NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
NSG552 / NSG 552 EXAM 1 (LATEST )
PSYCHOPHARMACOLOGY
Grade A Questions and Verified Answers — 100% Correct
Wilkes University | Graduate Nursing & Advanced Practice Education
Examination Instructions: This comprehensive examination contains 100 multiple-choice questions across eight (8)
content domains aligned with the Wilkes University NSG 552 Psychopharmacology syllabus, AACN Essentials of
Master’s Education, and Advanced Psychopharmacology Competencies (2026/2027 Edition). Cognitive distribution: 20%
recall, 50% application, 30% analysis. Each item has exactly one (1) best answer. Rationales incorporate NSG 552
curriculum content, AACN standards, and established psychopharmacology principles. Black box warnings, controlled
substance scheduling, and FDA-approved monitoring parameters are emphasized throughout.
Section 1: Principles of Psychopharmacology
Q1. A 42-year-old patient with major depressive disorder is started on paroxetine 20 mg daily. The patient is a
CYP2D6 poor metabolizer identified through pharmacogenomic testing. Which pharmacokinetic consequence is
most expected, and what is the appropriate prescriptive action consistent with AACN Master’s Essentials and FDA
pharmacogenomic guidance?
A. Reduced paroxetine clearance with elevated plasma levels; initiate at the lowest effective dose and monitor
closely for serotonin syndrome and discontinuation symptoms. [CORRECT]
B. Increased paroxetine clearance; recommend dose escalation to 40 mg daily for therapeutic effect.
C. No change in metabolism because paroxetine is primarily renally excreted unchanged.
D. Induction of CYP2D6 activity requiring addition of a CYP2D6 inducer such as carbamazepine.
Correct Answer: A
Rationale: Paroxetine is metabolized predominantly by CYP2D6; poor metabolizers exhibit markedly reduced clearance,
leading to elevated plasma concentrations and increased risk of dose-dependent adverse effects including serotonin
syndrome. AACN Master’s Essentials and CPIC guidelines recommend initiating at the lowest effective dose, slow titration,
and enhanced therapeutic drug monitoring. Option A is contraindicated because dose escalation would amplify toxicity.
Option C is incorrect because paroxetine undergoes significant hepatic oxidative metabolism. Option D is unsafe;
carbamazepine induces CYP3A4 rather than CYP2D6 and would complicate the clinical picture.
Q2. An advanced practice psychiatric nurse is preparing to prescribe a Schedule II stimulant for an adult with
ADHD. According to DEA regulations and state prescriptive authority, which statement most accurately reflects
legal prescribing parameters?
A. Schedule II prescriptions may be refilled up to five times within six months if the patient remains clinically stable.
B. Schedule II stimulants require a new prescription for each dispense; refills are prohibited, and partial fills
are limited to a 30-day supply per dispensing event. [CORRECT]
C. Schedule II medications can be prescribed via telephone or electronic order without any written documentation if
verbal confirmation is obtained.
D. Schedule II prescribing requires only a state nursing license; no DEA registration is necessary for APRNs in any
jurisdiction.
Correct Answer: B
Rationale: Under the Controlled Substances Act, Schedule II stimulants (e.g., methylphenidate, amphetamines) cannot be
refilled; each dispense requires a new prescription, and partial fills are permitted but capped at a 30-day supply per fill.
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 1
,NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
APRNs must hold both state prescriptive authority and an active DEA registration. Option A describes Schedule III-V rules.
Option C is incorrect; telephone prescriptions for Schedule II are limited to emergency situations only. Option D is false;
federal DEA registration is universally required for Schedule II prescribing.
Q3. A patient with schizophrenia is prescribed oral olanzapine 20 mg daily. Concurrent administration of
fluvoxamine, a potent CYP1A2 inhibitor, is added for comorbid OCD. Which pharmacokinetic interaction is
anticipated, and what monitoring is essential per psychopharmacology best practices?
A. Decreased olanzapine plasma concentration due to CYP1A2 induction; increase olanzapine dose.
B. No clinically significant interaction because olanzapine is metabolized exclusively by CYP2D6.
C. Elevated olanzapine plasma concentration due to CYP1A2 inhibition; monitor for excessive sedation,
orthostatic hypotension, and metabolic decompensation, and consider dose reduction. [CORRECT]
D. Reduced fluvoxamine levels requiring upward titration of the SSRI.
Correct Answer: C
Rationale: Olanzapine is metabolized primarily by CYP1A2 (with minor contributions from CYP2D6 and glucuronidation).
Fluvoxamine is a strong CYP1A2 inhibitor, raising olanzapine exposure and increasing the risk of sedation, orthostasis, and
metabolic side effects. Best practice is to reduce olanzapine dose and monitor metabolic parameters. Option A is incorrect;
fluvoxamine inhibits rather than induces CYP1A2. Option C is false; CYP1A2 is the principal pathway. Option D
misattributes the interaction direction.
Q4. A 67-year-old patient with bipolar I disorder has been on lithium 900 mg twice daily for 15 years. Recent labs
reveal serum creatinine 1.8 mg/dL (baseline 0.9), eGFR 38 mL/min, and 24-hour urine showing impaired
concentrating ability. Which pathophysiologic process and clinical action are most appropriate?
A. Acute tubular necrosis from a single lithium overdose; initiate hemodialysis immediately.
B. Polyuria attributable to primary psychogenic polydipsia; restrict fluids and continue lithium unchanged.
C. Transient elevation due to NSAID co-administration; increase lithium dose to maintain therapeutic serum level.
D. Chronic lithium-induced nephrogenic diabetes insipidus and tubulointerstitial nephropathy; consult
nephrology, reduce or discontinue lithium, and consider alternative mood stabilizer such as lamotrigine or
aripiprazole. [CORRECT]
Correct Answer: D
Rationale: Long-term lithium therapy is associated with tubulointerstitial nephropathy and nephrogenic diabetes insipidus
due to lithium’s interference with aquaporin-2 function in collecting ducts. A persistent eGFR decline below 60 mL/min and
doubling of creatinine mandates nephrology consultation and consideration of alternative mood stabilization. Option A is
incorrect because the picture is chronic, not acute overdose. Option C fails to address structural renal injury. Option D is
dangerous; NSAIDs actually increase lithium levels, and dose escalation would worsen nephrotoxicity.
Q5. Which statement best describes the role of P-glycoprotein (P-gp) in psychopharmacology and its relevance to
therapeutic drug monitoring?
A. P-gp is a hepatic enzyme responsible for the Phase II glucuronidation of benzodiazepines.
B. P-gp is an efflux transporter at the blood-brain barrier that actively pumps certain drugs (e.g., risperidone,
loperamide) back into the systemic circulation, thereby limiting CNS penetration and influencing central
pharmacodynamics. [CORRECT]
C. P-gp enhances CNS penetration of all psychotropic medications, requiring reduced dosing.
D. P-gp is found exclusively in the renal proximal tubule and has no role at the blood-brain barrier.
Correct Answer: B
Rationale: P-glycoprotein (ABCB1) is an ATP-dependent efflux transporter expressed at the luminal membrane of brain
capillary endothelial cells; it limits CNS penetration of substrates including risperidone, loperamide, and many
antidepressants. Polymorphisms in ABCB1 alter treatment response and adverse effect risk. Options A, C, and D
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 2
,NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
mischaracterize P-gp’s function or location; it is not a Phase II enzyme and does not enhance CNS penetration. This
principle is foundational in NSG 552 neuropharmacology modules.
Q6. A prescriber is selecting an antidepressant for a patient with hepatic cirrhosis (Child-Pugh B) and concurrent
cardiovascular disease. Applying pharmacokinetic principles of first-pass metabolism and protein binding, which
agent is most appropriate?
A. Imipramine, due to its extensive first-pass metabolism and narrow therapeutic index.
B. Venlafaxine at standard doses, since it has no impact on blood pressure in patients with cardiac disease.
C. Sertraline, because it exhibits minimal CYP450 inhibition and a more favorable hepatic and cardiac safety
profile than TCAs. [CORRECT]
D. Phenelzine, due to its short half-life and predictable hepatic kinetics in cirrhosis.
Correct Answer: C
Rationale: Sertraline has minimal CYP450 inhibition (notably weaker CYP2D6 effects than paroxetine or fluoxetine), no
significant QT prolongation, and a relatively favorable profile in hepatic impairment when dose-adjusted. Option A is
inappropriate because TCAs have narrow therapeutic indices, are highly protein-bound, and prolong QT. Option C is
incorrect; venlafaxine can cause treatment-emergent hypertension. Option D is unsafe; MAOIs require strict dietary and
medication vigilance, and their metabolism in cirrhosis is unpredictable.
Q7. A 28-year-old female patient with treatment-resistant depression has failed two adequate SSRI trials.
Pharmacogenomic testing reveals a CYP2C19 ultra-rapid metabolizer phenotype. Which antidepressant selection and
dosing rationale is most appropriate?
A. Prescribe citalopram at standard dosing because CYP2C19 status does not affect SSRI metabolism.
B. Switch to a TCA and use standard dosing regardless of CYP2C19 phenotype.
C. Initiate phenelzine since MAOIs are not influenced by any cytochrome P450 enzyme.
D. Avoid citalopram and escitalopram (CYP2C19 substrates) or escalate dosing significantly; consider
bupropion (CYP2B6 metabolized) or mirtazapine, which are less affected by CYP2C19 status. [CORRECT]
Correct Answer: D
Rationale: CYP2C19 ultra-rapid metabolizers exhibit accelerated clearance of citalopram and escitalopram, leading to
subtherapeutic plasma concentrations and therapeutic failure. CPIC guidelines recommend either avoiding these agents or
substantially escalating dose with close monitoring. Bupropion (CYP2B6) and mirtazapine are reasonable alternatives.
Option A contradicts pharmacogenomic evidence. Option C ignores that TCAs (e.g., amitriptyline) are also CYP2C19
substrates with narrow therapeutic windows. Option D is incorrect; MAOI metabolism is still hepatically mediated and
phenelzine carries significant dietary risks.
Q8. A patient with schizophrenia has been stable on haloperidol decanoate 100 mg IM every 4 weeks for 2 years.
The patient develops new-onset Parkinsonism. Which pharmacodynamic mechanism explains this adverse effect,
and what is the most appropriate clinical response?
A. D2 receptor antagonism in the nigrostriatal pathway exceeding 80% occupancy; reduce dose, switch to a
lower-potency or partial agonist antipsychotic, or add an anticholinergic such as benztropine. [CORRECT]
B. Excessive 5-HT2A blockade producing secondary parkinsonism; switch to aripiprazole.
C. Dopamine D1 receptor hypersensitivity in the mesolimbic pathway; increase haloperidol dose.
D. Acetylcholine depletion in the basal ganglia; discontinue all anticholinergic agents.
Correct Answer: A
Rationale: Haloperidol produces parkinsonism through D2 blockade in the nigrostriatal pathway when occupancy exceeds
approximately 80%. Clinical response includes dose reduction, switching to a partial agonist (aripiprazole) or
lower-potency agent, or adding an anticholinergic. Option A is incorrect; 5-HT2A blockade is generally protective against
EPS. Option C is dangerously counter-therapeutic. Option D misattributes the mechanism; parkinsonism reflects
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 3
, NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
dopamine-acetylcholine imbalance, not acetylcholine depletion.
Q9. Which ethical principle most directly underpins the requirement for informed consent before initiating
long-acting injectable paliperidone in a patient with schizophrenia, and how should the APRN operationalize it?
A. Beneficence alone; the prescriber determines the medication and proceeds without disclosure.
B. Justice; allocation of paliperidone must prioritize cost over patient preference.
C. Autonomy; the patient must receive clear information about indications, expected benefits, risks (EPS,
metabolic syndrome, injection site reactions), alternatives, and the long-acting nature of the formulation, with
documented voluntary agreement. [CORRECT]
D. Non-maleficence limited to physical adverse effects without considering psychosocial implications.
Correct Answer: C
Rationale: Informed consent is grounded in the ethical principle of autonomy. Long-acting injectables carry additional
implications because, once administered, the medication cannot be rapidly discontinued. The APRN must disclose
indications, risks (EPS, metabolic effects, prolactin elevation, injection reactions), alternatives, and the prolonged
pharmacokinetic profile. Beneficence, non-maleficence, and justice remain relevant but cannot substitute for autonomous
informed consent. Options A, C, and D each overemphasize one principle at the expense of patient self-determination.
Q10. A patient asks the APRN why grapefruit juice was discontinued when prescribed oral buspirone. Which
pharmacokinetic mechanism explains this interaction, and what is the clinical concern?
A. Grapefruit induces CYP3A4, reducing buspirone plasma levels and therapeutic effect.
B. Grapefruit alters renal tubular secretion of buspirone, requiring creatinine clearance monitoring.
C. No clinically meaningful interaction exists; the restriction is unnecessary.
D. Grapefruit irreversibly inhibits intestinal CYP3A4, increasing buspirone bioavailability and risk of excess
sedation, dizziness, and serotonin toxicity, especially with concurrent SSRIs. [CORRECT]
Correct Answer: D
Rationale: Grapefruit juice irreversibly inhibits intestinal CYP3A4, significantly increasing oral bioavailability of buspirone
(a CYP3A4 substrate). This raises plasma concentrations and risk of CNS depression, dizziness, and serotonin toxicity when
combined with SSRIs. Option A is incorrect; grapefruit inhibits rather than induces CYP3A4. Option C misattributes the
mechanism to renal excretion. Option D contradicts established pharmacology.
Q11. A 35-year-old woman with bipolar I disorder is planning pregnancy. She is currently maintained on valproic
acid 1500 mg/day with therapeutic serum levels. Which evidence-based recommendation aligns with FDA and
ACOG guidance for psychopharmacologic management during pregnancy?
A. Discontinue valproic acid prior to conception due to high teratogenic risk (neural tube defects, ~6-9%),
neurodevelopmental risks (autism spectrum, lower IQ), and switch to a safer agent such as lamotrigine or an
antipsychotic. [CORRECT]
B. Continue valproic acid unchanged because the risk of relapse outweighs teratogenic risk.
C. Reduce valproic acid dose by 50% and add folate; this eliminates teratogenic risk.
D. Switch to carbamazepine as it has a lower teratogenic profile than valproic acid.
Correct Answer: A
Rationale: Valproic acid is a known human teratogen associated with neural tube defects, cardiac anomalies, and fetal
valproate syndrome; it also confers dose-independent risks of lower IQ and autism in offspring. FDA and ACOG strongly
advise against use in pregnancy. Lamotrigine (with folate supplementation) or pregnancy-category-compatible
antipsychotics (e.g., quetiapine) are preferred. Option A disregards teratogenicity. Option C falsely assumes dose reduction
eliminates risk. Option D is incorrect; carbamazepine is also a known teratogen with neural tube defect risk.
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 4
NSG552 / NSG 552 EXAM 1 (LATEST )
PSYCHOPHARMACOLOGY
Grade A Questions and Verified Answers — 100% Correct
Wilkes University | Graduate Nursing & Advanced Practice Education
Examination Instructions: This comprehensive examination contains 100 multiple-choice questions across eight (8)
content domains aligned with the Wilkes University NSG 552 Psychopharmacology syllabus, AACN Essentials of
Master’s Education, and Advanced Psychopharmacology Competencies (2026/2027 Edition). Cognitive distribution: 20%
recall, 50% application, 30% analysis. Each item has exactly one (1) best answer. Rationales incorporate NSG 552
curriculum content, AACN standards, and established psychopharmacology principles. Black box warnings, controlled
substance scheduling, and FDA-approved monitoring parameters are emphasized throughout.
Section 1: Principles of Psychopharmacology
Q1. A 42-year-old patient with major depressive disorder is started on paroxetine 20 mg daily. The patient is a
CYP2D6 poor metabolizer identified through pharmacogenomic testing. Which pharmacokinetic consequence is
most expected, and what is the appropriate prescriptive action consistent with AACN Master’s Essentials and FDA
pharmacogenomic guidance?
A. Reduced paroxetine clearance with elevated plasma levels; initiate at the lowest effective dose and monitor
closely for serotonin syndrome and discontinuation symptoms. [CORRECT]
B. Increased paroxetine clearance; recommend dose escalation to 40 mg daily for therapeutic effect.
C. No change in metabolism because paroxetine is primarily renally excreted unchanged.
D. Induction of CYP2D6 activity requiring addition of a CYP2D6 inducer such as carbamazepine.
Correct Answer: A
Rationale: Paroxetine is metabolized predominantly by CYP2D6; poor metabolizers exhibit markedly reduced clearance,
leading to elevated plasma concentrations and increased risk of dose-dependent adverse effects including serotonin
syndrome. AACN Master’s Essentials and CPIC guidelines recommend initiating at the lowest effective dose, slow titration,
and enhanced therapeutic drug monitoring. Option A is contraindicated because dose escalation would amplify toxicity.
Option C is incorrect because paroxetine undergoes significant hepatic oxidative metabolism. Option D is unsafe;
carbamazepine induces CYP3A4 rather than CYP2D6 and would complicate the clinical picture.
Q2. An advanced practice psychiatric nurse is preparing to prescribe a Schedule II stimulant for an adult with
ADHD. According to DEA regulations and state prescriptive authority, which statement most accurately reflects
legal prescribing parameters?
A. Schedule II prescriptions may be refilled up to five times within six months if the patient remains clinically stable.
B. Schedule II stimulants require a new prescription for each dispense; refills are prohibited, and partial fills
are limited to a 30-day supply per dispensing event. [CORRECT]
C. Schedule II medications can be prescribed via telephone or electronic order without any written documentation if
verbal confirmation is obtained.
D. Schedule II prescribing requires only a state nursing license; no DEA registration is necessary for APRNs in any
jurisdiction.
Correct Answer: B
Rationale: Under the Controlled Substances Act, Schedule II stimulants (e.g., methylphenidate, amphetamines) cannot be
refilled; each dispense requires a new prescription, and partial fills are permitted but capped at a 30-day supply per fill.
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 1
,NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
APRNs must hold both state prescriptive authority and an active DEA registration. Option A describes Schedule III-V rules.
Option C is incorrect; telephone prescriptions for Schedule II are limited to emergency situations only. Option D is false;
federal DEA registration is universally required for Schedule II prescribing.
Q3. A patient with schizophrenia is prescribed oral olanzapine 20 mg daily. Concurrent administration of
fluvoxamine, a potent CYP1A2 inhibitor, is added for comorbid OCD. Which pharmacokinetic interaction is
anticipated, and what monitoring is essential per psychopharmacology best practices?
A. Decreased olanzapine plasma concentration due to CYP1A2 induction; increase olanzapine dose.
B. No clinically significant interaction because olanzapine is metabolized exclusively by CYP2D6.
C. Elevated olanzapine plasma concentration due to CYP1A2 inhibition; monitor for excessive sedation,
orthostatic hypotension, and metabolic decompensation, and consider dose reduction. [CORRECT]
D. Reduced fluvoxamine levels requiring upward titration of the SSRI.
Correct Answer: C
Rationale: Olanzapine is metabolized primarily by CYP1A2 (with minor contributions from CYP2D6 and glucuronidation).
Fluvoxamine is a strong CYP1A2 inhibitor, raising olanzapine exposure and increasing the risk of sedation, orthostasis, and
metabolic side effects. Best practice is to reduce olanzapine dose and monitor metabolic parameters. Option A is incorrect;
fluvoxamine inhibits rather than induces CYP1A2. Option C is false; CYP1A2 is the principal pathway. Option D
misattributes the interaction direction.
Q4. A 67-year-old patient with bipolar I disorder has been on lithium 900 mg twice daily for 15 years. Recent labs
reveal serum creatinine 1.8 mg/dL (baseline 0.9), eGFR 38 mL/min, and 24-hour urine showing impaired
concentrating ability. Which pathophysiologic process and clinical action are most appropriate?
A. Acute tubular necrosis from a single lithium overdose; initiate hemodialysis immediately.
B. Polyuria attributable to primary psychogenic polydipsia; restrict fluids and continue lithium unchanged.
C. Transient elevation due to NSAID co-administration; increase lithium dose to maintain therapeutic serum level.
D. Chronic lithium-induced nephrogenic diabetes insipidus and tubulointerstitial nephropathy; consult
nephrology, reduce or discontinue lithium, and consider alternative mood stabilizer such as lamotrigine or
aripiprazole. [CORRECT]
Correct Answer: D
Rationale: Long-term lithium therapy is associated with tubulointerstitial nephropathy and nephrogenic diabetes insipidus
due to lithium’s interference with aquaporin-2 function in collecting ducts. A persistent eGFR decline below 60 mL/min and
doubling of creatinine mandates nephrology consultation and consideration of alternative mood stabilization. Option A is
incorrect because the picture is chronic, not acute overdose. Option C fails to address structural renal injury. Option D is
dangerous; NSAIDs actually increase lithium levels, and dose escalation would worsen nephrotoxicity.
Q5. Which statement best describes the role of P-glycoprotein (P-gp) in psychopharmacology and its relevance to
therapeutic drug monitoring?
A. P-gp is a hepatic enzyme responsible for the Phase II glucuronidation of benzodiazepines.
B. P-gp is an efflux transporter at the blood-brain barrier that actively pumps certain drugs (e.g., risperidone,
loperamide) back into the systemic circulation, thereby limiting CNS penetration and influencing central
pharmacodynamics. [CORRECT]
C. P-gp enhances CNS penetration of all psychotropic medications, requiring reduced dosing.
D. P-gp is found exclusively in the renal proximal tubule and has no role at the blood-brain barrier.
Correct Answer: B
Rationale: P-glycoprotein (ABCB1) is an ATP-dependent efflux transporter expressed at the luminal membrane of brain
capillary endothelial cells; it limits CNS penetration of substrates including risperidone, loperamide, and many
antidepressants. Polymorphisms in ABCB1 alter treatment response and adverse effect risk. Options A, C, and D
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 2
,NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
mischaracterize P-gp’s function or location; it is not a Phase II enzyme and does not enhance CNS penetration. This
principle is foundational in NSG 552 neuropharmacology modules.
Q6. A prescriber is selecting an antidepressant for a patient with hepatic cirrhosis (Child-Pugh B) and concurrent
cardiovascular disease. Applying pharmacokinetic principles of first-pass metabolism and protein binding, which
agent is most appropriate?
A. Imipramine, due to its extensive first-pass metabolism and narrow therapeutic index.
B. Venlafaxine at standard doses, since it has no impact on blood pressure in patients with cardiac disease.
C. Sertraline, because it exhibits minimal CYP450 inhibition and a more favorable hepatic and cardiac safety
profile than TCAs. [CORRECT]
D. Phenelzine, due to its short half-life and predictable hepatic kinetics in cirrhosis.
Correct Answer: C
Rationale: Sertraline has minimal CYP450 inhibition (notably weaker CYP2D6 effects than paroxetine or fluoxetine), no
significant QT prolongation, and a relatively favorable profile in hepatic impairment when dose-adjusted. Option A is
inappropriate because TCAs have narrow therapeutic indices, are highly protein-bound, and prolong QT. Option C is
incorrect; venlafaxine can cause treatment-emergent hypertension. Option D is unsafe; MAOIs require strict dietary and
medication vigilance, and their metabolism in cirrhosis is unpredictable.
Q7. A 28-year-old female patient with treatment-resistant depression has failed two adequate SSRI trials.
Pharmacogenomic testing reveals a CYP2C19 ultra-rapid metabolizer phenotype. Which antidepressant selection and
dosing rationale is most appropriate?
A. Prescribe citalopram at standard dosing because CYP2C19 status does not affect SSRI metabolism.
B. Switch to a TCA and use standard dosing regardless of CYP2C19 phenotype.
C. Initiate phenelzine since MAOIs are not influenced by any cytochrome P450 enzyme.
D. Avoid citalopram and escitalopram (CYP2C19 substrates) or escalate dosing significantly; consider
bupropion (CYP2B6 metabolized) or mirtazapine, which are less affected by CYP2C19 status. [CORRECT]
Correct Answer: D
Rationale: CYP2C19 ultra-rapid metabolizers exhibit accelerated clearance of citalopram and escitalopram, leading to
subtherapeutic plasma concentrations and therapeutic failure. CPIC guidelines recommend either avoiding these agents or
substantially escalating dose with close monitoring. Bupropion (CYP2B6) and mirtazapine are reasonable alternatives.
Option A contradicts pharmacogenomic evidence. Option C ignores that TCAs (e.g., amitriptyline) are also CYP2C19
substrates with narrow therapeutic windows. Option D is incorrect; MAOI metabolism is still hepatically mediated and
phenelzine carries significant dietary risks.
Q8. A patient with schizophrenia has been stable on haloperidol decanoate 100 mg IM every 4 weeks for 2 years.
The patient develops new-onset Parkinsonism. Which pharmacodynamic mechanism explains this adverse effect,
and what is the most appropriate clinical response?
A. D2 receptor antagonism in the nigrostriatal pathway exceeding 80% occupancy; reduce dose, switch to a
lower-potency or partial agonist antipsychotic, or add an anticholinergic such as benztropine. [CORRECT]
B. Excessive 5-HT2A blockade producing secondary parkinsonism; switch to aripiprazole.
C. Dopamine D1 receptor hypersensitivity in the mesolimbic pathway; increase haloperidol dose.
D. Acetylcholine depletion in the basal ganglia; discontinue all anticholinergic agents.
Correct Answer: A
Rationale: Haloperidol produces parkinsonism through D2 blockade in the nigrostriatal pathway when occupancy exceeds
approximately 80%. Clinical response includes dose reduction, switching to a partial agonist (aripiprazole) or
lower-potency agent, or adding an anticholinergic. Option A is incorrect; 5-HT2A blockade is generally protective against
EPS. Option C is dangerously counter-therapeutic. Option D misattributes the mechanism; parkinsonism reflects
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 3
, NSG 552 — Psychopharmacology | Exam 1 (2026/2027) Wilkes University | Grade A Verified
dopamine-acetylcholine imbalance, not acetylcholine depletion.
Q9. Which ethical principle most directly underpins the requirement for informed consent before initiating
long-acting injectable paliperidone in a patient with schizophrenia, and how should the APRN operationalize it?
A. Beneficence alone; the prescriber determines the medication and proceeds without disclosure.
B. Justice; allocation of paliperidone must prioritize cost over patient preference.
C. Autonomy; the patient must receive clear information about indications, expected benefits, risks (EPS,
metabolic syndrome, injection site reactions), alternatives, and the long-acting nature of the formulation, with
documented voluntary agreement. [CORRECT]
D. Non-maleficence limited to physical adverse effects without considering psychosocial implications.
Correct Answer: C
Rationale: Informed consent is grounded in the ethical principle of autonomy. Long-acting injectables carry additional
implications because, once administered, the medication cannot be rapidly discontinued. The APRN must disclose
indications, risks (EPS, metabolic effects, prolactin elevation, injection reactions), alternatives, and the prolonged
pharmacokinetic profile. Beneficence, non-maleficence, and justice remain relevant but cannot substitute for autonomous
informed consent. Options A, C, and D each overemphasize one principle at the expense of patient self-determination.
Q10. A patient asks the APRN why grapefruit juice was discontinued when prescribed oral buspirone. Which
pharmacokinetic mechanism explains this interaction, and what is the clinical concern?
A. Grapefruit induces CYP3A4, reducing buspirone plasma levels and therapeutic effect.
B. Grapefruit alters renal tubular secretion of buspirone, requiring creatinine clearance monitoring.
C. No clinically meaningful interaction exists; the restriction is unnecessary.
D. Grapefruit irreversibly inhibits intestinal CYP3A4, increasing buspirone bioavailability and risk of excess
sedation, dizziness, and serotonin toxicity, especially with concurrent SSRIs. [CORRECT]
Correct Answer: D
Rationale: Grapefruit juice irreversibly inhibits intestinal CYP3A4, significantly increasing oral bioavailability of buspirone
(a CYP3A4 substrate). This raises plasma concentrations and risk of CNS depression, dizziness, and serotonin toxicity when
combined with SSRIs. Option A is incorrect; grapefruit inhibits rather than induces CYP3A4. Option C misattributes the
mechanism to renal excretion. Option D contradicts established pharmacology.
Q11. A 35-year-old woman with bipolar I disorder is planning pregnancy. She is currently maintained on valproic
acid 1500 mg/day with therapeutic serum levels. Which evidence-based recommendation aligns with FDA and
ACOG guidance for psychopharmacologic management during pregnancy?
A. Discontinue valproic acid prior to conception due to high teratogenic risk (neural tube defects, ~6-9%),
neurodevelopmental risks (autism spectrum, lower IQ), and switch to a safer agent such as lamotrigine or an
antipsychotic. [CORRECT]
B. Continue valproic acid unchanged because the risk of relapse outweighs teratogenic risk.
C. Reduce valproic acid dose by 50% and add folate; this eliminates teratogenic risk.
D. Switch to carbamazepine as it has a lower teratogenic profile than valproic acid.
Correct Answer: A
Rationale: Valproic acid is a known human teratogen associated with neural tube defects, cardiac anomalies, and fetal
valproate syndrome; it also confers dose-independent risks of lower IQ and autism in offspring. FDA and ACOG strongly
advise against use in pregnancy. Lamotrigine (with folate supplementation) or pregnancy-category-compatible
antipsychotics (e.g., quetiapine) are preferred. Option A disregards teratogenicity. Option C falsely assumes dose reduction
eliminates risk. Option D is incorrect; carbamazepine is also a known teratogen with neural tube defect risk.
NSG 552 Psychopharmacology Exam 1 — 100 Questions — Page 4
