, HESI Pharmacology V2 Exam 2026/2027: Elsevier Evolve
NCSBN Clinical Judgment Model-Aligned Study Set with
Questions & Rationales - 130 Questions
Section 1: General (Questions 1-130)
1 A patient with chronic kidney disease (eGFR 25 mL/min/1.73m²) requires antibiotic therapy for a complicated
urinary tract infection. The prescriber considers gentamicin and ceftriaxone. Which statement accurately reflects
the pharmacodynamic principle of concentration-dependent killing and its application to dosing in renal
impairment?
A) Ceftriaxone exhibits concentration-dependent killing, requiring peak concentrations at least 10 times the MIC;
dose adjustment is based on renal function.
B) Gentamicin exhibits concentration-dependent killing, with a goal peak/MIC ratio of 8-10; extended-interval
dosing is preferred but requires monitoring of trough levels due to accumulation risk.
C) Both gentamicin and ceftriaxone are time-dependent antibiotics, so the duration above MIC is the key
parameter; renal impairment necessitates dose reduction.
D) Gentamicin exhibits time-dependent killing; therefore, maintaining trough levels below 2 mcg/mL is the
primary goal to prevent nephrotoxicity.
Answer: B
Rationale: Gentamicin is an aminoglycoside with concentration-dependent killing, where high peak/MIC ratios
(8-10) maximize efficacy. Extended-interval dosing is common, but in renal impairment, accumulation increases
toxicity risk, so trough monitoring is essential. Ceftriaxone has time-dependent killing, and its dosing is not
primarily adjusted for renal function. Option A incorrectly attributes concentration-dependent killing to
ceftriaxone. Option C misclassifies both drugs. Option D incorrectly describes gentamicin as time-dependent.
2 A researcher is designing a study to evaluate a new drug's effect on cardiac repolarization. Which of the
following electrophysiological parameters is the most specific surrogate marker for predicting the risk of
torsades de pointes?
A) Prolongation of the PR interval
B) Increase in QRS duration
C) Prolongation of the QT interval corrected for heart rate (QTc)
D) ST-segment elevation
Answer: C
Rationale: QTc prolongation is the most specific ECG marker for delayed ventricular repolarization, which
predisposes to torsades de pointes. PR interval reflects AV conduction, QRS duration indicates ventricular
depolarization, and ST elevation is associated with ischemia or injury, not drug-induced arrhythmia risk.
3 A patient with severe hepatic impairment (Child-Pugh class C) requires analgesia. Which of the following
statements about opioid pharmacokinetics is most accurate when considering fentanyl versus morphine?
A) Morphine is preferred because it undergoes glucuronidation, which is preserved in cirrhosis, whereas fentanyl
requires CYP3A4 metabolism, which is impaired.
B) Fentanyl is safer because its clearance is primarily via hepatic blood flow, which is less affected by
hepatocellular function than phase I metabolism.
C) Both drugs have similar pharmacokinetic profiles in liver disease; dose adjustments are not necessary if renal
function is normal.
,D) Morphine-6-glucuronide accumulation is a concern with morphine, but fentanyl's high first-pass metabolism
makes oral dosing unpredictable in cirrhosis.
Answer: B
Rationale: Fentanyl clearance is highly dependent on hepatic blood flow rather than hepatocellular function; in
cirrhosis, hepatic blood flow may be preserved, making fentanyl relatively safer. Morphine undergoes
glucuronidation (phase II), which is relatively preserved, but its active metabolite M6G accumulates in renal
impairment, which often coexists with liver disease. Option A overstates morphine's advantage. Option C is false.
Option D incorrectly emphasizes first-pass metabolism; fentanyl is not given orally.
4 A patient on warfarin therapy for mechanical heart valve requires a short course of antibiotics for a dental
procedure. The prescriber considers amoxicillin, clindamycin, or metronidazole. Which drug interaction
mechanism is most likely to potentiate warfarin's anticoagulant effect?
A) Amoxicillin reduces warfarin absorption by binding to it in the gut.
B) Clindamycin inhibits CYP2C9, reducing warfarin metabolism.
C) Metronidazole inhibits the vitamin K epoxide reductase complex indirectly, enhancing warfarin's effect.
D) All three antibiotics can potentiate warfarin by reducing gut flora that produce vitamin K.
Answer: D
Rationale: Broad-spectrum antibiotics reduce the intestinal flora that synthesize vitamin K, leading to decreased
vitamin K availability and enhanced warfarin effect. This is a common mechanism for many antibiotics. Option A
is incorrect; amoxicillin does not bind warfarin. Option B is incorrect; clindamycin does not inhibit CYP2C9.
Option C is partially correct for metronidazole (it inhibits warfarin metabolism via CYP2C9), but the broader
mechanism (option D) applies to all three, making it the best answer.
5 A patient with type 2 diabetes and obesity (BMI 38) is started on a GLP-1 receptor agonist. Which of the
following statements best explains the mechanism by which this drug class improves glycemic control and
promotes weight loss?
A) It increases insulin secretion in a glucose-dependent manner and delays gastric emptying, leading to reduced
postprandial glucose and increased satiety.
B) It inhibits the breakdown of incretin hormones, thereby increasing endogenous GLP-1 and GIP levels.
C) It directly activates AMP-kinase in skeletal muscle, enhancing glucose uptake independent of insulin.
D) It binds to the sulfonylurea receptor on pancreatic beta cells, causing insulin release regardless of glucose
level.
Answer: A
Rationale: GLP-1 receptor agonists (e.g., semaglutide, liraglutide) mimic endogenous GLP-1, which stimulates
glucose-dependent insulin secretion, suppresses glucagon, and slows gastric emptying. This results in lower
postprandial glucose and increased satiety, promoting weight loss. Option B describes DPP-4 inhibitors. Option C
describes metformin's mechanism. Option D describes sulfonylureas, which are not weight-neutral and can cause
hypoglycemia.
6 A patient with acute ischemic stroke receives alteplase within 3 hours of symptom onset. Which of the
following best explains the rationale for avoiding anticoagulant or antiplatelet therapy within 24 hours after
thrombolysis?
A) Alteplase depletes clotting factors, making anticoagulation unnecessary.
B) Concurrent use increases the risk of symptomatic intracranial hemorrhage due to impaired hemostasis from
fibrinogen depletion and ongoing clot lysis.
C) Antiplatelet agents are contraindicated because they inhibit the conversion of plasminogen to plasmin.
D) Anticoagulants enhance the metabolism of alteplase, reducing its efficacy.
, Answer: B
Rationale: Alteplase causes systemic fibrinogen depletion and lysis of fibrin clots, including hemostatic plugs.
Adding anticoagulants or antiplatelet agents within 24 hours significantly increases the risk of intracranial
hemorrhage. Option A is incorrect; clotting factors are not depleted. Option C is incorrect; antiplatelet agents do
not affect plasminogen conversion. Option D is incorrect; anticoagulants do not alter alteplase metabolism.
7 A patient with severe sepsis is started on norepinephrine for hemodynamic support. Which of the following best
describes the pharmacodynamic effect of norepinephrine on the vasculature and its impact on organ perfusion?
A) It is a selective alpha-1 agonist that causes vasodilation in splanchnic beds, improving renal blood flow.
B) It acts primarily on beta-2 receptors, causing bronchodilation and increased heart rate.
C) It is a potent alpha-1 and beta-1 agonist that increases mean arterial pressure through vasoconstriction, but
may reduce perfusion to some vascular beds at high doses.
D) It activates dopamine receptors in the renal vasculature, selectively increasing renal blood flow.
Answer: C
Rationale: Norepinephrine is a catecholamine with strong alpha-1 (vasoconstriction) and beta-1 (positive inotropy)
activity. It effectively increases MAP, but excessive vasoconstriction can compromise perfusion in renal,
splanchnic, and peripheral beds. Option A is incorrect; it causes vasoconstriction, not dilation. Option B describes
beta-2 effects (e.g., albuterol). Option D describes low-dose dopamine, which is no longer recommended.
8 A patient with bipolar I disorder is stabilized on lithium. After 6 months of therapy, routine labs show a serum
lithium level of 1.2 mEq/L (therapeutic range 0.6-1.2). The patient reports mild tremor and polyuria. Which of
the following is the most appropriate next step?
A) Increase the lithium dose to achieve a level of 1.5 mEq/L for better mood stabilization.
B) Discontinue lithium immediately and switch to valproate due to signs of toxicity.
C) Maintain the current dose but monitor renal function and consider dose reduction if symptoms worsen or if
creatinine rises.
D) Add a diuretic to enhance lithium excretion and lower the serum level.
Answer: C
Rationale: The lithium level is at the upper end of therapeutic range, and mild tremor and polyuria are common side
effects that may be tolerable. Dose reduction should be considered if symptoms become bothersome or if renal
function declines. Option A would increase toxicity risk. Option B is premature; symptoms are not severe. Option
D is dangerous; thiazide diuretics can increase lithium reabsorption and raise levels.
9 A patient with metastatic breast cancer is being treated with doxorubicin. Which of the following strategies is
most effective for preventing doxorubicin-induced cardiotoxicity?
A) Co-administration of dexrazoxane, an iron chelator that reduces free radical formation.
B) Limiting the cumulative dose to less than 550 mg/m², as cardiotoxicity is dose-dependent and irreversible.
C) Using a continuous infusion rather than bolus administration to lower peak plasma concentrations.
D) All of the above are recommended strategies.
Answer: D
Rationale: Doxorubicin cardiotoxicity is mediated by iron-dependent free radical generation. Dexrazoxane chelates
iron and reduces oxidative stress. Cumulative dose limitation (<550 mg/m²) is standard to minimize risk.
Continuous infusion reduces peak levels and has been shown to lower cardiotoxicity incidence. Therefore, all listed
strategies are recommended.
NCSBN Clinical Judgment Model-Aligned Study Set with
Questions & Rationales - 130 Questions
Section 1: General (Questions 1-130)
1 A patient with chronic kidney disease (eGFR 25 mL/min/1.73m²) requires antibiotic therapy for a complicated
urinary tract infection. The prescriber considers gentamicin and ceftriaxone. Which statement accurately reflects
the pharmacodynamic principle of concentration-dependent killing and its application to dosing in renal
impairment?
A) Ceftriaxone exhibits concentration-dependent killing, requiring peak concentrations at least 10 times the MIC;
dose adjustment is based on renal function.
B) Gentamicin exhibits concentration-dependent killing, with a goal peak/MIC ratio of 8-10; extended-interval
dosing is preferred but requires monitoring of trough levels due to accumulation risk.
C) Both gentamicin and ceftriaxone are time-dependent antibiotics, so the duration above MIC is the key
parameter; renal impairment necessitates dose reduction.
D) Gentamicin exhibits time-dependent killing; therefore, maintaining trough levels below 2 mcg/mL is the
primary goal to prevent nephrotoxicity.
Answer: B
Rationale: Gentamicin is an aminoglycoside with concentration-dependent killing, where high peak/MIC ratios
(8-10) maximize efficacy. Extended-interval dosing is common, but in renal impairment, accumulation increases
toxicity risk, so trough monitoring is essential. Ceftriaxone has time-dependent killing, and its dosing is not
primarily adjusted for renal function. Option A incorrectly attributes concentration-dependent killing to
ceftriaxone. Option C misclassifies both drugs. Option D incorrectly describes gentamicin as time-dependent.
2 A researcher is designing a study to evaluate a new drug's effect on cardiac repolarization. Which of the
following electrophysiological parameters is the most specific surrogate marker for predicting the risk of
torsades de pointes?
A) Prolongation of the PR interval
B) Increase in QRS duration
C) Prolongation of the QT interval corrected for heart rate (QTc)
D) ST-segment elevation
Answer: C
Rationale: QTc prolongation is the most specific ECG marker for delayed ventricular repolarization, which
predisposes to torsades de pointes. PR interval reflects AV conduction, QRS duration indicates ventricular
depolarization, and ST elevation is associated with ischemia or injury, not drug-induced arrhythmia risk.
3 A patient with severe hepatic impairment (Child-Pugh class C) requires analgesia. Which of the following
statements about opioid pharmacokinetics is most accurate when considering fentanyl versus morphine?
A) Morphine is preferred because it undergoes glucuronidation, which is preserved in cirrhosis, whereas fentanyl
requires CYP3A4 metabolism, which is impaired.
B) Fentanyl is safer because its clearance is primarily via hepatic blood flow, which is less affected by
hepatocellular function than phase I metabolism.
C) Both drugs have similar pharmacokinetic profiles in liver disease; dose adjustments are not necessary if renal
function is normal.
,D) Morphine-6-glucuronide accumulation is a concern with morphine, but fentanyl's high first-pass metabolism
makes oral dosing unpredictable in cirrhosis.
Answer: B
Rationale: Fentanyl clearance is highly dependent on hepatic blood flow rather than hepatocellular function; in
cirrhosis, hepatic blood flow may be preserved, making fentanyl relatively safer. Morphine undergoes
glucuronidation (phase II), which is relatively preserved, but its active metabolite M6G accumulates in renal
impairment, which often coexists with liver disease. Option A overstates morphine's advantage. Option C is false.
Option D incorrectly emphasizes first-pass metabolism; fentanyl is not given orally.
4 A patient on warfarin therapy for mechanical heart valve requires a short course of antibiotics for a dental
procedure. The prescriber considers amoxicillin, clindamycin, or metronidazole. Which drug interaction
mechanism is most likely to potentiate warfarin's anticoagulant effect?
A) Amoxicillin reduces warfarin absorption by binding to it in the gut.
B) Clindamycin inhibits CYP2C9, reducing warfarin metabolism.
C) Metronidazole inhibits the vitamin K epoxide reductase complex indirectly, enhancing warfarin's effect.
D) All three antibiotics can potentiate warfarin by reducing gut flora that produce vitamin K.
Answer: D
Rationale: Broad-spectrum antibiotics reduce the intestinal flora that synthesize vitamin K, leading to decreased
vitamin K availability and enhanced warfarin effect. This is a common mechanism for many antibiotics. Option A
is incorrect; amoxicillin does not bind warfarin. Option B is incorrect; clindamycin does not inhibit CYP2C9.
Option C is partially correct for metronidazole (it inhibits warfarin metabolism via CYP2C9), but the broader
mechanism (option D) applies to all three, making it the best answer.
5 A patient with type 2 diabetes and obesity (BMI 38) is started on a GLP-1 receptor agonist. Which of the
following statements best explains the mechanism by which this drug class improves glycemic control and
promotes weight loss?
A) It increases insulin secretion in a glucose-dependent manner and delays gastric emptying, leading to reduced
postprandial glucose and increased satiety.
B) It inhibits the breakdown of incretin hormones, thereby increasing endogenous GLP-1 and GIP levels.
C) It directly activates AMP-kinase in skeletal muscle, enhancing glucose uptake independent of insulin.
D) It binds to the sulfonylurea receptor on pancreatic beta cells, causing insulin release regardless of glucose
level.
Answer: A
Rationale: GLP-1 receptor agonists (e.g., semaglutide, liraglutide) mimic endogenous GLP-1, which stimulates
glucose-dependent insulin secretion, suppresses glucagon, and slows gastric emptying. This results in lower
postprandial glucose and increased satiety, promoting weight loss. Option B describes DPP-4 inhibitors. Option C
describes metformin's mechanism. Option D describes sulfonylureas, which are not weight-neutral and can cause
hypoglycemia.
6 A patient with acute ischemic stroke receives alteplase within 3 hours of symptom onset. Which of the
following best explains the rationale for avoiding anticoagulant or antiplatelet therapy within 24 hours after
thrombolysis?
A) Alteplase depletes clotting factors, making anticoagulation unnecessary.
B) Concurrent use increases the risk of symptomatic intracranial hemorrhage due to impaired hemostasis from
fibrinogen depletion and ongoing clot lysis.
C) Antiplatelet agents are contraindicated because they inhibit the conversion of plasminogen to plasmin.
D) Anticoagulants enhance the metabolism of alteplase, reducing its efficacy.
, Answer: B
Rationale: Alteplase causes systemic fibrinogen depletion and lysis of fibrin clots, including hemostatic plugs.
Adding anticoagulants or antiplatelet agents within 24 hours significantly increases the risk of intracranial
hemorrhage. Option A is incorrect; clotting factors are not depleted. Option C is incorrect; antiplatelet agents do
not affect plasminogen conversion. Option D is incorrect; anticoagulants do not alter alteplase metabolism.
7 A patient with severe sepsis is started on norepinephrine for hemodynamic support. Which of the following best
describes the pharmacodynamic effect of norepinephrine on the vasculature and its impact on organ perfusion?
A) It is a selective alpha-1 agonist that causes vasodilation in splanchnic beds, improving renal blood flow.
B) It acts primarily on beta-2 receptors, causing bronchodilation and increased heart rate.
C) It is a potent alpha-1 and beta-1 agonist that increases mean arterial pressure through vasoconstriction, but
may reduce perfusion to some vascular beds at high doses.
D) It activates dopamine receptors in the renal vasculature, selectively increasing renal blood flow.
Answer: C
Rationale: Norepinephrine is a catecholamine with strong alpha-1 (vasoconstriction) and beta-1 (positive inotropy)
activity. It effectively increases MAP, but excessive vasoconstriction can compromise perfusion in renal,
splanchnic, and peripheral beds. Option A is incorrect; it causes vasoconstriction, not dilation. Option B describes
beta-2 effects (e.g., albuterol). Option D describes low-dose dopamine, which is no longer recommended.
8 A patient with bipolar I disorder is stabilized on lithium. After 6 months of therapy, routine labs show a serum
lithium level of 1.2 mEq/L (therapeutic range 0.6-1.2). The patient reports mild tremor and polyuria. Which of
the following is the most appropriate next step?
A) Increase the lithium dose to achieve a level of 1.5 mEq/L for better mood stabilization.
B) Discontinue lithium immediately and switch to valproate due to signs of toxicity.
C) Maintain the current dose but monitor renal function and consider dose reduction if symptoms worsen or if
creatinine rises.
D) Add a diuretic to enhance lithium excretion and lower the serum level.
Answer: C
Rationale: The lithium level is at the upper end of therapeutic range, and mild tremor and polyuria are common side
effects that may be tolerable. Dose reduction should be considered if symptoms become bothersome or if renal
function declines. Option A would increase toxicity risk. Option B is premature; symptoms are not severe. Option
D is dangerous; thiazide diuretics can increase lithium reabsorption and raise levels.
9 A patient with metastatic breast cancer is being treated with doxorubicin. Which of the following strategies is
most effective for preventing doxorubicin-induced cardiotoxicity?
A) Co-administration of dexrazoxane, an iron chelator that reduces free radical formation.
B) Limiting the cumulative dose to less than 550 mg/m², as cardiotoxicity is dose-dependent and irreversible.
C) Using a continuous infusion rather than bolus administration to lower peak plasma concentrations.
D) All of the above are recommended strategies.
Answer: D
Rationale: Doxorubicin cardiotoxicity is mediated by iron-dependent free radical generation. Dexrazoxane chelates
iron and reduces oxidative stress. Cumulative dose limitation (<550 mg/m²) is standard to minimize risk.
Continuous infusion reduces peak levels and has been shown to lower cardiotoxicity incidence. Therefore, all listed
strategies are recommended.
