Pharmacology Actual Questions and Answers (PDF)
SECTION 1: PHARMACOKINETICS & PHARMACODYNAMICS
(Questions 1-20)
Question 1
A 55-year-old man with chronic kidney disease has an estimated glomerular filtration
rate of 28 mL/min. His prescriber is considering initiating a medication that is 80%
renally cleared. What is the most important pharmacokinetic consideration when
prescribing this medication?
A. Monitor drug levels and adjust the dose based on renal function
B. Increase the dose to compensate for reduced clearance
C. Switch to an intravenous route to bypass the kidneys
D. Add a second agent to enhance renal excretion
Correct Answer: A
Rationale: Medications that are primarily renally cleared require dose adjustment based
on renal function to prevent drug accumulation and toxicity. Increasing the dose would
worsen accumulation; IV route does not bypass renal elimination; adding a second
agent to enhance excretion is not a standard approach.
Question 2
A 42-year-old woman is taking warfarin 5 mg daily for atrial fibrillation. She is newly
prescribed fluconazole for a vaginal yeast infection. The nurse practitioner reviews the
interaction profile before dispensing. By which cytochrome P450 enzyme is warfarin
primarily metabolized?
A. CYP3A4
B. CYP2D6
C. CYP2C9
D. CYP1A2
,Correct Answer: C
Rationale: Warfarin is primarily metabolized by CYP2C9. Fluconazole is a potent CYP2C9
inhibitor that will increase warfarin levels and bleeding risk. CYP3A4 metabolizes many
drugs but is not the primary enzyme for warfarin. CYP2D6 and CYP1A2 are not
significantly involved in warfarin metabolism.
Question 3
A 68-year-old man takes simvastatin 40 mg daily for hyperlipidemia. His new provider
prescribes clarithromycin for community-acquired pneumonia. He presents three days
later with diffuse myalgias and dark-colored urine. Which pharmacokinetic interaction
best explains these findings?
A. Clarithromycin inhibits CYP3A4, raising simvastatin to toxic levels
B. Clarithromycin induces CYP3A4, increasing simvastatin activation
C. Clarithromycin displaces simvastatin from plasma protein binding sites
D. Clarithromycin reduces renal clearance of simvastatin metabolites
Correct Answer: A
Rationale: Clarithromycin is a strong CYP3A4 inhibitor that reduces simvastatin
metabolism, leading to elevated statin levels and rhabdomyolysis. CYP3A4 induction
would decrease statin levels; simvastatin has low protein binding displacement potential;
simvastatin is hepatically cleared, not renally.
Question 4
A 30-year-old woman who is a poor CYP2D6 metabolizer is prescribed codeine for
postoperative pain after a dental extraction. She reports no analgesic effect despite
taking the maximum recommended dose. What is the most likely pharmacogenomic
explanation for the treatment failure?
A. CYP2D6 converts codeine to its active metabolite morphine, and poor metabolizers
produce insufficient morphine for analgesia
B. CYP2D6 metabolizes codeine to a toxic metabolite causing sedation rather than
analgesia
,C. Poor CYP2D6 metabolizers clear codeine too rapidly for therapeutic effect
D. Codeine is a prodrug activated by CYP3A4, not CYP2D6
Correct Answer: A
Rationale: Codeine is a prodrug that requires O-demethylation by CYP2D6 to form
morphine for analgesic effect. Poor CYP2D6 metabolizers cannot convert codeine to
morphine effectively, resulting in treatment failure.
Question 5
Which statement best explains why amphotericin B must be given intravenously for
systemic mycoses?
A. It is rapidly metabolized by first-pass hepatic metabolism
B. It has very poor gastrointestinal absorption, so therapeutic serum levels cannot be
achieved orally
C. It causes severe gastric irritation when taken orally
D. It requires the presence of bile salts for absorption
Correct Answer: B
Rationale: Amphotericin B has very poor GI absorption, so therapeutic serum levels for
systemic mycoses can only be achieved with IV administration. After leaving the vascular
space, it binds extensively to sterol-containing membranes, but oral dosing does not
provide adequate bioavailability for systemic infection.
Question 6
Which intervention most effectively reduces the risk of amphotericin B–induced
nephrotoxicity?
A. Premedicating with acetaminophen
B. Administering the drug by rapid IV bolus
C. Infusing 1 liter of normal saline on days of treatment
D. Giving a loop diuretic before each dose
, Correct Answer: C
Rationale: Saline loading with 500 mL to 1 liter of IV normal saline before and after
amphotericin B infusion dilutes drug concentration in renal tubules and reduces
nephrotoxicity. Rapid administration and loop diuretics increase nephrotoxicity risk.
Question 7
Which statement best describes the mechanism of action of acyclovir?
A. It blocks viral entry by binding to cell surface receptors
B. It inhibits viral protease, preventing maturation of virions
C. It suppresses synthesis of viral DNA by inhibiting DNA polymerase and terminating
chain growth
D. It stimulates host interferon production to block viral replication
Correct Answer: C
Rationale: After activation to acyclo-GTP, acyclovir inhibits viral DNA polymerase and is
incorporated into viral DNA, blocking further strand elongation. This dual effect
suppresses viral DNA synthesis and replication.
Question 8
A patient being treated with IV acyclovir develops rising creatinine and decreased urine
output. What is the priority nursing action?
A. Hold the dose and notify the prescriber
B. Slow the infusion rate to 30 minutes
C. Administer a loop diuretic
D. Switch to oral acyclovir immediately
Correct Answer: A
Rationale: IV acyclovir carries a risk of renal failure, especially in patients with renal
disease or dehydration. Worsening renal function warrants holding the drug and
contacting the prescriber for possible dose adjustment or discontinuation.