Wilkes University NSG 552
Psychopharmacology for Advanced Practice
ACTUAL EXAM 2025/2026 | Exam 1 2 & 3
Comprehensive Review | 250 Questions |
Verified Answers | Verified Q&A | Pass
Guaranteed - A+ Graded
EXAM 1: NEUROBIOLOGY AND BASIC PRINCIPLES
Q1: A patient with treatment-resistant depression is prescribed phenelzine (Nardil). The patient
asks about dietary restrictions. Which food should be strictly avoided to prevent hypertensive
crisis?
A. Fresh apples
B. Aged cheese [CORRECT]
C. Steamed broccoli
D. White rice
Correct Answer: B
Rationale: MAOIs (phenelzine, tranylcypromine, isocarboxazid) irreversibly inhibit MAO-A and
MAO-B, preventing the breakdown of tyramine. Tyramine-rich foods (aged cheeses, cured meats,
fermented foods, soy sauce, fava beans, tap beers, red wine) can cause dangerous hypertension
through catecholamine release. Fresh foods (A, C, D) are safe.
Wilkes Note: Remember "AGED" foods = dangerous with MAOIs. The 14-day washout period
applies when switching from MAOIs to SSRIs/SNRIs (5 weeks for fluoxetine due to its long half-life).
Q2: A 68-year-old patient with schizophrenia is started on haloperidol 5mg daily. Within 48 hours,
the patient develops torticollis, oculogyric crisis, and tongue protrusion. Which neurotransmitter
imbalance explains these symptoms?
,A. Excessive dopamine in the nigrostriatal pathway
B. Dopamine blockade in the nigrostriatal pathway [CORRECT]
C. Excessive acetylcholine in the mesolimbic pathway
D. Serotonin excess in the raphe nuclei
Correct Answer: B
Rationale: Acute dystonia (torticollis, oculogyric crisis) results from D2 antagonism in the
nigrostriatal pathway, creating a relative cholinergic excess. First-generation antipsychotics (FGAs)
like haloperidol strongly block D2 receptors here. Treatment involves anticholinergics (benztropine,
diphenhydramine) to restore balance.
Wilkes Note: FGAs = high risk for EPS. Think "D2 blockade = EPS." Nigrostriatal pathway is for
movement; mesolimbic is for psychosis (target), tuberoinfundibular affects prolactin.
Q3: A patient taking fluoxetine (Prozac) 20mg daily for major depressive disorder reports nausea,
anxiety, and insomnia two days after starting therapy. What is the most appropriate response?
A. Discontinue fluoxetine immediately due to allergic reaction
B. Reassure the patient these are common initial side effects that improve in 1-2 weeks
[CORRECT]
C. Add lorazepam for anxiety and switch to bedtime dosing
D. Increase fluoxetine to 40mg to overcome activation symptoms
Correct Answer: B
Rationale: SSRIs commonly cause activation syndrome (anxiety, agitation, insomnia) and GI
symptoms (nausea, diarrhea) initially due to rapid serotonin increase. These typically resolve within
1-2 weeks as the brain adapts. This is not an allergic reaction (A) or serotonin syndrome
(hyperthermia, myoclonus, autonomic instability). Increasing the dose (D) would worsen symptoms.
Wilkes Note: "Start low, go slow" applies to initiation. Activation side effects are temporary, not
treatment failures.
Q4: Which CYP450 enzyme is responsible for metabolizing the majority of psychotropic
medications, including many antipsychotics, benzodiazepines, and antidepressants?
A. CYP1A2
B. CYP2D6
C. CYP3A4 [CORRECT]
D. CYP2E1
Correct Answer: C
Rationale: CYP3A4 metabolizes approximately 50% of all drugs, including quetiapine, aripiprazole,
ziprasidone, alprazolam, midazolam, triazolam, sertraline, and carbamazepine. CYP2D6 (B)
metabolizes risperidone, haloperidol, paroxetine, fluoxetine, atomoxetine, and tamoxifen. CYP1A2
(A) is induced by smoking and metabolizes clozapine and olanzapine.
Wilkes Note: CYP3A4 = "The Big One." Inhibitors: grapefruit juice, ketoconazole. Inducers:
carbamazepine, rifampin, St. John's wort.
,Q5: A patient with bipolar disorder on lithium carbonate develops polyuria, polydipsia, and a fine
tremor. Laboratory studies reveal a serum lithium level of 1.4 mEq/L. What is the most appropriate
intervention?
A. Continue current dose and add valproic acid
B. Decrease lithium dose and monitor renal function [CORRECT]
C. Discontinue lithium permanently and switch to carbamazepine
D. Increase lithium to achieve level of 1.8 mEq/L for better mood stabilization
Correct Answer: B
Rationale: Lithium toxicity begins at >1.5 mEq/L, but symptoms can occur at lower levels if
dehydrated or elderly. Therapeutic range: acute mania 0.8-1.2 mEq/L; maintenance 0.6-0.8 mEq/L.
Polyuria suggests nephrogenic diabetes insipidus (lithium reduces ADH response in collecting
ducts). The dose should be reduced, and renal function (Cr, eGFR) monitored.
Wilkes Note: Lithium levels >1.5 = toxic (coarse tremor, ataxia, confusion). >2.0 = medical
emergency (seizures, coma). Always monitor Cr/eGFR and TSH every 3-6 months.
Q6: Which neurotransmitter is synthesized from tryptophan via 5-HTP, plays a critical role in mood
regulation, and has receptors (5-HT2A) implicated in hallucinations and psychosis?
A. Dopamine
B. Norepinephrine
C. Serotonin [CORRECT]
D. Glutamate
Correct Answer: C
Rationale: Serotonin (5-HT) synthesis: tryptophan → 5-HTP → serotonin → melatonin. 5-HT2A
receptor stimulation causes hallucinations (psychedelics like LSD are 5-HT2A agonists); blockade
by atypical antipsychotics treats psychosis. Serotonin regulates mood, anxiety, sleep, appetite, and
impulse control.
Wilkes Note: "2A = Trippy." 5-HT2A blockade = antipsychotic effect + reduced EPS. 5-HT2C
blockade = appetite increase (mirtazapine, olanzapine).
Q7: A patient with ADHD is prescribed atomoxetine (Strattera). The patient is also on paroxetine
(Paxil) for anxiety. What is the primary concern with this combination?
A. Increased risk of serotonin syndrome
B. Atomoxetine toxicity due to CYP2D6 inhibition [CORRECT]
C. Decreased efficacy of atomoxetine
D. Increased risk of seizures
Correct Answer: B
Rationale: Atomoxetine is metabolized by CYP2D6. Paroxetine is a potent CYP2D6 inhibitor.
Co-administration increases atomoxetine levels 3-4 fold, increasing cardiovascular risks (BP, HR).
This is a pharmacokinetic interaction, not pharmacodynamic (A). Consider CYP2D6 genotype
testing or dose reduction.
, Wilkes Note: Paroxetine and fluoxetine are strong CYP2D6 inhibitors. They inhibit their own
metabolism (non-linear kinetics) and significantly increase levels of CYP2D6 substrates.
Q8: Which brain structure serves as the major relay station for sensory information (except smell)
and connects to the cerebral cortex?
A. Hypothalamus
B. Hippocampus
C. Thalamus [CORRECT]
D. Amygdala
Correct Answer: C
Rationale: The thalamus receives sensory input (visual, auditory, tactile) and relays it to
appropriate cortical areas. It also regulates consciousness, sleep, and alertness. The
hypothalamus (A) regulates autonomic and endocrine functions. Hippocampus (B) is for memory
consolidation. Amygdala (D) processes fear and emotional memories.
Wilkes Note: Thalamus = "Sensory Switchboard." Lesions can cause sensory neglect or thalamic
pain syndrome.
Q9: A patient with epilepsy is started on carbamazepine (Tegretol). After two weeks, the patient
develops confusion, ataxia, and hyponatremia (Na+ 128). What is the mechanism of this adverse
effect?
A. SIADH (Syndrome of Inappropriate Antidiuretic Hormone) [CORRECT]
B. Diabetes insipidus
C. Hyperaldosteronism
D. Acute tubular necrosis
Correct Answer: A
Rationale: Carbamazepine and oxcarbazepine commonly cause SIADH through ADH release or
potentiation, leading to water retention and dilutional hyponatremia. Monitor sodium levels,
especially in elderly. Treat with fluid restriction or discontinuation if severe. This is distinct from
lithium-induced nephrogenic DI (B).
Wilkes Note: "Carba-messy-nerves" = blood dyscrasias, SIADH, autoinduction of metabolism, and
many drug interactions.
Q10: Which receptor antagonism explains the weight gain and metabolic side effects seen with
atypical antipsychotics like olanzapine and clozapine?
A. D2 antagonism
B. 5-HT2A antagonism
C. Histamine H1 antagonism and 5-HT2C antagonism [CORRECT]
D. Alpha-1 antagonism
Correct Answer: C
Rationale: H1 antagonism causes sedation and appetite stimulation. 5-HT2C antagonism disinhibits
appetite regulation (increases food intake). Olanzapine and clozapine have the highest H1 and
Psychopharmacology for Advanced Practice
ACTUAL EXAM 2025/2026 | Exam 1 2 & 3
Comprehensive Review | 250 Questions |
Verified Answers | Verified Q&A | Pass
Guaranteed - A+ Graded
EXAM 1: NEUROBIOLOGY AND BASIC PRINCIPLES
Q1: A patient with treatment-resistant depression is prescribed phenelzine (Nardil). The patient
asks about dietary restrictions. Which food should be strictly avoided to prevent hypertensive
crisis?
A. Fresh apples
B. Aged cheese [CORRECT]
C. Steamed broccoli
D. White rice
Correct Answer: B
Rationale: MAOIs (phenelzine, tranylcypromine, isocarboxazid) irreversibly inhibit MAO-A and
MAO-B, preventing the breakdown of tyramine. Tyramine-rich foods (aged cheeses, cured meats,
fermented foods, soy sauce, fava beans, tap beers, red wine) can cause dangerous hypertension
through catecholamine release. Fresh foods (A, C, D) are safe.
Wilkes Note: Remember "AGED" foods = dangerous with MAOIs. The 14-day washout period
applies when switching from MAOIs to SSRIs/SNRIs (5 weeks for fluoxetine due to its long half-life).
Q2: A 68-year-old patient with schizophrenia is started on haloperidol 5mg daily. Within 48 hours,
the patient develops torticollis, oculogyric crisis, and tongue protrusion. Which neurotransmitter
imbalance explains these symptoms?
,A. Excessive dopamine in the nigrostriatal pathway
B. Dopamine blockade in the nigrostriatal pathway [CORRECT]
C. Excessive acetylcholine in the mesolimbic pathway
D. Serotonin excess in the raphe nuclei
Correct Answer: B
Rationale: Acute dystonia (torticollis, oculogyric crisis) results from D2 antagonism in the
nigrostriatal pathway, creating a relative cholinergic excess. First-generation antipsychotics (FGAs)
like haloperidol strongly block D2 receptors here. Treatment involves anticholinergics (benztropine,
diphenhydramine) to restore balance.
Wilkes Note: FGAs = high risk for EPS. Think "D2 blockade = EPS." Nigrostriatal pathway is for
movement; mesolimbic is for psychosis (target), tuberoinfundibular affects prolactin.
Q3: A patient taking fluoxetine (Prozac) 20mg daily for major depressive disorder reports nausea,
anxiety, and insomnia two days after starting therapy. What is the most appropriate response?
A. Discontinue fluoxetine immediately due to allergic reaction
B. Reassure the patient these are common initial side effects that improve in 1-2 weeks
[CORRECT]
C. Add lorazepam for anxiety and switch to bedtime dosing
D. Increase fluoxetine to 40mg to overcome activation symptoms
Correct Answer: B
Rationale: SSRIs commonly cause activation syndrome (anxiety, agitation, insomnia) and GI
symptoms (nausea, diarrhea) initially due to rapid serotonin increase. These typically resolve within
1-2 weeks as the brain adapts. This is not an allergic reaction (A) or serotonin syndrome
(hyperthermia, myoclonus, autonomic instability). Increasing the dose (D) would worsen symptoms.
Wilkes Note: "Start low, go slow" applies to initiation. Activation side effects are temporary, not
treatment failures.
Q4: Which CYP450 enzyme is responsible for metabolizing the majority of psychotropic
medications, including many antipsychotics, benzodiazepines, and antidepressants?
A. CYP1A2
B. CYP2D6
C. CYP3A4 [CORRECT]
D. CYP2E1
Correct Answer: C
Rationale: CYP3A4 metabolizes approximately 50% of all drugs, including quetiapine, aripiprazole,
ziprasidone, alprazolam, midazolam, triazolam, sertraline, and carbamazepine. CYP2D6 (B)
metabolizes risperidone, haloperidol, paroxetine, fluoxetine, atomoxetine, and tamoxifen. CYP1A2
(A) is induced by smoking and metabolizes clozapine and olanzapine.
Wilkes Note: CYP3A4 = "The Big One." Inhibitors: grapefruit juice, ketoconazole. Inducers:
carbamazepine, rifampin, St. John's wort.
,Q5: A patient with bipolar disorder on lithium carbonate develops polyuria, polydipsia, and a fine
tremor. Laboratory studies reveal a serum lithium level of 1.4 mEq/L. What is the most appropriate
intervention?
A. Continue current dose and add valproic acid
B. Decrease lithium dose and monitor renal function [CORRECT]
C. Discontinue lithium permanently and switch to carbamazepine
D. Increase lithium to achieve level of 1.8 mEq/L for better mood stabilization
Correct Answer: B
Rationale: Lithium toxicity begins at >1.5 mEq/L, but symptoms can occur at lower levels if
dehydrated or elderly. Therapeutic range: acute mania 0.8-1.2 mEq/L; maintenance 0.6-0.8 mEq/L.
Polyuria suggests nephrogenic diabetes insipidus (lithium reduces ADH response in collecting
ducts). The dose should be reduced, and renal function (Cr, eGFR) monitored.
Wilkes Note: Lithium levels >1.5 = toxic (coarse tremor, ataxia, confusion). >2.0 = medical
emergency (seizures, coma). Always monitor Cr/eGFR and TSH every 3-6 months.
Q6: Which neurotransmitter is synthesized from tryptophan via 5-HTP, plays a critical role in mood
regulation, and has receptors (5-HT2A) implicated in hallucinations and psychosis?
A. Dopamine
B. Norepinephrine
C. Serotonin [CORRECT]
D. Glutamate
Correct Answer: C
Rationale: Serotonin (5-HT) synthesis: tryptophan → 5-HTP → serotonin → melatonin. 5-HT2A
receptor stimulation causes hallucinations (psychedelics like LSD are 5-HT2A agonists); blockade
by atypical antipsychotics treats psychosis. Serotonin regulates mood, anxiety, sleep, appetite, and
impulse control.
Wilkes Note: "2A = Trippy." 5-HT2A blockade = antipsychotic effect + reduced EPS. 5-HT2C
blockade = appetite increase (mirtazapine, olanzapine).
Q7: A patient with ADHD is prescribed atomoxetine (Strattera). The patient is also on paroxetine
(Paxil) for anxiety. What is the primary concern with this combination?
A. Increased risk of serotonin syndrome
B. Atomoxetine toxicity due to CYP2D6 inhibition [CORRECT]
C. Decreased efficacy of atomoxetine
D. Increased risk of seizures
Correct Answer: B
Rationale: Atomoxetine is metabolized by CYP2D6. Paroxetine is a potent CYP2D6 inhibitor.
Co-administration increases atomoxetine levels 3-4 fold, increasing cardiovascular risks (BP, HR).
This is a pharmacokinetic interaction, not pharmacodynamic (A). Consider CYP2D6 genotype
testing or dose reduction.
, Wilkes Note: Paroxetine and fluoxetine are strong CYP2D6 inhibitors. They inhibit their own
metabolism (non-linear kinetics) and significantly increase levels of CYP2D6 substrates.
Q8: Which brain structure serves as the major relay station for sensory information (except smell)
and connects to the cerebral cortex?
A. Hypothalamus
B. Hippocampus
C. Thalamus [CORRECT]
D. Amygdala
Correct Answer: C
Rationale: The thalamus receives sensory input (visual, auditory, tactile) and relays it to
appropriate cortical areas. It also regulates consciousness, sleep, and alertness. The
hypothalamus (A) regulates autonomic and endocrine functions. Hippocampus (B) is for memory
consolidation. Amygdala (D) processes fear and emotional memories.
Wilkes Note: Thalamus = "Sensory Switchboard." Lesions can cause sensory neglect or thalamic
pain syndrome.
Q9: A patient with epilepsy is started on carbamazepine (Tegretol). After two weeks, the patient
develops confusion, ataxia, and hyponatremia (Na+ 128). What is the mechanism of this adverse
effect?
A. SIADH (Syndrome of Inappropriate Antidiuretic Hormone) [CORRECT]
B. Diabetes insipidus
C. Hyperaldosteronism
D. Acute tubular necrosis
Correct Answer: A
Rationale: Carbamazepine and oxcarbazepine commonly cause SIADH through ADH release or
potentiation, leading to water retention and dilutional hyponatremia. Monitor sodium levels,
especially in elderly. Treat with fluid restriction or discontinuation if severe. This is distinct from
lithium-induced nephrogenic DI (B).
Wilkes Note: "Carba-messy-nerves" = blood dyscrasias, SIADH, autoinduction of metabolism, and
many drug interactions.
Q10: Which receptor antagonism explains the weight gain and metabolic side effects seen with
atypical antipsychotics like olanzapine and clozapine?
A. D2 antagonism
B. 5-HT2A antagonism
C. Histamine H1 antagonism and 5-HT2C antagonism [CORRECT]
D. Alpha-1 antagonism
Correct Answer: C
Rationale: H1 antagonism causes sedation and appetite stimulation. 5-HT2C antagonism disinhibits
appetite regulation (increases food intake). Olanzapine and clozapine have the highest H1 and
