,NSG 552 Psychopharmacology Exam 2 Study
Guide Wilkes University Medication Classes +
150 Clinical Q&A | 2026/2027
1. A 32-year-old patient with schizophrenia has been taking a dopamine D2 receptor antagonist
for 6 weeks. The nurse practitioner notes the patient exhibits bradykinesia, a shuffling gait, and
a mask-like facial expression. Which mechanism best explains these findings?
A. Blockade of dopamine receptors in the nigrostriatal pathway produces extrapyramidal motor
symptoms
B. Excessive dopamine stimulation of the mesolimbic pathway leads to positive symptom
worsening
C. Reduced serotonin activity at 5-HT2A receptors causes impaired mood regulation
D. Increased acetylcholine release in the basal ganglia results in cognitive blunting
Correct Answer: A. Blockade of dopamine receptors in the nigrostriatal pathway produces
extrapyramidal motor symptoms
Rationale: Dopamine antagonists block D2 receptors not only in the mesolimbic pathway (target
for antipsychotic effect) but also in the nigrostriatal pathway, where dopamine is essential for
motor control. This off-target blockade produces extrapyramidal symptoms such as
parkinsonism.
2. A 45-year-old patient with major depressive disorder is prescribed an SSRI. The nurse
educator explains that the full therapeutic effect may take 2 to 4 weeks to become evident.
Which mechanism explains this delayed onset?
,A. Serotonin receptor downregulation occurs within 24 hours of initiating treatment
B. Neuroadaptive changes including postsynaptic receptor desensitization require prolonged
exposure
C. Norepinephrine reuptake inhibition is the primary mechanism driving delayed onset
D. GABA receptor modulation takes several weeks to reach therapeutic levels in the synapse
Correct Answer: B. Neuroadaptive changes including postsynaptic receptor desensitization
require prolonged exposure
Rationale: SSRIs immediately block serotonin reuptake, but the therapeutic antidepressant
effect requires neuroadaptive changes over weeks, including desensitization of presynaptic
autoreceptors and downstream signaling adaptations. This delay explains why patients do not
experience immediate relief despite the rapid pharmacological action at the synapse.
3. A psychiatric nurse practitioner is teaching a graduate student about the blood-brain barrier
and its impact on psychotropic drug delivery. The student asks why some medications require
higher doses to achieve central nervous system effects. Which statement is most accurate?
A. Lipid-soluble molecules are actively pumped out of the central nervous system by P-
glycoprotein
B. Highly protein-bound drugs cross more easily due to albumin receptor-mediated transport
C. The blood-brain barrier limits passage of large, ionized, and water-soluble molecules into the
brain
D. Drugs with high molecular weight readily diffuse across endothelial cell tight junctions
Correct Answer: C. The blood-brain barrier limits passage of large, ionized, and water-soluble
molecules into the brain
, Rationale: The blood-brain barrier consists of tight endothelial junctions that restrict passage to
small, lipid-soluble, non-ionized molecules. Highly ionized, water-soluble, or large-molecule
drugs have limited CNS penetration, often requiring higher systemic doses.
4. A patient with generalized anxiety disorder is started on buspirone. The nurse practitioner
explains that this medication has a delayed onset of action. Which mechanism accounts for this
delay?
A. Buspirone requires hepatic conversion to an active metabolite
B. Buspirone acts as a 5-HT1A partial agonist requiring neuroadaptive changes over 2–4 weeks
C. Buspirone inhibits serotonin reuptake, which requires steady-state concentrations
D. Buspirone enhances GABA-A receptor activity only after chronic administration
Correct Answer: B. Buspirone acts as a 5-HT1A partial agonist requiring neuroadaptive changes
over 2–4 weeks
Rationale: Buspirone is a 5-HT1A receptor partial agonist used for generalized anxiety disorder.
It has a delayed onset of 2–4 weeks and does not cause dependence or withdrawal. It is not
effective for acute anxiety.
5. Which of the following neurotransmitters is the primary inhibitory neurotransmitter in the
central nervous system?
A. Glutamate
Guide Wilkes University Medication Classes +
150 Clinical Q&A | 2026/2027
1. A 32-year-old patient with schizophrenia has been taking a dopamine D2 receptor antagonist
for 6 weeks. The nurse practitioner notes the patient exhibits bradykinesia, a shuffling gait, and
a mask-like facial expression. Which mechanism best explains these findings?
A. Blockade of dopamine receptors in the nigrostriatal pathway produces extrapyramidal motor
symptoms
B. Excessive dopamine stimulation of the mesolimbic pathway leads to positive symptom
worsening
C. Reduced serotonin activity at 5-HT2A receptors causes impaired mood regulation
D. Increased acetylcholine release in the basal ganglia results in cognitive blunting
Correct Answer: A. Blockade of dopamine receptors in the nigrostriatal pathway produces
extrapyramidal motor symptoms
Rationale: Dopamine antagonists block D2 receptors not only in the mesolimbic pathway (target
for antipsychotic effect) but also in the nigrostriatal pathway, where dopamine is essential for
motor control. This off-target blockade produces extrapyramidal symptoms such as
parkinsonism.
2. A 45-year-old patient with major depressive disorder is prescribed an SSRI. The nurse
educator explains that the full therapeutic effect may take 2 to 4 weeks to become evident.
Which mechanism explains this delayed onset?
,A. Serotonin receptor downregulation occurs within 24 hours of initiating treatment
B. Neuroadaptive changes including postsynaptic receptor desensitization require prolonged
exposure
C. Norepinephrine reuptake inhibition is the primary mechanism driving delayed onset
D. GABA receptor modulation takes several weeks to reach therapeutic levels in the synapse
Correct Answer: B. Neuroadaptive changes including postsynaptic receptor desensitization
require prolonged exposure
Rationale: SSRIs immediately block serotonin reuptake, but the therapeutic antidepressant
effect requires neuroadaptive changes over weeks, including desensitization of presynaptic
autoreceptors and downstream signaling adaptations. This delay explains why patients do not
experience immediate relief despite the rapid pharmacological action at the synapse.
3. A psychiatric nurse practitioner is teaching a graduate student about the blood-brain barrier
and its impact on psychotropic drug delivery. The student asks why some medications require
higher doses to achieve central nervous system effects. Which statement is most accurate?
A. Lipid-soluble molecules are actively pumped out of the central nervous system by P-
glycoprotein
B. Highly protein-bound drugs cross more easily due to albumin receptor-mediated transport
C. The blood-brain barrier limits passage of large, ionized, and water-soluble molecules into the
brain
D. Drugs with high molecular weight readily diffuse across endothelial cell tight junctions
Correct Answer: C. The blood-brain barrier limits passage of large, ionized, and water-soluble
molecules into the brain
, Rationale: The blood-brain barrier consists of tight endothelial junctions that restrict passage to
small, lipid-soluble, non-ionized molecules. Highly ionized, water-soluble, or large-molecule
drugs have limited CNS penetration, often requiring higher systemic doses.
4. A patient with generalized anxiety disorder is started on buspirone. The nurse practitioner
explains that this medication has a delayed onset of action. Which mechanism accounts for this
delay?
A. Buspirone requires hepatic conversion to an active metabolite
B. Buspirone acts as a 5-HT1A partial agonist requiring neuroadaptive changes over 2–4 weeks
C. Buspirone inhibits serotonin reuptake, which requires steady-state concentrations
D. Buspirone enhances GABA-A receptor activity only after chronic administration
Correct Answer: B. Buspirone acts as a 5-HT1A partial agonist requiring neuroadaptive changes
over 2–4 weeks
Rationale: Buspirone is a 5-HT1A receptor partial agonist used for generalized anxiety disorder.
It has a delayed onset of 2–4 weeks and does not cause dependence or withdrawal. It is not
effective for acute anxiety.
5. Which of the following neurotransmitters is the primary inhibitory neurotransmitter in the
central nervous system?
A. Glutamate
