Page |1
NUR 521 Advanced Pharmacology – Exam 3 Practice Questions complete
Exam 3 TEST BANK Practice Questions with 100% correct Answers and
Rationale 2026|2027 UPDATED!!!!! University of Alabama
Exam Coverage: This exam assesses graduate-level advanced pharmacology
competencies across cardiovascular, endocrine, antimicrobial, psychotropic, and
autonomic pharmacotherapy, emphasizing mechanism-based reasoning,
evidence-based guideline application, drug-drug/drug-disease interactions, and
safe prescribing in complex patient scenarios. You are responsible for the name,
MOA, indication, common adverse effects, serious adverse effects, dosing,
administration, contraindications, interactions, and patient education for all
prototype drugs presented in each module.
Section 1: Cardiovascular Pharmacology (Questions)
Heart Failure Pharmacology
1. A patient with systolic heart failure and reduced ejection
fraction (HFrEF) is optimized on guideline-directed medical
therapy. Which combination produces the greatest mortality
benefit by targeting complementary neurohormonal
pathways?
A) Sacubitril/valsartan plus a beta-blocker plus a
mineralocorticoid receptor antagonist
B) Hydralazine plus isosorbide dinitrate plus furosemide
, Page |2
C) Digoxin plus a loop diuretic plus a thiazide diuretic
D) Amlodipine plus an ACE inhibitor plus a statin
Answer: A
Rationale: Sacubitril/valsartan (ARNI), beta-blockers, and MRAs
each reduce mortality via distinct neurohormonal mechanisms
and are core GDMT for HFrEF. Hydralazine/nitrate is reserved
for specific populations (e.g., ACEi/ARB intolerance), while
digoxin and amlodipine do not reduce mortality.
2. A patient with HFrEF (EF 28%) is optimized on
sacubitril/valsartan, carvedilol, and spironolactone but
remains symptomatic. Which addition best reduces
cardiovascular death and HF hospitalization?
A) Ivabradine
B) Dapagliflozin
C) Digoxin
D) Hydralazine/isosorbide dinitrate
Answer: B
Rationale: SGLT2 inhibitors (dapagliflozin/empagliflozin) are
now a pillar of guideline-directed medical therapy for HFrEF,
reducing CV death and HF hospitalization regardless of diabetes
status (DAPA-HF, EMPEROR-Reduced). Ivabradine reduces
hospitalization but not mortality; digoxin reduces
hospitalizations only; hydralazine/ISDN improves outcomes
primarily in self-identified Black patients or when
ACEi/ARB/ARNI is not tolerated.
, Page |3
3. Which statement best describes the pharmacodynamic
basis for using a beta-blocker in heart failure with reduced
ejection fraction?
A) Beta-blockers acutely increase cardiac output by enhancing
contractility
B) Beta-blockers blunt chronic sympathetic overactivation,
reversing adverse remodeling and reducing mortality
C) Beta-blockers selectively block beta-2 receptors to reduce
heart rate
D) Beta-blockers increase renin release to improve renal
perfusion
Answer: B
Rationale: In HFrEF, chronic sympathetic activation drives
adverse remodeling; beta-blockers (e.g., carvedilol, metoprolol
succinate, bisoprolol) blunt this, improving survival. They do not
acutely increase contractility (in fact, they may transiently
worsen symptoms), they block beta-1 predominantly, and they
decrease renin release.
4. A patient with heart failure with reduced ejection fraction
(HFrEF) is transitioning from IV furosemide to oral therapy.
Which pharmacologic principle best explains why the oral
dose must be substantially higher than the IV dose to achieve
equivalent diuresis?
A) Oral furosemide has a high first-pass hepatic extraction,
reducing systemic bioavailability to approximately 10-20%
, Page |4
B) Oral furosemide is a weak acid that is ionized in the stomach,
preventing absorption
C) Oral furosemide undergoes extensive renal tubular secretion,
which competes with its own reabsorption
D) Oral furosemide binds to plasma albumin more avidly than
the IV formulation
Answer: A
Rationale: Oral furosemide bioavailability averages only 10-
20% (and is erratic) due to extensive first-pass metabolism and
incomplete absorption; therefore, oral doses must be roughly 2-
2.5 times the IV dose. Absorption is not primarily limited by
gastric ionization; tubular secretion delivers drug to the site of
action rather than limiting systemic availability; protein binding
is similar between routes.
5. A patient with HFrEF is prescribed sacubitril/valsartan. The
nurse practitioner should monitor for:
A) Hyperkalemia and hypotension
B) Hypokalemia and hypertension
C) Bradycardia
D) Hyperglycemia
Answer: A
Rationale: Sacubitril/valsartan (Entresto) can cause
hyperkalemia and hypotension. It is contraindicated with ACE
inhibitors due to angioedema risk.
NUR 521 Advanced Pharmacology – Exam 3 Practice Questions complete
Exam 3 TEST BANK Practice Questions with 100% correct Answers and
Rationale 2026|2027 UPDATED!!!!! University of Alabama
Exam Coverage: This exam assesses graduate-level advanced pharmacology
competencies across cardiovascular, endocrine, antimicrobial, psychotropic, and
autonomic pharmacotherapy, emphasizing mechanism-based reasoning,
evidence-based guideline application, drug-drug/drug-disease interactions, and
safe prescribing in complex patient scenarios. You are responsible for the name,
MOA, indication, common adverse effects, serious adverse effects, dosing,
administration, contraindications, interactions, and patient education for all
prototype drugs presented in each module.
Section 1: Cardiovascular Pharmacology (Questions)
Heart Failure Pharmacology
1. A patient with systolic heart failure and reduced ejection
fraction (HFrEF) is optimized on guideline-directed medical
therapy. Which combination produces the greatest mortality
benefit by targeting complementary neurohormonal
pathways?
A) Sacubitril/valsartan plus a beta-blocker plus a
mineralocorticoid receptor antagonist
B) Hydralazine plus isosorbide dinitrate plus furosemide
, Page |2
C) Digoxin plus a loop diuretic plus a thiazide diuretic
D) Amlodipine plus an ACE inhibitor plus a statin
Answer: A
Rationale: Sacubitril/valsartan (ARNI), beta-blockers, and MRAs
each reduce mortality via distinct neurohormonal mechanisms
and are core GDMT for HFrEF. Hydralazine/nitrate is reserved
for specific populations (e.g., ACEi/ARB intolerance), while
digoxin and amlodipine do not reduce mortality.
2. A patient with HFrEF (EF 28%) is optimized on
sacubitril/valsartan, carvedilol, and spironolactone but
remains symptomatic. Which addition best reduces
cardiovascular death and HF hospitalization?
A) Ivabradine
B) Dapagliflozin
C) Digoxin
D) Hydralazine/isosorbide dinitrate
Answer: B
Rationale: SGLT2 inhibitors (dapagliflozin/empagliflozin) are
now a pillar of guideline-directed medical therapy for HFrEF,
reducing CV death and HF hospitalization regardless of diabetes
status (DAPA-HF, EMPEROR-Reduced). Ivabradine reduces
hospitalization but not mortality; digoxin reduces
hospitalizations only; hydralazine/ISDN improves outcomes
primarily in self-identified Black patients or when
ACEi/ARB/ARNI is not tolerated.
, Page |3
3. Which statement best describes the pharmacodynamic
basis for using a beta-blocker in heart failure with reduced
ejection fraction?
A) Beta-blockers acutely increase cardiac output by enhancing
contractility
B) Beta-blockers blunt chronic sympathetic overactivation,
reversing adverse remodeling and reducing mortality
C) Beta-blockers selectively block beta-2 receptors to reduce
heart rate
D) Beta-blockers increase renin release to improve renal
perfusion
Answer: B
Rationale: In HFrEF, chronic sympathetic activation drives
adverse remodeling; beta-blockers (e.g., carvedilol, metoprolol
succinate, bisoprolol) blunt this, improving survival. They do not
acutely increase contractility (in fact, they may transiently
worsen symptoms), they block beta-1 predominantly, and they
decrease renin release.
4. A patient with heart failure with reduced ejection fraction
(HFrEF) is transitioning from IV furosemide to oral therapy.
Which pharmacologic principle best explains why the oral
dose must be substantially higher than the IV dose to achieve
equivalent diuresis?
A) Oral furosemide has a high first-pass hepatic extraction,
reducing systemic bioavailability to approximately 10-20%
, Page |4
B) Oral furosemide is a weak acid that is ionized in the stomach,
preventing absorption
C) Oral furosemide undergoes extensive renal tubular secretion,
which competes with its own reabsorption
D) Oral furosemide binds to plasma albumin more avidly than
the IV formulation
Answer: A
Rationale: Oral furosemide bioavailability averages only 10-
20% (and is erratic) due to extensive first-pass metabolism and
incomplete absorption; therefore, oral doses must be roughly 2-
2.5 times the IV dose. Absorption is not primarily limited by
gastric ionization; tubular secretion delivers drug to the site of
action rather than limiting systemic availability; protein binding
is similar between routes.
5. A patient with HFrEF is prescribed sacubitril/valsartan. The
nurse practitioner should monitor for:
A) Hyperkalemia and hypotension
B) Hypokalemia and hypertension
C) Bradycardia
D) Hyperglycemia
Answer: A
Rationale: Sacubitril/valsartan (Entresto) can cause
hyperkalemia and hypotension. It is contraindicated with ACE
inhibitors due to angioedema risk.
