W IL K E S UN IVE RSITY · N SG 552 · E XAM 2
Psychopharmacology
Comprehensive
Examination
One hundred board-style multiple-choice
questions with verified answers and detailed
rationales, aligned with the Wilkes University
NSG 552 syllabus, the AACN Essentials of
Master's Education, and advanced
psychopharmacology competencies for the
2026/2027 academic year.
Latest Edition
100 Questions · Verified Answers · 100% Correct ·
Grade A
,NSG552 / NSG 552 Exam 2 () - Psychopharmacology 100 Questions | Verified Answers
Section 1: Principles of Psychopharmacology
Q1. A psychiatric-mental health nurse practitioner (PMHNP) is counseling a patient who is switching
from the intramuscular form of chlorpromazine to the oral form and asks why the oral dose is
significantly higher. Which pharmacokinetic principle best explains this difference?
A. Oral absorption is incomplete because gastric acid destroys most of the dose
B. The drug undergoes active tubular secretion before reaching the systemic circulation
C. Extensive first-pass hepatic metabolism reduces oral bioavailability [CORRECT]
D. Protein binding is much lower with the oral formulation
Correct Answer: C
Rationale: Orally administered chlorpromazine is absorbed into the portal circulation and extensively
metabolized by hepatic enzymes before reaching the systemic circulation (first-pass effect), lowering
bioavailability and requiring a higher oral dose. Gastric acid destruction, renal secretion, and reduced
protein binding do not explain the route-specific dose difference. NSG 552 emphasizes linking
bioavailability directly to route-based dosing decisions.
Q2. A patient begins sertraline 50 mg daily, a medication with an average elimination half-life of
approximately 26 hours. The patient asks when the drug will reach steady-state concentration. Which
response is most accurate?
A. Within 24 to 48 hours of the first dose
B. After approximately 4 to 5 half-lives, or about 5 days of regular dosing [CORRECT]
C. Only after 3 or more weeks of continuous dosing
D. Steady state cannot be predicted for drugs with half-lives longer than 12 hours
Correct Answer: B
Rationale: A drug reaches steady state after approximately 4 to 5 half-lives; with a 26-hour half-life,
sertraline reaches steady state in roughly 5 days of regular dosing. The 3-week timeframe refers to
onset of therapeutic effect, not pharmacokinetic steady state. Distinguishing these two concepts is a
core NSG 552 pharmacokinetic competency.
Q3. A patient stabilized on clozapine 300 mg daily is prescribed fluvoxamine for comorbid
obsessive-compulsive symptoms. Two weeks later the patient reports excessive sedation,
hypersalivation, and dizziness. Which mechanism best explains this presentation?
A. Fluvoxamine competitively antagonizes clozapine at dopamine D2 receptors
B. Fluvoxamine induces CYP3A4, accelerating clozapine clearance
C. Fluvoxamine displaces clozapine from alpha-1 adrenergic binding sites
D. Fluvoxamine potently inhibits CYP1A2, raising clozapine plasma concentrations [CORRECT]
Correct Answer: D
Rationale: Fluvoxamine is a potent CYP1A2 inhibitor, and clozapine is primarily metabolized by
CYP1A2, so co-administration markedly elevates clozapine levels and produces dose-dependent
toxicity such as sedation, hypersalivation, hypotension, and seizures. The correct response is to reduce
the clozapine dose and monitor levels. Enzyme induction and receptor antagonism are mechanistically
incorrect explanations.
Wilkes University - Graduate Nursing and Advanced Practice Education 1
,NSG552 / NSG 552 Exam 2 () - Psychopharmacology 100 Questions | Verified Answers
Q4. A patient with depression shows no clinical improvement after 8 weeks on nortriptyline 100 mg
daily, and a serum level is subtherapeutic despite documented adherence. Pharmacogenomic testing
reveals a CYP2D6 ultrarapid metabolizer phenotype. What is the most appropriate interpretation?
A. The patient clears nortriptyline so rapidly that therapeutic levels cannot be reached at usual
doses [CORRECT]
B. The patient is covertly skipping doses despite self-reported adherence
C. The medication should simply be continued unchanged because response is merely delayed
D. Nortriptyline is contraindicated in ultrarapid metabolizers and must be stopped immediately
Correct Answer: A
Rationale: CYP2D6 ultrarapid metabolizers clear nortriptyline extremely quickly, so standard doses
produce subtherapeutic plasma levels; genotype-guided strategies include cautious dose escalation or
selection of a less genetically influenced agent. This pattern is not evidence of nonadherence, and
simply waiting longer cannot raise the level. Pharmacogenomic interpretation is an AACN Essentials
competency for precision prescribing.
Q5. Which molecular characteristic most directly allows a psychotropic medication to cross the
blood-brain barrier?
A. High ionization at physiological pH
B. High lipid solubility at physiological pH [CORRECT]
C. Strong binding to plasma albumin
D. A large molecular weight above 1000 daltons
Correct Answer: B
Rationale: The blood-brain barrier consists of tight junctions between capillary endothelial cells, so
only small, un-ionized, lipid-soluble molecules cross readily; most psychotropics are deliberately
designed to be lipophilic. Highly ionized drugs, heavily protein-bound drugs, and large molecules
remain largely excluded from the central nervous system.
Q6. A patient taking loperamide for diarrhea is started on quinidine, and the PMHNP warns that the
combination can produce central opioid effects. Which mechanism explains this warning?
A. Quinidine induces hepatic CYP3A4, converting loperamide into morphine
B. Quinidine competes with loperamide for plasma protein binding sites
C. Quinidine inhibits P-glycoprotein efflux at the blood-brain barrier, allowing loperamide to
enter the central nervous system [CORRECT]
D. Quinidine doubles gastrointestinal absorption of loperamide
Correct Answer: C
Rationale: P-glycoprotein at the blood-brain barrier normally pumps loperamide back into the capillary
lumen, keeping it out of the central nervous system; quinidine inhibits this efflux transporter, allowing
loperamide to reach central mu-opioid receptors and produce central effects. This illustrates
transporter-mediated drug interactions highlighted in advanced psychopharmacology.
Wilkes University - Graduate Nursing and Advanced Practice Education 2
, NSG552 / NSG 552 Exam 2 () - Psychopharmacology 100 Questions | Verified Answers
Q7. Positron emission tomography studies show that antipsychotic efficacy and extrapyramidal
symptoms correlate with different degrees of striatal dopamine D2 receptor occupancy. Which
conclusion follows for antipsychotic dosing?
A. Optimal dosing targets roughly 65 to 72 percent D2 occupancy, because blockade exceeding 80
percent sharply increases extrapyramidal symptoms [CORRECT]
B. Antipsychotic efficacy requires near-total (100 percent) D2 receptor occupancy
C. D2 occupancy is unrelated to both therapeutic effect and motor side effects
D. Therapeutic response begins only when D2 occupancy falls below 20 percent
Correct Answer: A
Rationale: Striatal D2 occupancy of approximately 65 to 72 percent is associated with antipsychotic
response, whereas occupancy above 80 percent is strongly associated with extrapyramidal symptoms,
supporting the principle of using the lowest effective dose. The remaining options contradict
well-established occupancy imaging data taught in NSG 552.
Q8. A patient stabilized on lithium 900 mg daily is scheduled for a serum level. The PMHNP should
instruct the patient to have the blood drawn at which time?
A. Exactly 2 hours after the morning dose
B. Any time of day as long as the patient is fasting
C. Immediately after taking the evening dose
D. Just before the morning dose, approximately 12 hours after the last evening dose [CORRECT]
Correct Answer: D
Rationale: Lithium levels are drawn as 12-hour post-dose troughs, typically just before the morning
dose, because distribution continues for several hours after ingestion and earlier sampling falsely
elevates results. Consistent trough timing allows valid comparison across visits, a central principle of
therapeutic drug monitoring.
Q9. Pharmacogenomic testing of a 68-year-old patient before starting citalopram reveals a CYP2C19
poor metabolizer phenotype. How should the PMHNP apply this result?
A. Prescribe the standard maximum of 40 mg daily because older adults metabolize drugs faster
B. Substitute phenelzine as the safer first-line option
C. Limit citalopram to 20 mg daily because poor metabolism increases exposure and
QT-prolongation risk [CORRECT]
D. Start at 40 mg daily and double the dose if response is inadequate
Correct Answer: C
Rationale: CYP2C19 poor metabolizers clear citalopram slowly, raising plasma exposure and the risk
of QT prolongation; FDA labeling recommends a maximum of 20 mg daily in such patients, and
citalopram is additionally capped at 20 mg in adults over 60. Doubling the dose would compound
toxicity risk, and nothing in this presentation justifies an MAOI.
Wilkes University - Graduate Nursing and Advanced Practice Education 3
Psychopharmacology
Comprehensive
Examination
One hundred board-style multiple-choice
questions with verified answers and detailed
rationales, aligned with the Wilkes University
NSG 552 syllabus, the AACN Essentials of
Master's Education, and advanced
psychopharmacology competencies for the
2026/2027 academic year.
Latest Edition
100 Questions · Verified Answers · 100% Correct ·
Grade A
,NSG552 / NSG 552 Exam 2 () - Psychopharmacology 100 Questions | Verified Answers
Section 1: Principles of Psychopharmacology
Q1. A psychiatric-mental health nurse practitioner (PMHNP) is counseling a patient who is switching
from the intramuscular form of chlorpromazine to the oral form and asks why the oral dose is
significantly higher. Which pharmacokinetic principle best explains this difference?
A. Oral absorption is incomplete because gastric acid destroys most of the dose
B. The drug undergoes active tubular secretion before reaching the systemic circulation
C. Extensive first-pass hepatic metabolism reduces oral bioavailability [CORRECT]
D. Protein binding is much lower with the oral formulation
Correct Answer: C
Rationale: Orally administered chlorpromazine is absorbed into the portal circulation and extensively
metabolized by hepatic enzymes before reaching the systemic circulation (first-pass effect), lowering
bioavailability and requiring a higher oral dose. Gastric acid destruction, renal secretion, and reduced
protein binding do not explain the route-specific dose difference. NSG 552 emphasizes linking
bioavailability directly to route-based dosing decisions.
Q2. A patient begins sertraline 50 mg daily, a medication with an average elimination half-life of
approximately 26 hours. The patient asks when the drug will reach steady-state concentration. Which
response is most accurate?
A. Within 24 to 48 hours of the first dose
B. After approximately 4 to 5 half-lives, or about 5 days of regular dosing [CORRECT]
C. Only after 3 or more weeks of continuous dosing
D. Steady state cannot be predicted for drugs with half-lives longer than 12 hours
Correct Answer: B
Rationale: A drug reaches steady state after approximately 4 to 5 half-lives; with a 26-hour half-life,
sertraline reaches steady state in roughly 5 days of regular dosing. The 3-week timeframe refers to
onset of therapeutic effect, not pharmacokinetic steady state. Distinguishing these two concepts is a
core NSG 552 pharmacokinetic competency.
Q3. A patient stabilized on clozapine 300 mg daily is prescribed fluvoxamine for comorbid
obsessive-compulsive symptoms. Two weeks later the patient reports excessive sedation,
hypersalivation, and dizziness. Which mechanism best explains this presentation?
A. Fluvoxamine competitively antagonizes clozapine at dopamine D2 receptors
B. Fluvoxamine induces CYP3A4, accelerating clozapine clearance
C. Fluvoxamine displaces clozapine from alpha-1 adrenergic binding sites
D. Fluvoxamine potently inhibits CYP1A2, raising clozapine plasma concentrations [CORRECT]
Correct Answer: D
Rationale: Fluvoxamine is a potent CYP1A2 inhibitor, and clozapine is primarily metabolized by
CYP1A2, so co-administration markedly elevates clozapine levels and produces dose-dependent
toxicity such as sedation, hypersalivation, hypotension, and seizures. The correct response is to reduce
the clozapine dose and monitor levels. Enzyme induction and receptor antagonism are mechanistically
incorrect explanations.
Wilkes University - Graduate Nursing and Advanced Practice Education 1
,NSG552 / NSG 552 Exam 2 () - Psychopharmacology 100 Questions | Verified Answers
Q4. A patient with depression shows no clinical improvement after 8 weeks on nortriptyline 100 mg
daily, and a serum level is subtherapeutic despite documented adherence. Pharmacogenomic testing
reveals a CYP2D6 ultrarapid metabolizer phenotype. What is the most appropriate interpretation?
A. The patient clears nortriptyline so rapidly that therapeutic levels cannot be reached at usual
doses [CORRECT]
B. The patient is covertly skipping doses despite self-reported adherence
C. The medication should simply be continued unchanged because response is merely delayed
D. Nortriptyline is contraindicated in ultrarapid metabolizers and must be stopped immediately
Correct Answer: A
Rationale: CYP2D6 ultrarapid metabolizers clear nortriptyline extremely quickly, so standard doses
produce subtherapeutic plasma levels; genotype-guided strategies include cautious dose escalation or
selection of a less genetically influenced agent. This pattern is not evidence of nonadherence, and
simply waiting longer cannot raise the level. Pharmacogenomic interpretation is an AACN Essentials
competency for precision prescribing.
Q5. Which molecular characteristic most directly allows a psychotropic medication to cross the
blood-brain barrier?
A. High ionization at physiological pH
B. High lipid solubility at physiological pH [CORRECT]
C. Strong binding to plasma albumin
D. A large molecular weight above 1000 daltons
Correct Answer: B
Rationale: The blood-brain barrier consists of tight junctions between capillary endothelial cells, so
only small, un-ionized, lipid-soluble molecules cross readily; most psychotropics are deliberately
designed to be lipophilic. Highly ionized drugs, heavily protein-bound drugs, and large molecules
remain largely excluded from the central nervous system.
Q6. A patient taking loperamide for diarrhea is started on quinidine, and the PMHNP warns that the
combination can produce central opioid effects. Which mechanism explains this warning?
A. Quinidine induces hepatic CYP3A4, converting loperamide into morphine
B. Quinidine competes with loperamide for plasma protein binding sites
C. Quinidine inhibits P-glycoprotein efflux at the blood-brain barrier, allowing loperamide to
enter the central nervous system [CORRECT]
D. Quinidine doubles gastrointestinal absorption of loperamide
Correct Answer: C
Rationale: P-glycoprotein at the blood-brain barrier normally pumps loperamide back into the capillary
lumen, keeping it out of the central nervous system; quinidine inhibits this efflux transporter, allowing
loperamide to reach central mu-opioid receptors and produce central effects. This illustrates
transporter-mediated drug interactions highlighted in advanced psychopharmacology.
Wilkes University - Graduate Nursing and Advanced Practice Education 2
, NSG552 / NSG 552 Exam 2 () - Psychopharmacology 100 Questions | Verified Answers
Q7. Positron emission tomography studies show that antipsychotic efficacy and extrapyramidal
symptoms correlate with different degrees of striatal dopamine D2 receptor occupancy. Which
conclusion follows for antipsychotic dosing?
A. Optimal dosing targets roughly 65 to 72 percent D2 occupancy, because blockade exceeding 80
percent sharply increases extrapyramidal symptoms [CORRECT]
B. Antipsychotic efficacy requires near-total (100 percent) D2 receptor occupancy
C. D2 occupancy is unrelated to both therapeutic effect and motor side effects
D. Therapeutic response begins only when D2 occupancy falls below 20 percent
Correct Answer: A
Rationale: Striatal D2 occupancy of approximately 65 to 72 percent is associated with antipsychotic
response, whereas occupancy above 80 percent is strongly associated with extrapyramidal symptoms,
supporting the principle of using the lowest effective dose. The remaining options contradict
well-established occupancy imaging data taught in NSG 552.
Q8. A patient stabilized on lithium 900 mg daily is scheduled for a serum level. The PMHNP should
instruct the patient to have the blood drawn at which time?
A. Exactly 2 hours after the morning dose
B. Any time of day as long as the patient is fasting
C. Immediately after taking the evening dose
D. Just before the morning dose, approximately 12 hours after the last evening dose [CORRECT]
Correct Answer: D
Rationale: Lithium levels are drawn as 12-hour post-dose troughs, typically just before the morning
dose, because distribution continues for several hours after ingestion and earlier sampling falsely
elevates results. Consistent trough timing allows valid comparison across visits, a central principle of
therapeutic drug monitoring.
Q9. Pharmacogenomic testing of a 68-year-old patient before starting citalopram reveals a CYP2C19
poor metabolizer phenotype. How should the PMHNP apply this result?
A. Prescribe the standard maximum of 40 mg daily because older adults metabolize drugs faster
B. Substitute phenelzine as the safer first-line option
C. Limit citalopram to 20 mg daily because poor metabolism increases exposure and
QT-prolongation risk [CORRECT]
D. Start at 40 mg daily and double the dose if response is inadequate
Correct Answer: C
Rationale: CYP2C19 poor metabolizers clear citalopram slowly, raising plasma exposure and the risk
of QT prolongation; FDA labeling recommends a maximum of 20 mg daily in such patients, and
citalopram is additionally capped at 20 mg in adults over 60. Doubling the dose would compound
toxicity risk, and nothing in this presentation justifies an MAOI.
Wilkes University - Graduate Nursing and Advanced Practice Education 3
