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Wilkes NSG 552 Exam 1 Psychopharmacology EXAM QUESTIONS AND CORRECT ANSWERS WITH RATIONALES.pdf

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**TAP ON "AVAILABLE IN BUNDLE / PACKAGE DEAL" TO UNLOCK FREE BONUS EXAMS AND EVERYTHING YOU NEED.** **WILKES NSG 552 EXAM 1 PSYCHOPHARMACOLOGY EXAM QUESTIONS AND CORRECT ANSWERS WITH RATIONALES JUST RELEASED** This study guide covers key Wilkes NSG 552 Exam 1 concepts, including pharmacokinetics (absorption, distribution, metabolism, excretion) versus pharmacodynamics (what the drug does to the body), the six general principles of psychopharmacological treatment (pharmacokinetics, safety, tolerability, efficacy, practicality, treatment accessibility, treatment compliance), CYP450 enzyme system including inducers (decrease serum levels of substrate drugs) and inhibitors (increase serum levels causing toxic levels), CYP3A4 metabolizing approximately 50% of all clinically used medications, CYP2D6 metabolizing approximately 25% of psychiatric medications and its polymorphic nature affecting drug efficacy, first-pass metabolism and its effect on bioavailability, steady state achievement after 4-5 half-lives, half-life as the time needed to clear 50% of drug from plasma, receptor theory including full agonists (maximum biological response), partial agonists, antagonists, and inverse agonists, neurotransmitter systems including serotonin derived from tryptophan in the raphe nuclei, norepinephrine produced in the locus ceruleus, dopamine produced in the VTA, GABA as the primary inhibitory neurotransmitter, glutamate as the primary excitatory neurotransmitter, the four dopamine pathways (mesolimbic associated with positive symptoms, mesocortical associated with negative symptoms, nigrostriatal associated with motor symptoms and EPS, tuberoinfundibular inhibiting prolactin), neuroanatomy including amygdala (fear and rage), thalamus (sensory relay), hypothalamus (homeostasis and sleep-wake cycles), and frontal lobe/prefrontal cortex (executive functioning and working memory), first-generation antipsychotics (D2 receptor antagonism in mesolimbic pathway) versus second-generation antipsychotics (5-HT2A antagonism), extrapyramidal symptoms including acute dystonia, akathisia, pseudo-Parkinsonism, and tardive dyskinesia, neuroleptic malignant syndrome recognition using the FALTERED mnemonic, antidepressant classes including SSRIs (fluoxetine, sertraline, escitalopram, citalopram, paroxetine, fluvoxamine), SNRIs, NDRIs (bupropion), SARIs (trazodone), TCAs (with 3A's anticholinergic effects and 3C's cardiotoxic effects), and MAOIs (requiring tyramine-restricted diet and washout periods), serotonin syndrome recognition including neuromuscular excitability and clonus, hyponatremia risk with SSRIs especially in elderly patients, discontinuation syndrome, and applicable Wilkes University NSG 552 course competencies and PMHNP prescribing standards. It features exam-style practice questions with verified correct answers and detailed rationales to reinforce technical knowledge, strengthen clinical decision-making and psychopharmacological reasoning skills, and support focused Wilkes NSG 552 Exam 1 preparation.

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Wilkes NSG 552 Exam 1 Psychopharmacology EXAM


Exam Coverage

• Foundations of psychopharmacology, including pharmacokinetics, pharmacodynamics,

therapeutic response, and medication safety principles.

• Neurotransmitter systems involving dopamine, serotonin, norepinephrine, glutamate, GABA,

acetylcholine, and their psychiatric relevance.

• Neuroanatomy and dopamine pathways, including mesolimbic, mesocortical, nigrostriatal, and

tuberoinfundibular pathways.

• Cytochrome P450 metabolism, enzyme induction and inhibition, half-life, steady state,

bioavailability, and clinically important interactions.

• Antipsychotic pharmacology, including first-generation and second-generation agents,

receptor actions, indications, and monitoring.

• Extrapyramidal symptoms, tardive dyskinesia, akathisia, dystonia, pseudoparkinsonism,

neuroleptic malignant syndrome, and treatment approaches.

• Antidepressant pharmacology, including SSRIs, SNRIs, bupropion, mirtazapine, trazodone,

TCAs, MAOIs, and newer multimodal agents.

• Serotonin syndrome, antidepressant discontinuation, hypertensive reactions, overdose risks,

sexual adverse effects, and patient counseling.

• Mood-stabilizing pharmacology, including lithium, valproate, carbamazepine, and lamotrigine,

with emphasis on toxicity and laboratory monitoring.

• Clinical prescribing principles, adherence, treatment response, adverse-effect management,

special precautions, and evidence-based medication selection.

,1. A patient taking trazodone develops a prolonged painful erection and seeks urgent

evaluation. Which adverse effect is classically associated with this medication?

A. Priapism

B. Agranulocytosis

C. Severe hyperprolactinemia in all patients

D. Tardive dyskinesia

Answer: A

Rationale: Priapism is a rare but important adverse effect of trazodone and requires urgent

medical evaluation because prolonged ischemia can cause tissue injury.


2. A patient with treatment-resistant schizophrenia is being considered for clozapine. Which

serious adverse effect requires ongoing blood monitoring?

A. Mild dry mouth

B. Severe neutropenia or agranulocytosis

C. Transient headache

D. Increased appetite alone

Answer: B

Rationale: Clozapine can cause severe neutropenia or agranulocytosis, so appropriate

blood-count monitoring is required to reduce the risk of serious infection.


3. In an advanced-practice nursing assessment, the nurse practitioner wants to select the

explanation that is most consistent with psychopharmacology. when comparing two

medications by their receptor actions and resulting clinical effects rather than their absorption or

elimination, which concept is being assessed?

,A. Pharmacokinetics

B. Bioavailability

C. Pharmacodynamics

D. Clearance

Answer: C

Rationale: Receptor action and the resulting biologic response are pharmacodynamic

concepts. Pharmacokinetics instead addresses how drug concentrations change in the body.

This interpretation is clinically useful because it links the medication's mechanism with the

patient's observable response and guides appropriate monitoring.


4. During a psychiatric medication review, the patient asks which pharmacologic principle most

directly explains the finding described. why are medication washout periods important when

switching between an MAOI and another serotonergic antidepressant?

A. Washout periods prevent all weight gain

B. They eliminate the need for blood pressure monitoring

C. They increase CYP induction

D. The combination can produce serious toxicity, including serotonin syndrome

Answer: D

Rationale: MAO inhibition persists beyond the last dose for some agents. Inadequate

separation from serotonergic medications can produce severe serotonin toxicity. This

interpretation is clinically useful because it links the medication's mechanism with the patient's

observable response and guides appropriate monitoring.

, 5. A patient taking a dopamine-blocking antipsychotic develops severe rigidity, hyperthermia,

altered mental status, and autonomic instability. Which emergency is most likely?

A. Neuroleptic malignant syndrome

B. Serotonin syndrome

C. Tardive dyskinesia

D. Acute dystonia

Answer: A

Rationale: Neuroleptic malignant syndrome is a potentially life-threatening reaction to

dopamine blockade characterized by severe rigidity, hyperthermia, altered mental status, and

autonomic instability.


6. In a clinical decision-making encounter, the patient asks which pharmacologic principle most

directly explains the finding described. a patient taking a typical antipsychotic develops rigidity

and tremor. Which neurotransmitter pathway is most directly affected by the medication's

therapeutic mechanism and this adverse effect?

A. Only acetylcholine pathways

B. Dopaminergic pathways

C. Only glutamate pathways

D. Only GABA pathways

Answer: B

Rationale: Typical antipsychotics primarily block dopamine receptors. Their clinical and

adverse effects reflect dopamine signaling across several pathways. This interpretation is

clinically useful because it links the medication's mechanism with the patient's observable

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