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NSG 555 Exam 3 Study Guide — Wilkes University
Nurse Practitioners in Primary Care II | 2026/2027
Curriculum | Complete Solutions
Welcome to your comprehensive exam preparation resource. This guide synthesizes high-yield
content across eight clinical domains, formatted for active learning and exam success. Let's work
through each section together.
PART A: CARDIOLOGY & PULMONOLOGY DRILL (Questions 1–12)
Question 1 A 58-year-old male with hypertension reports substernal chest pressure when
walking uphill that is relieved by rest. His resting ECG is normal. What is the most appropriate
next step?
A. Admit for emergent cardiac catheterization
B. Order stress testing (exercise treadmill or nuclear)
C. Start nitroglycerin PRN and reassess in 3 months
D. Prescribe aspirin and schedule routine follow-up
Correct Answer: B
Rationale: This is classic stable angina: exertional chest discomfort relieved by rest. A normal
resting ECG does not rule out coronary artery disease. Stress testing (exercise treadmill ECG or
pharmacologic stress with imaging) is the standard next step for risk stratification in patients
with intermediate pretest probability. Emergent catheterization is reserved for acute coronary
syndromes. Starting nitroglycerin without diagnosis is premature.
High-Yield Pearl: "Normal ECG does not exclude CAD." In stable angina, stress testing is the
gatekeeper to invasive evaluation. The Duke Treadmill Score helps risk-stratify results.
Question 2 A patient with chronic stable angina remains symptomatic weekly despite
metoprolol and sublingual nitroglycerin PRN. Which is the best next step?
, 2
A. Increase metoprolol to maximum tolerated dose
B. Add a long-acting nitrate, ranolazine, or amlodipine
C. Refer for coronary artery bypass grafting immediately
D. Discontinue metoprolol and switch to diltiazem
Correct Answer: B
Rationale: Beta-blockers are first-line for stable angina, but if symptoms persist, a second anti-
anginal agent is indicated. Options include long-acting nitrates (isosorbide mononitrate),
ranolazine (inhibits late sodium current, no effect on heart rate or blood pressure), or
dihydropyridine calcium channel blockers (amlodipine). CABG is reserved for high-risk anatomy
or refractory symptoms despite optimal medical therapy. Switching from beta-blocker to
diltiazem loses the mortality benefit of beta-blockers.
High-Yield Pearl: "Beta-blocker first, then add on." Ranolazine is unique—it reduces angina
without affecting hemodynamics, making it ideal for patients with low blood pressure or
bradycardia.
Question 3 A 72-year-old female has a mid-systolic click followed by a late systolic murmur at
the apex. What is the most likely diagnosis?
A. Aortic stenosis
B. Mitral valve prolapse
C. Mitral regurgitation
D. Tricuspid regurgitation
Correct Answer: B
Rationale: The mid-systolic click with late systolic murmur is pathognomonic for mitral valve
prolapse (MVP). The click represents the tensing of chordae tendineae as the valve leaflets
billow into the left atrium. The late systolic murmur reflects regurgitation that worsens as the
valve prolapses further during systole. Aortic stenosis produces a crescendo-decrescendo
systolic murmur at the right upper sternal border. Mitral regurgitation produces a holosystolic
murmur.
High-Yield Pearl: "Click then murmur = MVP." The click may vary with position (louder standing,
softer squatting). Most MVP is benign, but severe prolapse can progress to regurgitation
requiring surgery.
, 3
Question 4 A 78-year-old male has a harsh crescendo-decrescendo systolic murmur at the right
upper sternal border radiating to the carotids. He reports syncope with exertion. Which
statement is correct?
A. Nitrates are the drug of choice for angina in this patient
B. This is aortic stenosis; nitrates are contraindicated
C. This is mitral regurgitation; surgery is never indicated
D. This is hypertrophic cardiomyopathy; beta-blockers are contraindicated
Correct Answer: B
Rationale: The murmur description (harsh, crescendo-decrescendo, RUSB, radiating to carotids)
with pulsus parvus et tardus (weak, delayed pulse) is classic for aortic stenosis (AS). Syncope
during exertion occurs because the fixed stenotic valve cannot increase cardiac output with
demand, causing cerebral hypoperfusion. Nitrates are contraindicated because they reduce
preload, worsening the already compromised cardiac output. Valve replacement is indicated for
symptomatic AS.
High-Yield Pearl: "Syncope + AS murmur = bad valve, don't vasodilate." The three cardinal
symptoms of severe AS are angina, syncope, and heart failure. Once symptomatic, prognosis
without valve replacement is poor.
Question 5 A patient with HFrEF (EF 30%, NYHA Class III) is on lisinopril and metoprolol
succinate. Which medication should be added next per guideline-directed therapy?
A. Digoxin
B. Spironolactone
C. Amlodipine
D. Hydralazine-isosorbide dinitrate
Correct Answer: B
Rationale: Guideline-directed medical therapy (GDMT) for HFrEF (EF ≤35%) consists of triple
therapy: ACE inhibitor (or ARB/ARNI), evidence-based beta-blocker (carvedilol, metoprolol
succinate, or bisoprolol), and mineralocorticoid receptor antagonist (spironolactone or
eplerenone). This triple therapy reduces mortality and hospitalization. Digoxin is for symptom
control in persistent symptoms. Amlodipine has no mortality benefit in HFrEF. Hydralazine-
isosorbide is for Black patients with persistent symptoms or ACE inhibitor intolerance.
, 4
High-Yield Pearl: "ACEi + BB + MRA = the HFrEF trinity." This combination is the foundation of
GDMT. SGLT2 inhibitors (dapagliflozin, empagliflozin) are now also standard—making it
quadruple therapy.
Question 6 A patient with HFpEF presents with dyspnea and peripheral edema. Which therapy
is now recommended per updated guidelines?
A. ACE inhibitor alone
B. Diuretics for volume management plus SGLT2 inhibitor
C. Beta-blocker as monotherapy
D. Digoxin for symptom control
Correct Answer: B
Rationale: HFpEF (EF ≥50%) historically lacked disease-modifying therapy. Updated guidelines
(ACC/AHA/HFSA) now recommend SGLT2 inhibitors (dapagliflozin) for HFpEF to reduce
hospitalization and cardiovascular death. Diuretics remain essential for volume management.
ACE inhibitors and beta-blockers improve outcomes in HFrEF but have limited benefit in HFpEF.
Spironolactone may be considered in select HFpEF patients.
High-Yield Pearl: "SGLT2 inhibitors are the breakthrough for HFpEF." Dapagliflozin is the first
therapy proven to reduce heart failure events in HFpEF—memorize this for the exam.
Question 7 A patient with HFrEF has ferritin 85 ng/mL and transferrin saturation 15%. Which
intervention is indicated?
A. Oral iron supplementation
B. IV iron (ferric carboxymaltose)
C. Erythropoietin stimulating agents
D. Blood transfusion
Correct Answer: B
Rationale: Iron deficiency in HFrEF is defined as ferritin <100 ng/mL OR ferritin 100–299 ng/mL
with TSAT <20%. IV iron (ferric carboxymaltose or iron sucrose) improves quality of life,
functional capacity, and reduces hospitalizations—even in patients without anemia. Oral iron is
poorly absorbed in heart failure due to intestinal edema and hepcidin elevation. ESAs and
transfusion are not indicated for iron deficiency without severe anemia.
NSG 555 Exam 3 Study Guide — Wilkes University
Nurse Practitioners in Primary Care II | 2026/2027
Curriculum | Complete Solutions
Welcome to your comprehensive exam preparation resource. This guide synthesizes high-yield
content across eight clinical domains, formatted for active learning and exam success. Let's work
through each section together.
PART A: CARDIOLOGY & PULMONOLOGY DRILL (Questions 1–12)
Question 1 A 58-year-old male with hypertension reports substernal chest pressure when
walking uphill that is relieved by rest. His resting ECG is normal. What is the most appropriate
next step?
A. Admit for emergent cardiac catheterization
B. Order stress testing (exercise treadmill or nuclear)
C. Start nitroglycerin PRN and reassess in 3 months
D. Prescribe aspirin and schedule routine follow-up
Correct Answer: B
Rationale: This is classic stable angina: exertional chest discomfort relieved by rest. A normal
resting ECG does not rule out coronary artery disease. Stress testing (exercise treadmill ECG or
pharmacologic stress with imaging) is the standard next step for risk stratification in patients
with intermediate pretest probability. Emergent catheterization is reserved for acute coronary
syndromes. Starting nitroglycerin without diagnosis is premature.
High-Yield Pearl: "Normal ECG does not exclude CAD." In stable angina, stress testing is the
gatekeeper to invasive evaluation. The Duke Treadmill Score helps risk-stratify results.
Question 2 A patient with chronic stable angina remains symptomatic weekly despite
metoprolol and sublingual nitroglycerin PRN. Which is the best next step?
, 2
A. Increase metoprolol to maximum tolerated dose
B. Add a long-acting nitrate, ranolazine, or amlodipine
C. Refer for coronary artery bypass grafting immediately
D. Discontinue metoprolol and switch to diltiazem
Correct Answer: B
Rationale: Beta-blockers are first-line for stable angina, but if symptoms persist, a second anti-
anginal agent is indicated. Options include long-acting nitrates (isosorbide mononitrate),
ranolazine (inhibits late sodium current, no effect on heart rate or blood pressure), or
dihydropyridine calcium channel blockers (amlodipine). CABG is reserved for high-risk anatomy
or refractory symptoms despite optimal medical therapy. Switching from beta-blocker to
diltiazem loses the mortality benefit of beta-blockers.
High-Yield Pearl: "Beta-blocker first, then add on." Ranolazine is unique—it reduces angina
without affecting hemodynamics, making it ideal for patients with low blood pressure or
bradycardia.
Question 3 A 72-year-old female has a mid-systolic click followed by a late systolic murmur at
the apex. What is the most likely diagnosis?
A. Aortic stenosis
B. Mitral valve prolapse
C. Mitral regurgitation
D. Tricuspid regurgitation
Correct Answer: B
Rationale: The mid-systolic click with late systolic murmur is pathognomonic for mitral valve
prolapse (MVP). The click represents the tensing of chordae tendineae as the valve leaflets
billow into the left atrium. The late systolic murmur reflects regurgitation that worsens as the
valve prolapses further during systole. Aortic stenosis produces a crescendo-decrescendo
systolic murmur at the right upper sternal border. Mitral regurgitation produces a holosystolic
murmur.
High-Yield Pearl: "Click then murmur = MVP." The click may vary with position (louder standing,
softer squatting). Most MVP is benign, but severe prolapse can progress to regurgitation
requiring surgery.
, 3
Question 4 A 78-year-old male has a harsh crescendo-decrescendo systolic murmur at the right
upper sternal border radiating to the carotids. He reports syncope with exertion. Which
statement is correct?
A. Nitrates are the drug of choice for angina in this patient
B. This is aortic stenosis; nitrates are contraindicated
C. This is mitral regurgitation; surgery is never indicated
D. This is hypertrophic cardiomyopathy; beta-blockers are contraindicated
Correct Answer: B
Rationale: The murmur description (harsh, crescendo-decrescendo, RUSB, radiating to carotids)
with pulsus parvus et tardus (weak, delayed pulse) is classic for aortic stenosis (AS). Syncope
during exertion occurs because the fixed stenotic valve cannot increase cardiac output with
demand, causing cerebral hypoperfusion. Nitrates are contraindicated because they reduce
preload, worsening the already compromised cardiac output. Valve replacement is indicated for
symptomatic AS.
High-Yield Pearl: "Syncope + AS murmur = bad valve, don't vasodilate." The three cardinal
symptoms of severe AS are angina, syncope, and heart failure. Once symptomatic, prognosis
without valve replacement is poor.
Question 5 A patient with HFrEF (EF 30%, NYHA Class III) is on lisinopril and metoprolol
succinate. Which medication should be added next per guideline-directed therapy?
A. Digoxin
B. Spironolactone
C. Amlodipine
D. Hydralazine-isosorbide dinitrate
Correct Answer: B
Rationale: Guideline-directed medical therapy (GDMT) for HFrEF (EF ≤35%) consists of triple
therapy: ACE inhibitor (or ARB/ARNI), evidence-based beta-blocker (carvedilol, metoprolol
succinate, or bisoprolol), and mineralocorticoid receptor antagonist (spironolactone or
eplerenone). This triple therapy reduces mortality and hospitalization. Digoxin is for symptom
control in persistent symptoms. Amlodipine has no mortality benefit in HFrEF. Hydralazine-
isosorbide is for Black patients with persistent symptoms or ACE inhibitor intolerance.
, 4
High-Yield Pearl: "ACEi + BB + MRA = the HFrEF trinity." This combination is the foundation of
GDMT. SGLT2 inhibitors (dapagliflozin, empagliflozin) are now also standard—making it
quadruple therapy.
Question 6 A patient with HFpEF presents with dyspnea and peripheral edema. Which therapy
is now recommended per updated guidelines?
A. ACE inhibitor alone
B. Diuretics for volume management plus SGLT2 inhibitor
C. Beta-blocker as monotherapy
D. Digoxin for symptom control
Correct Answer: B
Rationale: HFpEF (EF ≥50%) historically lacked disease-modifying therapy. Updated guidelines
(ACC/AHA/HFSA) now recommend SGLT2 inhibitors (dapagliflozin) for HFpEF to reduce
hospitalization and cardiovascular death. Diuretics remain essential for volume management.
ACE inhibitors and beta-blockers improve outcomes in HFrEF but have limited benefit in HFpEF.
Spironolactone may be considered in select HFpEF patients.
High-Yield Pearl: "SGLT2 inhibitors are the breakthrough for HFpEF." Dapagliflozin is the first
therapy proven to reduce heart failure events in HFpEF—memorize this for the exam.
Question 7 A patient with HFrEF has ferritin 85 ng/mL and transferrin saturation 15%. Which
intervention is indicated?
A. Oral iron supplementation
B. IV iron (ferric carboxymaltose)
C. Erythropoietin stimulating agents
D. Blood transfusion
Correct Answer: B
Rationale: Iron deficiency in HFrEF is defined as ferritin <100 ng/mL OR ferritin 100–299 ng/mL
with TSAT <20%. IV iron (ferric carboxymaltose or iron sucrose) improves quality of life,
functional capacity, and reduces hospitalizations—even in patients without anemia. Oral iron is
poorly absorbed in heart failure due to intestinal edema and hepcidin elevation. ESAs and
transfusion are not indicated for iron deficiency without severe anemia.
