STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Presynaptic
Autoreceptors & Reuptake
Stem
A 45-year-old patient with major depressive disorder reports
partial improvement on an SSRI but persistent psychomotor
slowing and sexual dysfunction. The patient previously had poor
tolerability to an MAO inhibitor. As a PMHNP you consider
switching strategies that preserve antidepressant efficacy while
reducing serotonergic side effects by targeting different
presynaptic mechanisms discussed in Stahl. Which
pharmacologic strategy best fits this goal?
,Options
A. Switch to a selective norepinephrine–dopamine reuptake
inhibitor (NDRI) to reduce serotonergic excess.
B. Add a 5-HT1A partial agonist to increase serotonin release
presynaptically.
C. Initiate a high-affinity SERT booster to increase synaptic
serotonin further.
D. Use an irreversible MAO inhibitor to increase monoamine
levels broadly.
Correct answer
A
Rationales
Correct (A): NDRI drugs primarily block NET and DAT without
central SERT blockade, reducing reliance on serotonergic
enhancement; this can preserve antidepressant benefit via
catecholaminergic mechanisms while lowering SSRI-mediated
sexual dysfunction and psychomotor activation/sedation linked
to excessive serotonin. Stahl emphasizes that targeting different
transporters alters the neurotransmitter balance and side-effect
profile.
Incorrect (B): A 5-HT1A partial agonist can modulate
serotonergic tone but may not reliably reduce SSRI-related
sexual side effects because it still acts within serotonergic
pathways.
Incorrect (C): A SERT booster (increase of SERT function) is not a
clinically used mechanism and would further increase
,serotonergic activity, worsening sexual side effects.
Incorrect (D): Irreversible MAO inhibition raises all monoamines
and is contraindicated given prior poor tolerability and risks
(e.g., hypertensive interactions); it would not selectively reduce
serotonergic adverse effects.
Teaching point
Switching to non-serotonergic reuptake inhibition can reduce
SSRI-linked sexual and motor side effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular Storage
(VMAT) and Release
Stem
A 60-year-old patient with long-standing depression develops
severe orthostatic hypotension and increased risk of falls after
starting an older antihypertensive known to deplete vesicular
monoamine stores. Using Stahl’s description of vesicular
storage, which agent class best explains this adverse effect and
why it would worsen depressive symptoms?
Options
A. VMAT inhibitors (e.g., reserpine-like agents) that deplete
, vesicular monoamines.
B. Selective serotonin reuptake inhibitors that increase synaptic
serotonin.
C. Cholinesterase inhibitors that increase acetylcholine
availability.
D. Benzodiazepines enhancing GABA_A receptor function.
Correct answer
A
Rationales
Correct (A): VMAT inhibition prevents monoamines (NE, DA, 5-
HT) from being stored in synaptic vesicles, leading to cytosolic
degradation and reduced synaptic release—Stahl links VMAT
blockade to depressive symptoms and autonomic effects like
orthostatic hypotension due to reduced noradrenergic tone.
Incorrect (B): SSRIs raise synaptic serotonin and are not
associated with vesicular depletion or direct orthostatic
hypotension from monoamine depletion.
Incorrect (C): Cholinesterase inhibitors increase acetylcholine
and may cause autonomic effects but do not deplete
monoamines stored in vesicles.
Incorrect (D): Benzodiazepines modulate GABAergic tone and
cause sedation but do not deplete monoamine stores or
specifically cause orthostatic hypotension by that mechanism.
Teaching point
VMAT blockade depletes monoamines, worsening mood and
causing autonomic instability.
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Presynaptic
Autoreceptors & Reuptake
Stem
A 45-year-old patient with major depressive disorder reports
partial improvement on an SSRI but persistent psychomotor
slowing and sexual dysfunction. The patient previously had poor
tolerability to an MAO inhibitor. As a PMHNP you consider
switching strategies that preserve antidepressant efficacy while
reducing serotonergic side effects by targeting different
presynaptic mechanisms discussed in Stahl. Which
pharmacologic strategy best fits this goal?
,Options
A. Switch to a selective norepinephrine–dopamine reuptake
inhibitor (NDRI) to reduce serotonergic excess.
B. Add a 5-HT1A partial agonist to increase serotonin release
presynaptically.
C. Initiate a high-affinity SERT booster to increase synaptic
serotonin further.
D. Use an irreversible MAO inhibitor to increase monoamine
levels broadly.
Correct answer
A
Rationales
Correct (A): NDRI drugs primarily block NET and DAT without
central SERT blockade, reducing reliance on serotonergic
enhancement; this can preserve antidepressant benefit via
catecholaminergic mechanisms while lowering SSRI-mediated
sexual dysfunction and psychomotor activation/sedation linked
to excessive serotonin. Stahl emphasizes that targeting different
transporters alters the neurotransmitter balance and side-effect
profile.
Incorrect (B): A 5-HT1A partial agonist can modulate
serotonergic tone but may not reliably reduce SSRI-related
sexual side effects because it still acts within serotonergic
pathways.
Incorrect (C): A SERT booster (increase of SERT function) is not a
clinically used mechanism and would further increase
,serotonergic activity, worsening sexual side effects.
Incorrect (D): Irreversible MAO inhibition raises all monoamines
and is contraindicated given prior poor tolerability and risks
(e.g., hypertensive interactions); it would not selectively reduce
serotonergic adverse effects.
Teaching point
Switching to non-serotonergic reuptake inhibition can reduce
SSRI-linked sexual and motor side effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular Storage
(VMAT) and Release
Stem
A 60-year-old patient with long-standing depression develops
severe orthostatic hypotension and increased risk of falls after
starting an older antihypertensive known to deplete vesicular
monoamine stores. Using Stahl’s description of vesicular
storage, which agent class best explains this adverse effect and
why it would worsen depressive symptoms?
Options
A. VMAT inhibitors (e.g., reserpine-like agents) that deplete
, vesicular monoamines.
B. Selective serotonin reuptake inhibitors that increase synaptic
serotonin.
C. Cholinesterase inhibitors that increase acetylcholine
availability.
D. Benzodiazepines enhancing GABA_A receptor function.
Correct answer
A
Rationales
Correct (A): VMAT inhibition prevents monoamines (NE, DA, 5-
HT) from being stored in synaptic vesicles, leading to cytosolic
degradation and reduced synaptic release—Stahl links VMAT
blockade to depressive symptoms and autonomic effects like
orthostatic hypotension due to reduced noradrenergic tone.
Incorrect (B): SSRIs raise synaptic serotonin and are not
associated with vesicular depletion or direct orthostatic
hypotension from monoamine depletion.
Incorrect (C): Cholinesterase inhibitors increase acetylcholine
and may cause autonomic effects but do not deplete
monoamines stored in vesicles.
Incorrect (D): Benzodiazepines modulate GABAergic tone and
cause sedation but do not deplete monoamine stores or
specifically cause orthostatic hypotension by that mechanism.
Teaching point
VMAT blockade depletes monoamines, worsening mood and
causing autonomic instability.
