ACG CXA EXAM PREP QUESTIONS AND ANSWERS A+
GRADED WITH EXPERT SOLUTIONS - 110 Questions
with Answers
Page 1
,Q1. A 48-year-old man with chronic hepatitis C (genotype 1a) and compensated
cirrhosis (Child-Pugh A) has completed 8 weeks of glecaprevir-pibrentasvir therapy.
At week 4 his HCV RNA was 15 IU/mL, and at end of treatment it is undetectable.
Which of the following best describes the recommended monitoring and outcome of
this regimen?
A. Continue therapy for 4 additional weeks due to detectable viremia at week 4
B. Stop therapy at week 8 and obtain sustained virologic response (SVR12) at 12
weeks post-treatment
C. Switch to sofosbuvir/velpatasvir plus ribavirin for 24 weeks because of cirrhosis
D. Add ribavirin and extend therapy to 16 weeks due to prior non-response
Correct Answer: B. Stop therapy at week 8 and obtain sustained virologic response
(SVR12) at 12 weeks post-treatment
Rationale: Glecaprevir-pibrentasvir is approved for 8 weeks in treatment-naive patients
with compensated cirrhosis and HCV genotype 1. Detectable HCV RNA at week 4 does not
require extension; the goal is SVR12, which is assessed 12 weeks after the end of
treatment. Continuing or switching is not indicated in this scenario.
Why Wrong:
A - Week 4 viremia is not a criterion for extending therapy; the regimen duration is
fixed at 8 weeks for this population.
C - Sofosbuvir/velpatasvir plus ribavirin is not the standard of care for treatment-naive
genotype 1a with compensated cirrhosis, and glecaprevir-pibrentasvir is already
optimal.
D - Ribavirin is not added for treatment-naive patients on glecaprevir-pibrentasvir,
and there is no history of prior non-response.
Reference: AASLD-IDSA HCV Guidance, 2023; Panel on Treatment of HCV. Hepatology.
2023.
Q2. A patient with primary biliary cholangitis and a baseline alkaline phosphatase
(ALP) of 2.5 times the upper limit of normal is started on obeticholic acid (OCA) 5
mg daily. After 3 months, ALP has decreased by 20%. Which of the following is the
most appropriate next step in management?
A. Discontinue OCA and refer for liver transplantation
B. Increase OCA to 10 mg daily if tolerated, with continued monitoring
C. Add ursodeoxycholic acid (UDCA) 13-15 mg/kg/day
D. Switch to bezafibrate 400 mg daily
Correct Answer: B. Increase OCA to 10 mg daily if tolerated, with continued
monitoring
Rationale: OCA is indicated for PBC with an inadequate response to UDCA or as
monotherapy. The starting dose is 5 mg, and if there is an inadequate reduction in ALP
Page 2
,after 3 months, the dose can be increased to 10 mg. A 20% reduction is not sufficient to
declare non-response, and UDCA would have been used first-line before OCA.
Why Wrong:
A - A 20% reduction is not a failure requiring transplantation; dose escalation is the
standard next step.
C - UDCA is first-line therapy and should have been initiated before OCA; adding it
now is not the immediate next step.
D - Bezafibrate is a second-line option but not the preferred next step after only 3
months of OCA at a submaximal dose.
Reference: Lindor KD, et al. Hepatology. 2019; AASLD PBC Guidance.
Q3. Which of the following best explains the pharmacodynamic basis for the use of
naloxone in the management of opioid-induced respiratory depression?
A. Naloxone is a competitive antagonist at mu-opioid receptors, displacing opioids and
reversing their effects
B. Naloxone is a partial agonist at mu-opioid receptors, providing mild respiratory
stimulation
C. Naloxone enhances the metabolism of opioids via CYP3A4 induction
D. Naloxone increases respiratory drive by activating central chemoreceptors directly
Correct Answer: A. Naloxone is a competitive antagonist at mu-opioid receptors,
displacing opioids and reversing their effects
Rationale: Naloxone is a competitive antagonist at mu-opioid receptors, with high affinity
but no intrinsic activity. It displaces opioid agonists, rapidly reversing respiratory
depression and other opioid effects. Its action is competitive, so higher doses are needed in
the presence of high opioid concentrations.
Why Wrong:
B - Naloxone is an antagonist, not a partial agonist; it does not have intrinsic activity
to stimulate respiration.
C - Naloxone does not induce CYP3A4 or alter opioid metabolism; it acts at the
receptor level.
D - Naloxone does not directly stimulate chemoreceptors; it acts by blocking opioid
receptors.
Reference: Lehne RA. Pharmacology for Nursing Care. 12th ed. Ch. 21.
Q4. A patient with atrial fibrillation is prescribed digoxin. Which of the following best
describes the mechanism of action of digoxin in this context?
A. Inhibition of Na+/K+-ATPase leading to increased intracellular calcium and
enhanced vagal tone
B. Blockade of L-type calcium channels in the sinoatrial node
Page 3
, C. Activation of potassium channels in atrial myocytes
D. Inhibition of the funny current (If) in the sinoatrial node
Correct Answer: A. Inhibition of Na+/K+-ATPase leading to increased intracellular
calcium and enhanced vagal tone
Rationale: Digoxin inhibits Na+/K+-ATPase, increasing intracellular sodium, which via
the Na+/Ca2+ exchanger raises intracellular calcium, enhancing contractility. It also
increases vagal tone, slowing AV conduction, which is beneficial in atrial fibrillation. The
other options describe mechanisms of other antiarrhythmics (e.g., verapamil, amiodarone,
ivabradine).
Why Wrong:
B - L-type calcium channel blockade is the mechanism of non-dihydropyridine
calcium channel blockers, not digoxin.
C - Potassium channel activation is not a primary mechanism of digoxin.
D - Inhibition of the funny current is the mechanism of ivabradine, not digoxin.
Reference: Lehne RA. Pharmacology for Nursing Care. 12th ed. Ch. 44.
Q5. A patient with type 2 diabetes and chronic kidney disease (eGFR 35 mL/min/1.73
m²) is being started on an SGLT2 inhibitor. Which agent is most appropriate at this
level of renal function?
A. Canagliflozin
B. Dapagliflozin
C. Empagliflozin
D. Ertugliflozin
Correct Answer: C. Empagliflozin
Rationale: Empagliflozin is approved for use in patients with eGFR as low as 30
mL/min/1.73 m² and has demonstrated cardiovascular and renal benefits in the
EMPA-REG OUTCOME trial. Canagliflozin is not recommended below eGFR 45,
dapagliflozin is not recommended below eGFR 25 (but in some regions down to 25), and
ertugliflozin is not recommended below eGFR 60.
Why Wrong:
A - Canagliflozin is not recommended when eGFR is below 45 mL/min/1.73 m².
B - Dapagliflozin is approved down to eGFR 25, but empagliflozin is the preferred
choice at 35 because of stronger evidence and labeling.
D - Ertugliflozin is not recommended when eGFR is below 60 mL/min/1.73 m².
Reference: FDA Prescribing Information; ADA Standards of Medical Care in Diabetes,
2024.
Q6. A patient with congestive heart failure is receiving furosemide. Which of the
following best describes the mechanism of action of furosemide?
Page 4
GRADED WITH EXPERT SOLUTIONS - 110 Questions
with Answers
Page 1
,Q1. A 48-year-old man with chronic hepatitis C (genotype 1a) and compensated
cirrhosis (Child-Pugh A) has completed 8 weeks of glecaprevir-pibrentasvir therapy.
At week 4 his HCV RNA was 15 IU/mL, and at end of treatment it is undetectable.
Which of the following best describes the recommended monitoring and outcome of
this regimen?
A. Continue therapy for 4 additional weeks due to detectable viremia at week 4
B. Stop therapy at week 8 and obtain sustained virologic response (SVR12) at 12
weeks post-treatment
C. Switch to sofosbuvir/velpatasvir plus ribavirin for 24 weeks because of cirrhosis
D. Add ribavirin and extend therapy to 16 weeks due to prior non-response
Correct Answer: B. Stop therapy at week 8 and obtain sustained virologic response
(SVR12) at 12 weeks post-treatment
Rationale: Glecaprevir-pibrentasvir is approved for 8 weeks in treatment-naive patients
with compensated cirrhosis and HCV genotype 1. Detectable HCV RNA at week 4 does not
require extension; the goal is SVR12, which is assessed 12 weeks after the end of
treatment. Continuing or switching is not indicated in this scenario.
Why Wrong:
A - Week 4 viremia is not a criterion for extending therapy; the regimen duration is
fixed at 8 weeks for this population.
C - Sofosbuvir/velpatasvir plus ribavirin is not the standard of care for treatment-naive
genotype 1a with compensated cirrhosis, and glecaprevir-pibrentasvir is already
optimal.
D - Ribavirin is not added for treatment-naive patients on glecaprevir-pibrentasvir,
and there is no history of prior non-response.
Reference: AASLD-IDSA HCV Guidance, 2023; Panel on Treatment of HCV. Hepatology.
2023.
Q2. A patient with primary biliary cholangitis and a baseline alkaline phosphatase
(ALP) of 2.5 times the upper limit of normal is started on obeticholic acid (OCA) 5
mg daily. After 3 months, ALP has decreased by 20%. Which of the following is the
most appropriate next step in management?
A. Discontinue OCA and refer for liver transplantation
B. Increase OCA to 10 mg daily if tolerated, with continued monitoring
C. Add ursodeoxycholic acid (UDCA) 13-15 mg/kg/day
D. Switch to bezafibrate 400 mg daily
Correct Answer: B. Increase OCA to 10 mg daily if tolerated, with continued
monitoring
Rationale: OCA is indicated for PBC with an inadequate response to UDCA or as
monotherapy. The starting dose is 5 mg, and if there is an inadequate reduction in ALP
Page 2
,after 3 months, the dose can be increased to 10 mg. A 20% reduction is not sufficient to
declare non-response, and UDCA would have been used first-line before OCA.
Why Wrong:
A - A 20% reduction is not a failure requiring transplantation; dose escalation is the
standard next step.
C - UDCA is first-line therapy and should have been initiated before OCA; adding it
now is not the immediate next step.
D - Bezafibrate is a second-line option but not the preferred next step after only 3
months of OCA at a submaximal dose.
Reference: Lindor KD, et al. Hepatology. 2019; AASLD PBC Guidance.
Q3. Which of the following best explains the pharmacodynamic basis for the use of
naloxone in the management of opioid-induced respiratory depression?
A. Naloxone is a competitive antagonist at mu-opioid receptors, displacing opioids and
reversing their effects
B. Naloxone is a partial agonist at mu-opioid receptors, providing mild respiratory
stimulation
C. Naloxone enhances the metabolism of opioids via CYP3A4 induction
D. Naloxone increases respiratory drive by activating central chemoreceptors directly
Correct Answer: A. Naloxone is a competitive antagonist at mu-opioid receptors,
displacing opioids and reversing their effects
Rationale: Naloxone is a competitive antagonist at mu-opioid receptors, with high affinity
but no intrinsic activity. It displaces opioid agonists, rapidly reversing respiratory
depression and other opioid effects. Its action is competitive, so higher doses are needed in
the presence of high opioid concentrations.
Why Wrong:
B - Naloxone is an antagonist, not a partial agonist; it does not have intrinsic activity
to stimulate respiration.
C - Naloxone does not induce CYP3A4 or alter opioid metabolism; it acts at the
receptor level.
D - Naloxone does not directly stimulate chemoreceptors; it acts by blocking opioid
receptors.
Reference: Lehne RA. Pharmacology for Nursing Care. 12th ed. Ch. 21.
Q4. A patient with atrial fibrillation is prescribed digoxin. Which of the following best
describes the mechanism of action of digoxin in this context?
A. Inhibition of Na+/K+-ATPase leading to increased intracellular calcium and
enhanced vagal tone
B. Blockade of L-type calcium channels in the sinoatrial node
Page 3
, C. Activation of potassium channels in atrial myocytes
D. Inhibition of the funny current (If) in the sinoatrial node
Correct Answer: A. Inhibition of Na+/K+-ATPase leading to increased intracellular
calcium and enhanced vagal tone
Rationale: Digoxin inhibits Na+/K+-ATPase, increasing intracellular sodium, which via
the Na+/Ca2+ exchanger raises intracellular calcium, enhancing contractility. It also
increases vagal tone, slowing AV conduction, which is beneficial in atrial fibrillation. The
other options describe mechanisms of other antiarrhythmics (e.g., verapamil, amiodarone,
ivabradine).
Why Wrong:
B - L-type calcium channel blockade is the mechanism of non-dihydropyridine
calcium channel blockers, not digoxin.
C - Potassium channel activation is not a primary mechanism of digoxin.
D - Inhibition of the funny current is the mechanism of ivabradine, not digoxin.
Reference: Lehne RA. Pharmacology for Nursing Care. 12th ed. Ch. 44.
Q5. A patient with type 2 diabetes and chronic kidney disease (eGFR 35 mL/min/1.73
m²) is being started on an SGLT2 inhibitor. Which agent is most appropriate at this
level of renal function?
A. Canagliflozin
B. Dapagliflozin
C. Empagliflozin
D. Ertugliflozin
Correct Answer: C. Empagliflozin
Rationale: Empagliflozin is approved for use in patients with eGFR as low as 30
mL/min/1.73 m² and has demonstrated cardiovascular and renal benefits in the
EMPA-REG OUTCOME trial. Canagliflozin is not recommended below eGFR 45,
dapagliflozin is not recommended below eGFR 25 (but in some regions down to 25), and
ertugliflozin is not recommended below eGFR 60.
Why Wrong:
A - Canagliflozin is not recommended when eGFR is below 45 mL/min/1.73 m².
B - Dapagliflozin is approved down to eGFR 25, but empagliflozin is the preferred
choice at 35 because of stronger evidence and labeling.
D - Ertugliflozin is not recommended when eGFR is below 60 mL/min/1.73 m².
Reference: FDA Prescribing Information; ADA Standards of Medical Care in Diabetes,
2024.
Q6. A patient with congestive heart failure is receiving furosemide. Which of the
following best describes the mechanism of action of furosemide?
Page 4
