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Wilkes NSG 552 Exam 2 Psychopharmacology (2026/2027) Questions & Answers | Guarantee Pass

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Wilkes NSG 552 Exam 2 Psychopharmacology study guide delivers real Q&A with detailed rationales covering antipsychotics, mood stabilizers, anxiolytics, and psychiatric medication management for advanced practice nurses. What You Will Get: verified practice questions, answer rationales, key concept breakdowns, and exam-focused review for guaranteed success.Wilkes NSG 552 exam 2 questions and answers, NSG 552 psychopharmacology exam 2 study guide, Wilkes University NSG 552 exam 2 prep, NSG 552 exam 2 practice questions with rationales, psychopharmacology NSG 552 exam 2 quizlet, NSG 552 exam 2 antipsychotic questions, Wilkes NSG 552 exam 2 review, NSG 552 psychopharmacology practice test exam 2, NSG 552 exam 2 answers, Wilkes nursing NSG 552 study guide exam 2, NSG 552 mood stabilizer quiz, NSG 552 anxiolytic drugs exam, NSG 552 antidepressant management test, NSG 552 bipolar disorder medications questions, NSG 552 schizophrenia pharmacology exam, NSG 552 psychiatric medication quiz, Wilkes NSG 552 exam 2 review guide, NSG 552 psychopharmacology prep exam 2#NSG552 #NSG552Exam2 #WilkesUniversity #WilkesNursing #Psychopharmacology #PsychiatricNursing #PMHNPStudent #PsychNPStudent #GraduateNursing #NursingExamPrep #ExamPrep #StudyGuide

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Wilkes University NSG 552 Exam 2 (pdf) | 2026/2027 |
Psychopharmacology Q&A | Nursing
1. Which benzodiazepine is preferred for a patient with severe hepatic impairment due to its
lack of extensive liver metabolism?

A) Diazepam

B) Lorazepam

C) Chlordiazepoxide

D) Clorazepate

Correct Answer: Lorazepam

Rationale: Lorazepam undergoes glucuronidation, making it safer for patients with liver disease
because it does not rely on hepatic oxidation. Diazepam and chlordiazepoxide are long-acting and
hepatically metabolized. This pharmacokinetic distinction reduces the risk of drug accumulation and
toxicity in hepatic impairment.

2. What is the primary mechanism of action of buspirone in treating generalized anxiety
disorder?

A) GABA-A receptor positive allosteric modulation

B) Serotonin 5-HT1A receptor partial agonism

C) Norepinephrine reuptake inhibition

D) Dopamine D2 receptor blockade

Correct Answer: Serotonin 5-HT1A receptor partial agonism

Rationale: Buspirone acts as a partial agonist at 5-HT1A receptors, modulating serotonergic
transmission without direct GABAergic activity. This mechanism explains its delayed onset and lack of
abuse potential compared to benzodiazepines. It is not effective as a PRN medication for acute
anxiety.

3. According to the NSG 552 study guide, which three benzodiazepines are recommended for
patients with alcohol use disorder due to their safer metabolic profile?

A) Diazepam, chlordiazepoxide, clonazepam

B) Lorazepam, oxazepam, temazepam

C) Alprazolam, triazolam, flurazepam

D) Clorazepate, prazepam, halazepam

Correct Answer: Lorazepam, oxazepam, temazepam

Rationale: These benzodiazepines are conjugated rather than extensively oxidized by the liver, making
them safer for patients with hepatic impairment or alcohol use disorder. The “OTL” mnemonic
(Outside The Liver) highlights lorazepam, oxazepam, and temazepam. Their simplified metabolism
reduces the risk of accumulation and adverse effects.

, 4. A patient with panic disorder is initiated on sertraline. Which statement best explains why a
benzodiazepine may be temporarily co-prescribed?

A) Benzodiazepines enhance the long-term efficacy of SSRIs

B) Benzodiazepines provide rapid symptom relief while the SSRI reaches therapeutic levels

C) Benzodiazepines prevent serotonin syndrome during SSRI initiation

D) Benzodiazepines are required to prevent SSRI discontinuation syndrome

Correct Answer: Benzodiazepines provide rapid symptom relief while the SSRI reaches therapeutic
levels

Rationale: SSRIs require several weeks to achieve full therapeutic effect, leaving a gap in symptom
control. Benzodiazepines bridge this gap by offering immediate anxiolysis during the initiation phase.
They are not intended for long-term use due to dependence risks and do not enhance SSRI efficacy.

5. Which antidepressant class is associated with the highest anticholinergic side effect burden?

A) Selective serotonin reuptake inhibitors

B) Serotonin-norepinephrine reuptake inhibitors

C) Tricyclic antidepressants

D) Monoamine oxidase inhibitors

Correct Answer: Tricyclic antidepressants

Rationale: TCAs such as amitriptyline and clomipramine possess significant anticholinergic properties,
causing dry mouth, constipation, urinary retention, and blurred vision. SSRIs and SNRIs have minimal
anticholinergic effects. This side effect profile makes TCAs less favorable for older adults and patients
sensitive to anticholinergic burden.

6. Which activating antidepressant is most likely to exacerbate anxiety symptoms, particularly
at higher doses?

A) Mirtazapine

B) Venlafaxine

C) Trazodone

D) Amitriptyline

Correct Answer: Venlafaxine

Rationale: Venlafaxine, an SNRI, increases norepinephrine activity at higher doses, which can
precipitate agitation, restlessness, and heightened anxiety. Mirtazapine and trazodone are generally
sedating rather than activating. This noradrenergic effect requires careful dose titration in anxious
patients.

7. What is the recommended treatment strategy for obsessive-compulsive disorder according
to NSG 552 materials?

A) Benzodiazepines as first-line monotherapy

, B) SSRIs combined with cognitive-behavioral therapy

C) Bupropion as the preferred agent

D) Antipsychotics alone for all severity levels

Correct Answer: SSRIs combined with cognitive-behavioral therapy

Rationale: OCD treatment guidelines recommend SSRIs (fluoxetine, sertraline, fluvoxamine,
paroxetine) combined with CBT, particularly exposure and response prevention. Benzodiazepines are
not effective for core OCD obsessions and carry dependence risk. Bupropion is not indicated for OCD.

8. A patient with severe OCD has an inadequate response to high-dose fluoxetine and intensive
CBT. Which augmentation strategy is most appropriate before considering ECT?

A) Add methylphenidate

B) Add an atypical antipsychotic

C) Add buspirone

D) Switch to bupropion

Correct Answer: Add an atypical antipsychotic

Rationale: For treatment-resistant OCD, augmentation with an atypical antipsychotic is supported
before pursuing ECT. Stimulants, buspirone, and bupropion are not established augmentation
strategies for OCD. ECT is reserved for debilitating, refractory cases after other options are exhausted.

9. Which medication is FDA-approved for OCD and commonly causes nausea and vomiting as
side effects?

A) Clomipramine

B) Fluvoxamine

C) Bupropion

D) Trazodone

Correct Answer: Fluvoxamine

Rationale: Fluvoxamine is an SSRI specifically FDA-approved for OCD, with gastrointestinal side effects
including nausea and vomiting being common. Clomipramine is a TCA also approved for OCD but has
a different side effect profile. Bupropion and trazodone are not indicated for OCD.

10. A patient on stable fluoxetine therapy develops serotonin syndrome after starting linezolid.
What is the primary mechanism of this toxicity?

A) CYP2D6 inhibition increasing fluoxetine levels

B) MAO-A inhibition combined with serotonin reuptake blockade

C) CYP3A4 inhibition increasing linezolid levels

D) Direct 5-HT3 receptor stimulation by linezolid

Correct Answer: MAO-A inhibition combined with serotonin reuptake blockade

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