Stahl's Essential Psychopharmacology
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient stabilized on haloperidol, a potent D2
receptor antagonist, presents with galactorrhea and menstrual
irregularities. The psychiatric-mental health nurse practitioner
(PMHNP) understands that this adverse effect is a direct result
of which neurobiological event?
A. Upregulation of 5-HT2A receptors in the cortex
B. Blockade of D2 receptors in the nigrostriatal pathway
C. Antagonism of D2 receptors in the tuberoinfundibular
pathway
D. Inhibition of dopamine reuptake in the mesolimbic pathway
Correct Answer: C
Rationales:
• Correct: In the tuberoinfundibular pathway, dopamine
tonically inhibits prolactin release. Antagonism of D2
, receptors here removes this inhibition, leading to
hyperprolactinemia, which can cause galactorrhea and
menstrual disturbances.
• Incorrect A: While 5-HT2A modulation is relevant to other
drug actions (e.g., atypical antipsychotics), it is not the
primary mechanism for hyperprolactinemia caused by
potent D2 antagonists like haloperidol.
• Incorrect B: Blockade of D2 receptors in the nigrostriatal
pathway is associated with extrapyramidal side effects
(EPS), not endocrine disturbances.
• Incorrect D: Inhibition of dopamine reuptake (e.g., by
stimulants) would increase dopamine signaling, which
would decrease, not increase, prolactin levels.
Teaching Point: Tuberoinfundibular D2 blockade disinhibits
prolactin, causing endocrine side effects.
Citation: Ch. 1, Chemical Neurotransmission
Question 2
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A new antidepressant is described as a
"serotonin reuptake pump inhibitor." Based on Stahl's teaching,
the PMHNP knows this drug's primary mechanism is to:
A. Directly stimulate postsynaptic serotonin receptors.
B. Block the enzymatic breakdown of serotonin in the synaptic
,cleft.
C. Bind to the vesicular monoamine transporter (VMAT2).
D. Block the serotonin transporter (SERT) on the presynaptic
neuron.
Correct Answer: D
Rationales:
• Correct: The "reuptake pump" is the serotonin transporter
(SERT). Inhibiting this transporter prevents the reuptake of
serotonin from the synapse, increasing its concentration
and duration of action.
• Incorrect A: This describes a serotonin receptor agonist,
not a reuptake inhibitor.
• Incorrect B: This describes the mechanism of a
monoamine oxidase inhibitor (MAOI), which blocks the
metabolism of monoamines inside the presynaptic neuron.
• Incorrect C: Binding to VMAT2 (e.g., by reserpine) depletes
monoamine vesicles, which is the opposite effect of a
reuptake inhibitor.
Teaching Point: Reuptake inhibitors work at the transporter, not
the receptor or enzyme.
Citation: Ch. 1, Chemical Neurotransmission
Question 3
, Reference: Ch. 1, Chemical Neurotransmission
Question Stem: According to the principles of chemical
neurotransmission, the therapeutic action of a benzodiazepine
positive allosteric modulator is best explained by its effect on:
A. Increasing the synthesis of GABA.
B. Directly opening the chloride ion channel.
C. Enhancing the affinity of GABA for its receptor.
D. Blocking the reuptake of GABA into glial cells and presynaptic
neurons.
Correct Answer: C
Rationales:
• Correct: Benzodiazepines are positive allosteric modulators
that bind to a site distinct from the GABA binding site. This
binding increases the frequency of chloride channel
opening when GABA is present, thereby enhancing
inhibitory neurotransmission.
• Incorrect A: Benzodiazepines do not affect the synthesis or
metabolism of GABA itself.
• Incorrect B: This describes the action of a direct receptor
agonist (e.g., muscimol), not a positive allosteric
modulator.
• Incorrect D: This is not a known mechanism of action for
benzodiazepines.
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient stabilized on haloperidol, a potent D2
receptor antagonist, presents with galactorrhea and menstrual
irregularities. The psychiatric-mental health nurse practitioner
(PMHNP) understands that this adverse effect is a direct result
of which neurobiological event?
A. Upregulation of 5-HT2A receptors in the cortex
B. Blockade of D2 receptors in the nigrostriatal pathway
C. Antagonism of D2 receptors in the tuberoinfundibular
pathway
D. Inhibition of dopamine reuptake in the mesolimbic pathway
Correct Answer: C
Rationales:
• Correct: In the tuberoinfundibular pathway, dopamine
tonically inhibits prolactin release. Antagonism of D2
, receptors here removes this inhibition, leading to
hyperprolactinemia, which can cause galactorrhea and
menstrual disturbances.
• Incorrect A: While 5-HT2A modulation is relevant to other
drug actions (e.g., atypical antipsychotics), it is not the
primary mechanism for hyperprolactinemia caused by
potent D2 antagonists like haloperidol.
• Incorrect B: Blockade of D2 receptors in the nigrostriatal
pathway is associated with extrapyramidal side effects
(EPS), not endocrine disturbances.
• Incorrect D: Inhibition of dopamine reuptake (e.g., by
stimulants) would increase dopamine signaling, which
would decrease, not increase, prolactin levels.
Teaching Point: Tuberoinfundibular D2 blockade disinhibits
prolactin, causing endocrine side effects.
Citation: Ch. 1, Chemical Neurotransmission
Question 2
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A new antidepressant is described as a
"serotonin reuptake pump inhibitor." Based on Stahl's teaching,
the PMHNP knows this drug's primary mechanism is to:
A. Directly stimulate postsynaptic serotonin receptors.
B. Block the enzymatic breakdown of serotonin in the synaptic
,cleft.
C. Bind to the vesicular monoamine transporter (VMAT2).
D. Block the serotonin transporter (SERT) on the presynaptic
neuron.
Correct Answer: D
Rationales:
• Correct: The "reuptake pump" is the serotonin transporter
(SERT). Inhibiting this transporter prevents the reuptake of
serotonin from the synapse, increasing its concentration
and duration of action.
• Incorrect A: This describes a serotonin receptor agonist,
not a reuptake inhibitor.
• Incorrect B: This describes the mechanism of a
monoamine oxidase inhibitor (MAOI), which blocks the
metabolism of monoamines inside the presynaptic neuron.
• Incorrect C: Binding to VMAT2 (e.g., by reserpine) depletes
monoamine vesicles, which is the opposite effect of a
reuptake inhibitor.
Teaching Point: Reuptake inhibitors work at the transporter, not
the receptor or enzyme.
Citation: Ch. 1, Chemical Neurotransmission
Question 3
, Reference: Ch. 1, Chemical Neurotransmission
Question Stem: According to the principles of chemical
neurotransmission, the therapeutic action of a benzodiazepine
positive allosteric modulator is best explained by its effect on:
A. Increasing the synthesis of GABA.
B. Directly opening the chloride ion channel.
C. Enhancing the affinity of GABA for its receptor.
D. Blocking the reuptake of GABA into glial cells and presynaptic
neurons.
Correct Answer: C
Rationales:
• Correct: Benzodiazepines are positive allosteric modulators
that bind to a site distinct from the GABA binding site. This
binding increases the frequency of chloride channel
opening when GABA is present, thereby enhancing
inhibitory neurotransmission.
• Incorrect A: Benzodiazepines do not affect the synthesis or
metabolism of GABA itself.
• Incorrect B: This describes the action of a direct receptor
agonist (e.g., muscimol), not a positive allosteric
modulator.
• Incorrect D: This is not a known mechanism of action for
benzodiazepines.
