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NR565 Advanced Pharmacology Fundamentals Master Quiz Bank - Chamberlain College Academic Year | Complete Question Bank & Rationales

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Master NR565 Advanced Pharmacology Fundamentals with this comprehensive Master Quiz Bank from Chamberlain College for the Academic Year. This complete question bank features applied scenarios with detailed rationales covering core pharmacological principles, drug therapies, clinical applications, and evidence-based prescribing. Essential for nursing students building pharmacological expertise and preparing for assessments.

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NR565 Advanced Pharmacology Fundamentals
Master Quiz Bank - Chamberlain College
2026-2027 Academic Year | Complete Question
Bank & Rationales


| 120 Applied Questions & 100 % Correct Rationales



DOMAIN 1 – PHARMACOKINETICS / PHARMACODYNAMICS & AUTONOMIC
PHARMACOLOGY (24 Qs)

Q1

A patient taking warfarin for AFib is started on cimetidine for GERD. The APRN
understands cimetidine may increase warfarin’s effect by which mechanism?

A. Inducing CYP2C9 metabolism

B. Inhibiting CYP2C9 metabolism

C. Competing for plasma-protein binding sites

D. Increasing warfarin’s renal excretion

Correct: B

,Rationale: Cimetidine is a non-selective CYP450 inhibitor; ↓ warfarin metabolism via
CYP2C9 → ↑ INR/bleeding. Induction (A) would lower levels; protein binding (C) is
minor; renal (D) irrelevant.

Q2

A 28-year-old woman with asthma uses inhaled albuterol PRN. She reports palpitations
and tremors within 5 minutes of use. These effects are best explained by activation of
which receptor subtype?

A. β1-adrenergic

B. β2-adrenergic

C. α1-adrenergic

D. Muscarinic M3

Correct: B

Rationale: Albuterol is selective β2 agonist; skeletal-muscle tremor and cardiac β2
(minor) cause symptoms. β1 (A) would cause more chronotropy; α1 (C)
vasoconstriction; M3 (D) bronchoconstriction.

Q3

A 55-year-old man with hypertension is switched from immediate-release nifedipine to
extended-release. His trough BP is now better controlled. Which PK parameter is MOST
affected by the formulation change?

A. Bioavailability (F)

B. Half-life (t½)

,C. Volume of distribution (Vd)

D. Clearance (Cl)

Correct: B

Rationale: ER formulation prolongs absorption → apparent t½ increases, allowing
smoother 24-h control. Bioavailability (A) usually unchanged; Vd/Cl (C,D) are
drug-intrinsic.

Q4

An APRN considers adding ketoconazole to a patient on simvastatin. The concern is
best explained by which PK interaction?

A. CYP3A4 inhibition → ↑ simvastatin AUC → rhabdomyolysis risk

B. CYP2C19 induction → ↓ simvastatin levels → loss of efficacy

C. P-gp induction → ↓ simvastatin brain levels → seizures

D. UGT1A1 inhibition → ↑ bilirubin → jaundice

Correct: A

Rationale: Ketoconazole potently inhibits CYP3A4; simvastatin is 3A4 substrate → ↑
exposure/myopathy. Induction (B) is opposite; P-gp/UGT (C,D) are minor.

Q5

A 70-kg patient receives IV lidocaine 100 mg bolus followed by 2 mg/min infusion.
Lidocaine t½ = 1.5 h, Vd = 1 L/kg. Approximately how long to reach steady-state plasma
levels?

, A. 30 min

B. 1 h

C. 4–5 h

D. 8 h

Correct: C

Rationale: Time to steady-state ≈ 4–5 × t½ = 6–7.5 h (closest 4–5 h). Half-life governs
accumulation, not Vd.

Q6

A patient on digoxin develops hypokalemia (K⁺ 3.0 mEq/L). The risk of digoxin toxicity
increases because hypokalemia

A. Induces digoxin-metabolizing enzymes.

B. Decreases renal tubular secretion of digoxin.

C. Increases digoxin binding to Na⁺/K⁺-ATPase.

D. Competes with digoxin for plasma-protein binding.

Correct: C

Rationale: K⁺ competes with digoxin for the receptor; low K⁺ → more digoxin binding →
toxicity. Enzymes (A) irrelevant; secretion (B) minor; protein binding (D) unaffected.

Q7
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