NR 565 ADVANCED PHARMACOLOGY FINAL EXAM REVIEW
2026/2027 | 100+ Questions and Answers | Rated A |
Chamberlain College | Pass Guaranteed
Unit 1: Pharmacokinetics & Pharmacodynamics (12 Questions)
Q1: A 68-year-old male with heart failure (EF 35%) and severe renal impairment (CrCl 22
mL/min) is prescribed digoxin 0.25 mg daily for atrial fibrillation rate control. After 5
days, he presents with nausea, vomiting, and visual disturbances. Serum digoxin level is
3.8 ng/mL (therapeutic 0.5-0.9 ng/mL for AF). What pharmacokinetic parameter is
primarily responsible for this toxicity, and what is the appropriate management?
A. Increased absorption; administer activated charcoal
B. Decreased volume of distribution; continue current dose and monitor
C. Decreased renal elimination; hold digoxin and consider digoxin-specific antibody
fragments [CORRECT]
D. Increased hepatic metabolism; reduce dose by 25%
Correct Answer: C
,Rationale: Digoxin is eliminated primarily unchanged by renal excretion (60-80%). In
severe renal impairment (CrCl <30), elimination half-life prolongs from 36 hours to 4-6
days, causing accumulation. The narrow therapeutic index (0.5-0.9 ng/mL for AF, <1.2
ng/mL for HF) and patient presentation (GI symptoms, visual
changes—xanthopsia/yellow vision) indicate severe toxicity (>3.0 ng/mL).
Digoxin-specific antibody fragments (DigiFab) bind digoxin for elimination in
life-threatening toxicity (arrhythmias, hyperkalemia >5 mEq/L). A is incorrect because
absorption is not significantly altered in renal failure; activated charcoal is for acute
overdose <2 hours. B is incorrect because volume of distribution actually decreases in
renal failure (reduced tissue binding), increasing plasma concentration, but the primary
issue is elimination; continuing the dose would worsen toxicity. D is incorrect because
digoxin undergoes minimal hepatic metabolism (<15%); hepatic impairment has
minimal effect.
Q2: A 45-year-old female with epilepsy on phenytoin 300 mg daily has a breakthrough
seizure. Serum phenytoin level is 8 μg/mL (therapeutic 10-20). She recently started
omeprazole 20 mg daily for GERD. What pharmacokinetic interaction explains this
subtherapeutic level, and what adjustment is needed?
A. Omeprazole inhibits CYP2C19, decreasing phenytoin metabolism; increase phenytoin
dose
B. Omeprazole induces CYP2C9, increasing phenytoin clearance; increase phenytoin
dose
,C. Omeprazole inhibits CYP2C19, increasing phenytoin metabolism via CYP2C9
autoinduction; increase phenytoin dose [CORRECT]
D. Omeprazole induces CYP3A4, increasing phenytoin protein binding; no change
needed
Correct Answer: C
Rationale: Phenytoin undergoes metabolism by CYP2C9 (primary) and CYP2C19
(secondary). Omeprazole is a potent CYP2C19 inhibitor, shunting metabolism to
CYP2C9. However, phenytoin exhibits autoinduction—it induces its own metabolism
over 2-3 weeks. The net effect of CYP2C19 inhibition with autoinduction through
CYP2C9 often results in unpredictable levels, but in this case, the interaction and
autoinduction have decreased levels, requiring dose increase and close monitoring. A is
incorrect because while omeprazole inhibits CYP2C19, this would initially increase
phenytoin levels, not decrease them; the autoinduction complicates this. B is incorrect
because omeprazole inhibits, not induces, CYP2C9 is not significantly induced by
omeprazole. D is incorrect because phenytoin is not a CYP3A4 substrate, and protein
binding changes don't explain this magnitude of level reduction.
Q3: A 72-year-old male with liver cirrhosis (Child-Pugh C) requires analgesia for severe
osteoarthritis pain. Which opioid should be avoided due to significantly altered
pharmacokinetics in hepatic impairment?
A. Morphine
, B. Oxycodone
C. Hydromorphone
D. Meperidine [CORRECT]
Correct Answer: D
Rationale: Meperidine is metabolized to normeperidine (neurotoxic metabolite) via
hepatic demethylation. In severe hepatic impairment, accumulation of normeperidine
causes seizures, myoclonus, and delirium. Additionally, meperidine has poor oral
bioavailability, erratic absorption, and multiple drug interactions (MAOI
contraindication). A is incorrect because morphine undergoes glucuronidation
(preserved in cirrhosis) though clearance is reduced; dose reduction suffices. B is
incorrect as oxycodone undergoes CYP3A4/2D6 metabolism with reduced clearance in
cirrhosis but is not absolutely contraindicated. C is incorrect because hydromorphone
undergoes glucuronidation and is actually preferred in hepatic impairment due to lack of
active metabolites.
Q4: A 55-year-old male with normal renal function is started on lithium 300 mg TID for
bipolar disorder. How many days are required to achieve steady-state concentration,
and what is the rationale for this timeline?
A. 2-3 days; based on absorption half-life
B. 5-7 days; based on distribution half-life
2026/2027 | 100+ Questions and Answers | Rated A |
Chamberlain College | Pass Guaranteed
Unit 1: Pharmacokinetics & Pharmacodynamics (12 Questions)
Q1: A 68-year-old male with heart failure (EF 35%) and severe renal impairment (CrCl 22
mL/min) is prescribed digoxin 0.25 mg daily for atrial fibrillation rate control. After 5
days, he presents with nausea, vomiting, and visual disturbances. Serum digoxin level is
3.8 ng/mL (therapeutic 0.5-0.9 ng/mL for AF). What pharmacokinetic parameter is
primarily responsible for this toxicity, and what is the appropriate management?
A. Increased absorption; administer activated charcoal
B. Decreased volume of distribution; continue current dose and monitor
C. Decreased renal elimination; hold digoxin and consider digoxin-specific antibody
fragments [CORRECT]
D. Increased hepatic metabolism; reduce dose by 25%
Correct Answer: C
,Rationale: Digoxin is eliminated primarily unchanged by renal excretion (60-80%). In
severe renal impairment (CrCl <30), elimination half-life prolongs from 36 hours to 4-6
days, causing accumulation. The narrow therapeutic index (0.5-0.9 ng/mL for AF, <1.2
ng/mL for HF) and patient presentation (GI symptoms, visual
changes—xanthopsia/yellow vision) indicate severe toxicity (>3.0 ng/mL).
Digoxin-specific antibody fragments (DigiFab) bind digoxin for elimination in
life-threatening toxicity (arrhythmias, hyperkalemia >5 mEq/L). A is incorrect because
absorption is not significantly altered in renal failure; activated charcoal is for acute
overdose <2 hours. B is incorrect because volume of distribution actually decreases in
renal failure (reduced tissue binding), increasing plasma concentration, but the primary
issue is elimination; continuing the dose would worsen toxicity. D is incorrect because
digoxin undergoes minimal hepatic metabolism (<15%); hepatic impairment has
minimal effect.
Q2: A 45-year-old female with epilepsy on phenytoin 300 mg daily has a breakthrough
seizure. Serum phenytoin level is 8 μg/mL (therapeutic 10-20). She recently started
omeprazole 20 mg daily for GERD. What pharmacokinetic interaction explains this
subtherapeutic level, and what adjustment is needed?
A. Omeprazole inhibits CYP2C19, decreasing phenytoin metabolism; increase phenytoin
dose
B. Omeprazole induces CYP2C9, increasing phenytoin clearance; increase phenytoin
dose
,C. Omeprazole inhibits CYP2C19, increasing phenytoin metabolism via CYP2C9
autoinduction; increase phenytoin dose [CORRECT]
D. Omeprazole induces CYP3A4, increasing phenytoin protein binding; no change
needed
Correct Answer: C
Rationale: Phenytoin undergoes metabolism by CYP2C9 (primary) and CYP2C19
(secondary). Omeprazole is a potent CYP2C19 inhibitor, shunting metabolism to
CYP2C9. However, phenytoin exhibits autoinduction—it induces its own metabolism
over 2-3 weeks. The net effect of CYP2C19 inhibition with autoinduction through
CYP2C9 often results in unpredictable levels, but in this case, the interaction and
autoinduction have decreased levels, requiring dose increase and close monitoring. A is
incorrect because while omeprazole inhibits CYP2C19, this would initially increase
phenytoin levels, not decrease them; the autoinduction complicates this. B is incorrect
because omeprazole inhibits, not induces, CYP2C9 is not significantly induced by
omeprazole. D is incorrect because phenytoin is not a CYP3A4 substrate, and protein
binding changes don't explain this magnitude of level reduction.
Q3: A 72-year-old male with liver cirrhosis (Child-Pugh C) requires analgesia for severe
osteoarthritis pain. Which opioid should be avoided due to significantly altered
pharmacokinetics in hepatic impairment?
A. Morphine
, B. Oxycodone
C. Hydromorphone
D. Meperidine [CORRECT]
Correct Answer: D
Rationale: Meperidine is metabolized to normeperidine (neurotoxic metabolite) via
hepatic demethylation. In severe hepatic impairment, accumulation of normeperidine
causes seizures, myoclonus, and delirium. Additionally, meperidine has poor oral
bioavailability, erratic absorption, and multiple drug interactions (MAOI
contraindication). A is incorrect because morphine undergoes glucuronidation
(preserved in cirrhosis) though clearance is reduced; dose reduction suffices. B is
incorrect as oxycodone undergoes CYP3A4/2D6 metabolism with reduced clearance in
cirrhosis but is not absolutely contraindicated. C is incorrect because hydromorphone
undergoes glucuronidation and is actually preferred in hepatic impairment due to lack of
active metabolites.
Q4: A 55-year-old male with normal renal function is started on lithium 300 mg TID for
bipolar disorder. How many days are required to achieve steady-state concentration,
and what is the rationale for this timeline?
A. 2-3 days; based on absorption half-life
B. 5-7 days; based on distribution half-life
