NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
NSG 552 Exam 1 Study Guide + Review
Psychopharmacology
Wilkes University | 2026/2027 Academic Year
Graduate PMHNP Program | 150 Comprehensive Questions with Rationales
This study guide and review examination contains 150 multiple-choice questions organized
into nine content sections aligned with the NSG 552 Exam 1 blueprint. Each question is
followed by four options (A-D), the correct answer, and a detailed psychopharmacology
rationale incorporating receptor pharmacology, pharmacokinetic principles, and clinical
reasoning. The rationales are designed to reinforce study-guide concepts for Exam 1
preparation. Cognitive levels: ~30% recall, ~50% application, ~20% analysis.
Approximately 70% of items are scenario-based, 30% are direct recall of pharmacological
principles.
Section 1: Neuroanatomy and Neurotransmission (Q1-Q18)
Q1: A PMHNP student is explaining neuronal structure to a peer. Which neuronal
component receives excitatory input from other neurons and conducts it toward the
cell body?
A. Axon hillock
B. Myelin sheath
C. Dendrites [CORRECT]
D. Terminal bouton
Correct Answer: C
Rationale: Dendrites are tree-like extensions from the neuron cell body that receive synaptic input
from upstream neurons via neurotransmitter binding to receptors on their spines. The axon hillock
integrates these signals and initiates action potentials, while myelin insulates the axon for saltatory
conduction. Terminal boutons (presynaptic endings) release neurotransmitter, not receive it. Study
guide note: knowing signal flow (dendrite -> soma -> axon hillock -> axon -> terminal) is
foundational for Exam 1.
Q2: A patient with multiple sclerosis exhibits slowed nerve conduction due to
demyelination. Myelin in the central nervous system is produced by which cell
type?
A. Schwann cells
B. Oligodendrocytes [CORRECT]
C. Astrocytes
D. Microglia
Correct Answer: B
Rationale: Oligodendrocytes produce myelin in the CNS, with each cell myelinating multiple axon
segments. Schwann cells myelinate axons in the PNS, with one Schwann cell per internode.
Astrocytes maintain blood-brain barrier and synaptic support, while microglia are CNS immune cells.
This distinction matters pharmacologically because MS demyelination disrupts saltatory conduction
at Nodes of Ranvier, slowing signal transmission and producing the characteristic motor and sensory
deficits.
Page 1
,NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
Q3: During an action potential, depolarization occurs when voltage-gated sodium
channels open. What is the approximate threshold potential at which these
channels typically open?
A. -90 mV
B. -70 mV
C. -55 mV [CORRECT]
D. +30 mV
Correct Answer: C
Rationale: The threshold potential of approximately -55 mV is the critical depolarization point at
which voltage-gated Na+ channels rapidly open, initiating the rising phase of the action potential.
Resting membrane potential is approximately -70 mV, and -90 mV is below resting (hyperpolarized).
+30 mV is the peak of the action potential, not the threshold. Once threshold is reached, the action
potential is "all or nothing" - a key concept for understanding neuronal signaling and drug effects on
excitability.
Q4: A patient is prescribed lithium, which has a narrow therapeutic index. The
sodium-potassium pump (Na+/K+-ATPase) is essential for restoring which ion
gradient after action potential firing?
A. Na+ in / K+ out
B. Na+ out / K+ in [CORRECT]
C. Ca2+ in / Na+ out
D. Cl- in / K+ out
Correct Answer: B
Rationale: The Na+/K+-ATPase pumps 3 Na+ out of the cell and 2 K+ into the cell against their
concentration gradients, using ATP. This maintains the resting membrane potential and restores
gradients after repeated action potentials. The pump is electrogenic (net positive charge out),
contributing directly to resting potential. Lithium can substitute for Na+ in some transport
processes, which is relevant to its pharmacology, toxicity, and interaction with sodium-wasting
conditions such as dehydration or thiazide diuretic use.
Q5: The absolute refractory period prevents backward propagation of action
potentials. Which mechanism is primarily responsible?
A. Voltage-gated K+ channels remain closed
B. Voltage-gated Na+ channels are inactivated [CORRECT]
C. Cl- channels remain open
D. Ca2+ channels are blocked
Correct Answer: B
Rationale: During the absolute refractory period, voltage-gated Na+ channels are in the inactivated
state and cannot reopen until the membrane repolarizes and channels reset to the closed state. This
prevents generation of a second action potential regardless of stimulus strength and ensures
unidirectional propagation. The relative refractory period follows, during which stronger-than-normal
stimuli can trigger impulses as K+ channels remain open, causing hyperpolarization. Local
anesthetics exploit Na+ channel inactivation to block conduction.
Page 2
,NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
Q6: Saltatory conduction increases conduction velocity in myelinated axons. Where
does depolarization actually occur during this process?
A. Along the entire axon membrane
B. Only at the axon hillock
C. Only at the Nodes of Ranvier [CORRECT]
D. Only at the terminal boutons
Correct Answer: C
Rationale: In saltatory conduction, the action potential "jumps" between Nodes of Ranvier, where
voltage-gated Na+ channels are concentrated. Myelin acts as an insulator, increasing membrane
resistance and allowing passive current spread to the next node. This dramatically increases
conduction velocity (up to 120 m/s) compared to unmyelinated fibers (~1 m/s). Demyelinating
diseases such as multiple sclerosis disrupt this process, producing slowed or blocked conduction and
clinical deficits.
Q7: A PMHNP is teaching about synaptic transmission. Calcium influx into the
presynaptic terminal triggers which event?
A. Reuptake of neurotransmitter
B. Enzymatic degradation of neurotransmitter
C. Synaptic vesicle fusion and exocytosis [CORRECT]
D. Opening of postsynaptic chloride channels
Correct Answer: C
Rationale: When an action potential reaches the presynaptic terminal, voltage-gated Ca2+
channels open, allowing Ca2+ influx. Calcium binds to synaptotagmin, triggering vesicle fusion with
the presynaptic membrane via the SNARE complex, releasing neurotransmitter into the synaptic
cleft. Reuptake and enzymatic degradation are mechanisms of neurotransmitter termination, not
release. Postsynaptic channels open in response to neurotransmitter binding, not calcium. Botulinum
toxin blocks this process by cleaving SNARE proteins.
Q8: Selective serotonin reuptake inhibitors (SSRIs) exert therapeutic effect by
blocking which protein?
A. Monoamine oxidase (MAO)
B. Serotonin transporter (SERT) [CORRECT]
C. 5-HT2A receptor
D. Tryptophan hydroxylase
Correct Answer: B
Rationale: SSRIs block the serotonin transporter (SERT), the presynaptic protein responsible for
reuptake of serotonin from the synaptic cleft back into the presynaptic neuron. This blockade
increases synaptic serotonin concentration, enhancing postsynaptic receptor activation. MAO
degrades serotonin intracellularly (target of MAOIs). 5-HT2A is a postsynaptic receptor. Tryptophan
hydroxylase is the rate-limiting enzyme in serotonin synthesis, not a reuptake target. Note:
therapeutic effect is delayed 2-6 weeks due to autoreceptor desensitization.
Page 3
, NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
Q9: Acetylcholinesterase inhibitors (e.g., donepezil) work by which mechanism?
A. Blocking muscarinic receptors
B. Inhibiting enzymatic degradation of acetylcholine [CORRECT]
C. Blocking acetylcholine release
D. Enhancing acetylcholine reuptake
Correct Answer: B
Rationale: Acetylcholinesterase inhibitors block the enzyme acetylcholinesterase, which normally
degrades acetylcholine in the synaptic cleft into choline and acetate. By inhibiting this enzyme, ACh
remains in the synapse longer, enhancing cholinergic transmission - useful in Alzheimer disease.
Note: there is no specific ACh reuptake transporter; termination is primarily via enzymatic
degradation. This contrasts with monoamines, which are terminated primarily by reuptake via
transporters such as SERT, NET, and DAT.
Q10: A neuron receives simultaneous excitatory (EPSP) and inhibitory (IPSP) inputs.
Where does spatial summation primarily occur?
A. Dendritic spines
B. Axon hillock [CORRECT]
C. Synaptic cleft
D. Terminal bouton
Correct Answer: B
Rationale: The axon hillock has the highest density of voltage-gated Na+ channels and the lowest
threshold, making it the site where EPSPs and IPSPs from various dendritic locations are spatially
and temporally summed. If the summated potential reaches threshold (~-55 mV), an action
potential is initiated. Dendritic spines receive input but do not initiate action potentials. This
integrative function is critical for understanding drug effects on neuronal firing patterns and
excitability.
Q11: GABA binding to GABA-A receptors opens chloride channels, causing which
effect on the postsynaptic neuron?
A. Depolarization
B. Hyperpolarization [CORRECT]
C. No change in membrane potential
D. Action potential firing
Correct Answer: B
Rationale: GABA-A receptor activation opens chloride channels, allowing Cl- influx, which
hyperpolarizes the postsynaptic membrane (brings it closer to ECl at approximately -65 to -70 mV),
making the neuron less excitable. This is the primary mechanism of fast inhibitory transmission in
the CNS and the target of benzodiazepines, which potentiate GABA-A function. Hyperpolarization
moves membrane potential away from action potential threshold. Barbiturates and alcohol also act
at GABA-A but at different sites.
Page 4
NSG 552 Exam 1 Study Guide + Review
Psychopharmacology
Wilkes University | 2026/2027 Academic Year
Graduate PMHNP Program | 150 Comprehensive Questions with Rationales
This study guide and review examination contains 150 multiple-choice questions organized
into nine content sections aligned with the NSG 552 Exam 1 blueprint. Each question is
followed by four options (A-D), the correct answer, and a detailed psychopharmacology
rationale incorporating receptor pharmacology, pharmacokinetic principles, and clinical
reasoning. The rationales are designed to reinforce study-guide concepts for Exam 1
preparation. Cognitive levels: ~30% recall, ~50% application, ~20% analysis.
Approximately 70% of items are scenario-based, 30% are direct recall of pharmacological
principles.
Section 1: Neuroanatomy and Neurotransmission (Q1-Q18)
Q1: A PMHNP student is explaining neuronal structure to a peer. Which neuronal
component receives excitatory input from other neurons and conducts it toward the
cell body?
A. Axon hillock
B. Myelin sheath
C. Dendrites [CORRECT]
D. Terminal bouton
Correct Answer: C
Rationale: Dendrites are tree-like extensions from the neuron cell body that receive synaptic input
from upstream neurons via neurotransmitter binding to receptors on their spines. The axon hillock
integrates these signals and initiates action potentials, while myelin insulates the axon for saltatory
conduction. Terminal boutons (presynaptic endings) release neurotransmitter, not receive it. Study
guide note: knowing signal flow (dendrite -> soma -> axon hillock -> axon -> terminal) is
foundational for Exam 1.
Q2: A patient with multiple sclerosis exhibits slowed nerve conduction due to
demyelination. Myelin in the central nervous system is produced by which cell
type?
A. Schwann cells
B. Oligodendrocytes [CORRECT]
C. Astrocytes
D. Microglia
Correct Answer: B
Rationale: Oligodendrocytes produce myelin in the CNS, with each cell myelinating multiple axon
segments. Schwann cells myelinate axons in the PNS, with one Schwann cell per internode.
Astrocytes maintain blood-brain barrier and synaptic support, while microglia are CNS immune cells.
This distinction matters pharmacologically because MS demyelination disrupts saltatory conduction
at Nodes of Ranvier, slowing signal transmission and producing the characteristic motor and sensory
deficits.
Page 1
,NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
Q3: During an action potential, depolarization occurs when voltage-gated sodium
channels open. What is the approximate threshold potential at which these
channels typically open?
A. -90 mV
B. -70 mV
C. -55 mV [CORRECT]
D. +30 mV
Correct Answer: C
Rationale: The threshold potential of approximately -55 mV is the critical depolarization point at
which voltage-gated Na+ channels rapidly open, initiating the rising phase of the action potential.
Resting membrane potential is approximately -70 mV, and -90 mV is below resting (hyperpolarized).
+30 mV is the peak of the action potential, not the threshold. Once threshold is reached, the action
potential is "all or nothing" - a key concept for understanding neuronal signaling and drug effects on
excitability.
Q4: A patient is prescribed lithium, which has a narrow therapeutic index. The
sodium-potassium pump (Na+/K+-ATPase) is essential for restoring which ion
gradient after action potential firing?
A. Na+ in / K+ out
B. Na+ out / K+ in [CORRECT]
C. Ca2+ in / Na+ out
D. Cl- in / K+ out
Correct Answer: B
Rationale: The Na+/K+-ATPase pumps 3 Na+ out of the cell and 2 K+ into the cell against their
concentration gradients, using ATP. This maintains the resting membrane potential and restores
gradients after repeated action potentials. The pump is electrogenic (net positive charge out),
contributing directly to resting potential. Lithium can substitute for Na+ in some transport
processes, which is relevant to its pharmacology, toxicity, and interaction with sodium-wasting
conditions such as dehydration or thiazide diuretic use.
Q5: The absolute refractory period prevents backward propagation of action
potentials. Which mechanism is primarily responsible?
A. Voltage-gated K+ channels remain closed
B. Voltage-gated Na+ channels are inactivated [CORRECT]
C. Cl- channels remain open
D. Ca2+ channels are blocked
Correct Answer: B
Rationale: During the absolute refractory period, voltage-gated Na+ channels are in the inactivated
state and cannot reopen until the membrane repolarizes and channels reset to the closed state. This
prevents generation of a second action potential regardless of stimulus strength and ensures
unidirectional propagation. The relative refractory period follows, during which stronger-than-normal
stimuli can trigger impulses as K+ channels remain open, causing hyperpolarization. Local
anesthetics exploit Na+ channel inactivation to block conduction.
Page 2
,NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
Q6: Saltatory conduction increases conduction velocity in myelinated axons. Where
does depolarization actually occur during this process?
A. Along the entire axon membrane
B. Only at the axon hillock
C. Only at the Nodes of Ranvier [CORRECT]
D. Only at the terminal boutons
Correct Answer: C
Rationale: In saltatory conduction, the action potential "jumps" between Nodes of Ranvier, where
voltage-gated Na+ channels are concentrated. Myelin acts as an insulator, increasing membrane
resistance and allowing passive current spread to the next node. This dramatically increases
conduction velocity (up to 120 m/s) compared to unmyelinated fibers (~1 m/s). Demyelinating
diseases such as multiple sclerosis disrupt this process, producing slowed or blocked conduction and
clinical deficits.
Q7: A PMHNP is teaching about synaptic transmission. Calcium influx into the
presynaptic terminal triggers which event?
A. Reuptake of neurotransmitter
B. Enzymatic degradation of neurotransmitter
C. Synaptic vesicle fusion and exocytosis [CORRECT]
D. Opening of postsynaptic chloride channels
Correct Answer: C
Rationale: When an action potential reaches the presynaptic terminal, voltage-gated Ca2+
channels open, allowing Ca2+ influx. Calcium binds to synaptotagmin, triggering vesicle fusion with
the presynaptic membrane via the SNARE complex, releasing neurotransmitter into the synaptic
cleft. Reuptake and enzymatic degradation are mechanisms of neurotransmitter termination, not
release. Postsynaptic channels open in response to neurotransmitter binding, not calcium. Botulinum
toxin blocks this process by cleaving SNARE proteins.
Q8: Selective serotonin reuptake inhibitors (SSRIs) exert therapeutic effect by
blocking which protein?
A. Monoamine oxidase (MAO)
B. Serotonin transporter (SERT) [CORRECT]
C. 5-HT2A receptor
D. Tryptophan hydroxylase
Correct Answer: B
Rationale: SSRIs block the serotonin transporter (SERT), the presynaptic protein responsible for
reuptake of serotonin from the synaptic cleft back into the presynaptic neuron. This blockade
increases synaptic serotonin concentration, enhancing postsynaptic receptor activation. MAO
degrades serotonin intracellularly (target of MAOIs). 5-HT2A is a postsynaptic receptor. Tryptophan
hydroxylase is the rate-limiting enzyme in serotonin synthesis, not a reuptake target. Note:
therapeutic effect is delayed 2-6 weeks due to autoreceptor desensitization.
Page 3
, NSG 552 Exam 1 Study Guide + Review | Psychopharmacology | Wilkes University 2026/2027
Q9: Acetylcholinesterase inhibitors (e.g., donepezil) work by which mechanism?
A. Blocking muscarinic receptors
B. Inhibiting enzymatic degradation of acetylcholine [CORRECT]
C. Blocking acetylcholine release
D. Enhancing acetylcholine reuptake
Correct Answer: B
Rationale: Acetylcholinesterase inhibitors block the enzyme acetylcholinesterase, which normally
degrades acetylcholine in the synaptic cleft into choline and acetate. By inhibiting this enzyme, ACh
remains in the synapse longer, enhancing cholinergic transmission - useful in Alzheimer disease.
Note: there is no specific ACh reuptake transporter; termination is primarily via enzymatic
degradation. This contrasts with monoamines, which are terminated primarily by reuptake via
transporters such as SERT, NET, and DAT.
Q10: A neuron receives simultaneous excitatory (EPSP) and inhibitory (IPSP) inputs.
Where does spatial summation primarily occur?
A. Dendritic spines
B. Axon hillock [CORRECT]
C. Synaptic cleft
D. Terminal bouton
Correct Answer: B
Rationale: The axon hillock has the highest density of voltage-gated Na+ channels and the lowest
threshold, making it the site where EPSPs and IPSPs from various dendritic locations are spatially
and temporally summed. If the summated potential reaches threshold (~-55 mV), an action
potential is initiated. Dendritic spines receive input but do not initiate action potentials. This
integrative function is critical for understanding drug effects on neuronal firing patterns and
excitability.
Q11: GABA binding to GABA-A receptors opens chloride channels, causing which
effect on the postsynaptic neuron?
A. Depolarization
B. Hyperpolarization [CORRECT]
C. No change in membrane potential
D. Action potential firing
Correct Answer: B
Rationale: GABA-A receptor activation opens chloride channels, allowing Cl- influx, which
hyperpolarizes the postsynaptic membrane (brings it closer to ECl at approximately -65 to -70 mV),
making the neuron less excitable. This is the primary mechanism of fast inhibitory transmission in
the CNS and the target of benzodiazepines, which potentiate GABA-A function. Hyperpolarization
moves membrane potential away from action potential threshold. Barbiturates and alcohol also act
at GABA-A but at different sites.
Page 4
