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PMHNP Board Certification Practice Examination V2.0 150 Advanced Practice Questions with Evidence-Based Rationales a well detailed one 2025 / 2026 written and graded A+ upgraded

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PMHNP Board Certification Practice Examination V2.0 150 Advanced Practice Questions with Evidence-Based Rationales a well detailed one 2025 / 2026 written and graded A+ upgraded

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PMHNP Board Certification Practice
Examination V2.0 150 Advanced Practice
Questions with Evidence-Based Rationales a
well detailed one written and
graded A+ upgraded




General Instructions

• Difficulty Level: Advanced/Hard

• Target Audience: PMHNP candidates preparing for board certification

• Format: Single best answer multiple-choice

• Coverage: Psychopharmacology, neurobiology, differential diagnosis, psychotherapy,
ethics, advanced clinical decision-making



Section 1: Advanced Psychopharmacology (Questions 1-30)

1. A 58-year-old patient with treatment-resistant depression has been on phenelzine 60
mg/day for 6 weeks with significant improvement. The patient now requires surgery and the
anesthesiologist requests discontinuation of the MAOI. What is the most appropriate
perioperative management strategy?

A. Discontinue phenelzine 24 hours before surgery and resume immediately postoperatively
B. Discontinue phenelzine 2 weeks before surgery and bridge with a short-acting SSRI
C. Continue phenelzine throughout the perioperative period with careful monitoring and
avoidance of meperidine and sympathomimetics

,D. Discontinue phenelzine 10 days before surgery and resume when the patient can tolerate
oral intake

Correct Answer: C

Rationale: MAOIs should ideally be continued through the perioperative period if possible, as
discontinuation can lead to depressive relapse and withdrawal. The most significant risk is drug
interactions with meperidine (which can cause serotonin syndrome) and sympathomimetics
(which can cause hypertensive crisis). Anesthesia teams should be informed and appropriate
agents selected. If discontinuation is necessary, phenelzine should be stopped 2 weeks prior
(not 24 hours or 10 days) due to irreversible MAO inhibition requiring new enzyme synthesis.
Bridging with SSRIs carries risks of serotonin syndrome.



2. A patient with bipolar I disorder on lithium 900 mg/day develops a severe maculopapular
rash, fever, and lymphadenopathy. Laboratory studies show elevated liver enzymes and
eosinophilia. What is the most likely diagnosis and appropriate management?

A. Lithium toxicity; discontinue lithium and administer normal saline
B. Drug reaction with eosinophilia and systemic symptoms (DRESS); discontinue lithium
immediately and initiate systemic corticosteroids
C. Stevens-Johnson syndrome; discontinue lithium and initiate IVIG
D. Serum sickness-like reaction; continue lithium and add antihistamines

Correct Answer: B

Rationale: The patient's presentation (maculopapular rash, fever, lymphadenopathy,
eosinophilia, elevated liver enzymes) is consistent with DRESS syndrome, a severe idiosyncratic
drug reaction that can be life-threatening. Lithium can cause DRESS, though it is rare. Immediate
discontinuation of the offending agent and systemic corticosteroids are the mainstays of
treatment. SJS is characterized by blistering and mucosal involvement, which are absent here.
Lithium toxicity presents with GI and neurological symptoms, not this systemic hypersensitivity
pattern.



3. Which cytochrome P450 enzyme is responsible for the conversion of codeine to its active
metabolite morphine, and what is the clinical significance of this pathway?

A. CYP2D6; poor metabolizers have reduced analgesic effect, while ultrarapid metabolizers have
increased risk of toxicity
B. CYP3A4; poor metabolizers have increased toxicity

,C. CYP2C19; poor metabolizers have reduced effect
D. CYP1A2; ultrarapid metabolizers have increased effect

Correct Answer: A

Rationale: Codeine is a prodrug that is metabolized to morphine by CYP2D6. Approximately 7-
10% of the population are poor metabolizers (PMs) and derive minimal analgesic benefit, while
1-2% are ultrarapid metabolizers (UMs) and are at risk of morphine toxicity, including
respiratory depression. The FDA has issued warnings about codeine use in children, especially
those who are UMs. This pharmacogenetic variability has significant clinical implications for pain
management.



4. A 42-year-old patient with panic disorder is started on clonazepam 0.5 mg BID. After 3
months, the patient reports that the medication is no longer effective and they require 1.0 mg
BID to achieve the same effect. What is the most appropriate next step?

A. Increase clonazepam to 1.0 mg BID
B. Switch to alprazolam due to faster onset
C. Cross-taper to a longer-acting benzodiazepine and initiate an SSRI for definitive treatment
D. Add buspirone to augment the clonazepam effect

Correct Answer: C

Rationale: The patient is developing tolerance to the benzodiazepine, requiring dose escalation
to achieve the same effect. While benzodiazepines are effective for acute treatment of panic
disorder, SSRIs are the first-line definitive treatment. The most appropriate strategy is to cross-
taper clonazepam to a longer-acting benzodiazepine (or maintain clonazepam) while initiating
an SSRI. Once the SSRI is effective, the benzodiazepine can be gradually tapered. Buspirone has
limited efficacy for panic disorder.



5. A 28-year-old patient with schizophrenia is on clozapine 300 mg/day. The patient develops
fever, tachycardia, and a new-onset murmur. Laboratory studies show elevated troponin and
C-reactive protein. What is the most likely diagnosis and appropriate management?

A. Neuroleptic malignant syndrome; discontinue clozapine and initiate dantrolene
B. Clozapine-induced myocarditis; discontinue clozapine and initiate cardiology consultation
C. Serotonin syndrome; discontinue clozapine and administer cyproheptadine
D. Malignant catatonia; initiate ECT

Correct Answer: B

, Rationale: The patient's presentation (fever, tachycardia, elevated troponin, new murmur,
elevated CRP) is concerning for clozapine-induced myocarditis, a rare but potentially fatal
adverse effect that typically occurs within the first 1-2 months of treatment. Immediate
discontinuation of clozapine and urgent cardiology consultation are essential. NMS presents
with rigidity and elevated creatine kinase; serotonin syndrome presents with myoclonus and
hyperreflexia. Clozapine should not be restarted after myocarditis.



6. A 65-year-old patient with Alzheimer's disease is on donepezil 10 mg/day and memantine
20 mg/day. The patient's caregiver reports that the patient has developed new-onset
bradycardia and syncope. What is the most likely medication-related cause?

A. Memantine-induced bradycardia
B. Donepezil-induced bradycardia via vagal stimulation
C. Drug interaction between donepezil and memantine
D. Donepezil-induced QT prolongation

Correct Answer: B

Rationale: Donepezil is a cholinesterase inhibitor that increases acetylcholine levels, leading to
vagal stimulation and bradycardia. This is a well-documented adverse effect that can cause
syncope, especially in elderly patients with underlying cardiac conditions. Memantine does not
cause bradycardia. The combination is generally safe, but the bradycardia is likely due to
donepezil. QT prolongation is not a primary effect of donepezil.



7. A 30-year-old patient with ADHD and comorbid tic disorder is being considered for
pharmacotherapy. Which medication is most appropriate given the comorbidity?

A. Immediate-release methylphenidate
B. Amphetamine/dextroamphetamine mixed salts
C. Guanfacine extended-release
D. Lisdexamfetamine

Correct Answer: C

Rationale: Guanfacine extended-release is a non-stimulant alpha-2A adrenergic agonist that is
FDA-approved for ADHD and does not exacerbate tics. In fact, alpha-2 agonists are also used to
treat tic disorders. Stimulants (methylphenidate, amphetamine products) can exacerbate tics in
some patients. Guanfacine is the preferred choice when ADHD and tic disorder are comorbid.
Clonidine is another option, but guanfacine has a more favorable side effect profile.

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