Stahl's Essential Psychopharmacology
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Question 1
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A nursing student is reviewing the mechanism
of action for a new antipsychotic medication described as a
"dopamine stabilizer." This drug acts as a functional antagonist
in the mesolimbic pathway but a functional agonist in the
mesocortical pathway. What is the primary presynaptic
mechanism that allows for this dual, pathway-specific action?
Options:
A. Direct blockade of postsynaptic D2 receptors
B. Selective inhibition of dopamine reuptake (DAT blockade)
C. Stimulation of presynaptic dopamine autoreceptors
D. Irreversible inhibition of monoamine oxidase (MAO)
Correct Answer: C
,Rationales:
• Correct (C): Dopamine stabilizers work primarily by acting
as partial agonists at presynaptic dopamine autoreceptors.
In hyperactive pathways (e.g., mesolimbic), this agonism
reduces dopamine release, functioning as an antagonist. In
hypoactive pathways (e.g., mesocortical), the blockade of
excessive autoreceptor signaling increases dopamine
release, functioning as an agonist.
• Incorrect (A): This describes a pure antagonist, like a
typical antipsychotic, which would block dopamine
indiscriminately in all pathways, not stabilize it in a
pathway-specific manner.
• Incorrect (B): DAT blockade increases synaptic dopamine,
which is the mechanism for stimulants like
methylphenidate, not for dopamine stabilizers.
• Incorrect (D): MAO inhibition increases the presynaptic
pool of monoamines but does not confer the pathway-
specific stabilizing action of a partial autoreceptor agonist.
Teaching Point: Presynaptic autoreceptors act like a thermostat,
regulating neurotransmitter release and enabling pathway-
specific drug effects.
Citation: Ch. 1, Chemical Neurotransmission
Question 2
,Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient with depression has been prescribed
a selective serotonin reuptake inhibitor (SSRI). The nurse
explains that the therapeutic effect on mood may take several
weeks. Which neurobiological process best explains this
delayed onset of action?
Options:
A. The time required for the drug to achieve steady-state
plasma concentration
B. The initial overstimulation and subsequent downregulation
of postsynaptic serotonin receptors
C. The time needed for the drug to saturate serotonin
transporters (SERT) in the gut
D. The slow process of presynaptic autoreceptor
downregulation, leading to increased serotonin release
Correct Answer: D
Rationales:
• Correct (D): The delay is primarily due to the
downregulation of presynaptic 5-HT1A autoreceptors.
Initially, increased synaptic serotonin activates these
autoreceptors, inhibiting further release. Over time, these
autoreceptors desensitize, allowing for a sustained
increase in serotonin release and neurotransmission.
, • Incorrect (A): While pharmacokinetics are a factor, steady-
state is typically reached in 4-5 half-lives (days), which does
not account for the week-long delay in therapeutic effect.
• Incorrect (B): Downregulation of postsynaptic receptors is
a consequence of sustained increased neurotransmission
and may contribute to the final therapeutic effect, but it is
not the primary rate-limiting step.
• Incorrect (C): SERT saturation in the CNS occurs rapidly,
within hours of dosing, which correlates with the onset of
side effects, not the therapeutic effect.
Teaching Point: Antidepressant efficacy requires long-term
neuroplasticity, primarily presynaptic autoreceptor
downregulation.
Citation: Ch. 1, Chemical Neurotransmission
Question 3
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient taking a medication for schizophrenia
develops galactorrhea. The nurse understands this adverse
effect is due to the drug's action as a D2 antagonist in a specific
neuroendocrine pathway. Blocking dopamine in this pathway
disinhibits the release of which hormone?
Options:
A. Adrenocorticotropic hormone (ACTH)
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Question 1
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A nursing student is reviewing the mechanism
of action for a new antipsychotic medication described as a
"dopamine stabilizer." This drug acts as a functional antagonist
in the mesolimbic pathway but a functional agonist in the
mesocortical pathway. What is the primary presynaptic
mechanism that allows for this dual, pathway-specific action?
Options:
A. Direct blockade of postsynaptic D2 receptors
B. Selective inhibition of dopamine reuptake (DAT blockade)
C. Stimulation of presynaptic dopamine autoreceptors
D. Irreversible inhibition of monoamine oxidase (MAO)
Correct Answer: C
,Rationales:
• Correct (C): Dopamine stabilizers work primarily by acting
as partial agonists at presynaptic dopamine autoreceptors.
In hyperactive pathways (e.g., mesolimbic), this agonism
reduces dopamine release, functioning as an antagonist. In
hypoactive pathways (e.g., mesocortical), the blockade of
excessive autoreceptor signaling increases dopamine
release, functioning as an agonist.
• Incorrect (A): This describes a pure antagonist, like a
typical antipsychotic, which would block dopamine
indiscriminately in all pathways, not stabilize it in a
pathway-specific manner.
• Incorrect (B): DAT blockade increases synaptic dopamine,
which is the mechanism for stimulants like
methylphenidate, not for dopamine stabilizers.
• Incorrect (D): MAO inhibition increases the presynaptic
pool of monoamines but does not confer the pathway-
specific stabilizing action of a partial autoreceptor agonist.
Teaching Point: Presynaptic autoreceptors act like a thermostat,
regulating neurotransmitter release and enabling pathway-
specific drug effects.
Citation: Ch. 1, Chemical Neurotransmission
Question 2
,Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient with depression has been prescribed
a selective serotonin reuptake inhibitor (SSRI). The nurse
explains that the therapeutic effect on mood may take several
weeks. Which neurobiological process best explains this
delayed onset of action?
Options:
A. The time required for the drug to achieve steady-state
plasma concentration
B. The initial overstimulation and subsequent downregulation
of postsynaptic serotonin receptors
C. The time needed for the drug to saturate serotonin
transporters (SERT) in the gut
D. The slow process of presynaptic autoreceptor
downregulation, leading to increased serotonin release
Correct Answer: D
Rationales:
• Correct (D): The delay is primarily due to the
downregulation of presynaptic 5-HT1A autoreceptors.
Initially, increased synaptic serotonin activates these
autoreceptors, inhibiting further release. Over time, these
autoreceptors desensitize, allowing for a sustained
increase in serotonin release and neurotransmission.
, • Incorrect (A): While pharmacokinetics are a factor, steady-
state is typically reached in 4-5 half-lives (days), which does
not account for the week-long delay in therapeutic effect.
• Incorrect (B): Downregulation of postsynaptic receptors is
a consequence of sustained increased neurotransmission
and may contribute to the final therapeutic effect, but it is
not the primary rate-limiting step.
• Incorrect (C): SERT saturation in the CNS occurs rapidly,
within hours of dosing, which correlates with the onset of
side effects, not the therapeutic effect.
Teaching Point: Antidepressant efficacy requires long-term
neuroplasticity, primarily presynaptic autoreceptor
downregulation.
Citation: Ch. 1, Chemical Neurotransmission
Question 3
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient taking a medication for schizophrenia
develops galactorrhea. The nurse understands this adverse
effect is due to the drug's action as a D2 antagonist in a specific
neuroendocrine pathway. Blocking dopamine in this pathway
disinhibits the release of which hormone?
Options:
A. Adrenocorticotropic hormone (ACTH)
