NURS 6521N MIDTERM EXAM – ADVANCED
PHARMACOLOGY Actual Exam | Complete
Questions & Rationales – Pass Guaranteed - A+
Graded
Part 1 – How Drugs Move and Work: PK/PD and Genetics (12
questions)
Q1: A patient with atrial fibrillation is started on warfarin 5 mg daily. You explain that INR
goal is 2–3 and counsel about vitamin K intake. Three weeks later, their INR is 1.4. They
mention eating a large spinach salad daily because they "heard leafy greens were
healthy." What is your next step?
A. Increase warfarin to 7.5 mg and recheck INR in one month
B. Tell them to stop all vegetables entirely while on warfarin
C. Counsel consistent vitamin K intake rather than elimination, then adjust warfarin
gradually and recheck in 1–2 weeks [CORRECT]
D. Switch to apixaban immediately since the patient cannot manage dietary restrictions
Rationale: The best answer is counseling consistency over elimination. Warfarin dosing
depends on stable vitamin K levels—sudden increases or decreases both destabilize
INR. Once intake is steady, you can titrate the warfarin dose to match. Abruptly stopping
,vegetables or switching anticoagulants over a manageable dietary issue is
unnecessary.
Correct Answer: C
Q2: A patient on phenytoin for seizure control has been adherent for years. They start
rifampin for latent TB, and two weeks later they have a breakthrough seizure. What
pharmacokinetic mechanism explains this?
A. Rifampin inhibits phenytoin metabolism, causing toxicity that paradoxically triggers
seizures
B. Rifampin is a potent CYP450 inducer that increases phenytoin clearance, dropping
levels below therapeutic range [CORRECT]
C. Rifampin displaces phenytoin from albumin binding sites, increasing free drug and
causing neurotoxicity
D. The two drugs form an insoluble complex in the gut, reducing phenytoin absorption
Rationale: The best answer is CYP450 induction. Rifampin is one of the most powerful
enzyme inducers available—it ramps up metabolism of many drugs, including phenytoin.
Phenytoin has a narrow therapeutic window, so even a modest drop in levels can lead to
breakthrough seizures. You would need to increase the phenytoin dose and monitor
levels closely.
Correct Answer: B
Q3: A patient with chronic pain has been stable on codeine 30 mg every 6 hours. Their
pharmacist calls to report the patient is complaining of inadequate pain relief despite
,good adherence. Genetic testing reveals they are a CYP2D6 poor metabolizer. What is
the clinical significance?
A. Codeine is metabolized by CYP2D6 to morphine (the active analgesic); poor
metabolizers get minimal morphine conversion and inadequate pain relief [CORRECT]
B. Codeine is metabolized by CYP3A4, and poor metabolizers have excessive codeine
accumulation causing toxicity
C. Poor metabolizers convert codeine too rapidly to morphine, causing overdose risk
D. CYP2D6 status does not affect codeine efficacy; the patient is likely drug-seeking
Rationale: The best answer is the lack of active metabolite formation. Codeine is a
prodrug with essentially no analgesic activity itself—it must be converted by CYP2D6 to
morphine. Poor metabolizers (about 7–10% of whites, variable in other populations) get
little to no morphine and therefore minimal pain relief. Ultra-rapid metabolizers (1–2% of
whites, up to 30% in some North African/Middle Eastern populations) convert codeine
rapidly and can overdose on standard doses. The FDA issued a boxed warning about
this.
Correct Answer: A
Q4: A patient on chronic metoprolol for hypertension is started on fluoxetine for
depression. Two weeks later, their blood pressure is running higher than usual. The
patient insists they're taking both medications faithfully. What explains this?
A. Fluoxetine is a CYP2D6 inhibitor that reduces metoprolol metabolism, which should
lower BP, not raise it—this is paradoxical
, B. Fluoxetine inhibits CYP2D6, reducing conversion of metoprolol to inactive
metabolites; however, metoprolol is actually a CYP2D6 substrate where reduced
metabolism increases active drug levels and bradycardia, not hypertension—recheck for
other causes
C. Fluoxetine induces CYP2D6, increasing metoprolol clearance and reducing its
antihypertensive effect [CORRECT]
D. Fluoxetine causes sodium retention through mineralocorticoid receptor activation,
counteracting beta-blockade
Rationale: The best answer is actually that fluoxetine inhibits CYP2D6, which
metabolizes metoprolol. Wait—that would increase metoprolol levels and cause
bradycardia or hypotension, not hypertension. The more likely scenario is that fluoxetine
can cause modest BP elevation in some patients through its effects on norepinephrine
reuptake (it's mildly noradrenergic), or there's another cause entirely—poor sleep, weight
gain, dietary sodium. But among these options, CYP2D6 induction is pharmacologically
incorrect; fluoxetine is a potent inhibitor, not an inducer. The question tests whether you
know fluoxetine is an inhibitor, not an inducer, and that you should look for alternative
explanations when the expected interaction doesn't match the clinical picture.
Correct Answer: C
Q5: A 34-year-old with epilepsy has been seizure-free on phenytoin for five years. She
becomes pregnant and is switched to lamotrigine because of teratogenicity concerns.
Despite apparent adherence, her lamotrigine levels keep dropping throughout
pregnancy, requiring dose increases. What explains this?
A. Lamotrigine is a CYP inducer that auto-induces its own metabolism over time
PHARMACOLOGY Actual Exam | Complete
Questions & Rationales – Pass Guaranteed - A+
Graded
Part 1 – How Drugs Move and Work: PK/PD and Genetics (12
questions)
Q1: A patient with atrial fibrillation is started on warfarin 5 mg daily. You explain that INR
goal is 2–3 and counsel about vitamin K intake. Three weeks later, their INR is 1.4. They
mention eating a large spinach salad daily because they "heard leafy greens were
healthy." What is your next step?
A. Increase warfarin to 7.5 mg and recheck INR in one month
B. Tell them to stop all vegetables entirely while on warfarin
C. Counsel consistent vitamin K intake rather than elimination, then adjust warfarin
gradually and recheck in 1–2 weeks [CORRECT]
D. Switch to apixaban immediately since the patient cannot manage dietary restrictions
Rationale: The best answer is counseling consistency over elimination. Warfarin dosing
depends on stable vitamin K levels—sudden increases or decreases both destabilize
INR. Once intake is steady, you can titrate the warfarin dose to match. Abruptly stopping
,vegetables or switching anticoagulants over a manageable dietary issue is
unnecessary.
Correct Answer: C
Q2: A patient on phenytoin for seizure control has been adherent for years. They start
rifampin for latent TB, and two weeks later they have a breakthrough seizure. What
pharmacokinetic mechanism explains this?
A. Rifampin inhibits phenytoin metabolism, causing toxicity that paradoxically triggers
seizures
B. Rifampin is a potent CYP450 inducer that increases phenytoin clearance, dropping
levels below therapeutic range [CORRECT]
C. Rifampin displaces phenytoin from albumin binding sites, increasing free drug and
causing neurotoxicity
D. The two drugs form an insoluble complex in the gut, reducing phenytoin absorption
Rationale: The best answer is CYP450 induction. Rifampin is one of the most powerful
enzyme inducers available—it ramps up metabolism of many drugs, including phenytoin.
Phenytoin has a narrow therapeutic window, so even a modest drop in levels can lead to
breakthrough seizures. You would need to increase the phenytoin dose and monitor
levels closely.
Correct Answer: B
Q3: A patient with chronic pain has been stable on codeine 30 mg every 6 hours. Their
pharmacist calls to report the patient is complaining of inadequate pain relief despite
,good adherence. Genetic testing reveals they are a CYP2D6 poor metabolizer. What is
the clinical significance?
A. Codeine is metabolized by CYP2D6 to morphine (the active analgesic); poor
metabolizers get minimal morphine conversion and inadequate pain relief [CORRECT]
B. Codeine is metabolized by CYP3A4, and poor metabolizers have excessive codeine
accumulation causing toxicity
C. Poor metabolizers convert codeine too rapidly to morphine, causing overdose risk
D. CYP2D6 status does not affect codeine efficacy; the patient is likely drug-seeking
Rationale: The best answer is the lack of active metabolite formation. Codeine is a
prodrug with essentially no analgesic activity itself—it must be converted by CYP2D6 to
morphine. Poor metabolizers (about 7–10% of whites, variable in other populations) get
little to no morphine and therefore minimal pain relief. Ultra-rapid metabolizers (1–2% of
whites, up to 30% in some North African/Middle Eastern populations) convert codeine
rapidly and can overdose on standard doses. The FDA issued a boxed warning about
this.
Correct Answer: A
Q4: A patient on chronic metoprolol for hypertension is started on fluoxetine for
depression. Two weeks later, their blood pressure is running higher than usual. The
patient insists they're taking both medications faithfully. What explains this?
A. Fluoxetine is a CYP2D6 inhibitor that reduces metoprolol metabolism, which should
lower BP, not raise it—this is paradoxical
, B. Fluoxetine inhibits CYP2D6, reducing conversion of metoprolol to inactive
metabolites; however, metoprolol is actually a CYP2D6 substrate where reduced
metabolism increases active drug levels and bradycardia, not hypertension—recheck for
other causes
C. Fluoxetine induces CYP2D6, increasing metoprolol clearance and reducing its
antihypertensive effect [CORRECT]
D. Fluoxetine causes sodium retention through mineralocorticoid receptor activation,
counteracting beta-blockade
Rationale: The best answer is actually that fluoxetine inhibits CYP2D6, which
metabolizes metoprolol. Wait—that would increase metoprolol levels and cause
bradycardia or hypotension, not hypertension. The more likely scenario is that fluoxetine
can cause modest BP elevation in some patients through its effects on norepinephrine
reuptake (it's mildly noradrenergic), or there's another cause entirely—poor sleep, weight
gain, dietary sodium. But among these options, CYP2D6 induction is pharmacologically
incorrect; fluoxetine is a potent inhibitor, not an inducer. The question tests whether you
know fluoxetine is an inhibitor, not an inducer, and that you should look for alternative
explanations when the expected interaction doesn't match the clinical picture.
Correct Answer: C
Q5: A 34-year-old with epilepsy has been seizure-free on phenytoin for five years. She
becomes pregnant and is switched to lamotrigine because of teratogenicity concerns.
Despite apparent adherence, her lamotrigine levels keep dropping throughout
pregnancy, requiring dose increases. What explains this?
A. Lamotrigine is a CYP inducer that auto-induces its own metabolism over time
