Cirrhosis and its complications

Question 1

Which of the following is a characteristic feature of decompensated cirrhosis?
A. Bridging fibrosis without nodularity
B. Jaundice, hypoalbuminemia, and coagulopathy
C. Presence of ascites, variceal bleeding, or hepatic encephalopathy
D. Stable liver function without complications

Answer 1

Correct Answer: C
Rationale: Decompensated cirrhosis is defined by clinical features such as ascites, variceal bleeding, or hepatic encephalopathy. These signify the failure of the liver to maintain its compensatory mechanisms. While jaundice, hypoalbuminemia, and coagulopathy (Answer B) are signs of liver dysfunction, they are more associated with hepatocellular failure than the defining clinical events of decompensation.

Question 2

What is the most appropriate management step for a patient with decompensated cirrhosis and uncontrolled ascites?
A. Observation and routine follow-up
B. Initiation of lifestyle modifications
C. Consideration for liver transplantation
D. Administration of antiviral therapy

Answer 2

Correct Answer: C
Rationale: Patients with decompensated cirrhosis and poorly controlled complications (e.g., ascites) should be evaluated for liver transplantation. Observation (Answer A) and lifestyle modifications (Answer B) alone are insufficient to address the severity of decompensation. Antiviral therapy (Answer D) may be appropriate in certain etiologies (e.g., hepatitis B or C), but the focus here should be on definitive treatment via transplantation.

Question 3

What is the defining characteristic of micronodular cirrhosis seen in alcohol-associated liver disease?
A. Nodules larger than 3 mm in diameter
B. Presence of both macro- and micronodules
C. Nodules smaller than 3 mm in diameter
D. Absence of fibrosis

Answer 3

Correct Answer: C
Rationale: Micronodular cirrhosis, commonly associated with alcohol-related liver disease, is characterized by nodules that are less than 3 mm in diameter. Larger nodules (>3 mm) are indicative of macronodular or mixed forms of cirrhosis, which can develop after cessation of alcohol use.

Question 4

How does cessation of alcohol use affect the morphology of cirrhosis in alcohol-associated liver disease?
A. Leads to the resolution of all nodules
B. Promotes the development of larger nodules, resulting in mixed cirrhosis
C. Prevents the progression of fibrosis but does not change nodule size
D. Causes an immediate reversal of liver damage

Answer 4

Correct Answer: B
Rationale: Cessation of alcohol use can lead to the development of larger nodules, resulting in a mixed micronodular and macronodular pattern of cirrhosis. This reflects ongoing liver remodeling and partial regeneration. Complete reversal of cirrhosis (Answer D) does not typically occur.

Question 5

Which of the following best describes the liver morphology in advanced alcohol-associated cirrhosis after sustained abstinence?
A. Uniformly micronodular cirrhosis
B. Mixed micronodular and macronodular cirrhosis
C. Complete resolution of cirrhosis
D. Fibrosis without nodularity

Answer 5

Correct Answer: B
Rationale: After sustained abstinence from alcohol, the liver may undergo remodeling, resulting in a mixed pattern of micronodular and macronodular cirrhosis. This reflects some regenerative capacity of the liver, though cirrhosis itself persists.

Question 6

Which of the following findings on physical examination is most suggestive of advanced alcohol-associated cirrhosis?
A. Enlarged, smooth liver edge
B. Scleral icterus, gynecomastia, and muscle wasting
C. Tender hepatomegaly with no nodularity
D. Isolated splenomegaly without other signs

Answer 6

Correct Answer: B
Rationale: Advanced alcohol-associated cirrhosis is characterized by multiple clinical signs, including scleral icterus (jaundice), gynecomastia, and muscle wasting, due to hormonal imbalances, liver dysfunction, and malnutrition. A smooth liver edge (Answer A) or isolated splenomegaly (Answer D) are less specific to cirrhosis, and tender hepatomegaly (Answer C) is more typical of alcoholic hepatitis

Question 7

What laboratory abnormality is commonly observed in advanced alcohol-associated cirrhosis?
A. Elevated ALT levels higher than AST levels
B. Prolonged prothrombin time unresponsive to parenteral vitamin K
C. Increased platelet count due to portal hypertension
D. Normal bilirubin levels in the presence of severe disease

Answer 7

Correct Answer: B
Rationale: In advanced alcohol-associated cirrhosis, prolonged prothrombin time that does not improve with vitamin K indicates significant liver dysfunction and impaired synthesis of clotting factors. AST levels are typically higher than ALT levels in a 2:1 ratio (Answer A), and platelet counts are often decreased due to hypersplenism (Answer C). Elevated bilirubin levels (Answer D) are common in severe disease.

Question 8

Which of the following is a unique hematologic complication associated with severe alcoholic hepatitis?
A. Iron deficiency anemia
B. Zieve’s syndrome with hemolytic anemia and spur cells
C. Thrombocytosis
D. Megaloblastic anemia due to folate deficiency

Answer 8

Correct Answer: B
Rationale: Zieve’s syndrome is a rare complication of severe alcoholic hepatitis characterized by hemolytic anemia, spur cells, and acanthocytes. While megaloblastic anemia (Answer D) can occur in alcohol-associated cirrhosis due to folate deficiency, Zieve’s syndrome is distinct to severe alcoholic liver disease.

Question 9

Which laboratory finding is most characteristic of ongoing alcohol use in a patient with alcohol-associated liver disease?
A. Elevated AST levels with an AST/ALT ratio of approximately 2:1
B. Low total bilirubin levels with normal liver enzymes
C. Elevated platelet counts with prolonged prothrombin time
D. High serum sodium levels despite ascites

Answer 9

Correct Answer: A
Rationale: The AST/ALT ratio of approximately 2:1 is a hallmark of ongoing alcohol use in alcohol-associated liver disease. Platelet counts (Answer C) are typically reduced due to portal hypertension, and sodium levels (Answer D) are often low in the presence of ascites due to free water retention.

Question 10

What is the cornerstone of therapy for patients with alcohol-associated liver disease?
A. Glucocorticoid therapy
B. Abstinence from alcohol
C. Long-term use of antioxidants
D. Regular administration of vitamin K

Answer 10

Correct Answer: B
Rationale: Abstinence from alcohol is the foundation of treatment for alcohol-associated liver disease, as continued alcohol use exacerbates liver damage and worsens prognosis. While glucocorticoids (Answer A) may be used in specific circumstances, abstinence remains the most critical determinant of long-term survival.

Question 11

In which scenario is glucocorticoid therapy indicated for patients with severe alcoholic hepatitis?
A. Presence of infection and discriminant function (DF) >32
B. DF >32 and absence of infection
C. Mild alcoholic hepatitis with DF <32
D. DF >32 regardless of infection status

Answer 11

Correct Answer: B
Rationale: Glucocorticoid therapy is indicated in patients with severe alcoholic hepatitis (DF >32) and no evidence of infection. Infection is a contraindication as glucocorticoids suppress immune function. DF <32 (Answer C) does not meet the criteria for severe disease requiring glucocorticoids.

Question 12

How is the discriminant function (DF) calculated in patients with severe alcoholic hepatitis?
A. DF = Serumtotalbilirubin + (Patient’sINR−NormalINR)×10
B. DF = (Serumtotalbilirubin×2) +(Prothrombintimedifference×3.5)
C. DF = Serumtotalbilirubin (Prothrombintimedifference) × 4.6
D. DF = (SerumALT+SerumAST)÷2

Answer 12

Correct Answer: C
Rationale: Serumtotalbilirubin(mg/dL)+(Patient’sprothrombintime(seconds)-Controlprothrombintime)×4.6
This formula is used to assess the severity of alcoholic hepatitis and guide treatment decisions.

Question 13

What is the appropriate action if a patient with severe alcoholic hepatitis does not show improvement in total bilirubin levels after 7 days of glucocorticoid therapy?
A. Continue therapy for an additional 7 days
B. Increase the dose of glucocorticoids
C. Discontinue glucocorticoid therapy
D. Start antiviral therapy

Answer 13

Correct Answer: C
Rationale: Failure of total bilirubin levels to improve after 7 days of glucocorticoid therapy predicts treatment failure, and glucocorticoids should be discontinued.

Failure to improve total bilirubin after 7 days predicts treatment failure, and glucocorticoids
can be stopped; otherwise, they are continued for 28 days.

Question 14

Which antiviral agents are preferred for treating hepatitis B in patients with cirrhosis due to their low risk of viral resistance?
A. Lamivudine and telbivudine
B. Adefovir and interferon α
C. Entecavir and tenofovir
D. Pegylated interferon and ribavirin

Answer 14

Correct Answer: C
Rationale: Entecavir and tenofovir are the preferred antiviral agents for treating hepatitis B in cirrhosis because they have a low risk of viral resistance. Lamivudine and telbivudine (Answer A) have higher rates of resistance, and interferon α (Answer B) is contraindicated in cirrhotic patients.

Question 15

What is a key reason direct-acting antiviral (DAA) therapy has revolutionized the treatment of hepatitis C?
A. It is affordable and widely accessible in all countries.
B. It is highly effective, with cure rates exceeding 95%, and is well tolerated.
C. It eliminates the need for liver transplantation in all cases.
D. It has no side effects and requires no monitoring during therapy.

Answer 15

Correct Answer: B
Rationale: Direct-acting antiviral (DAA) therapy has a >95% cure rate for hepatitis C, is well tolerated, and requires a short treatment duration of 8–12 weeks. While it has dramatically improved outcomes, it remains costly (Answer A) and does not eliminate the need for transplantation in advanced cases (Answer C). Some side effects and monitoring (Answer D) may still be necessary.

Question 16

What is a key diagnostic feature for autoimmune hepatitis (AIH) in patients with cirrhosis who do not show active inflammation on liver biopsy?
A. Elevated liver enzymes alone
B. Presence of antinuclear antibody (ANA) or anti-smooth-muscle antibody (ASMA)
C. Radiologic evidence of fatty liver disease
D. Positive viral hepatitis serologies

Answer 16

Correct Answer: B
Rationale: The diagnosis of AIH in cirrhotic patients without active inflammation on liver biopsy relies on positive autoimmune markers such as ANA or ASMA.

Question 17

What is the primary histologic characteristic of PBC?
A. Extensive fibrosis of large bile ducts
B. Portal inflammation and necrosis of cholangiocytes in small- and medium-sized bile ducts
C. Diffuse steatosis of hepatocytes
D. Lobular inflammation and massive hepatocyte necrosis

Answer 17

Correct Answer: B
Rationale: PBC is characterized by portal inflammation and necrosis of cholangiocytes in small- and medium-sized bile ducts. This distinguishes it from other liver diseases like NAFLD (Answer C) or acute viral hepatitis (Answer D).

Question 18

Which laboratory marker is most specific for the diagnosis of PBC?
A. Antinuclear antibodies (ANA)
B. Elevated serum bilirubin levels
C. Antimitochondrial antibodies (AMA)
D. Increased aspartate aminotransferase (AST)

Answer 18

Correct Answer: C
Rationale: AMA is present in approximately 95% of patients with PBC and is highly specific for the disease. Elevated bilirubin (Answer B) and AST (Answer D) are non-specific markers, and ANA (Answer A) is more commonly associated with autoimmune hepatitis.

Question 19

What is the first-line treatment for slowing disease progression in PBC?
A. Ursodeoxycholic acid (UDCA)
B. Liver transplantation
C. Glucocorticoid therapy
D. Interferon α

Answer 19

Correct Answer: A
Rationale: UDCA is the first-line treatment for PBC, as it slows the progression of the disease. Liver transplantation (Answer B) is reserved for patients with decompensated cirrhosis, while glucocorticoids (Answer C) and interferon α (Answer D) are not part of PBC management.

Question 20

Which laboratory findings are most characteristic of PBC?
A. Significant elevations in ALT and AST with normal ALP
B. Elevated γ-glutamyl transpeptidase (GGT) and alkaline phosphatase (ALP) with increased IgM levels
C. Severe hyperbilirubinemia in early disease
D. Normal liver enzymes with elevated IgG

Answer 20

Correct Answer: B
Rationale: PBC is characterized by cholestatic liver enzyme abnormalities, including elevated GGT and ALP, along with increased IgM levels. Significant ALT and AST elevations (Answer A) are not typical, hyperbilirubinemia (Answer C) is usually seen only once cirrhosis has developed, and elevated IgG (Answer D) is more characteristic of AIH or overlap syndrome.

Question 21

Which autoantibody is positive in approximately 65% of PSC patients?
A. Antinuclear antibody (ANA)
B. Antimitochondrial antibody (AMA)
C. Perinuclear antineutrophil cytoplasmic antibody (pANCA)
D. Anti-smooth-muscle antibody (ASMA)

Answer 21

Correct Answer: C
Rationale: Perinuclear antineutrophil cytoplasmic antibody (pANCA) is positive in about 65% of patients with PSC. AMA (Answer B) is associated with PBC, while ANA (Answer A) and ASMA (Answer D) are more typical of autoimmune hepatitis.

Question 22

What is a common overlap syndrome in patients with PSC?
A. PSC and PBC
B. PSC and autoimmune hepatitis (AIH)
C. PSC and NAFLD
D. PSC and hepatitis B

Answer 22

Correct Answer: B
Rationale: A small subset of PSC patients can have overlap syndrome with autoimmune hepatitis (AIH), presenting with aminotransferase elevations >5× the upper limit of normal and features of AIH on biopsy. Overlaps with PBC (Answer A) and NAFLD (Answer C) are not typical, and hepatitis B (Answer D) is unrelated.

Question 23

What is the imaging modality of choice for the initial evaluation of primary sclerosing cholangitis (PSC)?
A. Ultrasound
B. Endoscopic retrograde cholangiopancreatography (ERCP)
C. Computed tomography (CT)
D. Magnetic resonance cholangiopancreatography (MRCP)

Answer 23

Correct Answer: D
Rationale: Magnetic resonance cholangiopancreatography (MRCP) is the preferred imaging technique for the initial evaluation of PSC due to its non-invasive nature and high diagnostic accuracy. ERCP (Answer B) is reserved for cases where MRCP is inconclusive or if a dominant stricture is suspected.

Question 24

What are the characteristic cholangiographic findings in PSC?
A. Diffuse dilation of the entire biliary tree
B. Multifocal stricturing and beading involving both intrahepatic and extrahepatic bile ducts
C. Focal strictures in the extrahepatic bile ducts only
D. Uniform narrowing of all bile ducts

Answer 24

Correct Answer: B
Rationale: The hallmark cholangiographic findings in PSC are multifocal stricturing and beading of the intrahepatic and extrahepatic bile ducts, creating the classic “beaded appearance.”

Question 25

Which complication of PSC is a relative contraindication to liver transplantation?
A. Development of ascites
B. Cholangiocarcinoma
C. Hepatic encephalopathy
D. Portal hypertension

Answer 25

Correct Answer: B
Rationale: The development of cholangiocarcinoma in PSC patients is a relative contraindication to liver transplantation because it significantly complicates the transplant process and outcomes. Ascites (Answer A), hepatic encephalopathy (Answer C), and portal hypertension (Answer D) are common complications of cirrhosis but do not contraindicate transplantation.

Question 26

Which of the following treatments can be helpful in managing dominant strictures in PSC?
A. High-dose UDCA
B. Endoscopic dilatation
C. Liver transplantation
D. Antibiotics

Answer 26

Correct Answer: B
Rationale: Endoscopic dilatation of dominant strictures can provide symptomatic relief in PSC. UDCA (Answer A) has limited clinical benefit, and liver transplantation (Answer C) is reserved for decompensated cirrhosis, not specifically for strictures. Antibiotics (Answer D) are used to treat episodes of cholangitis, not strictures.

Question 27

Which of the following is the most common genetic susceptibility for hemochromatosis?
A. C282Y mutation of the HFE gene
B. Alpha-1 antitrypsin deficiency mutation
C. Mutation in the CFTR gene
D. PKD1 mutation

Answer 27

Correct Answer: A
Rationale: The C282Y mutation of the HFE gene is the most common genetic cause of hereditary hemochromatosis.

Question 28

What is the primary treatment for hemochromatosis?
A. Iron supplementation
B. Regular therapeutic phlebotomy
C. Hepatitis C antiviral therapy
D. Liver transplantation

Answer 28

Correct Answer: B
Rationale: The primary treatment for hemochromatosis is regular therapeutic phlebotomy to reduce iron levels in the body.

Question 29

What laboratory findings are suggestive of hemochromatosis?
A. Low transferrin saturation and ferritin levels
B. Elevated transferrin saturation and elevated ferritin levels
C. Low albumin and elevated bilirubin
D. Positive anti-nuclear antibody and elevated AST/ALT

Answer 29

Correct Answer: B
Rationale: In hemochromatosis, serum iron studies typically show elevated transferrin saturation and ferritin levels, indicating iron overload.

Question 30

What is the key diagnostic finding in Wilson’s disease?
A. High ceruloplasmin levels
B. Elevated serum ferritin levels
C. Low ceruloplasmin and elevated urine copper levels
D. Positive anti-nuclear antibodies

Answer 30

Correct Answer: C
Rationale: In Wilson’s disease, ceruloplasmin levels are typically low, and 24-hour urine copper levels are elevated. Elevated ferritin (Answer B) is seen in conditions like hemochromatosis, and anti-nuclear antibodies (Answer D) are usually found in autoimmune diseases.

Question 31

What is a classic physical examination finding in Wilson’s disease?
A. Butterfly-shaped rash
B. Kayser-Fleischer corneal rings
C. Spider angiomas
D. Palmar erythema

Answer 31

Correct Answer: B
Rationale: Kayser-Fleischer corneal rings are a hallmark of Wilson’s disease, representing copper deposition in the cornea. The other physical findings listed (Answer A, C, and D) are associated with other conditions, not Wilson’s disease.

Question 32

Which of the following is the most important treatment for Wilson’s disease?
A. Copper chelation therapy
B. Liver transplantation
C. High-dose corticosteroids
D. Vitamin K supplementation

Answer 32

Correct Answer: A
Rationale: The main treatment for Wilson’s disease is copper chelation therapy, which helps to remove excess copper from the body. Liver transplantation (Answer B) may be required for advanced liver disease, but it is not the first-line treatment. Corticosteroids (Answer C) are used in autoimmune diseases, not Wilson’s, and Vitamin K supplementation (Answer D) is used for clotting issues, not for copper overload.

Question 33

Portal hypertension is defined as a hepatic venous pressure gradient (HVPG) greater than:
A. 10 mmHg
B. 5 mmHg
C. 15 mmHg
D. 20 mmHg

Answer 33

Correct Answer: B
Rationale: Portal hypertension is specifically defined as an HVPG greater than 5 mmHg. This threshold is used to assess and diagnose portal hypertension.

Question 34

Which of the following contributes to the increased splanchnic blood flow in portal hypertension?
A. Vasoconstriction in the splanchnic vascular bed
B. Vasodilation in the splanchnic vascular bed
C. Decreased cardiac output
D. Increased hepatic venous pressure

Answer 34

Correct Answer: B
Rationale: In portal hypertension, there is increased splanchnic blood flow primarily due to vasodilation in the splanchnic vascular bed. This vasodilation contributes to the development of portal hypertension along with increased intrahepatic resistance. Decreased cardiac output (Answer C) and increased hepatic venous pressure (Answer D) are not the primary mechanisms for increased splanchnic blood flow.

Question 35

Which of the following is the most commonly used method for primary prophylaxis of variceal bleeding in patients with cirrhosis?
A. Endoscopic variceal ligation (EVL)
B. Nonselective beta blockade (NSBB)
C. Esophageal balloon tamponade
D. Liver transplantation

Answer 35

Correct Answer: B
Rationale: Nonselective beta blockers (NSBB), such as propranolol or nadolol, are commonly used for primary prophylaxis against variceal bleeding in cirrhosis. Endoscopic variceal ligation (EVL) (Answer A) is also effective but is typically used for patients who cannot tolerate or fail NSBB therapy. Esophageal balloon tamponade (Answer C) is used in acute bleeding situations, not for prophylaxis. Liver transplantation (Answer D) is not a primary prophylactic treatment but may be indicated in advanced cirrhosis with severe complications.

Question 36

What is the target heart rate when using nonselective beta blockers (NSBB) for primary prophylaxis of variceal bleeding?
A. 60-70 beats/min
B. 70-80 beats/min
C. 50-60 beats/min
D. 55-60 beats/min

Answer 36

Correct Answer: D
Rationale: When using NSBB like propranolol or nadolol for primary prophylaxis of variceal bleeding, the goal is to titrate the dose to achieve a heart rate of 55–60 beats/min. This target helps reduce the risk of bleeding without significantly affecting blood pressure.

Question 37

Which of the following statements is true regarding the efficacy of endoscopic variceal ligation (EVL) compared to nonselective beta blockers (NSBB)?
A. EVL is significantly more effective than NSBB in preventing variceal bleeding
B. NSBB and EVL have equivalent efficacy in preventing variceal bleeding
C. NSBB is significantly more effective than EVL in preventing variceal bleeding
D. EVL is not effective for primary prophylaxis

Answer 37

Correct Answer: B
Rationale: Studies have shown that endoscopic variceal ligation (EVL) has efficacy comparable to that of nonselective beta blockers (NSBB) for primary prophylaxis of variceal bleeding. Both methods are effective, and the choice between them is typically based on patient and physician preference and tolerability.

Question 38

Which of the following mechanisms primarily contributes to the development of ascites in patients with cirrhosis?
A. Increased portal pressure and splanchnic vasodilation
B. Decreased renal perfusion and increased fluid retention
C. Hypoalbuminemia and decreased plasma oncotic pressure
D. All of the above

Answer 38

Correct Answer: D
Rationale: The development of ascites in cirrhosis is multifactorial. Increased portal pressure and splanchnic vasodilation lead to increased production of splanchnic lymph and fluid accumulation. Hypoalbuminemia from reduced synthetic function in the cirrhotic liver contributes to decreased plasma oncotic pressure, facilitating the movement of fluid into the peritoneal cavity. Additionally, the activation of the renin-angiotensin-aldosterone system and sympathetic nervous system causes sodium retention and fluid expansion, leading to peripheral edema and ascites.

Question 39

What factor is responsible for the vasodilation of the splanchnic vascular bed in cirrhosis that contributes to ascites?
A. Renin
B. Nitric oxide
C. Angiotensin II
D. Aldosterone

Answer 39

Correct Answer: B
Rationale: Nitric oxide is the key vasodilator responsible for splanchnic vasodilation in cirrhosis. This vasodilation increases portal venous inflow, which, along with the increased intrahepatic resistance, contributes to the formation of ascites. Renin, angiotensin II, and aldosterone are involved in fluid retention and sodium balance but are not responsible for the initial vasodilation in the splanchnic vascular bed.

Question 40

Which of the following is a consequence of the underfilling of the arterial circulation in cirrhosis?
A. Decreased sympathetic nervous system activity
B. Activation of the renin-angiotensin-aldosterone system
C. Vasoconstriction in the splanchnic vasculature
D. Increased fluid loss from the intravascular compartment

Answer 40

Correct Answer: B
Rationale: The underfilling of the arterial circulation, which results from vasodilation in the splanchnic vascular bed, triggers compensatory mechanisms to maintain circulatory homeostasis. This includes the activation of the renin-angiotensin-aldosterone system, which promotes sodium retention and fluid accumulation. It does not result in decreased sympathetic nervous system activity or vasoconstriction in the splanchnic vasculature. The fluid loss from the intravascular compartment occurs due to other factors, such as hypoalbuminemia.

Question 41

What does a serum ascites-to-albumin gradient (SAAG) greater than 1.1 g/dL most likely indicate in a patient with ascites?
A. The presence of infection
B. Ascites caused by portal hypertension
C. Cardiac ascites with a protein concentration >2.5 g/dL
D. Malignant ascites

Answer 41

Correct Answer: B
Rationale: A SAAG greater than 1.1 g/dL suggests that ascites is most likely due to portal hypertension, which is typically seen in cirrhosis. This value helps to distinguish portal hypertension-related ascites from other causes, such as infection or malignancy.

Question 42

What is the significance of a low ascitic fluid protein concentration, typically <1.5 g/dL, in patients with cirrhosis?
A. It increases the risk of spontaneous bacterial peritonitis (SBP)
B. It indicates the presence of hepatocellular carcinoma
C. It suggests the ascites is caused by heart failure
D. It is a hallmark of malignant ascites

Answer 42

Correct Answer: A
Rationale: A low ascitic fluid protein concentration, typically <1.5 g/dL, is a risk factor for spontaneous bacterial peritonitis (SBP). The low protein concentration impairs the immune response, making patients more susceptible to infections in the ascitic fluid.

Question 43

When is the cause of ascites likely to be infectious or malignant, based on the serum ascites-to-albumin gradient (SAAG)?
A. SAAG >1.1 g/dL
B. SAAG <1.1 g/dL
C. Ascitic fluid protein >2.5 g/dL
D. The presence of >250 polymorphonuclear leukocytes/μL

Answer 43

Correct Answer: B
Rationale: A SAAG less than 1.1 g/dL typically suggests that ascites may be due to non-hepatic causes, such as infections or malignancy. This value helps differentiate from ascites due to portal hypertension, which has a SAAG greater than 1.1 g/dL.

Question 44

What is the significance of an elevated number of polymorphonuclear leukocytes (>250/μL) in ascitic fluid?
A. The patient is likely to have a traumatic tap
B. The patient likely has spontaneous bacterial peritonitis (SBP)
C. The ascites is probably due to malignancy
D. The patient’s ascites is due to portal hypertension

Answer 44

Correct Answer: B
Rationale: An elevated number of polymorphonuclear leukocytes (>250/μL) in ascitic fluid is a diagnostic criterion for spontaneous bacterial peritonitis (SBP). This finding suggests an infection of the ascitic fluid, which requires prompt treatment with antibiotics.

Question 45

In patients with ascites, when should diuretic therapy typically be initiated?
A. Only when ascitic fluid volume is large and requires paracentesis
B. For patients with moderate amounts of ascites
C. After failure of dietary sodium restriction
D. When there is evidence of spontaneous bacterial peritonitis (SBP)

Answer 45

Correct Answer: B
Rationale: Diuretic therapy is typically initiated in patients with moderate amounts of ascites. Spironolactone is often used initially, with furosemide added as necessary. Dietary sodium restriction alone is sufficient for patients with small amounts of ascites, while more significant ascites requires diuretics.

Question 46

What is the maximum recommended daily dose of spironolactone in patients with ascites who fail initial therapy and are compliant with a low-sodium diet?
A. 200 mg/d
B. 400 mg/d
C. 160 mg/d
D. 100 mg/d

Answer 46

Correct Answer: B
Rationale: For patients with refractory ascites who are compliant with a low-sodium diet and do not respond to initial diuretic therapy, the dose of spironolactone can be increased incrementally up to a maximum of 400 mg/d.

Question 47

What is defined as refractory ascites in patients with cirrhosis?
A. Ascites that persists despite diuretic therapy with high doses of spironolactone and furosemide
B. Ascites that occurs only in the setting of spontaneous bacterial peritonitis
C. Ascites that resolves after paracentesis
D. Ascites that develops after liver transplantation

Answer 47

Correct Answer: A
Rationale: Refractory ascites refers to ascites that remains present despite maximal medical management with diuretics (i.e., high doses of spironolactone and furosemide) in patients who are compliant with a low-sodium diet.

Question 48

What is the recommended management for patients with cirrhosis and refractory ascites who do not respond to diuretics?
A. Liver transplantation is immediately indicated
B. Repeated large-volume paracentesis (LVP) or a TIPS procedure may be considered
C. Systemic corticosteroids should be started to reduce fluid retention
D. Ascitic fluid should be drained continuously without albumin replacement

Answer 48

Correct Answer: B
Rationale: In cases of refractory ascites, when diuretic therapy fails, alternative treatments such as repeated large-volume paracentesis (LVP) or a transjugular intrahepatic portosystemic shunt (TIPS) procedure may be considered. However, TIPS is associated with an increased risk of hepatic encephalopathy and does not improve survival, so it must be used carefully.

Question 49

After performing a large-volume paracentesis (LVP) with the removal of ≥5 L of ascitic fluid, what is the recommended treatment to prevent circulatory dysfunction?
A. Administration of intravenous diuretics
B. Administration of 25% albumin IV at 8 g/L of removed ascites
C. Administration of broad-spectrum antibiotics
D. Continuous blood transfusion

Answer 49

Correct Answer: B
Rationale: After a large-volume paracentesis (≥5 L), it is recommended to administer intravenous 25% albumin at a dose of approximately 8 g/L of removed ascites to prevent circulatory dysfunction due to the sudden shift of fluid. This helps maintain plasma volume and prevent complications.

Question 50

Which of the following is the most common cause of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis and ascites?
A. Pseudomonas aeruginosa
B. Staphylococcus aureus
C. Escherichia coli
D. Candida albicans

Answer 50

Correct Answer: C
Rationale: Escherichia coli and other gut bacteria are the most common organisms responsible for spontaneous bacterial peritonitis (SBP) in patients with cirrhosis and ascites. Gram-positive organisms, such as Streptococcus viridans, Staphylococcus aureus, and Enterococcus spp., can also be involved, but E. coli is the primary pathogen.

Question 51

What is the diagnostic criterion for spontaneous bacterial peritonitis (SBP)?
A. Positive blood cultures and clinical signs of infection
B. An absolute neutrophil count >250/μL in ascitic fluid
C. Ascitic fluid amylase level >500 U/L
D. Presence of more than two organisms in ascitic fluid

Answer 51

Correct Answer: B
Rationale: The diagnosis of spontaneous bacterial peritonitis (SBP) is made when the ascitic fluid sample has an absolute neutrophil count >250/μL, which indicates infection. The presence of more than two organisms is a sign of secondary bacterial peritonitis due to a perforated viscus, not SBP.

Question 52

What is the recommended antibiotic treatment for spontaneous bacterial peritonitis (SBP) in hospitalized patients with cirrhosis and ascites?
A. Oral quinolones
B. Intravenous third-generation cephalosporins for 5 days
C. Intravenous vancomycin for 7 days
D. Intravenous piperacillin-tazobactam for 5 days

Answer 52

Correct Answer: B
Rationale: The standard treatment for spontaneous bacterial peritonitis (SBP) in hospitalized patients with cirrhosis and ascites is intravenous third-generation cephalosporins, such as cefotaxime or ceftriaxone, for 5 days. This helps treat the common organisms responsible for SBP, such as Escherichia coli.

Question 53

What additional therapy should be administered to patients with spontaneous bacterial peritonitis (SBP) to improve survival and prevent renal failure?
A. Intravenous broad-spectrum antibiotics
B. Intravenous albumin
C. Oral quinolones
D. Corticosteroids

Answer 53

Correct Answer: B
Rationale: In addition to antibiotics, intravenous albumin (1.5 g/kg body weight on day 1 and 1.0 g/kg on day 3) is recommended for patients with spontaneous bacterial peritonitis (SBP). Albumin reduces the risk of renal failure and improves survival in these patients.

Question 54

After a patient with cirrhosis and spontaneous bacterial peritonitis (SBP) recovers from an episode, what is recommended to prevent recurrent SBP?
A. Long-term IV antibiotics
B. Oral quinolone antibiotic prophylaxis
C. Prophylactic liver transplantation
D. Continuous diuretic therapy

Answer 54

Correct Answer: B
Rationale: For patients who have had an episode of spontaneous bacterial peritonitis (SBP) and recovered, prophylactic oral quinolones are recommended to prevent recurrent episodes of SBP. This helps reduce the risk of future infections.

Question 55

Which of the following statements is true regarding Type 1 Hepatorenal Syndrome (HRS)?
A. Type 1 HRS has a slow progression and a favorable outcome.
B. Type 1 HRS is characterized by a significant reduction in creatinine clearance within 1–2 weeks.
C. Type 1 HRS is most often reversible with diuretic therapy.
D. Liver transplantation is not an effective treatment for Type 1 HRS.

Answer 55

Correct Answer: B
Rationale: Type 1 HRS is characterized by rapid and progressive impairment in renal function, with a significant reduction in creatinine clearance occurring within 1–2 weeks. This form of renal failure has a poor prognosis unless liver transplantation is performed promptly.

Question 56

The best therapy for Hepatorenal Syndrome (HRS) is:
A. Diuretic therapy
B. Vasodilator therapy
C. Liver transplantation
D. Renal replacement therapy

Answer 56

Correct Answer: C
Rationale: Liver transplantation is the definitive treatment for HRS, as it not only addresses the underlying liver dysfunction but also typically results in recovery of renal function.

Question 57

A 55-year-old male with cirrhosis presents with confusion, asterixis, and disorientation. His ammonia levels are elevated, and he is diagnosed with hepatic encephalopathy. What is the mainstay of treatment for this condition?
A. Rifampin
B. Lactulose
C. Metronidazole
D. High-protein diet

Answer 57

Correct Answer: B
Rationale: Lactulose is the mainstay of treatment for hepatic encephalopathy. It works by acidifying the colon and promoting the elimination of nitrogenous products responsible for the development of encephalopathy. The goal is to achieve 2-3 soft stools per day.

Question 58

A patient with cirrhosis and recurrent episodes of hepatic encephalopathy is prescribed rifaximin at 550 mg twice daily. What is the primary purpose of this therapy?
A. To reduce gut flora and nitrogenous waste production
B. To enhance lactulose absorption
C. To prevent variceal bleeding
D. To improve liver function tests

Answer 58

Correct Answer: A
Rationale: Rifaximin is a poorly absorbed antibiotic used to reduce gut flora and nitrogenous waste production in patients with hepatic encephalopathy. It is effective in preventing recurrent episodes of encephalopathy.

Poorly absorbed antibiotics are often used as adjunctive therapies for patients who have a difficult time with lactulose. The alternating administration of neomycin and metronidazole has been used in the past to reduce the individual side effects of each: neomycin for renal insufficiency and ototoxicity and metronidazole for peripheral neuropathy. More recently, rifaximin at 550 mg twice daily has been very effective in preventing recurrent encephalopathy.