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NSG 6001 WEEK 4 QUIZ 1 ADVANCED PHARMACOLOGY 2026/2027 | Cardiovascular Therapeutics | 100% Correct Solutions | Pass Guaranteed - A+ Graded

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Master cardiovascular therapeutics with the 100% correct NSG 6001 Week 4 Quiz 1 solutions for 2026/2027. This A+ Graded resource for the Graduate Nursing Program NSG 6001 Advanced Pharmacology Week 4 Quiz 1 contains verified questions and answers covering cardiovascular therapeutics directly aligned with graduate-level advanced practice curriculum expectations and current clinical guidelines. Featuring antihypertensive agents, heart failure pharmacotherapy, antiarrhythmic drugs, antianginal medications, and lipid-lowering therapies with detailed rationales for mechanism of action, therapeutic indications, adverse effects, drug interactions, and clinical monitoring parameters, it provides an authentic replication of graduate nursing quiz rigor and advanced cardiovascular pharmacology preparation. With ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, diuretics, digoxin, statins, and anticoagulant considerations plus our Pass Guarantee, this is the definitive tool to master cardiovascular pharmacology and excel in your graduate nursing program. Download now and pass first try.

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NSG 6001 Week 4 Quiz 1
Advanced Pharmacology: Cardiovascular Therapeutics
Graduate Nursing Program – 100% Correct Solutions


Q1: A 68-year-old male with hypertension and type 2 diabetes is prescribed lisinopril
10mg daily. Two weeks later, he presents with a dry, nonproductive cough. His blood
pressure is well-controlled at 128/78 mmHg. Which mechanism explains this adverse
effect?

A. Bradykinin accumulation due to ACE inhibition
B. Direct irritation of bronchial mucosa by the drug molecule
C. Increased prostaglandin synthesis causing airway inflammation
D. Histamine release from mast cell degranulation

Correct Answer: A
Rationale: [CORRECT] A: Angiotensin-converting enzyme (ACE) inhibitors like lisinopril
block the conversion of angiotensin I to angiotensin II, but also inhibit the breakdown of
bradykinin, a potent vasodilator and inflammatory mediator. Bradykinin accumulation in
the pulmonary tree stimulates cough receptors, causing a dry, irritating cough in 5-20%
of patients. This is a class effect, not dose-dependent, and resolves within 1-4 weeks of
discontinuation. B: Direct chemical irritation is not the mechanism; ACE inhibitors are
well-absorbed and do not deposit in airways. C: Prostaglandins are not increased;
bradykinin stimulates prostacyclin and nitric oxide, but not airway inflammation. D:
Histamine release is not involved in ACE inhibitor cough; this describes type I
hypersensitivity reactions (e.g., penicillin allergy). Clinical Pearl: ARBs (losartan,
valsartan) do not affect bradykinin metabolism and are preferred in patients with ACE
inhibitor-induced cough.

,Q2: A patient with atrial fibrillation is prescribed warfarin 5mg daily. Which dietary
instruction is essential to prevent fluctuations in anticoagulation effect?

A. Avoid all green vegetables completely
B. Maintain consistent vitamin K intake from leafy greens
C. Eliminate all alcohol consumption permanently
D. Increase calcium-rich foods to enhance anticoagulation

Correct Answer: B
Rationale: [CORRECT] B: Warfarin inhibits vitamin K-dependent clotting factors (II, VII, IX,
X). The key to stable INR management is consistency in vitamin K intake rather than
avoidance. Patients should consume similar amounts of vitamin K-rich foods (leafy
greens, broccoli, Brussels sprouts) weekly to prevent INR fluctuations. Sudden
increases in vitamin K decrease INR; sudden decreases increase bleeding risk. A:
Complete avoidance causes vitamin deficiency and makes INR management impossible
when vegetables are reintroduced. C: Alcohol should be limited (≤1-2 drinks/day) and
consistent; complete elimination is unnecessary but binge drinking is dangerous
(increases INR and bleeding risk). D: Calcium has no effect on warfarin metabolism or
anticoagulation; this confuses warfarin with heparin (requires antithrombin III, not
calcium). Monitoring: INR target 2.0-3.0 for most indications; 2.5-3.5 for mechanical
valves.



Q3: A 72-year-old female with systolic heart failure (EF 35%) is prescribed metoprolol
succinate 25mg daily. Which parameter requires most careful monitoring during the first
2 weeks of therapy?

A. Serum potassium levels
B. Blood pressure and heart rate
C. Liver function enzymes
D. Complete blood count

, Correct Answer: B
Rationale: [CORRECT] B: Beta-blockers (metoprolol, carvedilol, bisoprolol) are
guideline-directed medical therapy for HFrEF but require careful titration. Metoprolol
succinate is a beta-1 selective blocker that reduces heart rate, myocardial oxygen
demand, and adverse remodeling. During initiation, monitor for bradycardia (HR <50
bpm), hypotension (SBP <90 mmHg), and worsening heart failure symptoms. Start low,
go slow, and uptitrate every 2 weeks to target doses (metoprolol succinate 200mg
daily). A: Potassium monitoring is critical with ACE inhibitors, ARBs, and spironolactone,
not beta-blockers. C: Hepatotoxicity is rare with metoprolol; carvedilol requires liver
monitoring due to alpha-1 blocking. D: Beta-blockers do not cause hematologic
abnormalities. Clinical Pearl: Never stop beta-blockers abruptly in heart failure
patients—risk of rebound tachycardia and decompensation.



Q4: Which antihypertensive agent is contraindicated in pregnancy due to risk of fetal
renal agenesis, oligohydramnios, and death?

A. Methyldopa
B. Labetalol
C. Lisinopril
D. Nifedipine

Correct Answer: C
Rationale: [CORRECT] C: ACE inhibitors (lisinopril, enalapril, captopril) are absolutely
contraindicated in pregnancy (FDA Category D, avoid in 2nd/3rd trimesters; Category C
in 1st trimester but generally avoided). They cause fetal renal tubular dysplasia,
oligohydramnios, pulmonary hypoplasia, intrauterine growth restriction, and fetal death
by inhibiting fetal renal perfusion and angiotensin II-mediated renal development. A:
Methyldopa is the historical drug of choice for pregnancy; safe but sedating. B:
Labetalol (alpha/beta-blocker) is first-line for pregnancy hypertension. D: Nifedipine

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