Wilkes University NSG 552
Psychopharmacology Exams 1 2 and 3 Latest
2026/2027 – Verified Revised Full Exam with
Detailed Explanations – Pass Guaranteed – A+
Graded
========================================
EXAM 1: Antidepressants & Foundational Principles
Q1: A 28-year-old patient with Major Depressive Disorder (MDD) asks how their new
medication works. You prescribe fluoxetine. What is the primary mechanism of action?
A. Blocks dopamine D2 receptors in the mesolimbic pathway
B. Selectively inhibits the serotonin transporter (SERT), increasing synaptic serotonin
[CORRECT]
C. Inhibits monoamine oxidase type A and type B irreversibly
D. Blocks presynaptic alpha-2 adrenergic autoreceptors
Correct Answer: B
Rationale: Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that selectively
blocks SERT, increasing serotonin (5-HT) concentration in the synaptic cleft. Choice A
describes antipsychotics; choice C describes MAOIs; choice D describes mirtazapine. A
key clinical pearl is that while synaptic serotonin increases immediately, downstream
receptor desensitization takes 2-4 weeks, explaining the delayed therapeutic onset.
Q2: Which neurotransmitter pathway, when activated, is most directly responsible for
the nausea and gastrointestinal distress commonly experienced by patients initiating
SSRI therapy?
A. Mesolimbic dopamine pathway
B. Tuberoinfundibular pathway
C. Dorsal raphe nucleus projecting to the gastrointestinal tract via the vagus nerve
[CORRECT]
D. Nigrostriatal pathway
Correct Answer: C
Rationale: Serotonin produced in the raphe nuclei travels down the vagus nerve to the
enteric nervous system, stimulating gastrointestinal motility and secretion.
,SSRI-induced increases in synaptic serotonin overstimulate this pathway, causing acute
nausea. The mesolimbic and nigrostriatal pathways are dopaminergic, while the
tuberoinfundibular pathway regulates prolactin.
Q3 (SATA): A 65-year-old patient with depression is prescribed nortriptyline. The
PMHNP educates the patient on anticholinergic side effects. Which of the following
symptoms should be included in this education? (Select All That Apply)
A. Urinary retention [CORRECT]
B. Diarrhea
C. Dry mouth [CORRECT]
D. Constipation [CORRECT]
E. Bradycardia
Correct Answer: A, C, D
Rationale: Tricyclic antidepressants (TCAs) like nortriptyline possess strong antagonistic
properties at muscarinic (M1) receptors, leading to classic anticholinergic effects: dry
mouth, constipation, urinary retention, and tachycardia (not bradycardia). Diarrhea is
incorrect because anticholinergics decrease GI motility, causing constipation. In geriatric
patients, these effects increase fall risk and can precipitate delirium.
Q4: A patient is prescribed a medication that is a strong inhibitor of the CYP2D6
isoenzyme. They are currently taking a prodrug metabolized entirely by CYP2D6 into its
active form. What is the expected clinical outcome?
A. Toxic levels of the active metabolite, increasing adverse effects
B. Reduced efficacy of the prodrug due to lack of conversion to the active form
[CORRECT]
C. Induction of CYP3A4, accelerating drug clearance
D. Decreased side effects of the prodrug
Correct Answer: B
Rationale: Prodrugs (e.g., codeine, tramadol) rely on hepatic enzymes (specifically
CYP2D6) for biotransformation into their active therapeutic metabolites (morphine,
O-desmethyltramadol). A strong CYP2D6 inhibitor (like paroxetine or fluoxetine) will
block this conversion, rendering the prodrug ineffective. This is a critical clinical pearl:
always check if a drug is an active parent compound or a prodrug before pairing it with
inhibitors.
Q5: A 32-year-old female with MDD and a history of bulimia nervosa is seeking
treatment. Which of the following antidepressants is FDA-approved for this specific
comorbidity and is the MOST appropriate choice?
A. Bupropion
B. Mirtazapine
C. Fluoxetine [CORRECT]
,D. Amitriptyline
Correct Answer: C
Rationale: Fluoxetine is the only antidepressant FDA-approved for bulimia nervosa,
shown to reduce binge-purge cycles. Bupropion is absolutely contraindicated in patients
with eating disorders due to a lowered seizure threshold associated with purging
behaviors. Mirtazapine and amitriptyline are not indicated for bulimia and carry risks of
significant weight gain.
Q6: A 45-year-old male with MDD is started on sertraline 50 mg daily. He returns to the
clinic in 4 weeks reporting minimal improvement in mood. His PMHNP decides to
increase the dose to 100 mg daily. He is also taking warfarin for atrial fibrillation. What is
the primary pharmacokinetic mechanism driving the potential drug interaction?
A. Sertraline induces CYP3A4, decreasing warfarin levels
B. Sertraline is a mild CYP2C9 inhibitor, potentially increasing INR [CORRECT]
C. Sertraline binds to plasma proteins, displacing warfarin
D. Sertraline inhibits renal excretion of warfarin
Correct Answer: B
Rationale: Sertraline exhibits mild inhibition of CYP2C9, the primary enzyme
responsible for metabolizing the more potent S-enantiomer of warfarin. Inhibiting this
enzyme reduces warfarin clearance, increasing its serum concentration and elevating
the INR, thereby increasing bleeding risk. SSRIs also independently impair platelet
aggregation via serotonin depletion, compounding bleed risk.
Q7: A 30-year-old female with Panic Disorder who is 8 weeks pregnant presents for
pharmacotherapy. Which of the following is considered the FIRST-LINE treatment
based on reproductive psychiatry guidelines due to the most robust safety data in
pregnancy?
A. Paroxetine
B. Sertraline [CORRECT]
C. Venlafaxine
D. Alprazolam
Correct Answer: B
Rationale: Sertraline is generally considered the first-line SSRI in pregnancy due to
extensive safety data showing no significant increase in teratogenicity. Paroxetine is
strictly contraindicated in the first trimester due to a 1.5 to 2-fold increased risk of
cardiac defects. Venlafaxine has less robust data, and alprazolam is a Category D
benzodiazepine associated with cleft palate and neonatal withdrawal.
Q8: A 52-year-old patient with depression, chronic pain, and severe insomnia is
prescribed trazodone 100 mg at bedtime. What is the primary receptor activity
responsible for its sedating and sleep-promoting effects?
, A. Potent serotonin reuptake inhibition
B. Strong 5-HT2A receptor antagonism and alpha-1 adrenergic antagonism
[CORRECT]
C. Histamine H1 receptor agonism
D. Dopamine D2 receptor blockade
Correct Answer: B
Rationale: At low doses (e.g., 50-150 mg), trazodone acts primarily as a 5-HT2A
antagonist and an alpha-1 adrenergic antagonist, which produces significant sedation,
making it a common off-label hypnotic. It is a weak serotonin reuptake inhibitor at these
doses; significant reuptake inhibition and 5-HT2C antagonism (which contributes to
weight gain) only occur at higher antidepressant doses (>300 mg).
Q9: A patient on fluoxetine 40 mg daily for 6 months is switched abruptly to duloxetine
due to insurance formulary changes. Three days later, the patient presents with severe
dizziness, "electric shock" sensations in the head, nausea, and crying spells. What is
the MOST accurate explanation for this presentation?
A. Relapse of Major Depressive Disorder
B. SSRI Discontinuation Syndrome [CORRECT]
C. Serotonin Syndrome
D. Conversion disorder
Correct Answer: B
Rationale: This patient is experiencing classic SSRI discontinuation syndrome,
characterized by the "four Ds": Dizziness, Diarrhea, Dream abnormalities, and
Dysphoria (including electric shock sensations/paresthesias). Fluoxetine has a very long
half-life (and active metabolite norfluoxetine), but abrupt cessation can still cause this.
Relapse takes weeks to manifest, not days. Serotonin syndrome presents with
hyperthermia, clonus, and hyperreflexia, not shock sensations.
Q10: A patient with MDD is taking phenelzine, an irreversible non-selective MAOI. They
inadvertently consume a large amount of aged cheddar cheese and red wine at a party.
What is the underlying pathophysiology of the subsequent hypertensive crisis?
A. Tyramine displaces norepinephrine from presynaptic vesicles
B. Unmetabolized tyramine enters the systemic circulation, displacing norepinephrine
from nerve terminals [CORRECT]
C. The cheese directly stimulates alpha-1 receptors
D. MAOIs directly sensitize vascular smooth muscle to catecholamines
Correct Answer: B
Rationale: Normally, dietary tyramine is extensively metabolized by intestinal and
hepatic monoamine oxidase (MAO). When MAO is inhibited, unmetabolized tyramine
enters the systemic circulation and acts as a false neurotransmitter, displacing massive
amounts of norepinephrine from presynaptic storage vesicles, causing a severe
Psychopharmacology Exams 1 2 and 3 Latest
2026/2027 – Verified Revised Full Exam with
Detailed Explanations – Pass Guaranteed – A+
Graded
========================================
EXAM 1: Antidepressants & Foundational Principles
Q1: A 28-year-old patient with Major Depressive Disorder (MDD) asks how their new
medication works. You prescribe fluoxetine. What is the primary mechanism of action?
A. Blocks dopamine D2 receptors in the mesolimbic pathway
B. Selectively inhibits the serotonin transporter (SERT), increasing synaptic serotonin
[CORRECT]
C. Inhibits monoamine oxidase type A and type B irreversibly
D. Blocks presynaptic alpha-2 adrenergic autoreceptors
Correct Answer: B
Rationale: Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that selectively
blocks SERT, increasing serotonin (5-HT) concentration in the synaptic cleft. Choice A
describes antipsychotics; choice C describes MAOIs; choice D describes mirtazapine. A
key clinical pearl is that while synaptic serotonin increases immediately, downstream
receptor desensitization takes 2-4 weeks, explaining the delayed therapeutic onset.
Q2: Which neurotransmitter pathway, when activated, is most directly responsible for
the nausea and gastrointestinal distress commonly experienced by patients initiating
SSRI therapy?
A. Mesolimbic dopamine pathway
B. Tuberoinfundibular pathway
C. Dorsal raphe nucleus projecting to the gastrointestinal tract via the vagus nerve
[CORRECT]
D. Nigrostriatal pathway
Correct Answer: C
Rationale: Serotonin produced in the raphe nuclei travels down the vagus nerve to the
enteric nervous system, stimulating gastrointestinal motility and secretion.
,SSRI-induced increases in synaptic serotonin overstimulate this pathway, causing acute
nausea. The mesolimbic and nigrostriatal pathways are dopaminergic, while the
tuberoinfundibular pathway regulates prolactin.
Q3 (SATA): A 65-year-old patient with depression is prescribed nortriptyline. The
PMHNP educates the patient on anticholinergic side effects. Which of the following
symptoms should be included in this education? (Select All That Apply)
A. Urinary retention [CORRECT]
B. Diarrhea
C. Dry mouth [CORRECT]
D. Constipation [CORRECT]
E. Bradycardia
Correct Answer: A, C, D
Rationale: Tricyclic antidepressants (TCAs) like nortriptyline possess strong antagonistic
properties at muscarinic (M1) receptors, leading to classic anticholinergic effects: dry
mouth, constipation, urinary retention, and tachycardia (not bradycardia). Diarrhea is
incorrect because anticholinergics decrease GI motility, causing constipation. In geriatric
patients, these effects increase fall risk and can precipitate delirium.
Q4: A patient is prescribed a medication that is a strong inhibitor of the CYP2D6
isoenzyme. They are currently taking a prodrug metabolized entirely by CYP2D6 into its
active form. What is the expected clinical outcome?
A. Toxic levels of the active metabolite, increasing adverse effects
B. Reduced efficacy of the prodrug due to lack of conversion to the active form
[CORRECT]
C. Induction of CYP3A4, accelerating drug clearance
D. Decreased side effects of the prodrug
Correct Answer: B
Rationale: Prodrugs (e.g., codeine, tramadol) rely on hepatic enzymes (specifically
CYP2D6) for biotransformation into their active therapeutic metabolites (morphine,
O-desmethyltramadol). A strong CYP2D6 inhibitor (like paroxetine or fluoxetine) will
block this conversion, rendering the prodrug ineffective. This is a critical clinical pearl:
always check if a drug is an active parent compound or a prodrug before pairing it with
inhibitors.
Q5: A 32-year-old female with MDD and a history of bulimia nervosa is seeking
treatment. Which of the following antidepressants is FDA-approved for this specific
comorbidity and is the MOST appropriate choice?
A. Bupropion
B. Mirtazapine
C. Fluoxetine [CORRECT]
,D. Amitriptyline
Correct Answer: C
Rationale: Fluoxetine is the only antidepressant FDA-approved for bulimia nervosa,
shown to reduce binge-purge cycles. Bupropion is absolutely contraindicated in patients
with eating disorders due to a lowered seizure threshold associated with purging
behaviors. Mirtazapine and amitriptyline are not indicated for bulimia and carry risks of
significant weight gain.
Q6: A 45-year-old male with MDD is started on sertraline 50 mg daily. He returns to the
clinic in 4 weeks reporting minimal improvement in mood. His PMHNP decides to
increase the dose to 100 mg daily. He is also taking warfarin for atrial fibrillation. What is
the primary pharmacokinetic mechanism driving the potential drug interaction?
A. Sertraline induces CYP3A4, decreasing warfarin levels
B. Sertraline is a mild CYP2C9 inhibitor, potentially increasing INR [CORRECT]
C. Sertraline binds to plasma proteins, displacing warfarin
D. Sertraline inhibits renal excretion of warfarin
Correct Answer: B
Rationale: Sertraline exhibits mild inhibition of CYP2C9, the primary enzyme
responsible for metabolizing the more potent S-enantiomer of warfarin. Inhibiting this
enzyme reduces warfarin clearance, increasing its serum concentration and elevating
the INR, thereby increasing bleeding risk. SSRIs also independently impair platelet
aggregation via serotonin depletion, compounding bleed risk.
Q7: A 30-year-old female with Panic Disorder who is 8 weeks pregnant presents for
pharmacotherapy. Which of the following is considered the FIRST-LINE treatment
based on reproductive psychiatry guidelines due to the most robust safety data in
pregnancy?
A. Paroxetine
B. Sertraline [CORRECT]
C. Venlafaxine
D. Alprazolam
Correct Answer: B
Rationale: Sertraline is generally considered the first-line SSRI in pregnancy due to
extensive safety data showing no significant increase in teratogenicity. Paroxetine is
strictly contraindicated in the first trimester due to a 1.5 to 2-fold increased risk of
cardiac defects. Venlafaxine has less robust data, and alprazolam is a Category D
benzodiazepine associated with cleft palate and neonatal withdrawal.
Q8: A 52-year-old patient with depression, chronic pain, and severe insomnia is
prescribed trazodone 100 mg at bedtime. What is the primary receptor activity
responsible for its sedating and sleep-promoting effects?
, A. Potent serotonin reuptake inhibition
B. Strong 5-HT2A receptor antagonism and alpha-1 adrenergic antagonism
[CORRECT]
C. Histamine H1 receptor agonism
D. Dopamine D2 receptor blockade
Correct Answer: B
Rationale: At low doses (e.g., 50-150 mg), trazodone acts primarily as a 5-HT2A
antagonist and an alpha-1 adrenergic antagonist, which produces significant sedation,
making it a common off-label hypnotic. It is a weak serotonin reuptake inhibitor at these
doses; significant reuptake inhibition and 5-HT2C antagonism (which contributes to
weight gain) only occur at higher antidepressant doses (>300 mg).
Q9: A patient on fluoxetine 40 mg daily for 6 months is switched abruptly to duloxetine
due to insurance formulary changes. Three days later, the patient presents with severe
dizziness, "electric shock" sensations in the head, nausea, and crying spells. What is
the MOST accurate explanation for this presentation?
A. Relapse of Major Depressive Disorder
B. SSRI Discontinuation Syndrome [CORRECT]
C. Serotonin Syndrome
D. Conversion disorder
Correct Answer: B
Rationale: This patient is experiencing classic SSRI discontinuation syndrome,
characterized by the "four Ds": Dizziness, Diarrhea, Dream abnormalities, and
Dysphoria (including electric shock sensations/paresthesias). Fluoxetine has a very long
half-life (and active metabolite norfluoxetine), but abrupt cessation can still cause this.
Relapse takes weeks to manifest, not days. Serotonin syndrome presents with
hyperthermia, clonus, and hyperreflexia, not shock sensations.
Q10: A patient with MDD is taking phenelzine, an irreversible non-selective MAOI. They
inadvertently consume a large amount of aged cheddar cheese and red wine at a party.
What is the underlying pathophysiology of the subsequent hypertensive crisis?
A. Tyramine displaces norepinephrine from presynaptic vesicles
B. Unmetabolized tyramine enters the systemic circulation, displacing norepinephrine
from nerve terminals [CORRECT]
C. The cheese directly stimulates alpha-1 receptors
D. MAOIs directly sensitize vascular smooth muscle to catecholamines
Correct Answer: B
Rationale: Normally, dietary tyramine is extensively metabolized by intestinal and
hepatic monoamine oxidase (MAO). When MAO is inhibited, unmetabolized tyramine
enters the systemic circulation and acts as a false neurotransmitter, displacing massive
amounts of norepinephrine from presynaptic storage vesicles, causing a severe
