STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Synaptic Release &
Autoreceptors
Stem
A 42-year-old outpatient with major depressive disorder reports
partial response to an SSRI (8 weeks) but persistent emotional
blunting and fatigue. He also experiences early-morning
activation (worse anxiety on waking). You consider switching or
augmenting based on presynaptic mechanisms. Which strategy
best addresses persistent low catecholaminergic tone while
minimizing serotonergic overstimulation?
,Options
A. Switch to an SNRI to increase synaptic norepinephrine and
dopamine via transporter blockade.
B. Augment SSRI with a norepinephrine–dopamine reuptake
inhibitor (bupropion) to increase catecholamine release without
boosting 5-HT.
C. Add a low-dose benzodiazepine to reduce anxiety and allow
SSRI dose escalation.
D. Switch to a serotonin antagonist to reduce postsynaptic 5-HT
receptor activation and thereby restore catecholamine tone.
Correct answer
B
Rationales
Correct (B): Augmenting with a norepinephrine–dopamine
reuptake inhibitor increases synaptic catecholamine levels by
blocking their transporters, addressing fatigue and blunting
linked to low catecholaminergic tone while preserving ongoing
serotonergic reuptake inhibition. Stahl’s framework emphasizes
transporter-level manipulations to adjust extracellular
transmitter balance.
Incorrect (A): Switching to an SNRI increases norepinephrine
but may also increase serotonergic tone depending on affinity;
switching loses the established SSRI response and risks
serotonergic adverse effects.
Incorrect (C): Benzodiazepine reduces anxiety via GABA_A
potentiation but does not correct catecholaminergic deficits
,driving blunted affect and fatigue.
Incorrect (D): A serotonin antagonist would block postsynaptic
5-HT receptors but may worsen depressive symptoms by
removing beneficial serotonergic signaling and does not directly
increase catecholamines.
Teaching point
Augment at transporter level to raise catecholamines while
preserving serotonergic gains.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular Storage and
VMAT
Stem
A 28-year-old woman with atypical depression has pronounced
anergia and psychomotor slowing despite SSRI therapy. She is
pregnant (first trimester) and concerned about fetal risk. You
consider pharmacologic options with an eye to mechanisms of
synaptic vesicular storage. Which option best targets
presynaptic vesicular monoamine availability while minimizing
fetal exposure to drugs that cross the placenta extensively?
, Options
A. Add a VMAT inhibitor to deplete vesicular monoamines and
lower synaptic levels.
B. Augment with a drug that increases cytosolic catecholamine
availability for vesicular uptake (precursor loading).
C. Switch to a norepinephrine reuptake inhibitor with low
placental transfer.
D. Add an agent that blocks monoamine oxidase (MAO) to raise
cytosolic monoamines available for vesicular storage.
Correct answer
B
Rationales
Correct (B): Increasing precursor availability raises cytosolic
monoamines that VMAT can package into vesicles, enhancing
synaptic release; in pregnancy, choosing precursors or
interventions with favorable placental profiles may be
preferable. Stahl highlights that vesicular storage and precursor
supply determine releasable transmitter pools.
Incorrect (A): VMAT inhibition depletes vesicular stores and
reduces neurotransmission, counterproductive for anergia.
Incorrect (C): An NRI increases extracellular norepinephrine by
blocking reuptake but does not directly augment vesicular
stores; placental transfer varies by agent and is not guaranteed
to be minimal.
Incorrect (D): MAO inhibition raises cytosolic monoamines but
carries dietary and drug interaction risks and significant
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Synaptic Release &
Autoreceptors
Stem
A 42-year-old outpatient with major depressive disorder reports
partial response to an SSRI (8 weeks) but persistent emotional
blunting and fatigue. He also experiences early-morning
activation (worse anxiety on waking). You consider switching or
augmenting based on presynaptic mechanisms. Which strategy
best addresses persistent low catecholaminergic tone while
minimizing serotonergic overstimulation?
,Options
A. Switch to an SNRI to increase synaptic norepinephrine and
dopamine via transporter blockade.
B. Augment SSRI with a norepinephrine–dopamine reuptake
inhibitor (bupropion) to increase catecholamine release without
boosting 5-HT.
C. Add a low-dose benzodiazepine to reduce anxiety and allow
SSRI dose escalation.
D. Switch to a serotonin antagonist to reduce postsynaptic 5-HT
receptor activation and thereby restore catecholamine tone.
Correct answer
B
Rationales
Correct (B): Augmenting with a norepinephrine–dopamine
reuptake inhibitor increases synaptic catecholamine levels by
blocking their transporters, addressing fatigue and blunting
linked to low catecholaminergic tone while preserving ongoing
serotonergic reuptake inhibition. Stahl’s framework emphasizes
transporter-level manipulations to adjust extracellular
transmitter balance.
Incorrect (A): Switching to an SNRI increases norepinephrine
but may also increase serotonergic tone depending on affinity;
switching loses the established SSRI response and risks
serotonergic adverse effects.
Incorrect (C): Benzodiazepine reduces anxiety via GABA_A
potentiation but does not correct catecholaminergic deficits
,driving blunted affect and fatigue.
Incorrect (D): A serotonin antagonist would block postsynaptic
5-HT receptors but may worsen depressive symptoms by
removing beneficial serotonergic signaling and does not directly
increase catecholamines.
Teaching point
Augment at transporter level to raise catecholamines while
preserving serotonergic gains.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular Storage and
VMAT
Stem
A 28-year-old woman with atypical depression has pronounced
anergia and psychomotor slowing despite SSRI therapy. She is
pregnant (first trimester) and concerned about fetal risk. You
consider pharmacologic options with an eye to mechanisms of
synaptic vesicular storage. Which option best targets
presynaptic vesicular monoamine availability while minimizing
fetal exposure to drugs that cross the placenta extensively?
, Options
A. Add a VMAT inhibitor to deplete vesicular monoamines and
lower synaptic levels.
B. Augment with a drug that increases cytosolic catecholamine
availability for vesicular uptake (precursor loading).
C. Switch to a norepinephrine reuptake inhibitor with low
placental transfer.
D. Add an agent that blocks monoamine oxidase (MAO) to raise
cytosolic monoamines available for vesicular storage.
Correct answer
B
Rationales
Correct (B): Increasing precursor availability raises cytosolic
monoamines that VMAT can package into vesicles, enhancing
synaptic release; in pregnancy, choosing precursors or
interventions with favorable placental profiles may be
preferable. Stahl highlights that vesicular storage and precursor
supply determine releasable transmitter pools.
Incorrect (A): VMAT inhibition depletes vesicular stores and
reduces neurotransmission, counterproductive for anergia.
Incorrect (C): An NRI increases extracellular norepinephrine by
blocking reuptake but does not directly augment vesicular
stores; placental transfer varies by agent and is not guaranteed
to be minimal.
Incorrect (D): MAO inhibition raises cytosolic monoamines but
carries dietary and drug interaction risks and significant
