WILK E S U NIVE RS ITY
PA SSA N SC HOOL OF NURSING
NSG 552 Exam 1:
Psychopharmacology
Course: NSG 552 - Advanced
Psychopharmacology
Exam: Examination 1
Questions: 75 Multiple Choice
Academic Year: 2026 - 2027
Lat est 2 02 6/2 02 7 Up d at e | Quest ions and Ver ified Answer s
, B. Mesolimbic pathway [CORRECT]
C. Mesocortical pathway
D. Tuberoinfundibular pathway
Correct Answer: B
Rationale: The mesolimbic dopamine pathway, which projects from the ventral tegmental area (VTA) to the nucleus accumbens and
other limbic structures, is the pathway most strongly associated with the positive symptoms of schizophrenia, including hallucinations,
delusions, and thought disorganization. Hyperactivity of dopamine transmission in this pathway is the basis of the dopamine
hypothesis of schizophrenia and is the primary target of antipsychotic medications, which function as D2 receptor antagonists. The
nigrostriatal pathway is involved in movement, the mesocortical pathway in cognition, and the tuberoinfundibular pathway in
prolactin regulation.
Q5: Norepinephrine is synthesized from dopamine through the action of which enzyme?
A. Tryptophan hydroxylase
B. Tyrosine hydroxylase
C. Dopamine beta-hydroxylase [CORRECT]
D. Monoamine oxidase (MAO)
Correct Answer: C
Rationale: Dopamine beta-hydroxylase (DBH) is the enzyme responsible for converting dopamine to norepinephrine within the
synaptic vesicles of noradrenergic neurons. This enzymatic conversion occurs in the presence of ascorbate (vitamin C) and copper as
cofactors. Tryptophan hydroxylase is the rate-limiting enzyme in serotonin synthesis, tyrosine hydroxylase is the rate-limiting enzyme
in dopamine synthesis (the first step from tyrosine to L-DOPA), and monoamine oxidase (MAO) is a catabolic enzyme that degrades
monoamine neurotransmitters rather than synthesizing them. Understanding DBH is important because genetic variations in this
enzyme can affect norepinephrine levels and influence psychiatric conditions and medication response.
Q6: A nurse practitioner is teaching a patient about their new medication that targets GABA-A receptors. The
patient asks how the medication works. Which response by the nurse practitioner is most accurate?
A. It blocks sodium channels to reduce neuronal excitability
B. It enhances chloride ion influx through a ligand-gated ion channel, producing inhibitory effects [CORRECT]
C. It activates G-protein coupled receptors to increase cAMP production
D. It inhibits glutamate release from presynaptic terminals
Correct Answer: B
Rationale: GABA-A receptors are ionotropic receptors, meaning they function as ligand-gated ion channels. When GABA (or a
GABA agonist such as a benzodiazepine) binds to the GABA-A receptor, it increases the frequency of chloride channel opening,
allowing chloride ions to flow into the neuron. This hyperpolarizes the neuronal membrane, making it less likely to fire an action
potential, thereby producing an inhibitory effect on CNS activity. This is the primary mechanism of action of benzodiazepines,
barbiturates, and alcohol. GABA-B receptors, by contrast, are metabotropic (G-protein coupled) and work through second messenger
systems. Sodium channel blockade describes the mechanism of anticonvulsants like phenytoin, not GABAergic drugs.
Q7: Glutamate is the primary excitatory neurotransmitter in the central nervous system. Which receptor type is
specifically targeted by memantine, an NMDA receptor antagonist used in Alzheimer disease?
A. AMPA receptor
B. Kainate receptor
C. NMDA receptor [CORRECT]
D. Metabotropic glutamate receptor (mGluR)
Correct Answer: C
Rationale: Memantine is a noncompetitive NMDA (N-methyl-D-aspartate) receptor antagonist approved for the treatment of
moderate to severe Alzheimer disease. The NMDA receptor is a ligand-gated ion channel (ionotropic) that, when activated by
glutamate and glycine, allows calcium influx into the postsynaptic neuron. Excessive glutamatergic stimulation of NMDA receptors
leads to excitotoxicity and neuronal damage, which is implicated in the pathophysiology of Alzheimer disease. Memantine blocks the
NMDA receptor channel, reducing excitotoxic calcium influx while preserving normal physiological glutamatergic neurotransmission.
AMPA and kainate receptors are other ionotropic glutamate receptors, and mGluRs are metabotropic glutamate receptors, none of
which are the primary targets of memantine.
, Q8: A patient prescribed an anticholinergic medication reports dry mouth, blurred vision, and constipation.
These effects are primarily due to blockade of which type of acetylcholine receptor?
A. Nicotinic receptors at the neuromuscular junction
B. Muscarinic receptors in parasympathetic target organs [CORRECT]
C. Nicotinic receptors in the central nervous system
D. Muscarinic receptors in the sympathetic ganglia
Correct Answer: B
Rationale: Muscarinic acetylcholine receptors are metabotropic (G-protein coupled) receptors found primarily in parasympathetic
target organs including the salivary glands, smooth muscle of the GI tract, and the ciliary muscle of the eye. Blockade of these
muscarinic receptors by anticholinergic medications (such as TCAs, antipsychotics, and benztropine) produces the classic
anticholinergic side effects of dry mouth (xerostomia), blurred vision (cycloplegia), constipation (decreased GI motility), urinary
retention, and tachycardia. Nicotinic receptors are ionotropic ligand-gated ion channels found at the neuromuscular junction and in
autonomic ganglia; their blockade produces neuromuscular weakness and ganglionic blockade, not the parasympathetic effects
described.
Q9: The psychiatric nurse practitioner is reviewing receptor types with students. Which of the following is an
example of a metabotropic (G-protein coupled) receptor?
A. GABA-A receptor
B. NMDA receptor
C. 5-HT2A receptor [CORRECT]
D. Nicotinic acetylcholine receptor
Correct Answer: C
Rationale: The 5-HT2A serotonin receptor is a metabotropic receptor, meaning it is a G-protein coupled receptor (GPCR) that signals
through second messenger systems rather than functioning as a direct ion channel. When serotonin binds to the 5-HT2A receptor, it
activates Gq proteins, which stimulate phospholipase C (PLC) to produce inositol triphosphate (IP3) and diacylglycerol (DAG),
leading to intracellular calcium release and protein kinase C activation. This is the receptor through which many atypical
antipsychotics exert part of their therapeutic effect. GABA-A, NMDA, and nicotinic acetylcholine receptors are all ionotropic
(ligand-gated ion channels), not metabotropic receptors.
Q10: Reuptake transporters are critical for terminating neurotransmitter signaling in the synaptic cleft. Which
reuptake transporter is responsible for removing serotonin from the synaptic cleft?
A. Dopamine transporter (DAT)
B. Norepinephrine transporter (NET)
C. Serotonin transporter (SERT) [CORRECT]
D. Vesicular monoamine transporter (VMAT)
Correct Answer: C
Rationale: The serotonin transporter (SERT) is a presynaptic membrane protein responsible for the active reuptake of serotonin from
the synaptic cleft back into the presynaptic neuron, thereby terminating serotonergic signaling. SERT is the primary pharmacologic
target of selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, sertraline, paroxetine, citalopram, and escitalopram, which
block this transporter and increase synaptic serotonin concentrations. DAT is responsible for dopamine reuptake, NET for
norepinephrine reuptake, and VMAT transports monoamines into synaptic vesicles for storage (not synaptic clearance), making SERT
the only correct answer for serotonin reuptake.
Q11: A second messenger system involving Gs proteins increases the production of cyclic adenosine
monophosphate (cAMP). Which of the following receptor activations would lead to increased cAMP levels?
A. Alpha-2 adrenergic receptor activation
B. Beta-1 adrenergic receptor activation [CORRECT]
C. 5-HT2A receptor activation
D. GABA-B receptor activation
Correct Answer: B
PA SSA N SC HOOL OF NURSING
NSG 552 Exam 1:
Psychopharmacology
Course: NSG 552 - Advanced
Psychopharmacology
Exam: Examination 1
Questions: 75 Multiple Choice
Academic Year: 2026 - 2027
Lat est 2 02 6/2 02 7 Up d at e | Quest ions and Ver ified Answer s
, B. Mesolimbic pathway [CORRECT]
C. Mesocortical pathway
D. Tuberoinfundibular pathway
Correct Answer: B
Rationale: The mesolimbic dopamine pathway, which projects from the ventral tegmental area (VTA) to the nucleus accumbens and
other limbic structures, is the pathway most strongly associated with the positive symptoms of schizophrenia, including hallucinations,
delusions, and thought disorganization. Hyperactivity of dopamine transmission in this pathway is the basis of the dopamine
hypothesis of schizophrenia and is the primary target of antipsychotic medications, which function as D2 receptor antagonists. The
nigrostriatal pathway is involved in movement, the mesocortical pathway in cognition, and the tuberoinfundibular pathway in
prolactin regulation.
Q5: Norepinephrine is synthesized from dopamine through the action of which enzyme?
A. Tryptophan hydroxylase
B. Tyrosine hydroxylase
C. Dopamine beta-hydroxylase [CORRECT]
D. Monoamine oxidase (MAO)
Correct Answer: C
Rationale: Dopamine beta-hydroxylase (DBH) is the enzyme responsible for converting dopamine to norepinephrine within the
synaptic vesicles of noradrenergic neurons. This enzymatic conversion occurs in the presence of ascorbate (vitamin C) and copper as
cofactors. Tryptophan hydroxylase is the rate-limiting enzyme in serotonin synthesis, tyrosine hydroxylase is the rate-limiting enzyme
in dopamine synthesis (the first step from tyrosine to L-DOPA), and monoamine oxidase (MAO) is a catabolic enzyme that degrades
monoamine neurotransmitters rather than synthesizing them. Understanding DBH is important because genetic variations in this
enzyme can affect norepinephrine levels and influence psychiatric conditions and medication response.
Q6: A nurse practitioner is teaching a patient about their new medication that targets GABA-A receptors. The
patient asks how the medication works. Which response by the nurse practitioner is most accurate?
A. It blocks sodium channels to reduce neuronal excitability
B. It enhances chloride ion influx through a ligand-gated ion channel, producing inhibitory effects [CORRECT]
C. It activates G-protein coupled receptors to increase cAMP production
D. It inhibits glutamate release from presynaptic terminals
Correct Answer: B
Rationale: GABA-A receptors are ionotropic receptors, meaning they function as ligand-gated ion channels. When GABA (or a
GABA agonist such as a benzodiazepine) binds to the GABA-A receptor, it increases the frequency of chloride channel opening,
allowing chloride ions to flow into the neuron. This hyperpolarizes the neuronal membrane, making it less likely to fire an action
potential, thereby producing an inhibitory effect on CNS activity. This is the primary mechanism of action of benzodiazepines,
barbiturates, and alcohol. GABA-B receptors, by contrast, are metabotropic (G-protein coupled) and work through second messenger
systems. Sodium channel blockade describes the mechanism of anticonvulsants like phenytoin, not GABAergic drugs.
Q7: Glutamate is the primary excitatory neurotransmitter in the central nervous system. Which receptor type is
specifically targeted by memantine, an NMDA receptor antagonist used in Alzheimer disease?
A. AMPA receptor
B. Kainate receptor
C. NMDA receptor [CORRECT]
D. Metabotropic glutamate receptor (mGluR)
Correct Answer: C
Rationale: Memantine is a noncompetitive NMDA (N-methyl-D-aspartate) receptor antagonist approved for the treatment of
moderate to severe Alzheimer disease. The NMDA receptor is a ligand-gated ion channel (ionotropic) that, when activated by
glutamate and glycine, allows calcium influx into the postsynaptic neuron. Excessive glutamatergic stimulation of NMDA receptors
leads to excitotoxicity and neuronal damage, which is implicated in the pathophysiology of Alzheimer disease. Memantine blocks the
NMDA receptor channel, reducing excitotoxic calcium influx while preserving normal physiological glutamatergic neurotransmission.
AMPA and kainate receptors are other ionotropic glutamate receptors, and mGluRs are metabotropic glutamate receptors, none of
which are the primary targets of memantine.
, Q8: A patient prescribed an anticholinergic medication reports dry mouth, blurred vision, and constipation.
These effects are primarily due to blockade of which type of acetylcholine receptor?
A. Nicotinic receptors at the neuromuscular junction
B. Muscarinic receptors in parasympathetic target organs [CORRECT]
C. Nicotinic receptors in the central nervous system
D. Muscarinic receptors in the sympathetic ganglia
Correct Answer: B
Rationale: Muscarinic acetylcholine receptors are metabotropic (G-protein coupled) receptors found primarily in parasympathetic
target organs including the salivary glands, smooth muscle of the GI tract, and the ciliary muscle of the eye. Blockade of these
muscarinic receptors by anticholinergic medications (such as TCAs, antipsychotics, and benztropine) produces the classic
anticholinergic side effects of dry mouth (xerostomia), blurred vision (cycloplegia), constipation (decreased GI motility), urinary
retention, and tachycardia. Nicotinic receptors are ionotropic ligand-gated ion channels found at the neuromuscular junction and in
autonomic ganglia; their blockade produces neuromuscular weakness and ganglionic blockade, not the parasympathetic effects
described.
Q9: The psychiatric nurse practitioner is reviewing receptor types with students. Which of the following is an
example of a metabotropic (G-protein coupled) receptor?
A. GABA-A receptor
B. NMDA receptor
C. 5-HT2A receptor [CORRECT]
D. Nicotinic acetylcholine receptor
Correct Answer: C
Rationale: The 5-HT2A serotonin receptor is a metabotropic receptor, meaning it is a G-protein coupled receptor (GPCR) that signals
through second messenger systems rather than functioning as a direct ion channel. When serotonin binds to the 5-HT2A receptor, it
activates Gq proteins, which stimulate phospholipase C (PLC) to produce inositol triphosphate (IP3) and diacylglycerol (DAG),
leading to intracellular calcium release and protein kinase C activation. This is the receptor through which many atypical
antipsychotics exert part of their therapeutic effect. GABA-A, NMDA, and nicotinic acetylcholine receptors are all ionotropic
(ligand-gated ion channels), not metabotropic receptors.
Q10: Reuptake transporters are critical for terminating neurotransmitter signaling in the synaptic cleft. Which
reuptake transporter is responsible for removing serotonin from the synaptic cleft?
A. Dopamine transporter (DAT)
B. Norepinephrine transporter (NET)
C. Serotonin transporter (SERT) [CORRECT]
D. Vesicular monoamine transporter (VMAT)
Correct Answer: C
Rationale: The serotonin transporter (SERT) is a presynaptic membrane protein responsible for the active reuptake of serotonin from
the synaptic cleft back into the presynaptic neuron, thereby terminating serotonergic signaling. SERT is the primary pharmacologic
target of selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, sertraline, paroxetine, citalopram, and escitalopram, which
block this transporter and increase synaptic serotonin concentrations. DAT is responsible for dopamine reuptake, NET for
norepinephrine reuptake, and VMAT transports monoamines into synaptic vesicles for storage (not synaptic clearance), making SERT
the only correct answer for serotonin reuptake.
Q11: A second messenger system involving Gs proteins increases the production of cyclic adenosine
monophosphate (cAMP). Which of the following receptor activations would lead to increased cAMP levels?
A. Alpha-2 adrenergic receptor activation
B. Beta-1 adrenergic receptor activation [CORRECT]
C. 5-HT2A receptor activation
D. GABA-B receptor activation
Correct Answer: B
