1|Page
NSG 552 Psychopharmacology Newest Exam
Preparation With Complete Questions And Correct
Answers With Rationales Already Graded A+Brand
New Version!!
Question 1
A 45-year-old male with major depressive disorder has been taking
fluoxetine 40 mg daily for six months. He reports feeling "emotionally
numb" and has lost interest in sexual activity. Which of the following
best describes the mechanism underlying these adverse effects?
A) Antagonism of histamine H1 receptors
B) Inhibition of nitric oxide synthase
C) Activation of 5-HT2C receptors
D) Downregulation of postsynaptic beta-adrenergic receptors
Answer: C
Activation of 5-HT2C receptors by increased serotonin concentrations is
implicated in sexual dysfunction and emotional blunting. SSRIs enhance
serotonergic transmission, and overstimulation of 5-HT2C receptors can
inhibit dopaminergic and noradrenergic pathways in the prefrontal
cortex and mesolimbic system. Histamine antagonism (A) causes
,2|Page
sedation, not sexual dysfunction. Nitric oxide inhibition (B) is not the
primary SSRI mechanism. Beta-adrenergic downregulation (D) is
associated with antidepressant effects, not these adverse effects.
Question 2
A 32-year-old woman with bipolar I disorder is prescribed lamotrigine
for maintenance therapy. Which pharmacokinetic property is most
critical when co-administering this drug with oral contraceptives?
A) Induction of CYP3A4 by lamotrigine
B) Glucuronidation induction by estrogen
C) Protein displacement of lamotrigine
D) Inhibition of P-glycoprotein by progestins
Answer: B
Estrogen-containing oral contraceptives induce the glucuronidation of
lamotrigine, reducing its serum concentration by approximately 50%.
This can lead to loss of efficacy and breakthrough mood episodes.
Lamotrigine does not significantly induce CYP3A4 (A). Protein
displacement (C) is not clinically significant with lamotrigine. P-
glycoprotein inhibition (D) is not the primary interaction mechanism.
Question 3
A patient with generalized anxiety disorder is started on buspirone. The
nurse explains that this drug differs from benzodiazepines in which
fundamental way?
,3|Page
A) It acts as a positive allosteric modulator at the GABA-A receptor
B) It has no affinity for the serotonin transporter
C) It is a partial agonist at 5-HT1A receptors and has no immediate
GABAergic effect
D) It blocks NMDA receptors to produce anxiolysis
Answer: C
Buspirone is a partial agonist at presynaptic and postsynaptic 5-HT1A
receptors, with a delayed onset of action and no direct GABAergic
modulation. Benzodiazepines are positive allosteric modulators of
GABA-A (A). Buspirone does not act on the serotonin transporter (B) as
SSRIs do. NMDA blockade (D) is characteristic of ketamine, not
buspirone.
Question 4
Which of the following best explains why clozapine requires weekly
white blood cell monitoring for the first six months?
A) It causes dose-dependent bone marrow suppression
B) It induces a hypersensitivity reaction leading to agranulocytosis
C) It inhibits the CYP2D6 enzyme, causing toxic metabolites
D) It produces irreversible thrombocytopenia
Answer: B
, 4|Page
Clozapine is associated with a 1-2% risk of agranulocytosis, which is
likely immune-mediated and idiosyncratic rather than dose-dependent.
The monitoring protocol is designed to detect early neutropenia. Dose-
dependent suppression (A) is not accurate. CYP2D6 inhibition (C) is not
the cause of agranulocytosis. Thrombocytopenia (D) is not the primary
hematologic concern.
Question 5
A patient with ADHD is switched from methylphenidate to
atomoxetine. The primary advantage of atomoxetine over
methylphenidate is:
A) Faster onset of therapeutic effect
B) Selective norepinephrine reuptake inhibition with no abuse potential
C) Greater efficacy for inattention compared to hyperactivity
D) Potentiation of dopamine release in the nucleus accumbens
Answer: B
Atomoxetine is a selective norepinephrine reuptake inhibitor that is not
a controlled substance and has no known abuse potential, unlike
methylphenidate, which is a schedule II stimulant. Atomoxetine has a
delayed onset (A). It treats both domains equally (C). It does not
potentiate dopamine release in the accumbens (D), which is a feature of
stimulants.
Question 6
NSG 552 Psychopharmacology Newest Exam
Preparation With Complete Questions And Correct
Answers With Rationales Already Graded A+Brand
New Version!!
Question 1
A 45-year-old male with major depressive disorder has been taking
fluoxetine 40 mg daily for six months. He reports feeling "emotionally
numb" and has lost interest in sexual activity. Which of the following
best describes the mechanism underlying these adverse effects?
A) Antagonism of histamine H1 receptors
B) Inhibition of nitric oxide synthase
C) Activation of 5-HT2C receptors
D) Downregulation of postsynaptic beta-adrenergic receptors
Answer: C
Activation of 5-HT2C receptors by increased serotonin concentrations is
implicated in sexual dysfunction and emotional blunting. SSRIs enhance
serotonergic transmission, and overstimulation of 5-HT2C receptors can
inhibit dopaminergic and noradrenergic pathways in the prefrontal
cortex and mesolimbic system. Histamine antagonism (A) causes
,2|Page
sedation, not sexual dysfunction. Nitric oxide inhibition (B) is not the
primary SSRI mechanism. Beta-adrenergic downregulation (D) is
associated with antidepressant effects, not these adverse effects.
Question 2
A 32-year-old woman with bipolar I disorder is prescribed lamotrigine
for maintenance therapy. Which pharmacokinetic property is most
critical when co-administering this drug with oral contraceptives?
A) Induction of CYP3A4 by lamotrigine
B) Glucuronidation induction by estrogen
C) Protein displacement of lamotrigine
D) Inhibition of P-glycoprotein by progestins
Answer: B
Estrogen-containing oral contraceptives induce the glucuronidation of
lamotrigine, reducing its serum concentration by approximately 50%.
This can lead to loss of efficacy and breakthrough mood episodes.
Lamotrigine does not significantly induce CYP3A4 (A). Protein
displacement (C) is not clinically significant with lamotrigine. P-
glycoprotein inhibition (D) is not the primary interaction mechanism.
Question 3
A patient with generalized anxiety disorder is started on buspirone. The
nurse explains that this drug differs from benzodiazepines in which
fundamental way?
,3|Page
A) It acts as a positive allosteric modulator at the GABA-A receptor
B) It has no affinity for the serotonin transporter
C) It is a partial agonist at 5-HT1A receptors and has no immediate
GABAergic effect
D) It blocks NMDA receptors to produce anxiolysis
Answer: C
Buspirone is a partial agonist at presynaptic and postsynaptic 5-HT1A
receptors, with a delayed onset of action and no direct GABAergic
modulation. Benzodiazepines are positive allosteric modulators of
GABA-A (A). Buspirone does not act on the serotonin transporter (B) as
SSRIs do. NMDA blockade (D) is characteristic of ketamine, not
buspirone.
Question 4
Which of the following best explains why clozapine requires weekly
white blood cell monitoring for the first six months?
A) It causes dose-dependent bone marrow suppression
B) It induces a hypersensitivity reaction leading to agranulocytosis
C) It inhibits the CYP2D6 enzyme, causing toxic metabolites
D) It produces irreversible thrombocytopenia
Answer: B
, 4|Page
Clozapine is associated with a 1-2% risk of agranulocytosis, which is
likely immune-mediated and idiosyncratic rather than dose-dependent.
The monitoring protocol is designed to detect early neutropenia. Dose-
dependent suppression (A) is not accurate. CYP2D6 inhibition (C) is not
the cause of agranulocytosis. Thrombocytopenia (D) is not the primary
hematologic concern.
Question 5
A patient with ADHD is switched from methylphenidate to
atomoxetine. The primary advantage of atomoxetine over
methylphenidate is:
A) Faster onset of therapeutic effect
B) Selective norepinephrine reuptake inhibition with no abuse potential
C) Greater efficacy for inattention compared to hyperactivity
D) Potentiation of dopamine release in the nucleus accumbens
Answer: B
Atomoxetine is a selective norepinephrine reuptake inhibitor that is not
a controlled substance and has no known abuse potential, unlike
methylphenidate, which is a schedule II stimulant. Atomoxetine has a
delayed onset (A). It treats both domains equally (C). It does not
potentiate dopamine release in the accumbens (D), which is a feature of
stimulants.
Question 6
