NSG552 / NSG 552 Exam 1: Psychopharmacology –
Wilkes University Actual Exam Complete Questions
& Rationales | Psychiatric Meds | Pass Guaranteed -
A+ Graded
[Neurotransmitters & Receptors in Psychiatry]
Q1: When teaching your PMHNP students about the foundational biochemistry of
psychiatric disorders, you ask them to trace the synthesis pathway of serotonin from its
dietary precursor. Which sequence correctly describes this process?
A. Phenylalanine is converted to tyrosine, which is then hydroxylated to form serotonin
B. Tryptophan is hydroxylated to 5-hydroxytryptophan (5-HTP), which is then
decarboxylated to serotonin
C. Tryptophan is decarboxylated to 5-HTP, which is then hydroxylated to form serotonin
D. Tyrosine is converted to L-DOPA, which is ultimately methylated to form serotonin
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: The best answer is the hydroxylation then decarboxylation of tryptophan, as
this is the exact enzymatic pathway the brain uses to produce serotonin. Remember
that tyrosine is the precursor for catecholamines like dopamine and norepinephrine, not
serotonin.
Q2: A 28-year-old patient with schizophrenia is started on a high-potency
first-generation antipsychotic. A few days later, they present with severe muscle
stiffness, a fever of 104°F, diaphoresis, and confusion. You explain to the students that
this reaction is primarily caused by extreme blockade of which neurotransmitter
pathway?
A. Excessive blockade of mesolimbic dopamine pathways
B. Excessive blockade of nigrostriatal dopamine pathways
C. Sudden surge in serotonin receptor activity in the brainstem
D. Depletion of norepinephrine in the peripheral nervous system
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: What you'd want to do in practice is immediately recognize neuroleptic
malignant syndrome (NMS), which is driven by profound dopamine blockade in the
nigrostriatal pathway, leading to severe rigidity and autonomic instability. While all
,antipsychotics block mesolimbic dopamine to treat psychosis, it's the extreme blockade
in the motor pathways that causes this life-threatening condition.
Q3: You are reviewing the mechanism of action of common anxiolytics with a student.
They ask which neurotransmitter is considered the primary inhibitory neurotransmitter in
the central nervous system, responsible for the majority of the brain's natural calming
effects. What is your response?
A. Glutamate
B. Acetylcholine
C. Gamma-aminobutyric acid (GABA)
D. Histamine
Correct Answer: C [CORRECT]
Correct Answer: C
Rationale: The best answer is GABA, because when this neurotransmitter binds to its
receptor, it allows chloride ions to enter the neuron, hyperpolarizing the cell and making
it much less likely to fire. This aligns with the receptor profile of benzodiazepines, which
work by enhancing GABA's natural inhibitory effect.
Q4: A patient with treatment-resistant depression is being considered for a trial of
ketamine. You explain to the student that unlike traditional antidepressants that focus on
monoamines, ketamine's rapid antidepressant effect is largely believed to be due to its
action on which receptor system?
A. NMDA glutamate receptor antagonism
B. 5-HT1A partial agonism
C. Alpha-2 adrenergic receptor antagonism
D. Nicotinic acetylcholine receptor modulation
Correct Answer: A [CORRECT]
Correct Answer: A
Rationale: The best answer is NMDA receptor antagonism, as ketamine works by
blocking this specific glutamate receptor, which rapidly triggers a cascade of synaptic
plasticity and connections in the brain. Given the side effect profile of traditional
antidepressants taking weeks to work, ketamine's unique mechanism on the glutamate
system provides a fast alternative for severe cases.
Q5: An 82-year-old patient is brought to the clinic by her family due to new-onset
confusion, dry mouth, constipation, and urinary retention. She recently started taking
over-the-counter diphenhydramine for sleep and oxybutynin for overactive bladder.
Which neurotransmitter is most responsible for this clinical presentation?
A. Dopamine
B. Serotonin
C. Acetylcholine
, D. Norepinephrine
Correct Answer: C [CORRECT]
Correct Answer: C
Rationale: What we're really looking at here is a classic anticholinergic toxidrome
caused by combining two highly anticholinergic medications in an older adult. The best
answer is acetylcholine, because blocking this neurotransmitter leads to the predictable
side effects of dry mouth, constipation, urinary retention, and notably, delirium in the
elderly.
Q6: A 45-year-old patient is started on venlafaxine for major depressive disorder. At
their follow-up visit two weeks later, they report feeling jittery and their home blood
pressure logs show an increase from 120/80 to 145/95 mmHg. You explain to the
student that this blood pressure elevation is directly linked to the reuptake inhibition of
which neurotransmitter?
A. Dopamine
B. Norepinephrine
C. Serotonin
D. GABA
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: The best answer is norepinephrine, because venlafaxine is an SNRI that
starts by inhibiting serotonin reuptake at lower doses but begins significantly inhibiting
norepinephrine reuptake at higher doses. This increase in synaptic norepinephrine
stimulates alpha-1 receptors on blood vessels, which is why you see the uptick in blood
pressure.
Q7: You are discussing buspirone with a student who asks why it doesn't cause the
same sedation or dependence as benzodiazepines. You explain that buspirone's
mechanism is entirely different, acting as a partial agonist at which specific receptor?
A. GABA-A receptor
B. 5-HT1A receptor
C. Dopamine D2 receptor
D. NMDA receptor
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: This aligns with the receptor profile of buspirone, which selectively targets
serotonin 5-HT1A autoreceptors and postsynaptic receptors to exert its anxiolytic effect
over time. Because it lacks the direct GABA-A modulation that benzos have, it simply
doesn't produce the rapid sedation or the neurological downregulation that leads to
dependence.
Wilkes University Actual Exam Complete Questions
& Rationales | Psychiatric Meds | Pass Guaranteed -
A+ Graded
[Neurotransmitters & Receptors in Psychiatry]
Q1: When teaching your PMHNP students about the foundational biochemistry of
psychiatric disorders, you ask them to trace the synthesis pathway of serotonin from its
dietary precursor. Which sequence correctly describes this process?
A. Phenylalanine is converted to tyrosine, which is then hydroxylated to form serotonin
B. Tryptophan is hydroxylated to 5-hydroxytryptophan (5-HTP), which is then
decarboxylated to serotonin
C. Tryptophan is decarboxylated to 5-HTP, which is then hydroxylated to form serotonin
D. Tyrosine is converted to L-DOPA, which is ultimately methylated to form serotonin
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: The best answer is the hydroxylation then decarboxylation of tryptophan, as
this is the exact enzymatic pathway the brain uses to produce serotonin. Remember
that tyrosine is the precursor for catecholamines like dopamine and norepinephrine, not
serotonin.
Q2: A 28-year-old patient with schizophrenia is started on a high-potency
first-generation antipsychotic. A few days later, they present with severe muscle
stiffness, a fever of 104°F, diaphoresis, and confusion. You explain to the students that
this reaction is primarily caused by extreme blockade of which neurotransmitter
pathway?
A. Excessive blockade of mesolimbic dopamine pathways
B. Excessive blockade of nigrostriatal dopamine pathways
C. Sudden surge in serotonin receptor activity in the brainstem
D. Depletion of norepinephrine in the peripheral nervous system
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: What you'd want to do in practice is immediately recognize neuroleptic
malignant syndrome (NMS), which is driven by profound dopamine blockade in the
nigrostriatal pathway, leading to severe rigidity and autonomic instability. While all
,antipsychotics block mesolimbic dopamine to treat psychosis, it's the extreme blockade
in the motor pathways that causes this life-threatening condition.
Q3: You are reviewing the mechanism of action of common anxiolytics with a student.
They ask which neurotransmitter is considered the primary inhibitory neurotransmitter in
the central nervous system, responsible for the majority of the brain's natural calming
effects. What is your response?
A. Glutamate
B. Acetylcholine
C. Gamma-aminobutyric acid (GABA)
D. Histamine
Correct Answer: C [CORRECT]
Correct Answer: C
Rationale: The best answer is GABA, because when this neurotransmitter binds to its
receptor, it allows chloride ions to enter the neuron, hyperpolarizing the cell and making
it much less likely to fire. This aligns with the receptor profile of benzodiazepines, which
work by enhancing GABA's natural inhibitory effect.
Q4: A patient with treatment-resistant depression is being considered for a trial of
ketamine. You explain to the student that unlike traditional antidepressants that focus on
monoamines, ketamine's rapid antidepressant effect is largely believed to be due to its
action on which receptor system?
A. NMDA glutamate receptor antagonism
B. 5-HT1A partial agonism
C. Alpha-2 adrenergic receptor antagonism
D. Nicotinic acetylcholine receptor modulation
Correct Answer: A [CORRECT]
Correct Answer: A
Rationale: The best answer is NMDA receptor antagonism, as ketamine works by
blocking this specific glutamate receptor, which rapidly triggers a cascade of synaptic
plasticity and connections in the brain. Given the side effect profile of traditional
antidepressants taking weeks to work, ketamine's unique mechanism on the glutamate
system provides a fast alternative for severe cases.
Q5: An 82-year-old patient is brought to the clinic by her family due to new-onset
confusion, dry mouth, constipation, and urinary retention. She recently started taking
over-the-counter diphenhydramine for sleep and oxybutynin for overactive bladder.
Which neurotransmitter is most responsible for this clinical presentation?
A. Dopamine
B. Serotonin
C. Acetylcholine
, D. Norepinephrine
Correct Answer: C [CORRECT]
Correct Answer: C
Rationale: What we're really looking at here is a classic anticholinergic toxidrome
caused by combining two highly anticholinergic medications in an older adult. The best
answer is acetylcholine, because blocking this neurotransmitter leads to the predictable
side effects of dry mouth, constipation, urinary retention, and notably, delirium in the
elderly.
Q6: A 45-year-old patient is started on venlafaxine for major depressive disorder. At
their follow-up visit two weeks later, they report feeling jittery and their home blood
pressure logs show an increase from 120/80 to 145/95 mmHg. You explain to the
student that this blood pressure elevation is directly linked to the reuptake inhibition of
which neurotransmitter?
A. Dopamine
B. Norepinephrine
C. Serotonin
D. GABA
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: The best answer is norepinephrine, because venlafaxine is an SNRI that
starts by inhibiting serotonin reuptake at lower doses but begins significantly inhibiting
norepinephrine reuptake at higher doses. This increase in synaptic norepinephrine
stimulates alpha-1 receptors on blood vessels, which is why you see the uptick in blood
pressure.
Q7: You are discussing buspirone with a student who asks why it doesn't cause the
same sedation or dependence as benzodiazepines. You explain that buspirone's
mechanism is entirely different, acting as a partial agonist at which specific receptor?
A. GABA-A receptor
B. 5-HT1A receptor
C. Dopamine D2 receptor
D. NMDA receptor
Correct Answer: B [CORRECT]
Correct Answer: B
Rationale: This aligns with the receptor profile of buspirone, which selectively targets
serotonin 5-HT1A autoreceptors and postsynaptic receptors to exert its anxiolytic effect
over time. Because it lacks the direct GABA-A modulation that benzos have, it simply
doesn't produce the rapid sedation or the neurological downregulation that leads to
dependence.
