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NSG 552 Exam 2 2026/2027 | Wilkes Psychopharmacology | Grade A Q&A | Pass Guaranteed

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Pass the NSG 552 Psychopharmacology Exam 2 at Wilkes University 2026/2027 with this comprehensive guide of verified questions and answers. This resource contains actual exam-style questions with accurate answers and detailed rationales covering psychopharmacology core concepts—including antidepressants (SSRIs, SNRIs, TCAs, MAOIs), antipsychotics (typical and atypical), mood stabilizers (lithium, anticonvulsants), anxiolytics and hypnotics (benzodiazepines, buspirone), stimulants for ADHD, and medications for substance use disorders. Topics also include pharmacokinetics and pharmacodynamics in psychiatric practice, drug interactions, adverse effect monitoring (serotonin syndrome, neuroleptic malignant syndrome, lithium toxicity), and patient education. Each solution is verified and Grade A to mirror the official Wilkes NSG 552 exam format. With authentic content and our Pass Guarantee, you will ace your NSG 552 Exam 2 with confidence. Download now and excel in Psychopharmacology!

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NSG 552 Exam 2 - Psychopharmacology | 2026/2027 Edition | Wilkes University




NSG552 / NSG 552 EXAM 2 (LATEST ):
PSYCHOPHARMACOLOGY
Grade A Questions and Verified Answers | 100% Correct - Wilkes
Wilkes University - Graduate Nursing Program | AACN Essentials Aligned


Instructions: This comprehensive examination consists of 100 multiple-choice questions distributed across seven (7)
sections aligned with the Wilkes University NSG 552 Psychopharmacology syllabus, AACN Essentials of Master's
Education, and the Advanced Psychopharmacology Competencies (2026/2027 Edition). Each question has one best
answer marked [CORRECT] and is followed by a rationale grounded in psychopharmacology principles and the NSG
552 curriculum. Cognitive distribution: 20% recall, 50% application, 30% analysis. Approximately 75% of items are
scenario-based clinical decision-making.




Section 1: Principles of Psychopharmacology

Q1: A 62-year-old patient with treatment-resistant depression is being started on amitriptyline. The
PMHNP orders pharmacogenomic testing prior to initiation. Which cytochrome P450 enzyme phenotype,
if identified as a poor metabolizer, would most significantly increase this patient's risk for severe
anticholinergic and cardiac toxicity?
A. CYP2C19 poor metabolizer
B. CYP2D6 poor metabolizer *[CORRECT]*
C. CYP3A4 ultrarapid metabolizer
D. CYP2C9 poor metabolizer
Correct Answer: B
Rationale: Amitriptyline is predominantly metabolized by CYP2D6, and poor metabolizers accumulate parent drug to
toxic levels, amplifying anticholinergic, sedative, and QT-prolonging effects. CYP2C19 is more relevant to
citalopram/escitalopram; CYP3A4 ultrarapid status would lower levels rather than increase them; CYP2C9 is primarily
relevant to warfarin and phenytoin, not TCA clearance. The NSG 552 curriculum emphasizes pre-treatment
pharmacogenomic profiling for TCAs to prevent avoidable adverse drug reactions.

Q2: A patient taking fluoxetine 20 mg daily for depression is newly prescribed tramadol 50 mg every 6
hours for post-operative pain. Within 48 hours, the patient presents with confusion, diaphoresis,
hyperreflexia, myoclonus, and a temperature of 38.9°C (102°F). Which underlying pharmacologic
mechanism best explains this presentation?
A. Competitive inhibition of CYP2D6 by tramadol reducing fluoxetine clearance
B. Synergistic serotonergic activity causing serotonin syndrome *[CORRECT]*
C. Anticholinergic toxicity from additive muscarinic blockade
D. Opioid-induced histamine release triggering mast cell degranulation
Correct Answer: B
Rationale: Fluoxetine is a potent SSRI and tramadol inhibits serotonin and norepinephrine reuptake while also weakly
acting on mu-opioid receptors; combined, they markedly increase synaptic serotonin, producing the classic serotonin
syndrome triad of autonomic instability, neuromuscular hyperactivity (hyperreflexia, myoclonus), and mental status
changes. This is not an anticholinergic nor a histamine-mediated picture, and tramadol does not meaningfully inhibit
fluoxetine clearance. AACN Essentials competency for advanced pharmacology requires the PMHNP to recognize
high-risk serotonergic combinations before prescribing.




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,NSG 552 Exam 2 - Psychopharmacology | 2026/2027 Edition | Wilkes University




Q3: The PMHNP is preparing to initiate therapy with a drug that has a narrow therapeutic index and
requires ongoing serum concentration monitoring. Which of the following psychotropic medications
requires the longest washout period before a safely tolerable switch to an MAOI such as phenelzine?
A. Sertraline
B. Fluoxetine *[CORRECT]*
C. Venlafaxine
D. Mirtazapine
Correct Answer: B
Rationale: Fluoxetine has an active metabolite, norfluoxetine, with a half-life of 7 to 15 days, requiring a minimum
5-week washout before initiating an MAOI to avoid precipitating serotonin syndrome. Sertraline, venlafaxine, and
mirtazapine require only a 2-week washout due to substantially shorter half-lives. This pharmacokinetic distinction is a
high-yield NSG 552 exam concept and is anchored in FDA labeling.

Q4: Which statement most accurately describes the role of P-glycoprotein (P-gp) in
psychopharmacotherapy?
A. P-gp facilitates hepatic phase I metabolism of selective serotonin reuptake inhibitors
B. P-gp is an efflux transporter at the blood-brain barrier that limits CNS penetration of many psychotropics
*[CORRECT]*
C. P-gp is a postsynaptic receptor that mediates the antipsychotic effect of risperidone
D. P-gp is the primary enzyme converting codeine to morphine
Correct Answer: B
Rationale: P-glycoprotein, encoded by ABCB1, is an ATP-dependent efflux transporter expressed at the blood-brain
barrier and intestinal epithelium; it actively pumps many drugs (including risperidone, olanzapine, and many
antidepressants) back into the lumen, limiting CNS bioavailability and influencing interpatient variability. It is not a
metabolic enzyme nor a receptor, and it has no role in codeine conversion (CYP2D6 does). Knowledge of P-gp is
foundational to understanding medication non-response in the NSG 552 curriculum.

Q5: A 34-year-old patient with schizophrenia on a stable dose of clozapine develops a urinary tract
infection and is prescribed ciprofloxacin 500 mg twice daily. Three days later the patient is sedated,
drooling, and tachycardic with a new-onset seizure. The PMHNP suspects an interaction. What is the
most likely pharmacokinetic mechanism?
A. Ciprofloxacin induces CYP1A2, lowering clozapine levels
B. Ciprofloxacin inhibits CYP1A2, raising clozapine levels *[CORRECT]*
C. Ciprofloxacin displaces clozapine from plasma proteins
D. Ciprofloxacin blocks renal tubular secretion of clozapine's metabolites
Correct Answer: B
Rationale: Clozapine is metabolized primarily by CYP1A2, and ciprofloxacin is a potent CYP1A2 inhibitor;
coadministration can double clozapine plasma concentrations, precipitating toxicity (sedation, hypersalivation, seizures,
orthostatic hypotension). The other mechanisms either decrease levels or are clinically insignificant. AACN Essentials
requires advanced practice nurses to anticipate and prevent CYP-mediated interactions when prescribing or co-managing
psychotropic regimens.




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,NSG 552 Exam 2 - Psychopharmacology | 2026/2027 Edition | Wilkes University




Q6: A patient on carbamazepine 600 mg twice daily for bipolar I disorder requests a prescription for oral
contraceptive pills. The PMHNP explains that carbamazepine reduces the efficacy of combined hormonal
contraceptives primarily through which mechanism?
A. Competitive binding at estrogen receptors in the endometrium
B. Induction of CYP3A4 leading to accelerated estrogen and progestin metabolism *[CORRECT]*
C. Increased renal clearance of ethinyl estradiol
D. Inhibition of P-glycoprotein at the intestinal mucosa
Correct Answer: B
Rationale: Carbamazepine is a broad-spectrum hepatic enzyme inducer that upregulates CYP3A4, dramatically
increasing the metabolism of ethinyl estradiol and progestins, which can lead to contraceptive failure and unplanned
pregnancy. It does not act at estrogen receptors, on renal clearance, or via P-gp. This pharmacokinetic principle is a
critical NSG 552 counseling point for women of reproductive potential.

Q7: A patient with major depressive disorder has been on a stable dose of paroxetine 40 mg daily for two
years and reports good response. The patient is newly diagnosed with breast cancer and will begin
tamoxifen therapy. What is the most appropriate pharmacologic action?
A. Continue paroxetine; no interaction is expected
B. Switch to fluoxetine to consolidate SSRI therapy
C. Switch to sertraline or venlafaxine to avoid CYP2D6 inhibition of tamoxifen activation *[CORRECT]*
D. Discontinue the SSRI entirely to avoid serotonin syndrome
Correct Answer: C
Rationale: Tamoxifen is a prodrug requiring CYP2D6-mediated conversion to endoxifen, its active anti-tumor
metabolite; paroxetine and fluoxetine are potent CYP2D6 inhibitors that substantially reduce endoxifen formation and
may increase breast cancer recurrence risk. Sertraline and venlafaxine are weak CYP2D6 inhibitors and are safer in this
context. Discontinuing the SSRI would risk depressive relapse. This is a classic pharmacogenomic-drug interaction
scenario emphasized in the NSG 552 curriculum.

Q8: Which of the following is a black box warning required on all antidepressant labeling in the United
States?
A. Increased risk of hepatotoxicity in patients over 65
B. Increased risk of suicidal thoughts and behaviors in children, adolescents, and young adults up to age 24
*[CORRECT]*
C. Increased risk of Stevens-Johnson syndrome in Asian populations
D. Increased risk of QT prolongation in patients with hypokalemia
Correct Answer: B
Rationale: In 2004 the FDA mandated a black box warning on all antidepressants regarding the increased risk of
suicidality in pediatric and young adult patients up to age 24, reflecting meta-analyses showing a roughly two-fold
increase in suicidal ideation compared with placebo. While QT prolongation, hepatotoxicity, and Stevens-Johnson
syndrome are recognized risks of specific agents, none carries a class-wide black box warning. The PMHNP must
balance this risk against the morbidity of untreated depression per AACN Essentials.




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, NSG 552 Exam 2 - Psychopharmacology | 2026/2027 Edition | Wilkes University




Q9: A patient with bipolar depression is prescribed lithium 600 mg twice daily. The PMHNP reviews
baseline labs prior to initiation. Which combination of monitoring studies is required at baseline and
periodically thereafter per AACN Essentials and standard psychopharmacology guidelines?
A. CBC, fasting lipid panel, and HbA1c only
B. BUN, creatinine, TSH, calcium, and a pregnancy test when applicable *[CORRECT]*
C. ALT, AST, GGT, and serum albumin only
D. Serum sodium, potassium, and chloride only
Correct Answer: B
Rationale: Lithium monitoring must include renal function (BUN/creatinine and urinalysis periodically), thyroid
function (TSH at baseline and every 6-12 months), calcium because of lithium-associated hyperparathyroidism, and a
pregnancy test in women of reproductive potential because lithium is teratogenic (Ebstein's anomaly). CBC, lipids, and
HbA1c are more relevant to atypical antipsychotic monitoring; LFTs are emphasized for valproate. This monitoring
schema is a high-yield NSG 552 concept.

Q10: A patient with schizophrenia who is a heavy smoker (1.5 packs/day) is stabilized on olanzapine 15
mg daily. The patient is admitted for a surgical procedure and required to stop smoking abruptly. The
PMHNP anticipates which change in olanzapine plasma concentration and what adjustment is most
appropriate?
A. Decrease in olanzapine levels; no adjustment needed
B. Increase in olanzapine levels; reduce olanzapine dose by 25-50% *[CORRECT]*
C. No change in olanzapine levels; smoking does not affect olanzapine metabolism
D. Decrease in olanzapine levels; increase olanzapine dose by 50%
Correct Answer: B
Rationale: Polycyclic aromatic hydrocarbons in tobacco smoke induce CYP1A2, which metabolizes olanzapine; abrupt
cessation of smoking removes this induction, raising olanzapine levels and increasing risk of sedation, weight gain, and
orthostatic hypotension. A proactive dose reduction of 25-50% over the first tobacco-free weeks is recommended. This
interaction is a classic NSG 552 application-level concept.

Q11: Under DEA Schedule II regulations applicable to a PMHNP with prescriptive authority, which
statement is most accurate regarding the prescribing of amphetamine mixed salts for an adult with
ADHD?
A. Schedule II stimulants may be refilled by telephone up to one time within 30 days
B. Schedule II prescriptions cannot be refilled; a new prescription is required for each dispensing
*[CORRECT]*
C. Schedule II prescriptions may be transmitted electronically without limitation
D. Schedule II prescriptions are valid for 12 months from the date of issuance
Correct Answer: B
Rationale: DEA regulations prohibit telephone refills of Schedule II stimulants; each dispensing requires a new
prescription, though electronic prescribing of controlled substances (EPCS) is now permitted for Schedule II. Partial fills
are allowed only in limited quantities and within strict time windows. State law may impose additional restrictions, but the
federal prohibition on refills is inviolable. This regulatory framework is a core NSG 552 competency linked to AACN
Essentials.




Wilkes University - Graduate Nursing Program Page 4

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