1
Barkley Psychiatric-Mental Health Nurse Practitioner (PMHNP)
Diagnostic Readiness Test (DRT) | 100 Actual Practice
Questions and Verified Answers
Barkley PMHNP Diagnostic Readiness Test – 100 Practice Questions
Section 1: Neurobiology & Foundations (Questions 1–10)
1. A PMHNP is explaining to a patient how selective serotonin reuptake
inhibitors (SSRIs) exert their therapeutic effect. Which of the following best
describes the initial mechanism of action?
A. Inhibition of monoamine oxidase enzymes
B. Blockade of postsynaptic serotonin receptors
C. Inhibition of presynaptic serotonin reuptake transporters (SERT)
D. Direct agonism at 5-HT1A receptors
: Answer : C
Rationale: SSRIs bind to and block the serotonin transporter (SERT) on the
presynaptic neuron, preventing reuptake of serotonin from the synaptic cleft. This
increases synaptic serotonin availability. Clinical effects are delayed due to
downstream receptor adaptations. Option A describes MAOIs; B describes
antagonists (e.g., some antipsychotics); D describes buspirone.
2. The mesolimbic dopamine pathway, when hyperactive, is most closely
associated with which symptoms of schizophrenia?
A. Negative symptoms (avolition, anhedonia)
B. Positive symptoms (hallucinations, delusions)
C. Cognitive symptoms (impaired working memory)
D. Affective symptoms (depression, anxiety)
: Answer : B
Rationale: Hyperactivity in the mesolimbic pathway (VTA to nucleus accumbens) is
linked to positive psychotic symptoms. Hypoactivity in the mesocortical pathway is
associated with negative and cognitive symptoms.
pg. 1
,2
3. A patient with generalized anxiety disorder has been on an SSRI for 8 weeks
with partial response. The PMHNP considers augmentation with buspirone.
Buspirone’s primary mechanism is:
A. GABA-A receptor positive allosteric modulation
B. Serotonin 5-HT1A receptor partial agonism
C. Dopamine D2 receptor antagonism
D. Norepinephrine reuptake inhibition
: Answer : B
*Rationale: Buspirone is a 5-HT1A partial agonist. It lacks GABAergic activity,
dependence potential, or significant sedation. It is not a D2 antagonist or NRI.*
4. Which of the following laboratory tests is essential to monitor in a patient
initiated on clozapine?
A. Liver function tests weekly
B. Absolute neutrophil count (ANC) weekly for 6 months, then every 2 weeks,
then monthly
C. Serum creatinine and BUN every 3 months
D. Thyroid stimulating hormone (TSH) every 6 months
: Answer : B
Rationale: Clozapine carries a risk of agranulocytosis. The REMS program requires
ANC monitoring: weekly for the first 6 months, every 2 weeks for the next 6
months, then monthly thereafter. LFTs, renal function, and thyroid are not specific
to clozapine REMS (though clozapine can affect metabolic parameters).
5. The therapeutic serum level range for lithium in the maintenance treatment
of bipolar disorder is typically:
A. 0.2–0.4 mEq/L
B. 0.6–1.2 mEq/L
C. 1.5–2.0 mEq/L
D. 2.5–3.5 mEq/L
: Answer : B
*Rationale: The therapeutic maintenance range is 0.6–1.2 mEq/L, with levels of
0.8–1.0 often targeted. Acute mania may require the higher end (1.0–1.2).
Toxicity generally begins above 1.5 mEq/L.*
pg. 2
,3
6. Which neurotransmitter system is primarily targeted by varenicline, a
medication used for smoking cessation?
A. Dopamine D2 receptors
B. Nicotinic acetylcholine receptors (partial agonist)
C. Opioid mu receptors
D. Cannabinoid CB1 receptors
: Answer : B
Rationale: Varenicline is a partial agonist at alpha4beta2 nicotinic acetylcholine
receptors. It reduces cravings and withdrawal symptoms while blocking the
rewarding effects of nicotine.
7. Which of the following antidepressants has the highest risk of discontinuation
syndrome due to its short half-life and lack of active metabolites?
A. Fluoxetine
B. Paroxetine
C. Citalopram
D. Escitalopram
: Answer : B
*Rationale: Paroxetine has the shortest half-life (~21 hours), no active metabolite,
and significant anticholinergic effects, making discontinuation syndrome more
severe. Fluoxetine’s long half-life provides self-tapering.*
8. A patient taking a monoamine oxidase inhibitor (MAOI) must avoid foods
high in tyramine to prevent:
A. Serotonin syndrome
B. Hypertensive crisis
C. Acute dystonia
D. Anticholinergic toxicity
: Answer : B
Rationale: Inhibition of MAO-A in the gut prevents breakdown of dietary tyramine,
which can cause massive norepinephrine release and severe hypertension.
Serotonin syndrome is due to excess serotonin, not tyramine.
9. What is the primary pharmacodynamic action of second-generation
antipsychotics (SGAs) that differentiates them from first-generation agents?
pg. 3
, 4
A. Pure D2 antagonism
B. D2 antagonism combined with 5-HT2A antagonism
C. Dopamine receptor agonism
D. GABA receptor potentiation
: Answer : B
*Rationale: SGAs have a dual mechanism: they block dopamine D2 receptors (less
tightly or more transiently than FGAs) and also block serotonin 5-HT2A receptors,
which mitigates some EPS and may improve negative symptoms.*
10. Which brain structure is critically involved in fear conditioning and the
pathophysiology of anxiety disorders?
A. Hippocampus
B. Amygdala
C. Prefrontal cortex
D. Thalamus
: Answer : B
Rationale: The amygdala processes fear and emotional salience, and is
hyperactive in many anxiety disorders. The hippocampus is more involved in
memory and context, the prefrontal cortex in executive function and regulation.
Section 2: Major Depressive and Bipolar Disorders (Questions 11–25)
11. A 45-year-old woman with MDD has failed two adequate trials of SSRIs. She
now has a partial response to an SNRI. Which augmentation strategy has the
strongest evidence for treatment-resistant depression?
A. Adding a benzodiazepine
B. Adding an atypical antipsychotic (e.g., aripiprazole)
C. Switching to an MAOI
D. Adding a beta-blocker
: Answer : B
Rationale: Atypical antipsychotics (aripiprazole, quetiapine, brexpiprazole,
olanzapine-fluoxetine) are FDA-approved augmenting agents for TRD.
Benzodiazepines are not effective for core depression. MAOIs are later-line
options.
pg. 4
Barkley Psychiatric-Mental Health Nurse Practitioner (PMHNP)
Diagnostic Readiness Test (DRT) | 100 Actual Practice
Questions and Verified Answers
Barkley PMHNP Diagnostic Readiness Test – 100 Practice Questions
Section 1: Neurobiology & Foundations (Questions 1–10)
1. A PMHNP is explaining to a patient how selective serotonin reuptake
inhibitors (SSRIs) exert their therapeutic effect. Which of the following best
describes the initial mechanism of action?
A. Inhibition of monoamine oxidase enzymes
B. Blockade of postsynaptic serotonin receptors
C. Inhibition of presynaptic serotonin reuptake transporters (SERT)
D. Direct agonism at 5-HT1A receptors
: Answer : C
Rationale: SSRIs bind to and block the serotonin transporter (SERT) on the
presynaptic neuron, preventing reuptake of serotonin from the synaptic cleft. This
increases synaptic serotonin availability. Clinical effects are delayed due to
downstream receptor adaptations. Option A describes MAOIs; B describes
antagonists (e.g., some antipsychotics); D describes buspirone.
2. The mesolimbic dopamine pathway, when hyperactive, is most closely
associated with which symptoms of schizophrenia?
A. Negative symptoms (avolition, anhedonia)
B. Positive symptoms (hallucinations, delusions)
C. Cognitive symptoms (impaired working memory)
D. Affective symptoms (depression, anxiety)
: Answer : B
Rationale: Hyperactivity in the mesolimbic pathway (VTA to nucleus accumbens) is
linked to positive psychotic symptoms. Hypoactivity in the mesocortical pathway is
associated with negative and cognitive symptoms.
pg. 1
,2
3. A patient with generalized anxiety disorder has been on an SSRI for 8 weeks
with partial response. The PMHNP considers augmentation with buspirone.
Buspirone’s primary mechanism is:
A. GABA-A receptor positive allosteric modulation
B. Serotonin 5-HT1A receptor partial agonism
C. Dopamine D2 receptor antagonism
D. Norepinephrine reuptake inhibition
: Answer : B
*Rationale: Buspirone is a 5-HT1A partial agonist. It lacks GABAergic activity,
dependence potential, or significant sedation. It is not a D2 antagonist or NRI.*
4. Which of the following laboratory tests is essential to monitor in a patient
initiated on clozapine?
A. Liver function tests weekly
B. Absolute neutrophil count (ANC) weekly for 6 months, then every 2 weeks,
then monthly
C. Serum creatinine and BUN every 3 months
D. Thyroid stimulating hormone (TSH) every 6 months
: Answer : B
Rationale: Clozapine carries a risk of agranulocytosis. The REMS program requires
ANC monitoring: weekly for the first 6 months, every 2 weeks for the next 6
months, then monthly thereafter. LFTs, renal function, and thyroid are not specific
to clozapine REMS (though clozapine can affect metabolic parameters).
5. The therapeutic serum level range for lithium in the maintenance treatment
of bipolar disorder is typically:
A. 0.2–0.4 mEq/L
B. 0.6–1.2 mEq/L
C. 1.5–2.0 mEq/L
D. 2.5–3.5 mEq/L
: Answer : B
*Rationale: The therapeutic maintenance range is 0.6–1.2 mEq/L, with levels of
0.8–1.0 often targeted. Acute mania may require the higher end (1.0–1.2).
Toxicity generally begins above 1.5 mEq/L.*
pg. 2
,3
6. Which neurotransmitter system is primarily targeted by varenicline, a
medication used for smoking cessation?
A. Dopamine D2 receptors
B. Nicotinic acetylcholine receptors (partial agonist)
C. Opioid mu receptors
D. Cannabinoid CB1 receptors
: Answer : B
Rationale: Varenicline is a partial agonist at alpha4beta2 nicotinic acetylcholine
receptors. It reduces cravings and withdrawal symptoms while blocking the
rewarding effects of nicotine.
7. Which of the following antidepressants has the highest risk of discontinuation
syndrome due to its short half-life and lack of active metabolites?
A. Fluoxetine
B. Paroxetine
C. Citalopram
D. Escitalopram
: Answer : B
*Rationale: Paroxetine has the shortest half-life (~21 hours), no active metabolite,
and significant anticholinergic effects, making discontinuation syndrome more
severe. Fluoxetine’s long half-life provides self-tapering.*
8. A patient taking a monoamine oxidase inhibitor (MAOI) must avoid foods
high in tyramine to prevent:
A. Serotonin syndrome
B. Hypertensive crisis
C. Acute dystonia
D. Anticholinergic toxicity
: Answer : B
Rationale: Inhibition of MAO-A in the gut prevents breakdown of dietary tyramine,
which can cause massive norepinephrine release and severe hypertension.
Serotonin syndrome is due to excess serotonin, not tyramine.
9. What is the primary pharmacodynamic action of second-generation
antipsychotics (SGAs) that differentiates them from first-generation agents?
pg. 3
, 4
A. Pure D2 antagonism
B. D2 antagonism combined with 5-HT2A antagonism
C. Dopamine receptor agonism
D. GABA receptor potentiation
: Answer : B
*Rationale: SGAs have a dual mechanism: they block dopamine D2 receptors (less
tightly or more transiently than FGAs) and also block serotonin 5-HT2A receptors,
which mitigates some EPS and may improve negative symptoms.*
10. Which brain structure is critically involved in fear conditioning and the
pathophysiology of anxiety disorders?
A. Hippocampus
B. Amygdala
C. Prefrontal cortex
D. Thalamus
: Answer : B
Rationale: The amygdala processes fear and emotional salience, and is
hyperactive in many anxiety disorders. The hippocampus is more involved in
memory and context, the prefrontal cortex in executive function and regulation.
Section 2: Major Depressive and Bipolar Disorders (Questions 11–25)
11. A 45-year-old woman with MDD has failed two adequate trials of SSRIs. She
now has a partial response to an SNRI. Which augmentation strategy has the
strongest evidence for treatment-resistant depression?
A. Adding a benzodiazepine
B. Adding an atypical antipsychotic (e.g., aripiprazole)
C. Switching to an MAOI
D. Adding a beta-blocker
: Answer : B
Rationale: Atypical antipsychotics (aripiprazole, quetiapine, brexpiprazole,
olanzapine-fluoxetine) are FDA-approved augmenting agents for TRD.
Benzodiazepines are not effective for core depression. MAOIs are later-line
options.
pg. 4
