STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission. Cambridge University
Press & Assessment
PMHNP-Level Question Stem (2–4 sentences)
A 42-year-old woman with major depressive disorder has
minimal improvement after 8 weeks of an SSRI. She reports
fatigue, poor concentration, and low motivation more so than
sadness. Prior treatment history includes a partial response to
an SNRI years ago. Considering presynaptic mechanisms of
monoaminergic transmission described by Stahl, which next
pharmacologic strategy most directly increases synaptic
monoamine availability by targeting presynaptic vesicular
storage?
,Options
A. Add a selective serotonin reuptake inhibitor (SSRI) at higher
dose
B. Switch to bupropion (a norepinephrine–dopamine reuptake
inhibitor)
C. Add a monoamine oxidase inhibitor (MAOI)
D. Add a vesicular monoamine transporter (VMAT2) inhibitor
Correct Answer
C
Rationales
Correct (C): MAOIs inhibit monoamine breakdown within
presynaptic terminals and mitochondria, increasing cytosolic
monoamine levels available for vesicular packaging and release;
in Stahl’s framework this raises overall monoaminergic tone and
can help partial SSRI responders.
Incorrect (A): Increasing SSRI dose only further blocks SERT
removal of serotonin from the synapse; it does not address
presynaptic catabolism or vesicular storage.
Incorrect (B): Bupropion inhibits DAT/NET and increases
synaptic catecholamines but does not directly increase
presynaptic vesicular storage or prevent intraterminal
monoamine breakdown.
Incorrect (D): VMAT2 inhibitors decrease vesicular storage of
monoamines, reducing release—opposite of the desired effect.
,Teaching Point (≤20 words)
MAO inhibition raises intraterminal monoamines; VMAT2
blockade reduces vesicular release—opposite clinical effects.
Citation (Simplified APA)
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1. Cambridge University Press & Assessment
2
Reference
Ch. 1 — Chemical Neurotransmission. Cambridge University
Press & Assessment
PMHNP-Level Question Stem
A 28-year-old patient with generalized anxiety disorder
becomes acutely agitated and tremulous after rapid titration of
a benzodiazepine for severe anxiety. The preceptor asks you to
explain why benzodiazepines can acutely sedate yet
paradoxically disinhibit in some patients. Based on receptor and
synaptic transmission principles in Stahl, which mechanism best
explains benzodiazepine-related paradoxical disinhibition?
Options
A. Nonselective blockade of GABA synthesis
B. Positive allosteric modulation of GABAA_AA receptors on
inhibitory interneurons causing disinhibition
C. Increased GABA reuptake via GAT transporters
, D. Direct agonism of GABAB_BB metabotropic receptors leading
to slow inhibition
Correct Answer
B
Rationales
Correct (B): Benzodiazepines are positive allosteric modulators
at GABAA_AA receptors. If they preferentially potentiate
GABAergic interneurons that inhibit other inhibitory neurons,
net network disinhibition can occur—explaining paradoxical
agitation. Stahl emphasizes receptor localization and network
effects.
Incorrect (A): Benzodiazepines do not block GABA synthesis.
Incorrect (C): GAT transporter upregulation would reduce
extracellular GABA, not explain benzodiazepine potentiation.
Incorrect (D): Benzodiazepines act at GABAA_AA (ionotropic)
receptors, not as direct GABAB_BB agonists.
Teaching Point
Allosteric modulation can produce network disinhibition
depending on receptor localization.
Citation (Simplified APA)
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1. Cambridge University Press & Assessment
3
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission. Cambridge University
Press & Assessment
PMHNP-Level Question Stem (2–4 sentences)
A 42-year-old woman with major depressive disorder has
minimal improvement after 8 weeks of an SSRI. She reports
fatigue, poor concentration, and low motivation more so than
sadness. Prior treatment history includes a partial response to
an SNRI years ago. Considering presynaptic mechanisms of
monoaminergic transmission described by Stahl, which next
pharmacologic strategy most directly increases synaptic
monoamine availability by targeting presynaptic vesicular
storage?
,Options
A. Add a selective serotonin reuptake inhibitor (SSRI) at higher
dose
B. Switch to bupropion (a norepinephrine–dopamine reuptake
inhibitor)
C. Add a monoamine oxidase inhibitor (MAOI)
D. Add a vesicular monoamine transporter (VMAT2) inhibitor
Correct Answer
C
Rationales
Correct (C): MAOIs inhibit monoamine breakdown within
presynaptic terminals and mitochondria, increasing cytosolic
monoamine levels available for vesicular packaging and release;
in Stahl’s framework this raises overall monoaminergic tone and
can help partial SSRI responders.
Incorrect (A): Increasing SSRI dose only further blocks SERT
removal of serotonin from the synapse; it does not address
presynaptic catabolism or vesicular storage.
Incorrect (B): Bupropion inhibits DAT/NET and increases
synaptic catecholamines but does not directly increase
presynaptic vesicular storage or prevent intraterminal
monoamine breakdown.
Incorrect (D): VMAT2 inhibitors decrease vesicular storage of
monoamines, reducing release—opposite of the desired effect.
,Teaching Point (≤20 words)
MAO inhibition raises intraterminal monoamines; VMAT2
blockade reduces vesicular release—opposite clinical effects.
Citation (Simplified APA)
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1. Cambridge University Press & Assessment
2
Reference
Ch. 1 — Chemical Neurotransmission. Cambridge University
Press & Assessment
PMHNP-Level Question Stem
A 28-year-old patient with generalized anxiety disorder
becomes acutely agitated and tremulous after rapid titration of
a benzodiazepine for severe anxiety. The preceptor asks you to
explain why benzodiazepines can acutely sedate yet
paradoxically disinhibit in some patients. Based on receptor and
synaptic transmission principles in Stahl, which mechanism best
explains benzodiazepine-related paradoxical disinhibition?
Options
A. Nonselective blockade of GABA synthesis
B. Positive allosteric modulation of GABAA_AA receptors on
inhibitory interneurons causing disinhibition
C. Increased GABA reuptake via GAT transporters
, D. Direct agonism of GABAB_BB metabotropic receptors leading
to slow inhibition
Correct Answer
B
Rationales
Correct (B): Benzodiazepines are positive allosteric modulators
at GABAA_AA receptors. If they preferentially potentiate
GABAergic interneurons that inhibit other inhibitory neurons,
net network disinhibition can occur—explaining paradoxical
agitation. Stahl emphasizes receptor localization and network
effects.
Incorrect (A): Benzodiazepines do not block GABA synthesis.
Incorrect (C): GAT transporter upregulation would reduce
extracellular GABA, not explain benzodiazepine potentiation.
Incorrect (D): Benzodiazepines act at GABAA_AA (ionotropic)
receptors, not as direct GABAB_BB agonists.
Teaching Point
Allosteric modulation can produce network disinhibition
depending on receptor localization.
Citation (Simplified APA)
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1. Cambridge University Press & Assessment
3
