NSG 552 Psychopharmacology
Exam 1, 2 & 3 Compilation — 180 Questions
Wilkes University • 2026/2027 Actual Questions & Verified Answers
Advanced Practice Psychopharmacology Examination
Exam 1, 2 & 3 Compilation — 180 Verified Questions with Detailed Rationales
This compilation consolidates NSG 552 Psychopharmacology Exams 1, 2, and 3 into a single comprehensive volume
aligned with the Wilkes University PMHNP curriculum and 2026/2027 advanced practice psychiatric pharmacology
standards. Content spans neuroanatomy and neurotransmission; antidepressants (SSRIs, SNRIs, TCAs, MAOIs,
atypicals); antipsychotics (FGA, SGA, long-acting injectables); mood stabilizers (lithium, valproate, lamotrigine,
carbamazepine); anxiolytics and hypnotics; stimulants and ADHD medications; substance use disorder
pharmacotherapy; and special populations (pediatrics, geriatrics, pregnancy, polypharmacy).
How to use this exam: Each item presents a clinical or conceptual stem, four response options (A–D), the single
correct answer marked [CORRECT], and a detailed rationale integrating receptor mechanisms, pharmacokinetic
principles, adverse-effect profiles, CYP450 interactions, therapeutic monitoring, and clinical guidelines. Cognitive
mix: 30% recall, 50% application, 20% analysis. 75% of items are scenario-based, reflecting entry-level PMHNP
practice.
Section Domain Items Count
1 Foundations of Psychopharmacology Q1–Q25 25
2 Antidepressants (SSRIs, SNRIs, TCAs, MAOIs, Atypicals) Q26–Q55 30
3 Antipsychotics (FGA, SGA, LAIs) Q56–Q85 30
4 Mood Stabilizers (Lithium, Valproate, Lamotrigine, CBZ) Q86–Q110 25
5 Anxiolytics and Hypnotics (BZDs, Buspirone, Z-drugs) Q111–Q130 20
6 Stimulants and ADHD Medications Q131–Q145 15
7 Substance Use Disorder Pharmacotherapy Q146–Q160 15
8 Special Populations and Clinical Applications Q161–Q180 20
TOTAL Q1–Q180 180
Cognitive blueprint: 30% recall • 50% application • 20% analysis
Item style: 75% scenario-based • 25% direct recall
Course alignment: Wilkes University NSG 552 — PMHNP Psychopharmacology
Advanced Practice Psychopharmacology • PMHNP Curriculum
,NSG 552 Psychopharmacology | Exam 1, 2 & 3 Compilation Wilkes University • 2026/2027
Section 1: Foundations of Psychopharmacology
Neuroanatomy, Neurotransmitters, Receptors, and Pharmacokinetics — Questions 1 through 25
Q1: The mesolimbic dopamine pathway originates in the ventral tegmental area (VTA) and projects to the:
A. Nucleus accumbens (reward, motivation, positive psychotic symptoms). [CORRECT]
B. Prefrontal cortex (cognition, negative symptoms).
C. Striatum (motor control).
D. Substantia nigra (movement).
Correct Answer: A
Rationale: The mesolimbic pathway (VTA → nucleus accumbens) is implicated in reward, motivation, addiction, and the
positive symptoms of psychosis (hallucinations, delusions). Antipsychotics reduce positive symptoms by blocking D2
receptors in this pathway. The mesocortical pathway (VTA → PFC) relates to negative/cognitive symptoms; nigrostriatal
(substantia nigra → striatum) to motor control (EPS); tuberoinfundibular to prolactin.
Q2: Blockade of the tuberoinfundibular dopamine pathway (D2 receptors in the pituitary) results in:
A. Hyperprolactinemia (galactorrhea, gynecomastia, amenorrhea, sexual dysfunction). [CORRECT]
B. Extrapyramidal symptoms (EPS).
C. Neuroleptic malignant syndrome (NMS).
D. Tardive dyskinesia (TD).
Correct Answer: A
Rationale: Dopamine normally inhibits prolactin release from the anterior pituitary via the tuberoinfundibular pathway.
Blocking D2 with antipsychotics (especially risperidone, haloperidol) removes this inhibition → hyperprolactinemia. EPS
results from nigrostriatal D2 blockade; NMS is an idiosyncratic reaction; TD is long-term D2 receptor upregulation.
Aripiprazole is partial agonist at D2 so causes less prolactin elevation.
Q3: A drug that binds to a receptor and produces a maximal response is a:
A. Full agonist. [CORRECT]
B. Partial agonist.
C. Antagonist.
D. Inverse agonist.
Correct Answer: A
Rationale: A full agonist produces the maximal possible response at the receptor (intrinsic efficacy = 1). A partial agonist
produces submaximal response even at full receptor occupancy (e.g., aripiprazole at D2, buprenorphine at mu-opioid). A
pure antagonist binds but produces no intrinsic response. An inverse agonist produces the opposite effect (reduces baseline
constitutive receptor activity).
Q4: Aripiprazole's mechanism of action is best described as:
A. Partial agonist at D2 receptors (functional antagonist in high-DA states, agonist in low-DA states).
[CORRECT]
B. Full D2 antagonist (like haloperidol).
C. Pure serotonin antagonist.
D. Dopamine reuptake inhibitor.
Correct Answer: A
Rationale: Aripiprazole is a partial agonist at D2 (and 5-HT1A) receptors. In high-dopamine states (mesolimbic, psychotic)
it acts as a functional antagonist, reducing positive symptoms. In low-dopamine states (nigrostriatal, tuberoinfundibular) it
provides agonist activity, minimizing EPS and prolactin elevation. This 'stabilizer' profile differentiates it from full D2
antagonists like haloperidol.
Actual Questions & Verified Correct Answers | Advanced Practice Psychopharmacology Page 2
,NSG 552 Psychopharmacology | Exam 1, 2 & 3 Compilation Wilkes University • 2026/2027
Q5: Which cytochrome P450 enzyme is most strongly inhibited by fluoxetine and paroxetine?
A. CYP2D6 (significantly raises levels of TCAs, antipsychotics, beta-blockers). [CORRECT]
B. CYP3A4.
C. CYP1A2.
D. CYP2C9.
Correct Answer: A
Rationale: Fluoxetine and paroxetine are potent CYP2D6 inhibitors. They dramatically raise levels of CYP2D6 substrates
including TCAs, risperidone, haloperidol, atomoxetine, codeine (reduces activation to morphine), and tamoxifen (reduces
activation to endoxifen). Sertraline is a weaker 2D6 inhibitor; fluvoxamine inhibits CYP1A2 and 2C19; none significantly
inhibit 3A4.
Q6: A patient on warfarin is started on fluconazole (a CYP2C9 inhibitor). The PMHNP should:
A. Anticipate increased warfarin levels and increased INR; monitor INR closely and consider warfarin dose
reduction. [CORRECT]
B. Increase warfarin dose because fluconazole induces metabolism.
C. Discontinue warfarin permanently.
D. Make no changes — there is no interaction.
Correct Answer: A
Rationale: Fluconazole inhibits CYP2C9, the primary enzyme metabolizing S-warfarin. This raises warfarin levels and
INR, increasing bleeding risk. Monitor INR more frequently and anticipate reducing warfarin dose ~25–50%. Similar
interactions occur with amiodarone, metronidazole, TMP-SMX (all CYP2C9 inhibitors). Always check interactions before
prescribing in anticoagulated patients.
Q7: GABA produces its inhibitory effect by:
A. Binding GABA-A receptors (ligand-gated chloride channels) → Cl influx → neuronal hyperpolarization.
[CORRECT]
B. Activating adenylate cyclase.
C. Blocking sodium channels.
D. Inhibiting serotonin reuptake.
Correct Answer: A
Rationale: GABA-A receptors are ligand-gated chloride channels. When GABA binds, Cl flows INTO the neuron,
hyperpolarizing the membrane and reducing excitability. Benzodiazepines bind to the α/γ subunit interface and potentiate
GABA (increase opening frequency). Barbiturates increase opening duration. Both produce CNS depression. GABA-B are
GPCRs (baclofen).
Q8: Glutamate excitotoxicity is mediated primarily through:
A. NMDA receptor overactivation → excessive Ca² influx → neuronal injury/death. [CORRECT]
B. GABA-A receptor activation.
C. Dopamine D2 blockade.
D. Serotonin 5-HT2A antagonism.
Correct Answer: A
Rationale: Excessive NMDA receptor activation allows pathological Ca² influx, triggering excitotoxic cascades (nitric
oxide, proteases, oxidative stress) implicated in stroke, Alzheimer's, schizophrenia, and ketamine's dissociative effects.
Memantine is a non-competitive NMDA antagonist used in Alzheimer's. Ketamine (NMDA antagonist) produces rapid
antidepressant effects via glutamate modulation.
Actual Questions & Verified Correct Answers | Advanced Practice Psychopharmacology Page 3
, NSG 552 Psychopharmacology | Exam 1, 2 & 3 Compilation Wilkes University • 2026/2027
Q9: A drug with a narrow therapeutic index means:
A. The dose required for efficacy is close to the dose producing toxicity; close monitoring is required.
[CORRECT]
B. The drug is always safe.
C. The drug has a wide dosing range.
D. The drug is water-soluble.
Correct Answer: A
Rationale: Narrow therapeutic index: the ratio of toxic dose to effective dose is small (close to 1). Examples in psychiatry:
lithium (0.6–1.2 mEq/L), TCAs, clozapine. These require serum drug monitoring. Wide therapeutic index drugs (e.g.,
SSRIs, penicillins) have a wide safety margin and don't require routine level monitoring.
Q10: Which antidepressant is most associated with QTc prolongation and torsades de pointes risk?
A. Citalopram and escitalopram (dose-dependent QTc prolongation, especially >40 mg citalopram or >20 mg
escitalopram). [CORRECT]
B. Sertraline.
C. Fluoxetine.
D. Bupropion.
Correct Answer: A
Rationale: Citalopram (max 40 mg/day, 20 mg in elderly or CYP2C19 poor metabolizers) and escitalopram (max 20
mg/day, 10 mg in elderly) carry FDA QTc prolongation warnings. Avoid in congenital long QT, hypokalemia,
hypomagnesemia, or with other QT-prolonging drugs (antipsychotics, macrolides, methadone). ECG monitoring in
high-risk patients. Sertraline has the least QT effect among SSRIs.
Q11: First-pass metabolism refers to:
A. Drug metabolism in the gut wall and liver before reaching systemic circulation, reducing oral bioavailability.
[CORRECT]
B. Renal excretion of the unchanged drug.
C. Distribution into fat tissue.
D. Binding to plasma proteins.
Correct Answer: A
Rationale: First-pass (presystemic) metabolism: orally administered drugs pass through the gut wall and portal circulation
to the liver before reaching systemic circulation. Substantial metabolism may occur, reducing bioavailability. Venlafaxine,
morphine, propranolol, and many others have significant first-pass effect. IV/IM/sublingual routes bypass first-pass,
increasing bioavailability. Prodrugs (e.g., codeine→morphine) require first-pass activation.
Q12: A medication with high protein binding (e.g., valproate 90% bound) has which characteristic?
A. Only the unbound (free) fraction is pharmacologically active; displacement by another drug can transiently
raise free levels. [CORRECT]
B. It cannot be metabolized.
C. It distributes only to plasma.
D. It has no side effects.
Correct Answer: A
Rationale: Only free (unbound) drug crosses membranes and produces effects. Highly protein-bound drugs (valproate,
warfarin, phenytoin) have small free fractions; displacement by competitors can transiently raise free levels (clinical
relevance is debated). In hypoalbuminemia (liver disease, malnutrition), free fraction rises — monitor free levels when
available. Drug-drug displacement interactions are typically most clinically relevant for narrow-therapeutic-index drugs.
Actual Questions & Verified Correct Answers | Advanced Practice Psychopharmacology Page 4
Exam 1, 2 & 3 Compilation — 180 Questions
Wilkes University • 2026/2027 Actual Questions & Verified Answers
Advanced Practice Psychopharmacology Examination
Exam 1, 2 & 3 Compilation — 180 Verified Questions with Detailed Rationales
This compilation consolidates NSG 552 Psychopharmacology Exams 1, 2, and 3 into a single comprehensive volume
aligned with the Wilkes University PMHNP curriculum and 2026/2027 advanced practice psychiatric pharmacology
standards. Content spans neuroanatomy and neurotransmission; antidepressants (SSRIs, SNRIs, TCAs, MAOIs,
atypicals); antipsychotics (FGA, SGA, long-acting injectables); mood stabilizers (lithium, valproate, lamotrigine,
carbamazepine); anxiolytics and hypnotics; stimulants and ADHD medications; substance use disorder
pharmacotherapy; and special populations (pediatrics, geriatrics, pregnancy, polypharmacy).
How to use this exam: Each item presents a clinical or conceptual stem, four response options (A–D), the single
correct answer marked [CORRECT], and a detailed rationale integrating receptor mechanisms, pharmacokinetic
principles, adverse-effect profiles, CYP450 interactions, therapeutic monitoring, and clinical guidelines. Cognitive
mix: 30% recall, 50% application, 20% analysis. 75% of items are scenario-based, reflecting entry-level PMHNP
practice.
Section Domain Items Count
1 Foundations of Psychopharmacology Q1–Q25 25
2 Antidepressants (SSRIs, SNRIs, TCAs, MAOIs, Atypicals) Q26–Q55 30
3 Antipsychotics (FGA, SGA, LAIs) Q56–Q85 30
4 Mood Stabilizers (Lithium, Valproate, Lamotrigine, CBZ) Q86–Q110 25
5 Anxiolytics and Hypnotics (BZDs, Buspirone, Z-drugs) Q111–Q130 20
6 Stimulants and ADHD Medications Q131–Q145 15
7 Substance Use Disorder Pharmacotherapy Q146–Q160 15
8 Special Populations and Clinical Applications Q161–Q180 20
TOTAL Q1–Q180 180
Cognitive blueprint: 30% recall • 50% application • 20% analysis
Item style: 75% scenario-based • 25% direct recall
Course alignment: Wilkes University NSG 552 — PMHNP Psychopharmacology
Advanced Practice Psychopharmacology • PMHNP Curriculum
,NSG 552 Psychopharmacology | Exam 1, 2 & 3 Compilation Wilkes University • 2026/2027
Section 1: Foundations of Psychopharmacology
Neuroanatomy, Neurotransmitters, Receptors, and Pharmacokinetics — Questions 1 through 25
Q1: The mesolimbic dopamine pathway originates in the ventral tegmental area (VTA) and projects to the:
A. Nucleus accumbens (reward, motivation, positive psychotic symptoms). [CORRECT]
B. Prefrontal cortex (cognition, negative symptoms).
C. Striatum (motor control).
D. Substantia nigra (movement).
Correct Answer: A
Rationale: The mesolimbic pathway (VTA → nucleus accumbens) is implicated in reward, motivation, addiction, and the
positive symptoms of psychosis (hallucinations, delusions). Antipsychotics reduce positive symptoms by blocking D2
receptors in this pathway. The mesocortical pathway (VTA → PFC) relates to negative/cognitive symptoms; nigrostriatal
(substantia nigra → striatum) to motor control (EPS); tuberoinfundibular to prolactin.
Q2: Blockade of the tuberoinfundibular dopamine pathway (D2 receptors in the pituitary) results in:
A. Hyperprolactinemia (galactorrhea, gynecomastia, amenorrhea, sexual dysfunction). [CORRECT]
B. Extrapyramidal symptoms (EPS).
C. Neuroleptic malignant syndrome (NMS).
D. Tardive dyskinesia (TD).
Correct Answer: A
Rationale: Dopamine normally inhibits prolactin release from the anterior pituitary via the tuberoinfundibular pathway.
Blocking D2 with antipsychotics (especially risperidone, haloperidol) removes this inhibition → hyperprolactinemia. EPS
results from nigrostriatal D2 blockade; NMS is an idiosyncratic reaction; TD is long-term D2 receptor upregulation.
Aripiprazole is partial agonist at D2 so causes less prolactin elevation.
Q3: A drug that binds to a receptor and produces a maximal response is a:
A. Full agonist. [CORRECT]
B. Partial agonist.
C. Antagonist.
D. Inverse agonist.
Correct Answer: A
Rationale: A full agonist produces the maximal possible response at the receptor (intrinsic efficacy = 1). A partial agonist
produces submaximal response even at full receptor occupancy (e.g., aripiprazole at D2, buprenorphine at mu-opioid). A
pure antagonist binds but produces no intrinsic response. An inverse agonist produces the opposite effect (reduces baseline
constitutive receptor activity).
Q4: Aripiprazole's mechanism of action is best described as:
A. Partial agonist at D2 receptors (functional antagonist in high-DA states, agonist in low-DA states).
[CORRECT]
B. Full D2 antagonist (like haloperidol).
C. Pure serotonin antagonist.
D. Dopamine reuptake inhibitor.
Correct Answer: A
Rationale: Aripiprazole is a partial agonist at D2 (and 5-HT1A) receptors. In high-dopamine states (mesolimbic, psychotic)
it acts as a functional antagonist, reducing positive symptoms. In low-dopamine states (nigrostriatal, tuberoinfundibular) it
provides agonist activity, minimizing EPS and prolactin elevation. This 'stabilizer' profile differentiates it from full D2
antagonists like haloperidol.
Actual Questions & Verified Correct Answers | Advanced Practice Psychopharmacology Page 2
,NSG 552 Psychopharmacology | Exam 1, 2 & 3 Compilation Wilkes University • 2026/2027
Q5: Which cytochrome P450 enzyme is most strongly inhibited by fluoxetine and paroxetine?
A. CYP2D6 (significantly raises levels of TCAs, antipsychotics, beta-blockers). [CORRECT]
B. CYP3A4.
C. CYP1A2.
D. CYP2C9.
Correct Answer: A
Rationale: Fluoxetine and paroxetine are potent CYP2D6 inhibitors. They dramatically raise levels of CYP2D6 substrates
including TCAs, risperidone, haloperidol, atomoxetine, codeine (reduces activation to morphine), and tamoxifen (reduces
activation to endoxifen). Sertraline is a weaker 2D6 inhibitor; fluvoxamine inhibits CYP1A2 and 2C19; none significantly
inhibit 3A4.
Q6: A patient on warfarin is started on fluconazole (a CYP2C9 inhibitor). The PMHNP should:
A. Anticipate increased warfarin levels and increased INR; monitor INR closely and consider warfarin dose
reduction. [CORRECT]
B. Increase warfarin dose because fluconazole induces metabolism.
C. Discontinue warfarin permanently.
D. Make no changes — there is no interaction.
Correct Answer: A
Rationale: Fluconazole inhibits CYP2C9, the primary enzyme metabolizing S-warfarin. This raises warfarin levels and
INR, increasing bleeding risk. Monitor INR more frequently and anticipate reducing warfarin dose ~25–50%. Similar
interactions occur with amiodarone, metronidazole, TMP-SMX (all CYP2C9 inhibitors). Always check interactions before
prescribing in anticoagulated patients.
Q7: GABA produces its inhibitory effect by:
A. Binding GABA-A receptors (ligand-gated chloride channels) → Cl influx → neuronal hyperpolarization.
[CORRECT]
B. Activating adenylate cyclase.
C. Blocking sodium channels.
D. Inhibiting serotonin reuptake.
Correct Answer: A
Rationale: GABA-A receptors are ligand-gated chloride channels. When GABA binds, Cl flows INTO the neuron,
hyperpolarizing the membrane and reducing excitability. Benzodiazepines bind to the α/γ subunit interface and potentiate
GABA (increase opening frequency). Barbiturates increase opening duration. Both produce CNS depression. GABA-B are
GPCRs (baclofen).
Q8: Glutamate excitotoxicity is mediated primarily through:
A. NMDA receptor overactivation → excessive Ca² influx → neuronal injury/death. [CORRECT]
B. GABA-A receptor activation.
C. Dopamine D2 blockade.
D. Serotonin 5-HT2A antagonism.
Correct Answer: A
Rationale: Excessive NMDA receptor activation allows pathological Ca² influx, triggering excitotoxic cascades (nitric
oxide, proteases, oxidative stress) implicated in stroke, Alzheimer's, schizophrenia, and ketamine's dissociative effects.
Memantine is a non-competitive NMDA antagonist used in Alzheimer's. Ketamine (NMDA antagonist) produces rapid
antidepressant effects via glutamate modulation.
Actual Questions & Verified Correct Answers | Advanced Practice Psychopharmacology Page 3
, NSG 552 Psychopharmacology | Exam 1, 2 & 3 Compilation Wilkes University • 2026/2027
Q9: A drug with a narrow therapeutic index means:
A. The dose required for efficacy is close to the dose producing toxicity; close monitoring is required.
[CORRECT]
B. The drug is always safe.
C. The drug has a wide dosing range.
D. The drug is water-soluble.
Correct Answer: A
Rationale: Narrow therapeutic index: the ratio of toxic dose to effective dose is small (close to 1). Examples in psychiatry:
lithium (0.6–1.2 mEq/L), TCAs, clozapine. These require serum drug monitoring. Wide therapeutic index drugs (e.g.,
SSRIs, penicillins) have a wide safety margin and don't require routine level monitoring.
Q10: Which antidepressant is most associated with QTc prolongation and torsades de pointes risk?
A. Citalopram and escitalopram (dose-dependent QTc prolongation, especially >40 mg citalopram or >20 mg
escitalopram). [CORRECT]
B. Sertraline.
C. Fluoxetine.
D. Bupropion.
Correct Answer: A
Rationale: Citalopram (max 40 mg/day, 20 mg in elderly or CYP2C19 poor metabolizers) and escitalopram (max 20
mg/day, 10 mg in elderly) carry FDA QTc prolongation warnings. Avoid in congenital long QT, hypokalemia,
hypomagnesemia, or with other QT-prolonging drugs (antipsychotics, macrolides, methadone). ECG monitoring in
high-risk patients. Sertraline has the least QT effect among SSRIs.
Q11: First-pass metabolism refers to:
A. Drug metabolism in the gut wall and liver before reaching systemic circulation, reducing oral bioavailability.
[CORRECT]
B. Renal excretion of the unchanged drug.
C. Distribution into fat tissue.
D. Binding to plasma proteins.
Correct Answer: A
Rationale: First-pass (presystemic) metabolism: orally administered drugs pass through the gut wall and portal circulation
to the liver before reaching systemic circulation. Substantial metabolism may occur, reducing bioavailability. Venlafaxine,
morphine, propranolol, and many others have significant first-pass effect. IV/IM/sublingual routes bypass first-pass,
increasing bioavailability. Prodrugs (e.g., codeine→morphine) require first-pass activation.
Q12: A medication with high protein binding (e.g., valproate 90% bound) has which characteristic?
A. Only the unbound (free) fraction is pharmacologically active; displacement by another drug can transiently
raise free levels. [CORRECT]
B. It cannot be metabolized.
C. It distributes only to plasma.
D. It has no side effects.
Correct Answer: A
Rationale: Only free (unbound) drug crosses membranes and produces effects. Highly protein-bound drugs (valproate,
warfarin, phenytoin) have small free fractions; displacement by competitors can transiently raise free levels (clinical
relevance is debated). In hypoalbuminemia (liver disease, malnutrition), free fraction rises — monitor free levels when
available. Drug-drug displacement interactions are typically most clinically relevant for narrow-therapeutic-index drugs.
Actual Questions & Verified Correct Answers | Advanced Practice Psychopharmacology Page 4
