic cholestatic liver disease is found to have alternating strictures and dilation of large bile ducts on imaging. Biopsy shows inflammation with periductal fibrosis. Which mechanism best explains the underlying disease process?
A. T cell–mediated immune injury to bile ducts
B. Obstruction of ducts by gallstones
C. Direct hepatocyte toxicity from bile acids
D. Increased bilirubin production from hemolysis

back 59

A. T cell–mediated immune injury to bile ducts

This describes Primary sclerosing cholangitis.

front 60

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

related to mitochondrial damage of hepatocytes

back 60

Reye syndrome

front 61

A 24-year-old woman using oral contraceptives is found to have a well-circumscribed benign liver mass. Which diagnosis is most likely?

A. Hepatocellular adenoma
B. Hepatoblastoma
C. Cholangiocarcinoma
D. Hemangioma

back 61

A. Hepatocellular adenoma

front 62

Hepatocellular adenoma is most strongly associated with oral contraceptives and:

A. Estrogen withdrawal
B. Anabolic steroids
C. Viral hepatitis
D. Pregnancy alone

back 62

B. Anabolic steroids

front 63

The most common liver tumor of early childhood is:

A. Hepatocellular adenoma
B. Hepatoblastoma
C. Angiosarcoma
D. Focal nodular hyperplasia

back 63

B. Hepatoblastoma

front 64

Widespread parenchymal injury causing zonal loss of contiguous hepatocytes is called:

A. Interface hepatitis
B. Confluent necrosis
C. Spotty necrosis
D. Ballooning degeneration

back 64

B. Confluent necrosis

front 65

The principal liver cell responsible for scar deposition is the:

A. Kupffer cell
B. Hepatocyte
C. Hepatic stellate cell
D. Cholangiocyte

back 65

C. Hepatic stellate cell

front 66

The most severe form of liver disease is:

A. Steatosis
B. Hepatitis
C. Cholestasis
D. Liver failure

back 66

D. Liver failure

front 67

Acute liver failure usually follows:

A. Slow portal fibrosis
B. Chronic biliary obstruction
C. Mild steatosis
D. Sudden massive destruction

back 67

D. Sudden massive destruction

front 68

Chronic liver failure more often follows:

A. Insidious progressive injury
B. Fulminant drug overdose
C. Isolated portal thrombosis
D. Acute bacterial sepsis

back 68

A. Insidious progressive injury

front 69

Acute liver failure is defined by acute liver illness with encephalopathy and:

A. Hyperbilirubinemia
B. Coagulopathy
C. Portal thrombosis
D. Neutropenia

back 69

B. Coagulopathy

front 70

Acute liver failure must occur within what time from the initial injury?

A. 12 weeks
B. 52 weeks
C. 26 weeks
D. 6 weeks

back 70

C. 26 weeks

front 71

Acute liver failure is usually associated with:

A. Massive hepatic necrosis
B. Portal lymphocytosis
C. Bile duct hyperplasia
D. Fatty sparing

back 71

A. Massive hepatic necrosis

front 72

Chronic liver failure is most often associated with advanced fibrosis and:

A. Steatohepatitis
B. Cholangitis
C. Cirrhosis
D. Hemochromatosis

back 72

C. Cirrhosis

front 73

Cirrhosis features diffuse remodeling into parenchymal nodules surrounded by:

A. Fat vacuoles
B. Fibrous bands
C. Sinusoidal thrombi
D. Bile lakes

back 73

B. Fibrous bands

front 74

Cirrhosis often includes a variable degree of:

A. Bacterial translocation
B. Arterial vasospasm
C. Lymphatic obstruction
D. Portosystemic shunting

back 74

D. Portosystemic shunting

front 75

Grossly, cirrhosis converts the smooth liver capsule into a:

A. Pale glassy sheet
B. Soft friable mass
C. Bumpy scarred surface
D. Uniform fatty surface

back 75

C. Bumpy scarred surface

front 76

The depressed scars and bulging nodules of cirrhosis reflect:

A. Necrotizing vasculitis
B. Regeneration and fibrosis
C. Iron deposition only
D. Acute cholestasis

back 76

B. Regeneration and fibrosis

front 77

Portal hypertension results partly from increased resistance to portal flow at the level of the:

A. Central veins
B. Portal venules
C. Hepatic arteries
D. Sinusoids

back 77

D. Sinusoids

front 78

Portal hypertension also involves increased portal flow due to:

A. Portal thrombosis
B. Hyperdynamic circulation
C. Hepatic infarction
D. Splenic rupture

back 78

B. Hyperdynamic circulation

front 79

Which is a major consequence of portal hypertension?

A. Ascites
B. Acute pancreatitis
C. Cholelithiasis
D. Hepatic adenoma

back 79

A. Ascites

front 80

Another major consequence of portal hypertension is formation of:

A. Regenerative nodules
B. Portosystemic shunts
C. Mallory bodies
D. Ground-glass cells

back 80

B. Portosystemic shunts

front 81

Portal hypertension commonly also causes congestive:

A. Hepatomegaly
B. Nephromegaly
C. Splenomegaly
D. Cardiomegaly

back 81

C. Splenomegaly

front 82

Which listed consequence of portal hypertension is commonly discussed under liver failure?

A. Ascites
B. Encephalopathy
C. Splenomegaly
D. Variceal bleeding

back 82

B. Encephalopathy

front 83

Hepatitis B can result in acute hepatitis followed by:

A. Carrier conversion only
B. Recovery and clearance
C. Immediate cirrhosis
D. Cholangiocarcinoma

back 83

B. Recovery and clearance

front 84

A severe possible consequence of hepatitis B is:

A. Massive liver necrosis
B. Amyloid deposition
C. Iron overload
D. Fat embolism

back 84

A. Massive liver necrosis

front 85

Hepatitis B may also produce chronic hepatitis with or without progression to:

A. Steatosis
B. Fibrosis only
C. Cirrhosis
D. Abscess

back 85

C. Cirrhosis

front 86

Which hepatitis B outcome may be clinically silent?

A. Healthy carrier state
B. Acute fatty liver
C. Fulminant cholangitis
D. Budd-Chiari syndrome

back 86

A. Healthy carrier state

front 87

Hepatitis C rarely causes:

A. Chronic hepatitis
B. Symptomatic acute hepatitis
C. Cirrhosis later
D. Persistent infection

back 87

B. Symptomatic acute hepatitis

front 88

Hepatitis C is the most common cause of:

A. Acute liver failure
B. Chronic viral hepatitis
C. Neonatal cholestasis
D. Hepatic adenoma

back 88

B. Chronic viral hepatitis

front 89

Chronic hepatitis requires continuing or relapsing hepatic disease for more than:

A. 3 months
B. 12 months
C. 6 months
D. 1 month

back 89

C. 6 months

front 90

Chronic hepatitis may also be defined morphologically by the presence of:

A. Steatosis
B. Fibrosis
C. Necrosis only
D. Bile plugs

back 90

B. Fibrosis

front 91

The defining histologic feature of chronic viral hepatitis is portal inflammation with:

A. Granulomas
B. Eosinophils
C. Neutrophils
D. Fibrosis

back 91

D. Fibrosis

front 92

The portal inflammatory infiltrate in chronic viral hepatitis is typically:

A. Lymphocytic or lymphoplasmacytic
B. Neutrophilic or eosinophilic
C. Histiocytic or giant-cell
D. Fibrinous or suppurative

back 92

A. Lymphocytic or lymphoplasmacytic

front 93

In chronic hepatitis B, hepatocytes may show a ground-glass appearance due to accumulation of:

A. HCV core protein
B. HBsAg in ER
C. Iron in lysosomes
D. Copper in cytosol

back 93

B. HBsAg in ER

front 94

Infectious agents that can involve the liver and biliary tree include bacteria, fungi, helminths, and:

A. Prions
B. Mycobacteria only
C. Protozoa/parasites
D. Rickettsiae only

back 94

C. Protozoa/parasites

front 95

Autoimmune hepatitis is a chronic progressive hepatitis associated with genetic predisposition, autoantibodies, and response to:

A. Antibiotics
B. Anticoagulation
C. Immunosuppression
D. Antivirals

back 95

C. Immunosuppression

front 96

Which finding supports the diagnosis of autoimmune hepatitis?

A. Low serum IgG
B. Elevated serum IgG
C. Undetectable antibodies
D. Portal vein thrombosis

back 96

B. Elevated serum IgG

front 97

Diagnosis of autoimmune hepatitis requires exclusion of other etiologies such as:

A. Viral hepatitis and drugs
B. Diabetes and obesity
C. Gallstones and pancreatitis
D. Trauma and ischemia

back 97

A. Viral hepatitis and drugs

front 98

A supportive study in autoimmune hepatitis is:

A. Renal biopsy
B. Bone marrow aspirate
C. Liver biopsy
D. ERCP

back 98

C. Liver biopsy

front 99

In the United States, a major cause of acute liver failure is:

A. Drug- or toxin-induced injury
B. Wilson disease only
C. Autoimmune cholangitis
D. Hepatoblastoma

back 99

A. Drug- or toxin-induced injury

front 100

The classic dose-dependent predictable hepatotoxin is:

A. Isoniazid
B. Methotrexate
C. Acetaminophen
D. Halothane

back 100

C. Acetaminophen

front 101

In the United States, the most common cause of acute liver failure requiring transplantation is:

A. Hepatitis B
B. Acetaminophen toxicity
C. Alcoholic hepatitis
D. Budd-Chiari syndrome

back 101

B. Acetaminophen toxicity

front 102

Excessive alcohol intake causes steatosis and dysfunction of mitochondria, microtubules, cellular membranes, and:

A. Cholangiolar transport
B. Oxidative stress pathways
C. Portal venous return
D. Urea excretion

back 102

B. Oxidative stress pathways

front 103

Alcohol-related liver injury ultimately leads to varying degrees of inflammation and:

A. Portal granulomas
B. Bile duct loss
C. Hepatocyte death
D. Splenic infarction

back 103

C. Hepatocyte death

front 104

Which finding is characteristic of hemochromatosis?

A. Hypopigmented skin
B. Pancreatic islet destruction
C. Decreased cardiac output only
D. Isolated nephropathy

back 104

B. Pancreatic islet destruction

front 105

A patient with iron overload has arrhythmias, diabetes, bronzed skin, and arthropathy. Which diagnosis is most likely?

A. Wilson disease
B. α1AT deficiency
C. Hemochromatosis
D. Preeclampsia

back 105

C. Hemochromatosis

front 106

α1-antitrypsin deficiency is characterized in hepatocytes by:

A. Ground-glass cytoplasm
B. Fat vacuoles
C. Mallory bodies
D. Cytoplasmic globular inclusions

back 106

D. Cytoplasmic globular inclusions

front 107

Obstruction of the major hepatic veins causing liver enlargement, pain, and ascites is called:

A. Budd-Chiari syndrome
B. Gilbert syndrome
C. Rotor syndrome
D. Fitz-Hugh-Curtis syndrome

back 107

A. Budd-Chiari syndrome

front 108

In preeclampsia, periportal sinusoids contain:

A. Copper granules
B. Fibrin deposits
C. Bile thrombi
D. Amyloid deposits

back 108

B. Fibrin deposits

front 109

In preeclampsia, hemorrhage into the space of Disse leads to periportal hepatocellular:

A. Apoptosis
B. Ballooning
C. Coagulative necrosis
D. Steatosis

back 109

C. Coagulative necrosis

front 110

Acute fatty liver of pregnancy can range from mild aminotransferase elevation to:

A. Portal fibrosis only
B. Hepatic failure and coma
C. Chronic hepatitis only
D. Budd-Chiari syndrome

back 110

B. Hepatic failure and coma