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NSG 552 Psychopharmacology Master Exam (2026/2027) | Wilkes University | 150 Q&A with Rationales | All 3 Exams Combined | PMHNP/FNP

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Complete NSG 552 Psychopharmacology Master Study Guide – Exams 1, 2 & 3 Combined – Wilkes University (2026/2027 Academic Year) This digital download is a comprehensive 150-question master practice exam for NSG 552 Psychopharmacology at Wilkes University. Unlike separate exam files, this consolidated master exam integrates key concepts from all three course exams into a single, streamlined 150-question study resource. Designed for graduate nursing students (PMHNP, FNP, AGNP) seeking efficient, high-yield review. What's included: 150 multiple-choice questions with detailed rationales (condensed from 450+ questions across 3 exams) 5 integrated sections covering all core psychopharmacology domains Answers with evidence-based rationales – learn the "why," not just the "what" High-yield, board-style questions – ideal for course exams and certification prep (ANCC, AANP) Section 1: Foundational Concepts (Q1–25) Pharmacokinetics vs. pharmacodynamics (ADME) Receptor theory: agonists, partial agonists, antagonists, inverse agonists Neurotransmitters: glutamate (excitatory), GABA (inhibitory), serotonin (Raphe nuclei), norepinephrine (locus coeruleus) Four dopamine pathways: mesolimbic (positive symptoms), mesocortical (negative symptoms), nigrostriatal (EPS), tuberoinfundibular (prolactin) CYP450 system: inducers (carbamazepine), inhibitors (valproate, grapefruit juice), substrates Half-life, therapeutic index, tolerance, receptor upregulation/downregulation Neuroanatomy: amygdala (emotion), thalamus (relay), frontal lobe (executive function) Section 2: Antipsychotics (Q26–50) First-generation (typical) vs. second-generation (atypical) antipsychotics FGAs: haloperidol – high EPS risk; SGAs: olanzapine, risperidone, quetiapine, aripiprazole, clozapine EPS: acute dystonia (treat with benztropine/diphenhydramine), akathisia (propranolol), pseudo-Parkinsonism, tardive dyskinesia (AIMS monitoring; VMAT2 inhibitors: valbenazine/Ingrezza, deutetrabenazine/Austedo) NMS: fever, lead pipe rigidity, autonomic instability – discontinue antipsychotic immediately Metabolic syndrome: olanzapine/clozapine highest risk; aripiprazole/ziprasidone weight-neutral; monitor weight/BMI, waist circumference, BP, glucose, lipids; metformin off-label for weight gain Clozapine: treatment-resistant schizophrenia, suicidal behavior; REMS ANC monitoring (weekly ×6 mo → q2wk ×6 mo → monthly); agranulocytosis (fever/sore throat → hold + STAT ANC), myocarditis (first 2 months), sialorrhea (glycopyrrolate), severe constipation/ileus (fatal), seizures (dose-dependent) LAIs: reduce relapse; risperidone LAI needs oral overlap 3–4 weeks; aripiprazole/paliperidone LAIs achieve levels without prolonged overlap Smoking (CYP1A2 inducer): reduces clozapine/olanzapine levels; cessation → levels rise 50–70% → dose reduction required CATIE trial: 74% discontinuation rate; olanzapine slightly superior but metabolic burden Pimavanserin (Nuplazid): 5-HT2A inverse agonist, FDA-approved for Parkinson's disease psychosis Section 3: Antidepressants & Mood Stabilizers (Q51–80) Monoamine theory: serotonin, norepinephrine, dopamine deficiency SSRIs: first-line for MDD; sexual dysfunction (#1 discontinuation reason); sertraline preferred in pregnancy/breastfeeding SNRIs: venlafaxine (dose-dependent hypertension), duloxetine Bupropion (NDRI): weight-neutral, no sexual side effects; contraindicated in seizure disorders/eating disorders TCAs: cardiotoxicity in overdose (QRS widening, arrhythmias) MAOIs: tyramine-free diet (aged cheese, cured meats, wine) to prevent hypertensive crisis Serotonin syndrome: AMS + autonomic instability + neuromuscular hyperreactivity (clonus, hyperreflexia) Discontinuation syndrome: paroxetine highest risk (short half-life); fluoxetine lowest risk (long half-life, self-tapering) Lithium: therapeutic range 0.6–1.2 mEq/L; toxicity (coarse tremor, nausea, vomiting, confusion); nephrogenic diabetes insipidus; hypothyroidism; Ebstein's anomaly risk ~0.1–0.2%; NSAIDs/thiazides ↑ lithium levels; hold 24–48 hours before ECT Valproate: effective for rapid cycling/mixed episodes; hepatotoxicity, thrombocytopenia; neural tube defects (pregnancy category D/X) – use effective contraception Lamotrigine: effective for bipolar depression/maintenance; slow titration to prevent SJS/TEN; dose reduce by 50% with valproate Carbamazepine: CYP3A4 inducer; reduces oral contraceptive efficacy (backup method required); agranulocytosis, hyponatremia Section 4: Anxiety Disorders, ADHD & Substance Use Disorders (Q81–110) GAD: SSRIs/SNRIs first-line; buspirone (5-HT1A partial agonist, no abuse potential, delayed onset 2–4 weeks) Panic disorder: SSRIs/SNRIs first-line; benzodiazepines as short-term bridge Performance anxiety: propranolol 30–60 minutes before event Benzodiazepines: avoid in substance use disorders; withdrawal can be life-threatening (seizures, delirium); slow taper required; Beers Criteria (avoid in elderly) ADHD: stimulants first-line (methylphenidate, amphetamines); common side effects: appetite suppression, insomnia, growth suppression (monitor height/weight) Lisdexamfetamine (Vyvanse): prodrug, lower abuse potential Non-stimulants: atomoxetine (NRI, black box warning for suicidal ideation, hepatotoxicity, CYP2D6 interaction with fluoxetine); guanfacine/clonidine (alpha-2 agonists – sedation, hypotension, rebound hypertension if stopped abruptly) Alcohol Use Disorder: naltrexone (mu-opioid antagonist), acamprosate (restores glutamate/GABA balance, renally excreted), disulfiram (aldehyde dehydrogenase inhibitor – avoid all alcohol sources) Opioid Use Disorder: buprenorphine/naloxone (Suboxone – deters IV misuse), methadone (OTP only, QTc prolongation); must be in withdrawal (COWS ≥8–12) before first buprenorphine dose to avoid precipitated withdrawal Nicotine Use Disorder: NRT, bupropion (start 1–2 weeks before quit date), varenicline (partial nicotinic agonist) Stimulant Use Disorder: no FDA-approved medications Naltrexone treats both OUD and AUD simultaneously Section 5: Advanced Treatment Strategies, Dementia & Special Populations (Q111–150) TRD: failure of ≥2 adequate antidepressant trials; augmentation with atypical antipsychotics (aripiprazole 2–5 mg, brexpiprazole, quetiapine XR 150–300 mg, olanzapine-fluoxetine combination) Esketamine (Spravato): NMDA antagonist; intranasal REMS program; requires 2-hour monitoring; must be on oral antidepressant ECT: gold standard for severe TRD, catatonia, suicidality; transient cognitive side effects (RUL placement minimizes) Alzheimer's disease: cholinesterase inhibitors (donepezil, rivastigmine patch, galantamine) first-line for mild-moderate; memantine (NMDA antagonist) for moderate-severe BPSD: non-pharmacologic first-line; antipsychotics black box warning (↑ mortality, CVA events) – use low-dose SGAs only when severe Lewy Body Dementia: extreme antipsychotic sensitivity; pimavanserin preferred Delirium: treat underlying cause; haloperidol or low-dose SGA if severe agitation Insomnia: CBT-I first-line; DORAs (suvorexant, lemborexant, daridorexant) – no respiratory depression, lower abuse potential; Z-drugs (zolpidem) – complex sleep behaviors (sleep-driving) – discontinue immediately; low-dose doxepin (3–6 mg) for sleep maintenance; ramelteon (melatonin agonist) – no abuse potential, safe in COPD Geriatrics: "start low, go slow" (1/4–1/2 adult dose); Beers Criteria; Anticholinergic Cognitive Burden (ACB) scale Pediatrics: SSRI black box warning (suicidal ideation); stimulants – monitor growth Polypharmacy: increased adverse events, interactions, non-adherence Key drug interactions: lithium + thiazides ↑ toxicity; carbamazepine + OCPs ↓ efficacy; clozapine + smoking cessation ↑ levels; warfarin + SSRIs ↑ INR; aripiprazole + CYP2D6 poor metabolizer → 50% dose reduction Shared decision-making: respect patient preferences (e.g., weight-neutral agents) Why this master exam works: 150 high-yield questions – integrated review of all 3 course exams Detailed rationales – understand complex mechanisms, side effects, drug interactions Efficient study – one file instead of three separate 150-question exams Exam & board ready – mirrors Wilkes University NSG 552 and ANCC/AANP certification style Format: PDF (150 questions + answer key + rationales) Institution: Wilkes University Course: NSG 552 – Psychopharmacology Term: 2026/2027 Type: Master Exam (Exams 1, 2 & 3 Combined) Instant download – study on any device or print for offline use.

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NSG 552 PSYCHOPHARMACOLOGY —
COMPLETE 150-QUESTION MASTER EXAM
Wilkes University | Exams 1, 2 & 3 Combined |
2026/2027 Questions with Answers & Rationales


SECTION 1: FOUNDATIONAL CONCEPTS (Questions 1-25)
Pharmacokinetics, Pharmacodynamics, Neurotransmitters,
CYP450, Principles
1. The study of what the body does to a drug, including absorption,
distribution, metabolism, and excretion, is known as:
A. Pharmacodynamics
B. Pharmacokinetics
C. Psychopharmacology
D. Pharmacogenomics
Correct Answer: B
Rationale: Pharmacokinetics describes how the body processes a
drug—specifically its absorption, distribution, metabolism, and
excretion (ADME). Pharmacodynamics studies what the drug does
to the body.
2. A drug that binds to a receptor and produces a full biologic
response is called a(n):
A. Antagonist
B. Partial agonist
C. Agonist
D. Inverse agonist

,Correct Answer: C
Rationale: An agonist binds to a receptor and fully activates it,
producing the maximum biologic response. A partial agonist
produces only a partial response even at full receptor occupancy.
3. A drug that binds to a receptor and blocks it, preventing a
biologic response, is called a(n):
A. Agonist
B. Partial agonist
C. Antagonist
D. Inverse agonist
Correct Answer: C
Rationale: An antagonist binds to a receptor without activating it,
thereby blocking agonists from binding and preventing a biologic
response.
4. The primary excitatory neurotransmitter in the central nervous
system is:
A. GABA
B. Glutamate
C. Dopamine
D. Serotonin
Correct Answer: B
Rationale: Glutamate is the main excitatory neurotransmitter in
the CNS, functioning as the "on switch" for neuronal activity.
Excessive glutamate can cause excitotoxicity.
5. The primary inhibitory neurotransmitter in the central nervous
system that induces calmness and relaxation is:
A. Glutamate

,B. Dopamine
C. Serotonin
D. GABA (Gamma-aminobutyric acid)
Correct Answer: D
Rationale: GABA is the main inhibitory neurotransmitter, acting as
the "off switch" to reduce neuronal excitability. Benzodiazepines
and barbiturates enhance GABA activity.
6. Serotonin is synthesized from which amino acid and in which
brain region?
A. Tyrosine; substantia nigra
B. Tryptophan; Raphe nuclei
C. Glutamate; cerebellum
D. Choline; basal forebrain
Correct Answer: B
*Rationale: Serotonin (5-HT) is synthesized from the amino acid
tryptophan primarily in the Raphe nuclei of the brainstem. It
regulates mood, anxiety, sleep, and appetite.*
7. Norepinephrine is synthesized in which brain region?
A. Raphe nuclei
B. Locus coeruleus
C. Substantia nigra
D. Ventral tegmental area
Correct Answer: B
Rationale: Norepinephrine is produced in the locus coeruleus and
is critical for attention, arousal, mood, and the stress response.

, 8. The four major dopamine pathways in the brain are:
A. Mesolimbic, Mesocortical, Nigrostriatal, Tuberoinfundibular
B. Mesolimbic, Mesocortical, Hypothalamic, Cerebellar
C. Nigrostriatal, Tuberoinfundibular, Thalamic, Cortical
D. Mesolimbic, Nigrostriatal, Amygdaloid, Hippocampal
Correct Answer: A
Rationale: The four dopamine pathways are: Mesolimbic (positive
symptoms, reward), Mesocortical (negative/cognitive symptoms),
Nigrostriatal (motor control/EPS), and Tuberoinfundibular
(prolactin regulation).
9. Increased dopamine in which pathway is associated with positive
symptoms of schizophrenia (hallucinations, delusions)?
A. Mesocortical
B. Nigrostriatal
C. Mesolimbic
D. Tuberoinfundibular
Correct Answer: C
Rationale: Hyperactivity of dopamine in the mesolimbic pathway is
linked to positive symptoms of psychosis. Antipsychotics block D2
receptors in this pathway.
10. Decreased dopamine in which pathway produces
extrapyramidal symptoms (EPS) and tardive dyskinesia?
A. Mesolimbic
B. Mesocortical
C. Nigrostriatal
D. Tuberoinfundibular

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