Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 1
NSG 552 / NSG552 — Exam 2 Study Guide
Psychopharmacology 2026/2027
Wilkes University — Graduate PMHNP Program
Examination Overview
This study guide and examination consists of 150 multiple-choice questions distributed across ten (10) content
domains aligned with the Wilkes University NSG 552 Exam 2 blueprint. Each question has four options (A–D) with
exactly one correct answer. Cognitive level distribution: ~25% recall, ~50% application, ~25% analysis.
Approximately 75% of items are scenario-based; 25% are direct recall. Rationales provide
psychopharmacology-specific reasoning, receptor mechanisms, monitoring parameters, and study-guide notes for
Exam 2 preparation.
Content Sections: (1) First-Generation Antipsychotics Q1–18 | (2) Second-Generation Antipsychotics Q19–38 | (3)
Third-Generation & LAIs Q39–52 | (4) EPS & Movement Disorders Q53–68 | (5) Metabolic & Endocrine AE
Q69–82 | (6) Lithium Q83–98 | (7) Anticonvulsant Mood Stabilizers Q99–116 | (8) ADHD Pharmacotherapy
Q117–132 | (9) Substance Use Disorder Pharmacotherapy Q133–144 | (10) Special Topics Q145–150.
Section 1: Antipsychotic Pharmacology — First-Generation Agents
(Haloperidol, Chlorpromazine, Fluphenazine, & Thioridazine)
Section 1 covers first-generation (typical) antipsychotics — Haloperidol, Chlorpromazine, Fluphenazine, and Thioridazine.
Mastery requires fluency with D2 antagonism potency differences (high-potency haloperidol/fluphenazine vs. low-potency
chlorpromazine), anticholinergic/sedative/orthostatic burden of low-potency agents, QTc prolongation (notably thioridazine
black box), pigmentary retinopathy, and the EPS risk profile that increases with dopamine D2 receptor occupancy above 80%.
Q1: A 28-year-old male with new-onset schizophrenia is started on haloperidol 5 mg PO BID. Two days
later he presents to the ED with torticollis, oculogyric crisis, and jaw trismus. Which pharmacologic
property of haloperidol best explains why this adverse effect occurred so rapidly at this dose?
A. High affinity for alpha-1 adrenergic receptors causing orthostatic hypotension
B. High D2 receptor potency producing greater than 80% D2 occupancy in the nigrostriatal pathway
[CORRECT]
C. Strong 5-HT2A antagonism that paradoxically worsens dystonia
D. Low anticholinergic activity that increases cholinergic-dopaminergic imbalance
Correct Answer: B
Rationale: Acute dystonia occurs within hours to days of initiating a high-potency D2 antagonist and reflects greater than
80% D2 receptor occupancy in the nigrostriatal pathway, producing a relative cholinergic excess. Haloperidol is a
high-potency first-generation antipsychotic (chlorpromazine equivalent ~50), so even modest milligram doses produce
near-threshold D2 blockade. Option A describes a low-potency effect (orthostasis). Option C is wrong because 5-HT2A
blockade is protective, not dystonia-worsening. Option D is partially true but is a downstream consequence, not the primary
mechanism. Wilkes NSG 552 Exam 2 emphasizes high-potency = high EPS risk.
Q2: A PMHNP student is comparing the receptor binding profiles of first-generation antipsychotics.
Which agent is correctly paired with its MOST characteristic side-effect profile based on potency?
A. Chlorpromazine — high EPS, low sedation, low orthostasis
B. Haloperidol — low EPS, high anticholinergic burden, weight gain
C. Thioridazine — moderate EPS, marked QTc prolongation, retinal pigmentary deposits [CORRECT]
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
,Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 2
D. Fluphenazine — high sedation, low EPS, hyperprolactinemia rare
Correct Answer: C
Rationale: Thioridazine carries an FDA black-box warning for QTc prolongation and dose-dependent pigmented
retinopathy; it is a low-to-mid potency phenothiazine. Chlorpromazine is a low-potency agent with high
anticholinergic/sedative/orthostatic burden but low EPS. Haloperidol is high potency with HIGH EPS, low anticholinergic
burden, and minimal weight gain. Fluphenazine (high potency) carries high EPS and frequent hyperprolactinemia —
sedation is minimal. The Exam 2 study guide stresses the inverse relationship between potency and
anticholinergic/sedative/orthostatic effects.
Q3: A 45-year-old inpatient on chlorpromazine 400 mg/day for schizophrenia complains of severe
dizziness when standing. Vitals: BP 140/88 supine, 102/64 standing, HR 96. Which receptor interaction is
the PRIMARY mechanism of this patient's orthostatic hypotension?
A. D2 blockade in the mesolimbic pathway
B. Alpha-1 adrenergic receptor blockade causing vasodilation [CORRECT]
C. Muscarinic-1 (M1) receptor blockade causing reflex tachycardia
D. Histamine-1 (H1) receptor blockade causing peripheral vasodilation
Correct Answer: B
Rationale: Orthostatic hypotension with reflex tachycardia is mediated primarily by alpha-1 adrenergic receptor blockade,
which prevents norepinephrine-mediated venous and arteriolar constriction on standing. Chlorpromazine, a low-potency
phenothiazine, has high alpha-1 affinity. M1 blockade produces anticholinergic effects (constipation, urinary retention) but
not orthostasis. H1 blockade produces sedation and weight gain. D2 blockade in mesolimbic pathways treats positive
symptoms. Wilkes NSG 552 Exam 2 expects students to map each receptor to its clinical effect.
Q4: Which statement CORRECTLY ranks the first-generation antipsychotics by approximate
chlorpromazine-equivalent potency (mg-for-mg D2 blockade)?
A. Haloperidol > fluphenazine > thioridazine > chlorpromazine
B. Fluphenazine > haloperidol > chlorpromazine > thioridazine [CORRECT]
C. Fluphenazine > haloperidol > thioridazine > chlorpromazine
D. Haloperidol > chlorpromazine > fluphenazine > thioridazine
Correct Answer: B
Rationale: Potency ranking of common FGAs by chlorpromazine equivalents: fluphenazine ~2 mg (highest potency),
haloperidol ~2–5 mg, thioridazine ~100 mg, chlorpromazine 100 mg (reference, lowest potency). Fluphenazine and
haloperidol are clinically interchangeable on potency; thioridazine and chlorpromazine are roughly equipotent. Higher
potency = more EPS but less sedation/orthostasis/anticholinergic burden. Wilkes NSG 552 Exam 2 study guide presents a
potency table that students must memorize for prescribing decisions.
Q5: A 35-year-old female on long-term haloperidol decanoate 100 mg IM monthly develops a 4-week
history of lip-smacking, tongue protrusion, and choreoathetoid finger movements. Symptoms worsen
when her haloperidol dose is increased. Which pathophysiologic process is most likely responsible?
A. Acute D2 hypersensitivity in the nigrostriatal pathway causing transient dyskinesia
B. Dopamine receptor supersensitivity from chronic D2 blockade leading to tardive dyskinesia
[CORRECT]
C. Serotonin 5-HT2A receptor upregulation causing choreiform movements
D. Anticholinergic-induced pseudoparkinsonism masked by haloperidol's low anticholinergic activity
Correct Answer: B
Rationale: Tardive dyskinesia (TD) results from chronic D2 receptor blockade producing postsynaptic supersensitivity in
the nigrostriatal pathway. The classical presentation includes orofacial choreoathetosis (lip-smacking, tongue protrusion),
and symptoms often WORSEN with antipsychotic dose increase as the supersensitive receptors are further denervated.
Acute dystonia (option A) is anticholinergic-responsive and short-lived. 5-HT2A (option C) is not the primary mechanism.
VMAT2 inhibitors (valbenazine, deutetrabenazine) are FDA-approved treatments. Wilkes NSG 552 Exam 2 stresses early
AIMS detection and differential from acute EPS.
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
,Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 3
Q6: A 19-year-old African American male receives haloperidol 10 mg IM for acute agitation. Six hours
later he develops neck hyperextension, upward eye deviation, and a torticollis-like posture. Vital signs
are stable. The MOST appropriate immediate intervention is:
A. Increase haloperidol dose to suppress the dystonia
B. Administer diphenhydramine 50 mg IM or benztropine 1–2 mg IM and reassess [CORRECT]
C. Discontinue all antipsychotics permanently and start lithium
D. Administer propranolol 20 mg PO for akathisia
Correct Answer: B
Rationale: Acute dystonia typically emerges within 24–72 hours of high-potency D2 antagonist initiation, especially after
IM administration in young males. The treatment is parenteral anticholinergic (diphenhydramine 25–50 mg IM/IV or
benztropine 1–2 mg IM/IV), which produces rapid resolution by restoring cholinergic-dopaminergic balance. Increasing
antipsychotic dose (A) would worsen dystonia. Propranolol (D) treats akathisia, not dystonia. Wilkes NSG 552 Exam 2
expects students to differentiate acute dystonia from akathisia and NMS and to know anticholinergic first-line therapy.
Q7: Which antipsychotic carries an FDA BLACK BOX WARNING specifically for QTc prolongation,
dose-dependent retinal pigmentation, and potentially irreversible retinopathy, and is therefore reserved
for treatment-resistant cases after other antipsychotics have failed?
A. Chlorpromazine (Thorazine)
B. Fluphenazine (Prolixin)
C. Haloperidol (Haldol)
D. Thioridazine (Mellaril) [CORRECT]
Correct Answer: D
Rationale: Thioridazine carries the strictest black box among FGAs — QTc prolongation with risk of torsades de pointes,
pigmentary retinopathy, and the recommendation to reserve for treatment-resistant patients who fail other agents. Baseline
and periodic ECG are required; daily doses above 800 mg are contraindicated. Chlorpromazine carries lower QTc risk.
Haloperidol IV is associated with QTc prolongation but thioridazine is the prototypical retinopathy/QTc black box agent.
Wilkes NSG 552 Exam 2 study guide lists thioridazine among medications requiring ECG monitoring.
Q8: A 60-year-old male with schizophrenia has been stable on fluphenazine decanoate 25 mg IM every 2
weeks for 10 years. He develops a pill-rolling tremor, shuffling gait, mask-like facies, and cogwheel
rigidity. The mechanism underlying this presentation is:
A. D2 blockade in the nigrostriatal pathway producing a relative acetylcholine excess [CORRECT]
B. Alpha-1 blockade producing parkinsonian gait via orthostatic hypotension
C. Serotonin 5-HT2A antagonism disrupting basal ganglia output
D. Chronic D2 receptor supersensitivity in the mesolimbic pathway
Correct Answer: A
Rationale: Pseudoparkinsonism is a parkinsonian triad (tremor, rigidity, bradykinesia) induced by D2 blockade in the
nigrostriatal pathway, creating a relative cholinergic (acetylcholine) excess. Onset is days to weeks. Management includes
dose reduction, switching to a lower-potency or atypical agent, or adding an anticholinergic (benztropine or
trihexyphenidyl). D2 supersensitivity (D) underlies tardive dyskinesia, not pseudoparkinsonism. Wilkes NSG 552 Exam 2
emphasizes the four EPS subtypes' onset timelines and management pathways.
Q9: A 24-year-old inpatient complains of intense inner restlessness 5 days after haloperidol initiation. He
paces the unit continuously and reports he 'cannot sit still.' Vitals: T 37.0°C, HR 80, BP 118/76. Mental
status is otherwise clear. The MOST accurate diagnostic interpretation and first-line treatment is:
A. Acute dystonia — treat with diphenhydramine 50 mg IM
B. Akathisia — treat with propranolol 10–30 mg TID or benzodiazepine; reduce antipsychotic dose
[CORRECT]
C. Tardive dyskinesia — discontinue antipsychotic and start valbenazine
D. Restless legs syndrome — prescribe pramipexole
Correct Answer: B
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
, Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 4
Rationale: Akathisia presents as subjective inner restlessness with objective motor compulsion to move, emerging days to
weeks after antipsychotic initiation or dose escalation. Differentiating from psychotic agitation is critical — increasing the
antipsychotic would worsen akathisia. First-line treatment is beta-blocker (propranolol 10–30 mg TID), benzodiazepine
(lorazepam), or anticholinergic if co-existing EPS; reduce antipsychotic dose or switch to lower-potency/atypical agent.
Acute dystonia (A) presents with sustained muscle spasm. Wilkes NSG 552 Exam 2 includes akathisia differentiation
scenarios.
Q10: Which statement BEST describes the comparative adverse-effect profile of high-potency (e.g.,
haloperidol) versus low-potency (e.g., chlorpromazine) first-generation antipsychotics?
A. High-potency agents cause more sedation, orthostatic hypotension, and anticholinergic effects than
low-potency agents
B. Low-potency agents cause more sedation, orthostatic hypotension, and anticholinergic effects than
high-potency agents [CORRECT]
C. Both classes have nearly identical side-effect profiles when dosed at chlorpromazine equivalents
D. High-potency agents cause more weight gain, while low-potency agents cause more EPS
Correct Answer: B
Rationale: The cardinal rule of FGA pharmacology: high-potency agents (haloperidol, fluphenazine) produce MORE EPS
but LESS sedation, orthostasis, anticholinergic effects, and weight gain. Low-potency agents (chlorpromazine, thioridazine)
produce MORE sedation, orthostasis, anticholinergic effects, and weight gain but LESS EPS. This inverse relationship
reflects receptor binding affinity — high-potency = high D2 affinity/low off-target binding, low-potency = low D2
affinity/high off-target alpha-1/H1/M1 binding. Wilkes NSG 552 Exam 2 mandates memorization of this rule.
Q11: A 32-year-old male on chlorpromazine 600 mg/day for 6 months presents with new-onset
galactorrhea, amenorrhea, and decreased libido. Prolactin level is 95 ng/mL (reference 4–23). The
mechanism of this adverse effect is:
A. D2 blockade in the tuberoinfundibular pathway removing the inhibitory dopaminergic tone on
lactotrophs [CORRECT]
B. 5-HT2A antagonism increasing prolactin-releasing hormone secretion
C. Alpha-1 blockade causing vasoconstriction of the pituitary portal system
D. H1 blockade producing indirect prolactin elevation via hypothalamic suppression
Correct Answer: A
Rationale: In the tuberoinfundibular pathway, dopamine normally inhibits prolactin release from anterior pituitary
lactotrophs via D2 receptors. D2 antagonism by antipsychotics removes this inhibition, producing hyperprolactinemia
(galactorrhea, gynecomastia, amenorrhea, sexual dysfunction). Prolactin-sparing agents include aripiprazole (D2 partial
agonist). Among FGAs, this is a class effect, but risperidone and paliperidone among SGAs produce the highest prolactin
elevation. Wilkes NSG 552 Exam 2 expects differentiation of pathway-specific D2 effects: mesolimbic = antipsychotic,
nigrostriatal = EPS, tuberoinfundibular = prolactin.
Q12: Which long-acting injectable (LAI) first-generation antipsychotic is correctly matched with its
administration interval?
A. Haloperidol decanoate — every 4 weeks IM (gluteal) [CORRECT]
B. Fluphenazine decanoate — every 12 weeks SC
C. Haloperidol decanoate — every 12 months IM
D. Fluphenazine decanoate — daily IM microdose
Correct Answer: A
Rationale: Haloperidol decanoate is administered IM (gluteal) every 4 weeks; the dose is approximately 10–15 times the
oral daily dose. Fluphenazine decanoate is also administered every 2–3 weeks IM or SC, not every 12 weeks. LAIs improve
adherence in patients with schizophrenia and reduce rehospitalization. Wilkes NSG 552 Exam 2 includes LAI dosing
intervals as a high-yield recall topic; students should memorize haloperidol decanoate (4 weeks), fluphenazine decanoate
(2–3 weeks), risperidone microspheres (2 weeks), paliperidone palmitate (monthly/3-monthly), and aripiprazole
monohydrate (monthly).
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
NSG 552 / NSG552 — Exam 2 Study Guide
Psychopharmacology 2026/2027
Wilkes University — Graduate PMHNP Program
Examination Overview
This study guide and examination consists of 150 multiple-choice questions distributed across ten (10) content
domains aligned with the Wilkes University NSG 552 Exam 2 blueprint. Each question has four options (A–D) with
exactly one correct answer. Cognitive level distribution: ~25% recall, ~50% application, ~25% analysis.
Approximately 75% of items are scenario-based; 25% are direct recall. Rationales provide
psychopharmacology-specific reasoning, receptor mechanisms, monitoring parameters, and study-guide notes for
Exam 2 preparation.
Content Sections: (1) First-Generation Antipsychotics Q1–18 | (2) Second-Generation Antipsychotics Q19–38 | (3)
Third-Generation & LAIs Q39–52 | (4) EPS & Movement Disorders Q53–68 | (5) Metabolic & Endocrine AE
Q69–82 | (6) Lithium Q83–98 | (7) Anticonvulsant Mood Stabilizers Q99–116 | (8) ADHD Pharmacotherapy
Q117–132 | (9) Substance Use Disorder Pharmacotherapy Q133–144 | (10) Special Topics Q145–150.
Section 1: Antipsychotic Pharmacology — First-Generation Agents
(Haloperidol, Chlorpromazine, Fluphenazine, & Thioridazine)
Section 1 covers first-generation (typical) antipsychotics — Haloperidol, Chlorpromazine, Fluphenazine, and Thioridazine.
Mastery requires fluency with D2 antagonism potency differences (high-potency haloperidol/fluphenazine vs. low-potency
chlorpromazine), anticholinergic/sedative/orthostatic burden of low-potency agents, QTc prolongation (notably thioridazine
black box), pigmentary retinopathy, and the EPS risk profile that increases with dopamine D2 receptor occupancy above 80%.
Q1: A 28-year-old male with new-onset schizophrenia is started on haloperidol 5 mg PO BID. Two days
later he presents to the ED with torticollis, oculogyric crisis, and jaw trismus. Which pharmacologic
property of haloperidol best explains why this adverse effect occurred so rapidly at this dose?
A. High affinity for alpha-1 adrenergic receptors causing orthostatic hypotension
B. High D2 receptor potency producing greater than 80% D2 occupancy in the nigrostriatal pathway
[CORRECT]
C. Strong 5-HT2A antagonism that paradoxically worsens dystonia
D. Low anticholinergic activity that increases cholinergic-dopaminergic imbalance
Correct Answer: B
Rationale: Acute dystonia occurs within hours to days of initiating a high-potency D2 antagonist and reflects greater than
80% D2 receptor occupancy in the nigrostriatal pathway, producing a relative cholinergic excess. Haloperidol is a
high-potency first-generation antipsychotic (chlorpromazine equivalent ~50), so even modest milligram doses produce
near-threshold D2 blockade. Option A describes a low-potency effect (orthostasis). Option C is wrong because 5-HT2A
blockade is protective, not dystonia-worsening. Option D is partially true but is a downstream consequence, not the primary
mechanism. Wilkes NSG 552 Exam 2 emphasizes high-potency = high EPS risk.
Q2: A PMHNP student is comparing the receptor binding profiles of first-generation antipsychotics.
Which agent is correctly paired with its MOST characteristic side-effect profile based on potency?
A. Chlorpromazine — high EPS, low sedation, low orthostasis
B. Haloperidol — low EPS, high anticholinergic burden, weight gain
C. Thioridazine — moderate EPS, marked QTc prolongation, retinal pigmentary deposits [CORRECT]
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
,Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 2
D. Fluphenazine — high sedation, low EPS, hyperprolactinemia rare
Correct Answer: C
Rationale: Thioridazine carries an FDA black-box warning for QTc prolongation and dose-dependent pigmented
retinopathy; it is a low-to-mid potency phenothiazine. Chlorpromazine is a low-potency agent with high
anticholinergic/sedative/orthostatic burden but low EPS. Haloperidol is high potency with HIGH EPS, low anticholinergic
burden, and minimal weight gain. Fluphenazine (high potency) carries high EPS and frequent hyperprolactinemia —
sedation is minimal. The Exam 2 study guide stresses the inverse relationship between potency and
anticholinergic/sedative/orthostatic effects.
Q3: A 45-year-old inpatient on chlorpromazine 400 mg/day for schizophrenia complains of severe
dizziness when standing. Vitals: BP 140/88 supine, 102/64 standing, HR 96. Which receptor interaction is
the PRIMARY mechanism of this patient's orthostatic hypotension?
A. D2 blockade in the mesolimbic pathway
B. Alpha-1 adrenergic receptor blockade causing vasodilation [CORRECT]
C. Muscarinic-1 (M1) receptor blockade causing reflex tachycardia
D. Histamine-1 (H1) receptor blockade causing peripheral vasodilation
Correct Answer: B
Rationale: Orthostatic hypotension with reflex tachycardia is mediated primarily by alpha-1 adrenergic receptor blockade,
which prevents norepinephrine-mediated venous and arteriolar constriction on standing. Chlorpromazine, a low-potency
phenothiazine, has high alpha-1 affinity. M1 blockade produces anticholinergic effects (constipation, urinary retention) but
not orthostasis. H1 blockade produces sedation and weight gain. D2 blockade in mesolimbic pathways treats positive
symptoms. Wilkes NSG 552 Exam 2 expects students to map each receptor to its clinical effect.
Q4: Which statement CORRECTLY ranks the first-generation antipsychotics by approximate
chlorpromazine-equivalent potency (mg-for-mg D2 blockade)?
A. Haloperidol > fluphenazine > thioridazine > chlorpromazine
B. Fluphenazine > haloperidol > chlorpromazine > thioridazine [CORRECT]
C. Fluphenazine > haloperidol > thioridazine > chlorpromazine
D. Haloperidol > chlorpromazine > fluphenazine > thioridazine
Correct Answer: B
Rationale: Potency ranking of common FGAs by chlorpromazine equivalents: fluphenazine ~2 mg (highest potency),
haloperidol ~2–5 mg, thioridazine ~100 mg, chlorpromazine 100 mg (reference, lowest potency). Fluphenazine and
haloperidol are clinically interchangeable on potency; thioridazine and chlorpromazine are roughly equipotent. Higher
potency = more EPS but less sedation/orthostasis/anticholinergic burden. Wilkes NSG 552 Exam 2 study guide presents a
potency table that students must memorize for prescribing decisions.
Q5: A 35-year-old female on long-term haloperidol decanoate 100 mg IM monthly develops a 4-week
history of lip-smacking, tongue protrusion, and choreoathetoid finger movements. Symptoms worsen
when her haloperidol dose is increased. Which pathophysiologic process is most likely responsible?
A. Acute D2 hypersensitivity in the nigrostriatal pathway causing transient dyskinesia
B. Dopamine receptor supersensitivity from chronic D2 blockade leading to tardive dyskinesia
[CORRECT]
C. Serotonin 5-HT2A receptor upregulation causing choreiform movements
D. Anticholinergic-induced pseudoparkinsonism masked by haloperidol's low anticholinergic activity
Correct Answer: B
Rationale: Tardive dyskinesia (TD) results from chronic D2 receptor blockade producing postsynaptic supersensitivity in
the nigrostriatal pathway. The classical presentation includes orofacial choreoathetosis (lip-smacking, tongue protrusion),
and symptoms often WORSEN with antipsychotic dose increase as the supersensitive receptors are further denervated.
Acute dystonia (option A) is anticholinergic-responsive and short-lived. 5-HT2A (option C) is not the primary mechanism.
VMAT2 inhibitors (valbenazine, deutetrabenazine) are FDA-approved treatments. Wilkes NSG 552 Exam 2 stresses early
AIMS detection and differential from acute EPS.
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
,Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 3
Q6: A 19-year-old African American male receives haloperidol 10 mg IM for acute agitation. Six hours
later he develops neck hyperextension, upward eye deviation, and a torticollis-like posture. Vital signs
are stable. The MOST appropriate immediate intervention is:
A. Increase haloperidol dose to suppress the dystonia
B. Administer diphenhydramine 50 mg IM or benztropine 1–2 mg IM and reassess [CORRECT]
C. Discontinue all antipsychotics permanently and start lithium
D. Administer propranolol 20 mg PO for akathisia
Correct Answer: B
Rationale: Acute dystonia typically emerges within 24–72 hours of high-potency D2 antagonist initiation, especially after
IM administration in young males. The treatment is parenteral anticholinergic (diphenhydramine 25–50 mg IM/IV or
benztropine 1–2 mg IM/IV), which produces rapid resolution by restoring cholinergic-dopaminergic balance. Increasing
antipsychotic dose (A) would worsen dystonia. Propranolol (D) treats akathisia, not dystonia. Wilkes NSG 552 Exam 2
expects students to differentiate acute dystonia from akathisia and NMS and to know anticholinergic first-line therapy.
Q7: Which antipsychotic carries an FDA BLACK BOX WARNING specifically for QTc prolongation,
dose-dependent retinal pigmentation, and potentially irreversible retinopathy, and is therefore reserved
for treatment-resistant cases after other antipsychotics have failed?
A. Chlorpromazine (Thorazine)
B. Fluphenazine (Prolixin)
C. Haloperidol (Haldol)
D. Thioridazine (Mellaril) [CORRECT]
Correct Answer: D
Rationale: Thioridazine carries the strictest black box among FGAs — QTc prolongation with risk of torsades de pointes,
pigmentary retinopathy, and the recommendation to reserve for treatment-resistant patients who fail other agents. Baseline
and periodic ECG are required; daily doses above 800 mg are contraindicated. Chlorpromazine carries lower QTc risk.
Haloperidol IV is associated with QTc prolongation but thioridazine is the prototypical retinopathy/QTc black box agent.
Wilkes NSG 552 Exam 2 study guide lists thioridazine among medications requiring ECG monitoring.
Q8: A 60-year-old male with schizophrenia has been stable on fluphenazine decanoate 25 mg IM every 2
weeks for 10 years. He develops a pill-rolling tremor, shuffling gait, mask-like facies, and cogwheel
rigidity. The mechanism underlying this presentation is:
A. D2 blockade in the nigrostriatal pathway producing a relative acetylcholine excess [CORRECT]
B. Alpha-1 blockade producing parkinsonian gait via orthostatic hypotension
C. Serotonin 5-HT2A antagonism disrupting basal ganglia output
D. Chronic D2 receptor supersensitivity in the mesolimbic pathway
Correct Answer: A
Rationale: Pseudoparkinsonism is a parkinsonian triad (tremor, rigidity, bradykinesia) induced by D2 blockade in the
nigrostriatal pathway, creating a relative cholinergic (acetylcholine) excess. Onset is days to weeks. Management includes
dose reduction, switching to a lower-potency or atypical agent, or adding an anticholinergic (benztropine or
trihexyphenidyl). D2 supersensitivity (D) underlies tardive dyskinesia, not pseudoparkinsonism. Wilkes NSG 552 Exam 2
emphasizes the four EPS subtypes' onset timelines and management pathways.
Q9: A 24-year-old inpatient complains of intense inner restlessness 5 days after haloperidol initiation. He
paces the unit continuously and reports he 'cannot sit still.' Vitals: T 37.0°C, HR 80, BP 118/76. Mental
status is otherwise clear. The MOST accurate diagnostic interpretation and first-line treatment is:
A. Acute dystonia — treat with diphenhydramine 50 mg IM
B. Akathisia — treat with propranolol 10–30 mg TID or benzodiazepine; reduce antipsychotic dose
[CORRECT]
C. Tardive dyskinesia — discontinue antipsychotic and start valbenazine
D. Restless legs syndrome — prescribe pramipexole
Correct Answer: B
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
, Wilkes University | NSG 552 — Psychopharmacology | Exam 2 Study Guide 2026/2027 Page 4
Rationale: Akathisia presents as subjective inner restlessness with objective motor compulsion to move, emerging days to
weeks after antipsychotic initiation or dose escalation. Differentiating from psychotic agitation is critical — increasing the
antipsychotic would worsen akathisia. First-line treatment is beta-blocker (propranolol 10–30 mg TID), benzodiazepine
(lorazepam), or anticholinergic if co-existing EPS; reduce antipsychotic dose or switch to lower-potency/atypical agent.
Acute dystonia (A) presents with sustained muscle spasm. Wilkes NSG 552 Exam 2 includes akathisia differentiation
scenarios.
Q10: Which statement BEST describes the comparative adverse-effect profile of high-potency (e.g.,
haloperidol) versus low-potency (e.g., chlorpromazine) first-generation antipsychotics?
A. High-potency agents cause more sedation, orthostatic hypotension, and anticholinergic effects than
low-potency agents
B. Low-potency agents cause more sedation, orthostatic hypotension, and anticholinergic effects than
high-potency agents [CORRECT]
C. Both classes have nearly identical side-effect profiles when dosed at chlorpromazine equivalents
D. High-potency agents cause more weight gain, while low-potency agents cause more EPS
Correct Answer: B
Rationale: The cardinal rule of FGA pharmacology: high-potency agents (haloperidol, fluphenazine) produce MORE EPS
but LESS sedation, orthostasis, anticholinergic effects, and weight gain. Low-potency agents (chlorpromazine, thioridazine)
produce MORE sedation, orthostasis, anticholinergic effects, and weight gain but LESS EPS. This inverse relationship
reflects receptor binding affinity — high-potency = high D2 affinity/low off-target binding, low-potency = low D2
affinity/high off-target alpha-1/H1/M1 binding. Wilkes NSG 552 Exam 2 mandates memorization of this rule.
Q11: A 32-year-old male on chlorpromazine 600 mg/day for 6 months presents with new-onset
galactorrhea, amenorrhea, and decreased libido. Prolactin level is 95 ng/mL (reference 4–23). The
mechanism of this adverse effect is:
A. D2 blockade in the tuberoinfundibular pathway removing the inhibitory dopaminergic tone on
lactotrophs [CORRECT]
B. 5-HT2A antagonism increasing prolactin-releasing hormone secretion
C. Alpha-1 blockade causing vasoconstriction of the pituitary portal system
D. H1 blockade producing indirect prolactin elevation via hypothalamic suppression
Correct Answer: A
Rationale: In the tuberoinfundibular pathway, dopamine normally inhibits prolactin release from anterior pituitary
lactotrophs via D2 receptors. D2 antagonism by antipsychotics removes this inhibition, producing hyperprolactinemia
(galactorrhea, gynecomastia, amenorrhea, sexual dysfunction). Prolactin-sparing agents include aripiprazole (D2 partial
agonist). Among FGAs, this is a class effect, but risperidone and paliperidone among SGAs produce the highest prolactin
elevation. Wilkes NSG 552 Exam 2 expects differentiation of pathway-specific D2 effects: mesolimbic = antipsychotic,
nigrostriatal = EPS, tuberoinfundibular = prolactin.
Q12: Which long-acting injectable (LAI) first-generation antipsychotic is correctly matched with its
administration interval?
A. Haloperidol decanoate — every 4 weeks IM (gluteal) [CORRECT]
B. Fluphenazine decanoate — every 12 weeks SC
C. Haloperidol decanoate — every 12 months IM
D. Fluphenazine decanoate — daily IM microdose
Correct Answer: A
Rationale: Haloperidol decanoate is administered IM (gluteal) every 4 weeks; the dose is approximately 10–15 times the
oral daily dose. Fluphenazine decanoate is also administered every 2–3 weeks IM or SC, not every 12 weeks. LAIs improve
adherence in patients with schizophrenia and reduce rehospitalization. Wilkes NSG 552 Exam 2 includes LAI dosing
intervals as a high-yield recall topic; students should memorize haloperidol decanoate (4 weeks), fluphenazine decanoate
(2–3 weeks), risperidone microspheres (2 weeks), paliperidone palmitate (monthly/3-monthly), and aripiprazole
monohydrate (monthly).
PMHNP Graduate Examination | 150 Questions | Cognitive Levels: 25% Recall / 50% Application / 25% Analysis
