Questions | 100% Correct Answers with Detailed Rationales
(2026/2027 Edition)
Chamberlain College of Nursing Advanced Pharmacology Examination
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SECTION 1: Pharmacokinetics and Pharmacodynamics
Question 1
A 68-year-old patient with a creatinine clearance of 30 mL/min is prescribed gentamicin
for a gram-negative infection. The standard dose is 1.7 mg/kg every 8 hours. Which
adjustment should the nurse practitioner recommend?
A. Reduce the dose by 50% and maintain the same dosing interval
B. Extend the dosing interval to every 24 hours while maintaining the standard dose
C. Reduce the dose by 25% and extend the interval to every 12 hours
D. Maintain standard dosing but increase monitoring of peak and trough levels only
Correct Answer: B
Rationale: In patients with renal impairment (CrCl < 40 mL/min), aminoglycosides
require interval extension rather than dose reduction to prevent accumulation and
nephrotoxicity. Extending the interval to every 24 hours allows for drug clearance while
,maintaining therapeutic peak concentrations. Dose reduction alone may result in
subtherapeutic peaks, and standard dosing risks accumulation and
ototoxicity/nephrotoxicity.
Question 2
A patient on chronic warfarin therapy is started on amiodarone for atrial fibrillation. The
nurse practitioner anticipates which pharmacokinetic interaction?
A. Amiodarone induces CYP2C9, decreasing warfarin plasma concentrations
B. Amiodarone inhibits CYP2C9 and CYP1A2, increasing warfarin plasma
concentrations
C. Amiodarone displaces warfarin from albumin binding sites, increasing free drug
D. Amiodarone increases warfarin renal clearance, decreasing its half-life
Correct Answer: B
Rationale: Amiodarone is a potent inhibitor of multiple CYP450 enzymes, including
CYP2C9 and CYP1A2, which are responsible for warfarin metabolism. This inhibition
decreases warfarin clearance, increases plasma concentrations, and significantly
elevates bleeding risk. The INR should be monitored closely, and warfarin dose typically
reduced by 30-50% when amiodarone is initiated.
Question 3
,A patient with hepatic cirrhosis (Child-Pugh Class C) requires analgesia following
surgery. Which opioid should be avoided due to its reliance on hepatic metabolism and
risk of accumulation?
A. Morphine
B. Oxycodone
C. Fentanyl
D. Meperidine
Correct Answer: D
Rationale: Meperidine is metabolized in the liver to normeperidine, a neurotoxic
metabolite that accumulates in hepatic impairment and can cause seizures.
Additionally, meperidine has a poor safety profile overall in advanced practice. Morphine
has active metabolites (M3G, M6G) that also accumulate in renal impairment, but
meperidine is specifically contraindicated in severe hepatic dysfunction due to
normeperidine accumulation.
Question 4
A patient with a history of poor CYP2D6 metabolism is prescribed codeine for
postoperative pain. What is the expected clinical outcome?
A. Enhanced analgesic effect due to increased parent drug concentration
B. Reduced analgesic effect due to decreased conversion to morphine
C. Increased risk of respiratory depression from excessive morphine production
D. No change in clinical effect because codeine is a prodrug for all patients
, Correct Answer: B
Rationale: Codeine is a prodrug that requires conversion via CYP2D6 to morphine for
analgesic effect. Poor metabolizers (approximately 7-10% of Caucasians, 1-2% of
Asians) have significantly reduced or absent CYP2D6 activity, resulting in minimal
morphine production and inadequate pain relief. These patients should receive
alternative analgesics such as morphine, oxycodone, or tramadol (with caution).
Question 5
A patient on digoxin develops toxicity manifesting as nausea, visual disturbances, and a
ventricular rate of 48 bpm. The serum potassium is 2.8 mEq/L. Which intervention is
most appropriate?
A. Administer potassium chloride immediately and hold digoxin
B. Administer digoxin immune Fab (Digibind) immediately
C. Start lidocaine for ventricular arrhythmias and continue digoxin
D. Administer calcium gluconate to stabilize the cardiac membrane
Correct Answer: A
Rationale: Hypokalemia potentiates digoxin toxicity by increasing myocardial binding of
digoxin. In the presence of hypokalemia and non-life-threatening digoxin toxicity,
potassium repletion is the first-line intervention. Digoxin immune Fab is reserved for
life-threatening arrhythmias, severe bradycardia unresponsive to atropine, or serum