PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
PharmD Cardiovascular
Pharmacotherapy
2026–2027 Clinical Case Practice Examination
110 original multiple-choice clinical cases | Correct answers | Detailed rationales | Incorrect-option explanations
An independently authored educational review for PharmD and advanced clinical pharmacy learners. This
is NOT an official university examination, licensed question bank, or guarantee of examination performance.
Individual medication decisions depend on patient factors, the current product label, institutional policies,
and up-to-date clinical guidelines.
How to use this resource
Attempt each case before revealing the answer; select one best response (A–D).
Review the correct-answer reasoning and each distractor explanation. Flag uncertainties for textbook or
guideline review.
For urgent symptoms (such as possible ACS, angioedema, major bleeding, or shock), the correct clinical
priority is prompt evaluation, not unsupervised medication changes.
Some scenarios use simplified, explicitly hypothetical numbers and U.S. guideline conventions for
educational purposes.
Content overview
01 | Hypertension and antihypertensive selection — Questions 1–10
02 | HFrEF guideline-directed pharmacotherapy — Questions 11–20
03 | HFpEF, diuretics, electrolytes, and monitoring — Questions 21–30
04 | Chronic coronary disease and antianginal drugs — Questions 31–40
05 | Acute coronary syndromes and PCI — Questions 41–50
06 | Dyslipidemia and ASCVD prevention (2026 context) — Questions 51–60
07 | Atrial fibrillation and anticoagulant choice — Questions 61–70
08 | Arrhythmia therapy and electrophysiology safety — Questions 71–80
09 | VTE, anticoagulants, and antithrombotic safety — Questions 81–90
10 | Drug interactions, adverse reactions, counseling — Questions 91–100
11 | Cardiovascular clinical calculations and integrated cases — Questions 101–110
Prepared October 2026. Guideline references are listed at the end of the document; recheck them for newer revisions.
Independent educational practice • Not an official examination | Page 1
, PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
01 | Hypertension and antihypertensive selection
Q001. A 56-year-old with repeated clinic blood pressures near 156/94 mm Hg has no compelling
comorbidity and normal renal function. Which is a guideline-supported initial drug class?
A. Digoxin
B. Amlodipine, a dihydropyridine calcium-channel blocker
C. Amiodarone
D. Clopidogrel
CORRECT ANSWER: B — Amlodipine, a dihydropyridine calcium-channel blocker
DETAILED RATIONALE: Long-acting dihydropyridine calcium-channel blockers are first-line options
for uncomplicated hypertension.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Digoxin treats selected cardiac conditions, not primary hypertension.
C. Amiodarone is an antiarrhythmic, not routine blood-pressure therapy.
D. Clopidogrel is an antiplatelet and does not lower blood pressure.
Q002. A 63-year-old with hypertension, diabetes, urine albumin-creatinine ratio 180 mg/g, and
eGFR 55 has potassium 4.2 mmol/L. Which medication class has particular renal benefit?
A. An angiotensin-receptor blocker such as losartan
B. An alpha-1 blocker as sole first-line therapy
C. A direct vasodilator as sole first-line therapy
D. A short-acting nitrate
CORRECT ANSWER: A — An angiotensin-receptor blocker such as losartan
DETAILED RATIONALE: Renin-angiotensin system blockade helps protect kidneys in hypertension
with albuminuric CKD; monitor creatinine and potassium.
WHY THE OTHER OPTIONS ARE INCORRECT:
B. Alpha-1 blockers are not the preferred kidney-protective choice.
C. Hydralazine alone lacks the same albuminuria-focused evidence.
D. Nitrates treat angina, not albuminuric CKD.
Q003. A patient starts lisinopril and develops a persistent dry cough without respiratory
infection. BP remains controlled. What change is most appropriate?
A. Add another ACE inhibitor
B. Double the lisinopril dose
C. Add an antibiotic without infectious findings
D. Replace lisinopril with an ARB after evaluating the cough
CORRECT ANSWER: D — Replace lisinopril with an ARB after evaluating the cough
DETAILED RATIONALE: ARBs do not inhibit bradykinin breakdown and are less likely than ACE
inhibitors to cause cough.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Another ACE inhibitor shares the cough mechanism.
B. Increasing lisinopril can worsen intolerance.
Independent educational practice • Not an official examination | Page 2
, PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
C. Antibiotics do not treat ACE-inhibitor cough.
Q004. A 50-year-old using hydrochlorothiazide reports weakness. Potassium is 3.0 mmol/L. What
adverse effect best explains this finding?
A. Drug-induced hyperkalemia
B. Increased calcium excretion causing hypocalcemia
C. Increased urinary potassium loss from thiazide therapy
D. Suppression of renal sodium excretion
CORRECT ANSWER: C — Increased urinary potassium loss from thiazide therapy
DETAILED RATIONALE: Thiazide diuretics increase distal sodium delivery and can cause
hypokalemia; assess severity and replenish as appropriate.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. The measured value is low, not high potassium.
B. Thiazides commonly reduce urinary calcium excretion.
D. Thiazides increase, rather than suppress, urinary sodium excretion.
Q005. A 71-year-old develops ankle edema after amlodipine titration, with clear lungs and no
weight gain. What is the most likely cause?
A. Acute left ventricular failure established by edema alone
B. Precapillary arteriolar dilation from amlodipine
C. Bradykinin-mediated angioedema
D. A direct increase in sodium retention from mineralocorticoid receptor activation
CORRECT ANSWER: B — Precapillary arteriolar dilation from amlodipine
DETAILED RATIONALE: Dihydropyridine CCBs can produce dependent peripheral edema through
arteriolar dilation; evaluate alternative causes.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Isolated dependent edema cannot establish acute HF.
C. Bradykinin angioedema involves deeper tissues, not typical ankle swelling.
D. Amlodipine does not act by activating mineralocorticoid receptors.
Q006. An adult receiving spironolactone for resistant hypertension starts trimethoprim-
sulfamethoxazole. Which risk requires particular attention?
A. Hyperkalemia
B. Hypoglycemia from beta-cell stimulation
C. Severe hypocalcemia
D. Drug-induced thrombocytosis
CORRECT ANSWER: A — Hyperkalemia
DETAILED RATIONALE: Spironolactone retains potassium and trimethoprim may further reduce
renal potassium excretion.
WHY THE OTHER OPTIONS ARE INCORRECT:
B. Neither drug combination primarily stimulates pancreatic insulin release.
Independent educational practice • Not an official examination | Page 3
, PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
C. Hypocalcemia is not the characteristic combined risk.
D. High platelets are not the main expected adverse effect.
Q007. A 45-year-old with hypertension is 10 weeks pregnant and currently taking lisinopril.
Which is the most important medication action?
A. Continue lisinopril because it protects the fetal kidneys
B. Add aliskiren to improve BP control
C. Change to valsartan without further review
D. Urgently review and replace the ACE inhibitor with a pregnancy-compatible regimen
CORRECT ANSWER: D — Urgently review and replace the ACE inhibitor with a pregnancy-compatible
regimen
DETAILED RATIONALE: ACE inhibitors and ARBs can cause fetal harm and should not be continued in
pregnancy; specialist evaluation is appropriate.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. ACE inhibitors are not fetal kidney protectants.
B. Aliskiren is also unsuitable in pregnancy.
C. ARBs also carry fetal toxicity concerns.
Q008. A patient treated with clonidine misses multiple doses and develops severe rebound
hypertension and tachycardia. What mechanism explains the episode?
A. Excess nitric oxide generation
B. Persistent sodium-channel blockade
C. Abrupt withdrawal of central alpha-2 adrenergic agonism
D. Increased prostacyclin release
CORRECT ANSWER: C — Abrupt withdrawal of central alpha-2 adrenergic agonism
DETAILED RATIONALE: Sudden clonidine cessation removes sympathetic suppression and can trigger
catecholamine-mediated rebound hypertension.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Nitric oxide vasodilation would not explain rebound hypertension.
B. Clonidine does not act primarily as a sodium-channel blocker.
D. Prostacyclin promotes vasodilation rather than sympathetic rebound.
Q009. A patient with resistant hypertension has BP above goal despite an ACE inhibitor,
amlodipine, and chlorthalidone at tolerated doses. Potassium is normal and eGFR is adequate.
Which add-on is often useful after confirming adherence and secondary causes?
A. Verapamil solely to duplicate calcium-channel blockade
B. Spironolactone with potassium and kidney-function monitoring
C. Aspirin solely to lower BP
D. Sublingual nitroglycerin as daily long-term monotherapy
CORRECT ANSWER: B — Spironolactone with potassium and kidney-function monitoring
DETAILED RATIONALE: Mineralocorticoid receptor antagonists can help resistant hypertension when
safe and appropriately monitored.
Independent educational practice • Not an official examination | Page 4
PharmD Cardiovascular
Pharmacotherapy
2026–2027 Clinical Case Practice Examination
110 original multiple-choice clinical cases | Correct answers | Detailed rationales | Incorrect-option explanations
An independently authored educational review for PharmD and advanced clinical pharmacy learners. This
is NOT an official university examination, licensed question bank, or guarantee of examination performance.
Individual medication decisions depend on patient factors, the current product label, institutional policies,
and up-to-date clinical guidelines.
How to use this resource
Attempt each case before revealing the answer; select one best response (A–D).
Review the correct-answer reasoning and each distractor explanation. Flag uncertainties for textbook or
guideline review.
For urgent symptoms (such as possible ACS, angioedema, major bleeding, or shock), the correct clinical
priority is prompt evaluation, not unsupervised medication changes.
Some scenarios use simplified, explicitly hypothetical numbers and U.S. guideline conventions for
educational purposes.
Content overview
01 | Hypertension and antihypertensive selection — Questions 1–10
02 | HFrEF guideline-directed pharmacotherapy — Questions 11–20
03 | HFpEF, diuretics, electrolytes, and monitoring — Questions 21–30
04 | Chronic coronary disease and antianginal drugs — Questions 31–40
05 | Acute coronary syndromes and PCI — Questions 41–50
06 | Dyslipidemia and ASCVD prevention (2026 context) — Questions 51–60
07 | Atrial fibrillation and anticoagulant choice — Questions 61–70
08 | Arrhythmia therapy and electrophysiology safety — Questions 71–80
09 | VTE, anticoagulants, and antithrombotic safety — Questions 81–90
10 | Drug interactions, adverse reactions, counseling — Questions 91–100
11 | Cardiovascular clinical calculations and integrated cases — Questions 101–110
Prepared October 2026. Guideline references are listed at the end of the document; recheck them for newer revisions.
Independent educational practice • Not an official examination | Page 1
, PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
01 | Hypertension and antihypertensive selection
Q001. A 56-year-old with repeated clinic blood pressures near 156/94 mm Hg has no compelling
comorbidity and normal renal function. Which is a guideline-supported initial drug class?
A. Digoxin
B. Amlodipine, a dihydropyridine calcium-channel blocker
C. Amiodarone
D. Clopidogrel
CORRECT ANSWER: B — Amlodipine, a dihydropyridine calcium-channel blocker
DETAILED RATIONALE: Long-acting dihydropyridine calcium-channel blockers are first-line options
for uncomplicated hypertension.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Digoxin treats selected cardiac conditions, not primary hypertension.
C. Amiodarone is an antiarrhythmic, not routine blood-pressure therapy.
D. Clopidogrel is an antiplatelet and does not lower blood pressure.
Q002. A 63-year-old with hypertension, diabetes, urine albumin-creatinine ratio 180 mg/g, and
eGFR 55 has potassium 4.2 mmol/L. Which medication class has particular renal benefit?
A. An angiotensin-receptor blocker such as losartan
B. An alpha-1 blocker as sole first-line therapy
C. A direct vasodilator as sole first-line therapy
D. A short-acting nitrate
CORRECT ANSWER: A — An angiotensin-receptor blocker such as losartan
DETAILED RATIONALE: Renin-angiotensin system blockade helps protect kidneys in hypertension
with albuminuric CKD; monitor creatinine and potassium.
WHY THE OTHER OPTIONS ARE INCORRECT:
B. Alpha-1 blockers are not the preferred kidney-protective choice.
C. Hydralazine alone lacks the same albuminuria-focused evidence.
D. Nitrates treat angina, not albuminuric CKD.
Q003. A patient starts lisinopril and develops a persistent dry cough without respiratory
infection. BP remains controlled. What change is most appropriate?
A. Add another ACE inhibitor
B. Double the lisinopril dose
C. Add an antibiotic without infectious findings
D. Replace lisinopril with an ARB after evaluating the cough
CORRECT ANSWER: D — Replace lisinopril with an ARB after evaluating the cough
DETAILED RATIONALE: ARBs do not inhibit bradykinin breakdown and are less likely than ACE
inhibitors to cause cough.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Another ACE inhibitor shares the cough mechanism.
B. Increasing lisinopril can worsen intolerance.
Independent educational practice • Not an official examination | Page 2
, PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
C. Antibiotics do not treat ACE-inhibitor cough.
Q004. A 50-year-old using hydrochlorothiazide reports weakness. Potassium is 3.0 mmol/L. What
adverse effect best explains this finding?
A. Drug-induced hyperkalemia
B. Increased calcium excretion causing hypocalcemia
C. Increased urinary potassium loss from thiazide therapy
D. Suppression of renal sodium excretion
CORRECT ANSWER: C — Increased urinary potassium loss from thiazide therapy
DETAILED RATIONALE: Thiazide diuretics increase distal sodium delivery and can cause
hypokalemia; assess severity and replenish as appropriate.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. The measured value is low, not high potassium.
B. Thiazides commonly reduce urinary calcium excretion.
D. Thiazides increase, rather than suppress, urinary sodium excretion.
Q005. A 71-year-old develops ankle edema after amlodipine titration, with clear lungs and no
weight gain. What is the most likely cause?
A. Acute left ventricular failure established by edema alone
B. Precapillary arteriolar dilation from amlodipine
C. Bradykinin-mediated angioedema
D. A direct increase in sodium retention from mineralocorticoid receptor activation
CORRECT ANSWER: B — Precapillary arteriolar dilation from amlodipine
DETAILED RATIONALE: Dihydropyridine CCBs can produce dependent peripheral edema through
arteriolar dilation; evaluate alternative causes.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Isolated dependent edema cannot establish acute HF.
C. Bradykinin angioedema involves deeper tissues, not typical ankle swelling.
D. Amlodipine does not act by activating mineralocorticoid receptors.
Q006. An adult receiving spironolactone for resistant hypertension starts trimethoprim-
sulfamethoxazole. Which risk requires particular attention?
A. Hyperkalemia
B. Hypoglycemia from beta-cell stimulation
C. Severe hypocalcemia
D. Drug-induced thrombocytosis
CORRECT ANSWER: A — Hyperkalemia
DETAILED RATIONALE: Spironolactone retains potassium and trimethoprim may further reduce
renal potassium excretion.
WHY THE OTHER OPTIONS ARE INCORRECT:
B. Neither drug combination primarily stimulates pancreatic insulin release.
Independent educational practice • Not an official examination | Page 3
, PHARMD | CARDIOVASCULAR PHARMACOTHERAPY | 2026–2027
C. Hypocalcemia is not the characteristic combined risk.
D. High platelets are not the main expected adverse effect.
Q007. A 45-year-old with hypertension is 10 weeks pregnant and currently taking lisinopril.
Which is the most important medication action?
A. Continue lisinopril because it protects the fetal kidneys
B. Add aliskiren to improve BP control
C. Change to valsartan without further review
D. Urgently review and replace the ACE inhibitor with a pregnancy-compatible regimen
CORRECT ANSWER: D — Urgently review and replace the ACE inhibitor with a pregnancy-compatible
regimen
DETAILED RATIONALE: ACE inhibitors and ARBs can cause fetal harm and should not be continued in
pregnancy; specialist evaluation is appropriate.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. ACE inhibitors are not fetal kidney protectants.
B. Aliskiren is also unsuitable in pregnancy.
C. ARBs also carry fetal toxicity concerns.
Q008. A patient treated with clonidine misses multiple doses and develops severe rebound
hypertension and tachycardia. What mechanism explains the episode?
A. Excess nitric oxide generation
B. Persistent sodium-channel blockade
C. Abrupt withdrawal of central alpha-2 adrenergic agonism
D. Increased prostacyclin release
CORRECT ANSWER: C — Abrupt withdrawal of central alpha-2 adrenergic agonism
DETAILED RATIONALE: Sudden clonidine cessation removes sympathetic suppression and can trigger
catecholamine-mediated rebound hypertension.
WHY THE OTHER OPTIONS ARE INCORRECT:
A. Nitric oxide vasodilation would not explain rebound hypertension.
B. Clonidine does not act primarily as a sodium-channel blocker.
D. Prostacyclin promotes vasodilation rather than sympathetic rebound.
Q009. A patient with resistant hypertension has BP above goal despite an ACE inhibitor,
amlodipine, and chlorthalidone at tolerated doses. Potassium is normal and eGFR is adequate.
Which add-on is often useful after confirming adherence and secondary causes?
A. Verapamil solely to duplicate calcium-channel blockade
B. Spironolactone with potassium and kidney-function monitoring
C. Aspirin solely to lower BP
D. Sublingual nitroglycerin as daily long-term monotherapy
CORRECT ANSWER: B — Spironolactone with potassium and kidney-function monitoring
DETAILED RATIONALE: Mineralocorticoid receptor antagonists can help resistant hypertension when
safe and appropriately monitored.
Independent educational practice • Not an official examination | Page 4
