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WGU D345 Psychopharmacology Pre-Assessment V2, Western Governors University, 2026/2027 – 150+ Questions with Verified Answers

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This document covers the Pre-Assessment V2 for WGU D345 Psychopharmacology for the 2026/2027 academic cycle. It includes 150+ questions with verified answers, focusing on psychopharmacologic principles, medication classifications, and clinical application in mental health care. The material supports exam preparation by reinforcing understanding of psychiatric medications, mechanisms of action, adverse effects, drug interactions, and safe prescribing practices within nursing and healthcare contexts.

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WGU D345 Psychopharmacology Pre-Assessment V2 | 2026-2027




WGU D345 PSYCHOPHARMACOLOGY

Pre-Assessment V2 | Questions & Verified Answers

150+ Questions | 2026-2027 Academic Cycle

Western Governors University | Nursing & Healthcare Focus




Page 1

, WGU D345 Psychopharmacology Pre-Assessment V2 | 2026-2027




Section 1: Neurotransmitter Systems & Receptor Pharmacology
This section assesses understanding of major neurotransmitter systems, receptor subtypes, and their
relevance to psychotropic medication mechanisms of action.



Question 1

Which neurotransmitter is the primary target of SSRIs and is most directly involved in mood regulation,
appetite, sleep, and impulse control?

A. Dopamine
B. Serotonin (5-HT)
C. Norepinephrine
D. GABA
Correct Answer: B. Serotonin (5-HT)
Rationale: Serotonin (5-HT) is the primary target of SSRIs, SNRIs, and MAOIs for mood and anxiety
disorders. It regulates mood, appetite, sleep-wake cycles, impulse control, pain perception, and GI
function through multiple receptor subtypes. The serotonergic system originates in the raphe nuclei and
projects widely throughout the brain.



Question 2

Dopamine D2 receptor antagonism in the mesolimbic pathway produces which therapeutic effect?

A. Antidepressant effect
B. Reduction of positive psychotic symptoms (hallucinations, delusions)
C. Anxiolytic effect
D. Mood stabilization in bipolar disorder
Correct Answer: B. Reduction of positive psychotic symptoms (hallucinations, delusions)
Rationale: D2 receptor antagonism in the mesolimbic pathway reduces excessive dopamine activity,
alleviating positive psychotic symptoms. However, D2 antagonism in the nigrostriatal pathway causes
EPS, and in the tuberoinfundibular pathway causes hyperprolactinemia. Understanding these
pathway-specific effects is essential for antipsychotic prescribing and monitoring.



Question 3

Which dopamine pathway regulates motor control, and its disruption by D2 antagonism causes
extrapyramidal symptoms?

A. Mesolimbic pathway



Page 2

, WGU D345 Psychopharmacology Pre-Assessment V2 | 2026-2027


B. Nigrostriatal pathway
C. Mesocortical pathway
D. Tuberoinfundibular pathway
Correct Answer: B. Nigrostriatal pathway
Rationale: The nigrostriatal pathway projects from the substantia nigra to the striatum and regulates
motor control. D2 antagonism in this pathway causes EPS including acute dystonia, parkinsonism,
akathisia, and tardive dyskinesia. High-potency FGAs cause more nigrostriatal D2 blockade and
therefore more EPS.



Question 4

The 5-HT2A receptor is the primary target of which class of medications, and its activation produces
psychedelic effects?

A. SSRIs
B. Second-generation antipsychotics (antagonism) and classic psychedelics
(activation)
C. Benzodiazepines
D. Mood stabilizers
Correct Answer: B. Second-generation antipsychotics (antagonism) and classic
psychedelics (activation)
Rationale: 5-HT2A antagonism by SGAs (risperidone, olanzapine, etc.) contributes to their improved
EPS profile compared to FGAs through modulation of dopamine release. Activation of 5-HT2A receptors
by LSD and psilocybin produces psychedelic effects. The D2/5-HT2A antagonism ratio is the hallmark
mechanism distinguishing SGAs from FGAs.



Question 5

Benzodiazepines act as positive allosteric modulators at which receptor complex?

A. GABA-B receptor
B. GABA-A receptor (alpha-gamma subunit interface)
C. NMDA receptor
D. 5-HT1A receptor
Correct Answer: B. GABA-A receptor (alpha-gamma subunit interface)
Rationale: Benzodiazepines bind at the interface of alpha and gamma subunits of the GABA-A
receptor pentamer, enhancing GABA's inhibitory effect by increasing chloride ion channel opening
frequency. Alpha-1 subunit-containing receptors mediate sedation and amnesia; alpha-2/3 subunit-
containing receptors mediate anxiolysis and myorelaxation.



Page 3

, WGU D345 Psychopharmacology Pre-Assessment V2 | 2026-2027




Question 6

Norepinephrine reuptake inhibition produces antidepressant effects but may also cause which adverse
effects?

A. Weight gain and sedation
B. Hypertension, tachycardia, diaphoresis, and insomnia
C. Bradycardia and hypotension
D. Anticholinergic effects
Correct Answer: B. Hypertension, tachycardia, diaphoresis, and insomnia
Rationale: NE reuptake inhibition increases synaptic norepinephrine, activating alpha-1 adrenergic
receptors (causing hypertension and tachycardia) and beta-adrenergic receptors (causing diaphoresis
and tremor). These effects are dose-dependent and more pronounced with SNRIs at higher doses
(venlafaxine >150 mg/day, duloxetine 60 mg/day).



Question 7

Acetylcholine receptor antagonism (muscarinic) from psychotropic medications produces which
constellation of effects?

A. Weight gain and metabolic changes
B. Dry mouth, constipation, urinary retention, blurred vision, cognitive
impairment, tachycardia
C. Sedation and respiratory depression
D. Extrapyramidal symptoms
Correct Answer: B. Dry mouth, constipation, urinary retention, blurred vision, cognitive
impairment, tachycardia
Rationale: Anticholinergic effects result from muscarinic receptor antagonism and are commonly
caused by TCAs, low-potency FGAs, olanzapine, quetiapine, and benztropine. These effects are
cumulative and particularly problematic in elderly patients, increasing risk of cognitive decline,
delirium, falls, and constipation.



Question 8

Ketamine and esketamine produce rapid antidepressant effects through which mechanism?

A. SSRI mechanism
B. NMDA receptor antagonism with downstream AMPA/BDNF activation
C. D2 receptor partial agonism




Page 4

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