NUR 6011 Exams 1–3 – Advanced
Pharmacology – (2026) Actual Questions
& Answers (WPU)
📘 NUR 6011 — EXAM 1
Cardiovascular, Renal & Related Pharmacology
1.1 KL is a 57-year-old male seen in the ED for suspected food poisoning with
nausea/vomiting for 2 days. Labs: K 5.6 mEq/L, SrCr 1.9, BUN 23. ECG shows second-
degree AV block. Digoxin level is 4.1 ng/mL taken ~3 hours post-dose. Based on this, which is
most accurate?
A. The digoxin level was taken too soon; wait at least 6–8 hours
B. With elevated SrCr, GI complaints are likely from uremia
C. It appears this patient is experiencing signs and symptoms of digoxin toxicity
D. The patient should immediately receive lipid rescue
✅ Answer: C. It appears this patient is experiencing signs and symptoms of digoxin
toxicity
Rationale: Bradyarrhythmia (AV block), hyperkalemia, GI symptoms, and a markedly elevated
digoxin level are classic for digoxin toxicity. Although timing of the level matters, the clinical
picture is consistent with toxicity and warrants treatment.
1.2 LP is a 56-year-old type 1 diabetic with HTN new to your practice. He stopped taking
enalapril 8 years ago due to a cough. He has been taking carvedilol for his BP, which is not
very well controlled. Which is correct?
A. Losartan may be an alternative; carvedilol can be abruptly stopped and losartan started
B. Enalapril should not be used in diabetics; losartan is safer with less risk of cough in
diabetics
C. Valsartan may be an alternative, so it can be started while the carvedilol is slowly weaned
off
D. Neither losartan nor valsartan is an option since the patient had cough with enalapril
✅ Answer: C. Valsartan may be an alternative, so it can be started while the carvedilol is
slowly weaned off
,Rationale: ACE-inhibitor–induced cough does not preclude ARB use, so valsartan (or another
ARB) is reasonable. Beta-blockers should not be stopped abruptly because of rebound
sympathetic activity; slow taper while introducing an ARB is appropriate.
1.3 WR is a 72-year-old male with a digoxin level of 1.8 mcg/mL on furosemide and
spironolactone. He now presents with bradycardia (HR 42), sluggishness, and loss of
appetite. Which statement about potassium and digoxin toxicity is correct?
A. Low serum potassium can lead to digoxin toxicity with normal digoxin levels
B. High serum potassium levels may be a marker of severe digoxin toxicity
C. Both A and B are correct
D. High serum potassium can lead to digoxin toxicity with normal digoxin levels
✅ Answer: C. Both A and B are correct
Rationale: Hypokalemia increases digoxin binding to Na ⁺/K ⁺-ATPase and predisposes to
toxicity even when total digoxin levels are "therapeutic." In severe digoxin poisoning,
hyperkalemia often emerges and is a poor prognostic marker.
1.4 KL is a 66-year-old female with vasospastic angina. Which of the following medications
may be the best option?
A. Metoprolol
B. Amlodipine
C. Ranolazine
D. Atenolol
✅ Answer: B. Amlodipine
Rationale: Prinzmetal (vasospastic) angina is treated with nitrates and calcium channel
blockers, particularly dihydropyridines like amlodipine that cause coronary vasodilation. Beta-
blockers can worsen vasospasm and are generally avoided.
1.5 DS has been receiving digoxin, furosemide, and lisinopril for several months to treat CHF.
At 3 months it was noted his SrCr went from 1.2 mg/dL to 2.4 mg/dL. What could explain this?
A. Digoxin led to pre-renal azotemia
B. Lisinopril caused an acute decompensation in renal function because the patient had
bilateral renal artery stenosis
C. A medication error occurred and the patient was actually given irbesartan
D. Lisinopril resulted in a high potassium level which then resulted in a decline in renal
function
, ✅ Answer: B. Lisinopril caused an acute decompensation in renal function because the
patient had bilateral renal artery stenosis
Rationale: ACE inhibitors can precipitate an acute rise in creatinine in patients with bilateral
renal artery stenosis because they reduce efferent arteriolar tone and intraglomerular
pressure. The timeline and doubling of SrCr are classic for ACEI-induced renal
decompensation in this setting.
1.6 Beta blockers are the drugs of choice for effort-induced angina because they primarily:
A. Improve myocardial oxygen supply by causing coronary artery vasodilation
B. Decrease myocardial oxygen demand by decreasing heart rate and force of contractility
C. Decrease oxygen demand by causing peripheral vasodilation
D. Are best for vasospastic angina and not effort-induced angina
✅ Answer: B. Decrease myocardial oxygen demand by decreasing heart rate and force of
contractility
Rationale: Beta-blockers reduce heart rate, blood pressure, and myocardial contractility,
thereby lowering myocardial oxygen demand during exertion. This makes them first-line
agents for stable (effort-induced) angina.
1.7 A patient with heart failure with reduced ejection fraction (HFrEF) is prescribed
sacubitril/valsartan (Entresto). Which of the following is the most important consideration
before initiating this therapy?
A. The patient must have a potassium level below 3.5 mEq/L
B. The patient must be off ACE inhibitors for at least 36 hours before starting
C. The patient must have an ejection fraction greater than 50%
D. The drug is only approved for patients over 75 years of age
✅ Answer: B. The patient must be off ACE inhibitors for at least 36 hours before starting
Rationale: Sacubitril/valsartan (ARNI) is contraindicated with concomitant ACE inhibitor use
due to the risk of angioedema. A washout period of at least 36 hours from the last ACE
inhibitor dose is required before initiation.
1.8 Which of the following is the mechanism of action of spironolactone in heart failure?
A. Blocks aldosterone receptors, preventing sodium retention and potassium loss
B. Inhibits the Na-K-2Cl cotransporter in the loop of Henle
C. Blocks beta-1 adrenergic receptors in the heart
D. Inhibits angiotensin-converting enzyme, reducing aldosterone release
Pharmacology – (2026) Actual Questions
& Answers (WPU)
📘 NUR 6011 — EXAM 1
Cardiovascular, Renal & Related Pharmacology
1.1 KL is a 57-year-old male seen in the ED for suspected food poisoning with
nausea/vomiting for 2 days. Labs: K 5.6 mEq/L, SrCr 1.9, BUN 23. ECG shows second-
degree AV block. Digoxin level is 4.1 ng/mL taken ~3 hours post-dose. Based on this, which is
most accurate?
A. The digoxin level was taken too soon; wait at least 6–8 hours
B. With elevated SrCr, GI complaints are likely from uremia
C. It appears this patient is experiencing signs and symptoms of digoxin toxicity
D. The patient should immediately receive lipid rescue
✅ Answer: C. It appears this patient is experiencing signs and symptoms of digoxin
toxicity
Rationale: Bradyarrhythmia (AV block), hyperkalemia, GI symptoms, and a markedly elevated
digoxin level are classic for digoxin toxicity. Although timing of the level matters, the clinical
picture is consistent with toxicity and warrants treatment.
1.2 LP is a 56-year-old type 1 diabetic with HTN new to your practice. He stopped taking
enalapril 8 years ago due to a cough. He has been taking carvedilol for his BP, which is not
very well controlled. Which is correct?
A. Losartan may be an alternative; carvedilol can be abruptly stopped and losartan started
B. Enalapril should not be used in diabetics; losartan is safer with less risk of cough in
diabetics
C. Valsartan may be an alternative, so it can be started while the carvedilol is slowly weaned
off
D. Neither losartan nor valsartan is an option since the patient had cough with enalapril
✅ Answer: C. Valsartan may be an alternative, so it can be started while the carvedilol is
slowly weaned off
,Rationale: ACE-inhibitor–induced cough does not preclude ARB use, so valsartan (or another
ARB) is reasonable. Beta-blockers should not be stopped abruptly because of rebound
sympathetic activity; slow taper while introducing an ARB is appropriate.
1.3 WR is a 72-year-old male with a digoxin level of 1.8 mcg/mL on furosemide and
spironolactone. He now presents with bradycardia (HR 42), sluggishness, and loss of
appetite. Which statement about potassium and digoxin toxicity is correct?
A. Low serum potassium can lead to digoxin toxicity with normal digoxin levels
B. High serum potassium levels may be a marker of severe digoxin toxicity
C. Both A and B are correct
D. High serum potassium can lead to digoxin toxicity with normal digoxin levels
✅ Answer: C. Both A and B are correct
Rationale: Hypokalemia increases digoxin binding to Na ⁺/K ⁺-ATPase and predisposes to
toxicity even when total digoxin levels are "therapeutic." In severe digoxin poisoning,
hyperkalemia often emerges and is a poor prognostic marker.
1.4 KL is a 66-year-old female with vasospastic angina. Which of the following medications
may be the best option?
A. Metoprolol
B. Amlodipine
C. Ranolazine
D. Atenolol
✅ Answer: B. Amlodipine
Rationale: Prinzmetal (vasospastic) angina is treated with nitrates and calcium channel
blockers, particularly dihydropyridines like amlodipine that cause coronary vasodilation. Beta-
blockers can worsen vasospasm and are generally avoided.
1.5 DS has been receiving digoxin, furosemide, and lisinopril for several months to treat CHF.
At 3 months it was noted his SrCr went from 1.2 mg/dL to 2.4 mg/dL. What could explain this?
A. Digoxin led to pre-renal azotemia
B. Lisinopril caused an acute decompensation in renal function because the patient had
bilateral renal artery stenosis
C. A medication error occurred and the patient was actually given irbesartan
D. Lisinopril resulted in a high potassium level which then resulted in a decline in renal
function
, ✅ Answer: B. Lisinopril caused an acute decompensation in renal function because the
patient had bilateral renal artery stenosis
Rationale: ACE inhibitors can precipitate an acute rise in creatinine in patients with bilateral
renal artery stenosis because they reduce efferent arteriolar tone and intraglomerular
pressure. The timeline and doubling of SrCr are classic for ACEI-induced renal
decompensation in this setting.
1.6 Beta blockers are the drugs of choice for effort-induced angina because they primarily:
A. Improve myocardial oxygen supply by causing coronary artery vasodilation
B. Decrease myocardial oxygen demand by decreasing heart rate and force of contractility
C. Decrease oxygen demand by causing peripheral vasodilation
D. Are best for vasospastic angina and not effort-induced angina
✅ Answer: B. Decrease myocardial oxygen demand by decreasing heart rate and force of
contractility
Rationale: Beta-blockers reduce heart rate, blood pressure, and myocardial contractility,
thereby lowering myocardial oxygen demand during exertion. This makes them first-line
agents for stable (effort-induced) angina.
1.7 A patient with heart failure with reduced ejection fraction (HFrEF) is prescribed
sacubitril/valsartan (Entresto). Which of the following is the most important consideration
before initiating this therapy?
A. The patient must have a potassium level below 3.5 mEq/L
B. The patient must be off ACE inhibitors for at least 36 hours before starting
C. The patient must have an ejection fraction greater than 50%
D. The drug is only approved for patients over 75 years of age
✅ Answer: B. The patient must be off ACE inhibitors for at least 36 hours before starting
Rationale: Sacubitril/valsartan (ARNI) is contraindicated with concomitant ACE inhibitor use
due to the risk of angioedema. A washout period of at least 36 hours from the last ACE
inhibitor dose is required before initiation.
1.8 Which of the following is the mechanism of action of spironolactone in heart failure?
A. Blocks aldosterone receptors, preventing sodium retention and potassium loss
B. Inhibits the Na-K-2Cl cotransporter in the loop of Henle
C. Blocks beta-1 adrenergic receptors in the heart
D. Inhibits angiotensin-converting enzyme, reducing aldosterone release
