NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
NR 546 Advanced Psychopharmacology
Final Examination - Two Latest Verified Versions (2026-2027)
Chamberlain University | Graduate PMHNP Program
200 Verified Questions | 100 Per Version | Advanced Practice Prescriptive Decision-Making
Coverage: Mood Disorders | Anxiety & Trauma | Psychotic Disorders | Neurodevelopmental Conditions | Special Populations |
Medication Safety
VERSION 1 - Questions 1 to 100
Section 1: Foundations of Psychopharmacology and Neurobiology
Q1: A 34-year-old patient is started on fluoxetine 20 mg daily for major depressive disorder. The PMHNP
understands that fluoxetine exerts its primary therapeutic effect by inhibiting reuptake at which synapse, and that
downstream clinical benefit over 2 to 4 weeks is most attributable to which neuroadaptive change?
A. Inhibiting serotonin reuptake; downregulation of postsynaptic 5-HT2A receptors [CORRECT]
B. Inhibiting dopamine reuptake; upregulation of D2 receptors in the mesolimbic pathway
C. Inhibiting norepinephrine reuptake; desensitization of presynaptic alpha-2 autoreceptors
D. Inhibiting GABA transaminase; increased GABA-B receptor expression
Correct Answer: A
Rationale: Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that blocks the serotonin transporter (SERT),
increasing synaptic serotonin in the raphe-cortical and raphe-limbic pathways. Acute reuptake blockade occurs within hours,
but therapeutic antidepressant effects require 2 to 4 weeks and are linked to desensitization of somatodendritic 5-HT1A
autoreceptors and downstream downregulation of postsynaptic 5-HT2A receptors. Option B describes stimulant mechanism,
option C describes SNRI/alpha-2 mechanisms, and option D describes GABAergic agents.
Q2: A graduate nursing student asks why second-generation antipsychotics differ in metabolic risk despite all
blocking dopamine D2 receptors. Which pharmacologic property best explains why clozapine and olanzapine carry
higher metabolic risk than aripiprazole or lurasidone?
A. Higher affinity for the histamine H1 receptor and 5-HT2C receptor, promoting appetite and weight gain
[CORRECT]
B. Stronger D2 antagonism in the nigrostriatal pathway, increasing extrapyramidal symptoms
C. Greater anticholinergic muscarinic M1 blockade, causing insulin dysregulation
D. Higher affinity for alpha-1 adrenergic receptors, producing orthostatic hypotension
Correct Answer: A
Rationale: Clozapine and olanzapine have high affinity for histamine H1 and serotonin 5-HT2C receptors, both of which
stimulate appetite and disrupt satiety signaling, leading to weight gain, insulin resistance, and dyslipidemia. Aripiprazole and
lurasidone have low H1 and 5-HT2C affinity, hence lower metabolic liability. D2 affinity (B) predicts EPS and prolactin risk,
not metabolic risk. Anticholinergic activity (C) causes constipation and cognitive blunting, while alpha-1 blockade (D)
causes orthostasis.
Page 1
,NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
Q3: A patient has been taking paroxetine 20 mg daily for 3 years and abruptly stops. Within 48 hours, the patient
reports dizziness, nausea, electric shock-like sensations, and insomnia. Which pharmacokinetic property of
paroxetine is the most important contributor to this presentation?
A. Short half-life and lack of active metabolites [CORRECT]
B. Strong inhibition of CYP2D6
C. High volume of distribution
D. Extensive renal elimination unchanged
Correct Answer: A
Rationale: Paroxetine has a short half-life of approximately 21 hours and no active metabolites, producing the most severe
discontinuation syndrome among SSRIs when stopped abruptly. Fluoxetine, in contrast, has a 1 to 4 day half-life with an
active metabolite (norfluoxetine) lasting 7 to 15 days, making discontinuation syndrome rare. CYP2D6 inhibition (B) affects
drug interactions, not withdrawal. Volume of distribution (C) and renal elimination (D) do not explain acute withdrawal
kinetics.
Q4: A PMHNP plans to initiate atomoxetine for adult ADHD in a patient already taking fluoxetine 20 mg daily.
What pharmacokinetic interaction must be anticipated, and what is the appropriate prescribing adjustment?
A. Fluoxetine inhibits CYP2D6, raising atomoxetine levels; initiate atomoxetine at a reduced dose and titrate
slowly [CORRECT]
B. Fluoxetine induces CYP3A4, lowering atomoxetine levels; increase atomoxetine dose by 50%
C. Fluoxetine displaces atomoxetine from plasma proteins, causing toxicity; space doses 12 hours apart
D. Fluoxetine inhibits P-glycoprotein at the blood-brain barrier; no dose adjustment needed
Correct Answer: A
Rationale: Atomoxetine is metabolized primarily by CYP2D6. Fluoxetine is a potent CYP2D6 inhibitor, which can raise
atomoxetine plasma concentrations 2- to 3-fold and increase adverse effects (dry mouth, insomnia, cardiovascular effects).
Dose reduction and slow titration are required. CYP3A4 induction (B) is incorrect as fluoxetine does not induce 3A4. Protein
displacement (C) is clinically negligible for atomoxetine, and P-glycoprotein (D) is not the relevant mechanism.
Q5: A 28-year-old with generalized anxiety disorder is prescribed buspirone 7.5 mg twice daily. The patient asks
when full anxiolytic effect will occur. The PMHNP correctly explains that buspirone's mechanism and onset are
best described by which statement?
A. Partial agonist at 5-HT1A receptors; full effect requires 2 to 4 weeks of continuous dosing [CORRECT]
B. Full agonist at GABA-A receptors; anxiolysis occurs within 30 minutes of administration
C. Antagonist at NMDA receptors; effect develops over 6 to 8 weeks
D. Reuptake inhibitor of norepinephrine; effect begins within 48 hours
Correct Answer: A
Rationale: Buspirone is a partial agonist at serotonin 5-HT1A autoreceptors and postsynaptic receptors, producing anxiolysis
through gradual serotonergic modulation rather than direct sedation. Onset requires 2 to 4 weeks of consistent dosing, similar
to SSRIs, making it unsuitable for acute anxiety. GABA-A agonism (B) describes benzodiazepines, NMDA antagonism (C)
describes ketamine, and norepinephrine reuptake inhibition (D) describes atomoxetine or reboxetine.
Page 2
,NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
Q6: A 45-year-old with treatment-resistant depression receives intranasal esketamine in conjunction with an oral
antidepressant. The PMHNP understands that the rapid antidepressant effect of esketamine within hours is
mediated primarily through which mechanism?
A. NMDA receptor antagonism enhancing glutamatergic signaling and synaptogenesis via mTOR pathway
activation [CORRECT]
B. Monoamine oxidase inhibition increasing synaptic serotonin, norepinephrine, and dopamine
C. Reversible inhibition of the serotonin transporter with downstream 5-HT1A receptor sensitization
D. Positive allosteric modulation of GABA-A receptors producing rapid sedation
Correct Answer: A
Rationale: Esketamine, the S-enantiomer of ketamine, is a noncompetitive NMDA receptor antagonist. Its rapid
antidepressant effect (within hours) is linked to glutamate surge in the prefrontal cortex, activation of the mTOR pathway,
and increased synaptogenesis and brain-derived neurotrophic factor (BDNF) expression. MAOI mechanism (B), SSRI
mechanism (C), and GABA-A potentiation (D) all have slower onsets and do not explain esketamine's unique rapid action.
Q7: A patient taking tranylcypromine, a monoamine oxidase inhibitor (MAOI), presents with hypertensive crisis
after eating aged cheese. Which neurotransmitter, accumulated in presynaptic terminals due to MAO inhibition
and released in excess by dietary tyramine, is primarily responsible for this life-threatening reaction?
A. Norepinephrine [CORRECT]
B. Serotonin
C. Acetylcholine
D. GABA
Correct Answer: A
Rationale: MAOIs inhibit monoamine oxidase, the enzyme that degrades norepinephrine, serotonin, and dopamine in
presynaptic terminals. Tyramine, found in aged cheeses, cured meats, and fermented foods, is normally metabolized by MAO
in the gut and liver. When MAO is inhibited, tyramine reaches systemic circulation, displaces norepinephrine from
sympathetic nerve terminals, and produces a massive pressor response. Serotonin (B) is associated with serotonin syndrome,
not hypertensive crisis. Acetylcholine (C) and GABA (D) are not tyramine-sensitive.
Q8: A 72-year-old patient with moderate Alzheimer's disease is started on donepezil 5 mg nightly. The PMHNP
counsels the patient that this medication works by which mechanism, and which common adverse effect should be
anticipated?
A. Acetylcholinesterase inhibition; anticipate gastrointestinal upset and vivid dreams [CORRECT]
B. NMDA receptor antagonism; anticipate dizziness and constipation
C. Selective serotonin reuptake inhibition; anticipate sexual dysfunction
D. Dopamine receptor agonism; anticipate impulse control disorders
Correct Answer: A
Rationale: Donepezil is a reversible acetylcholinesterase inhibitor that increases acetylcholine availability at central
cholinergic synapses, modestly improving cognition in Alzheimer's disease. Peripheral cholinergic excess produces common
adverse effects including nausea, diarrhea, abdominal cramping, vivid dreams, and bradycardia. NMDA antagonism (B)
describes memantine. SSRIs (C) and dopamine agonists (D) are not indicated for Alzheimer's dementia.
Page 3
, NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
Q9: A PMHNP is teaching about receptor pharmacology. Which statement correctly describes the concept of
receptor downregulation in the context of chronic SSRI therapy for depression?
A. Chronic serotonin reuptake blockade leads to desensitization and downregulation of somatodendritic
5-HT1A autoreceptors, permitting enhanced serotonergic neurotransmission [CORRECT]
B. Chronic SSRI therapy upregulates postsynaptic 5-HT2C receptors, explaining early-onset anxiolysis
C. Receptor downregulation occurs within 24 to 48 hours and explains immediate mood improvement
D. Downregulation of D2 receptors is the primary mechanism of SSRI antidepressant action
Correct Answer: A
Rationale: With chronic SSRI exposure, somatodendritic 5-HT1A autoreceptors on raphe neurons desensitize and
downregulate over 2 to 4 weeks, removing the brake on serotonin firing and allowing enhanced terminal serotonin release.
This time-dependent neuroadaptation explains the delayed onset of antidepressant action. Postsynaptic 5-HT2C changes (B)
do not explain anxiolysis, and the timeline (C) is incorrect. D2 receptors (D) are not the SSRI target.
Q10: Lithium has a narrow therapeutic index requiring close monitoring. Which pharmacokinetic property of
lithium necessitates dose adjustment in patients with impaired renal function or dehydration?
A. Lithium is excreted almost entirely unchanged by the kidneys, with clearance directly proportional to
glomerular filtration rate [CORRECT]
B. Lithium is extensively metabolized by hepatic CYP3A4 and accumulates in hepatic insufficiency
C. Lithium is highly protein-bound, and hypoalbuminemia increases free drug levels
D. Lithium undergoes significant enterohepatic recirculation and is affected by bile acid binders
Correct Answer: A
Rationale: Lithium is not metabolized and is excreted almost exclusively unchanged by the kidneys, with clearance closely
tracking glomerular filtration rate. Dehydration, sodium depletion, NSAIDs, ACE inhibitors, and thiazide diuretics all reduce
lithium clearance and increase toxicity risk. Hepatic metabolism (B) is irrelevant for lithium. Lithium is not protein-bound
(C), and enterohepatic recirculation (D) is not clinically significant.
Q11: A patient asks why oral clonazepam produces a slower onset of anxiolysis than sublingual alprazolam, even
though both are benzodiazepines. Which pharmacokinetic concept best explains this difference?
A. Sublingual administration bypasses first-pass hepatic metabolism, producing more rapid and complete
systemic availability [CORRECT]
B. Alprazolam has higher affinity for GABA-A receptors than clonazepam
C. Clonazepam is a partial agonist while alprazolam is a full agonist
D. Clonazepam is a CYP3A4 inducer, accelerating its own metabolism
Correct Answer: A
Rationale: Sublingual alprazolam is absorbed directly into systemic circulation via oral mucosa, bypassing intestinal and
hepatic first-pass metabolism and producing rapid peak concentrations (within 15 to 30 minutes). Oral clonazepam
undergoes first-pass effect, slowing onset. Receptor affinity (B) does not determine onset route. Both are full agonists (C).
Clonazepam is not a CYP inducer (D).
Page 4
NR 546 Advanced Psychopharmacology
Final Examination - Two Latest Verified Versions (2026-2027)
Chamberlain University | Graduate PMHNP Program
200 Verified Questions | 100 Per Version | Advanced Practice Prescriptive Decision-Making
Coverage: Mood Disorders | Anxiety & Trauma | Psychotic Disorders | Neurodevelopmental Conditions | Special Populations |
Medication Safety
VERSION 1 - Questions 1 to 100
Section 1: Foundations of Psychopharmacology and Neurobiology
Q1: A 34-year-old patient is started on fluoxetine 20 mg daily for major depressive disorder. The PMHNP
understands that fluoxetine exerts its primary therapeutic effect by inhibiting reuptake at which synapse, and that
downstream clinical benefit over 2 to 4 weeks is most attributable to which neuroadaptive change?
A. Inhibiting serotonin reuptake; downregulation of postsynaptic 5-HT2A receptors [CORRECT]
B. Inhibiting dopamine reuptake; upregulation of D2 receptors in the mesolimbic pathway
C. Inhibiting norepinephrine reuptake; desensitization of presynaptic alpha-2 autoreceptors
D. Inhibiting GABA transaminase; increased GABA-B receptor expression
Correct Answer: A
Rationale: Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that blocks the serotonin transporter (SERT),
increasing synaptic serotonin in the raphe-cortical and raphe-limbic pathways. Acute reuptake blockade occurs within hours,
but therapeutic antidepressant effects require 2 to 4 weeks and are linked to desensitization of somatodendritic 5-HT1A
autoreceptors and downstream downregulation of postsynaptic 5-HT2A receptors. Option B describes stimulant mechanism,
option C describes SNRI/alpha-2 mechanisms, and option D describes GABAergic agents.
Q2: A graduate nursing student asks why second-generation antipsychotics differ in metabolic risk despite all
blocking dopamine D2 receptors. Which pharmacologic property best explains why clozapine and olanzapine carry
higher metabolic risk than aripiprazole or lurasidone?
A. Higher affinity for the histamine H1 receptor and 5-HT2C receptor, promoting appetite and weight gain
[CORRECT]
B. Stronger D2 antagonism in the nigrostriatal pathway, increasing extrapyramidal symptoms
C. Greater anticholinergic muscarinic M1 blockade, causing insulin dysregulation
D. Higher affinity for alpha-1 adrenergic receptors, producing orthostatic hypotension
Correct Answer: A
Rationale: Clozapine and olanzapine have high affinity for histamine H1 and serotonin 5-HT2C receptors, both of which
stimulate appetite and disrupt satiety signaling, leading to weight gain, insulin resistance, and dyslipidemia. Aripiprazole and
lurasidone have low H1 and 5-HT2C affinity, hence lower metabolic liability. D2 affinity (B) predicts EPS and prolactin risk,
not metabolic risk. Anticholinergic activity (C) causes constipation and cognitive blunting, while alpha-1 blockade (D)
causes orthostasis.
Page 1
,NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
Q3: A patient has been taking paroxetine 20 mg daily for 3 years and abruptly stops. Within 48 hours, the patient
reports dizziness, nausea, electric shock-like sensations, and insomnia. Which pharmacokinetic property of
paroxetine is the most important contributor to this presentation?
A. Short half-life and lack of active metabolites [CORRECT]
B. Strong inhibition of CYP2D6
C. High volume of distribution
D. Extensive renal elimination unchanged
Correct Answer: A
Rationale: Paroxetine has a short half-life of approximately 21 hours and no active metabolites, producing the most severe
discontinuation syndrome among SSRIs when stopped abruptly. Fluoxetine, in contrast, has a 1 to 4 day half-life with an
active metabolite (norfluoxetine) lasting 7 to 15 days, making discontinuation syndrome rare. CYP2D6 inhibition (B) affects
drug interactions, not withdrawal. Volume of distribution (C) and renal elimination (D) do not explain acute withdrawal
kinetics.
Q4: A PMHNP plans to initiate atomoxetine for adult ADHD in a patient already taking fluoxetine 20 mg daily.
What pharmacokinetic interaction must be anticipated, and what is the appropriate prescribing adjustment?
A. Fluoxetine inhibits CYP2D6, raising atomoxetine levels; initiate atomoxetine at a reduced dose and titrate
slowly [CORRECT]
B. Fluoxetine induces CYP3A4, lowering atomoxetine levels; increase atomoxetine dose by 50%
C. Fluoxetine displaces atomoxetine from plasma proteins, causing toxicity; space doses 12 hours apart
D. Fluoxetine inhibits P-glycoprotein at the blood-brain barrier; no dose adjustment needed
Correct Answer: A
Rationale: Atomoxetine is metabolized primarily by CYP2D6. Fluoxetine is a potent CYP2D6 inhibitor, which can raise
atomoxetine plasma concentrations 2- to 3-fold and increase adverse effects (dry mouth, insomnia, cardiovascular effects).
Dose reduction and slow titration are required. CYP3A4 induction (B) is incorrect as fluoxetine does not induce 3A4. Protein
displacement (C) is clinically negligible for atomoxetine, and P-glycoprotein (D) is not the relevant mechanism.
Q5: A 28-year-old with generalized anxiety disorder is prescribed buspirone 7.5 mg twice daily. The patient asks
when full anxiolytic effect will occur. The PMHNP correctly explains that buspirone's mechanism and onset are
best described by which statement?
A. Partial agonist at 5-HT1A receptors; full effect requires 2 to 4 weeks of continuous dosing [CORRECT]
B. Full agonist at GABA-A receptors; anxiolysis occurs within 30 minutes of administration
C. Antagonist at NMDA receptors; effect develops over 6 to 8 weeks
D. Reuptake inhibitor of norepinephrine; effect begins within 48 hours
Correct Answer: A
Rationale: Buspirone is a partial agonist at serotonin 5-HT1A autoreceptors and postsynaptic receptors, producing anxiolysis
through gradual serotonergic modulation rather than direct sedation. Onset requires 2 to 4 weeks of consistent dosing, similar
to SSRIs, making it unsuitable for acute anxiety. GABA-A agonism (B) describes benzodiazepines, NMDA antagonism (C)
describes ketamine, and norepinephrine reuptake inhibition (D) describes atomoxetine or reboxetine.
Page 2
,NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
Q6: A 45-year-old with treatment-resistant depression receives intranasal esketamine in conjunction with an oral
antidepressant. The PMHNP understands that the rapid antidepressant effect of esketamine within hours is
mediated primarily through which mechanism?
A. NMDA receptor antagonism enhancing glutamatergic signaling and synaptogenesis via mTOR pathway
activation [CORRECT]
B. Monoamine oxidase inhibition increasing synaptic serotonin, norepinephrine, and dopamine
C. Reversible inhibition of the serotonin transporter with downstream 5-HT1A receptor sensitization
D. Positive allosteric modulation of GABA-A receptors producing rapid sedation
Correct Answer: A
Rationale: Esketamine, the S-enantiomer of ketamine, is a noncompetitive NMDA receptor antagonist. Its rapid
antidepressant effect (within hours) is linked to glutamate surge in the prefrontal cortex, activation of the mTOR pathway,
and increased synaptogenesis and brain-derived neurotrophic factor (BDNF) expression. MAOI mechanism (B), SSRI
mechanism (C), and GABA-A potentiation (D) all have slower onsets and do not explain esketamine's unique rapid action.
Q7: A patient taking tranylcypromine, a monoamine oxidase inhibitor (MAOI), presents with hypertensive crisis
after eating aged cheese. Which neurotransmitter, accumulated in presynaptic terminals due to MAO inhibition
and released in excess by dietary tyramine, is primarily responsible for this life-threatening reaction?
A. Norepinephrine [CORRECT]
B. Serotonin
C. Acetylcholine
D. GABA
Correct Answer: A
Rationale: MAOIs inhibit monoamine oxidase, the enzyme that degrades norepinephrine, serotonin, and dopamine in
presynaptic terminals. Tyramine, found in aged cheeses, cured meats, and fermented foods, is normally metabolized by MAO
in the gut and liver. When MAO is inhibited, tyramine reaches systemic circulation, displaces norepinephrine from
sympathetic nerve terminals, and produces a massive pressor response. Serotonin (B) is associated with serotonin syndrome,
not hypertensive crisis. Acetylcholine (C) and GABA (D) are not tyramine-sensitive.
Q8: A 72-year-old patient with moderate Alzheimer's disease is started on donepezil 5 mg nightly. The PMHNP
counsels the patient that this medication works by which mechanism, and which common adverse effect should be
anticipated?
A. Acetylcholinesterase inhibition; anticipate gastrointestinal upset and vivid dreams [CORRECT]
B. NMDA receptor antagonism; anticipate dizziness and constipation
C. Selective serotonin reuptake inhibition; anticipate sexual dysfunction
D. Dopamine receptor agonism; anticipate impulse control disorders
Correct Answer: A
Rationale: Donepezil is a reversible acetylcholinesterase inhibitor that increases acetylcholine availability at central
cholinergic synapses, modestly improving cognition in Alzheimer's disease. Peripheral cholinergic excess produces common
adverse effects including nausea, diarrhea, abdominal cramping, vivid dreams, and bradycardia. NMDA antagonism (B)
describes memantine. SSRIs (C) and dopamine agonists (D) are not indicated for Alzheimer's dementia.
Page 3
, NR 546 Advanced Psychopharmacology - Final Examination Chamberlain University | PMHNP
Q9: A PMHNP is teaching about receptor pharmacology. Which statement correctly describes the concept of
receptor downregulation in the context of chronic SSRI therapy for depression?
A. Chronic serotonin reuptake blockade leads to desensitization and downregulation of somatodendritic
5-HT1A autoreceptors, permitting enhanced serotonergic neurotransmission [CORRECT]
B. Chronic SSRI therapy upregulates postsynaptic 5-HT2C receptors, explaining early-onset anxiolysis
C. Receptor downregulation occurs within 24 to 48 hours and explains immediate mood improvement
D. Downregulation of D2 receptors is the primary mechanism of SSRI antidepressant action
Correct Answer: A
Rationale: With chronic SSRI exposure, somatodendritic 5-HT1A autoreceptors on raphe neurons desensitize and
downregulate over 2 to 4 weeks, removing the brake on serotonin firing and allowing enhanced terminal serotonin release.
This time-dependent neuroadaptation explains the delayed onset of antidepressant action. Postsynaptic 5-HT2C changes (B)
do not explain anxiolysis, and the timeline (C) is incorrect. D2 receptors (D) are not the SSRI target.
Q10: Lithium has a narrow therapeutic index requiring close monitoring. Which pharmacokinetic property of
lithium necessitates dose adjustment in patients with impaired renal function or dehydration?
A. Lithium is excreted almost entirely unchanged by the kidneys, with clearance directly proportional to
glomerular filtration rate [CORRECT]
B. Lithium is extensively metabolized by hepatic CYP3A4 and accumulates in hepatic insufficiency
C. Lithium is highly protein-bound, and hypoalbuminemia increases free drug levels
D. Lithium undergoes significant enterohepatic recirculation and is affected by bile acid binders
Correct Answer: A
Rationale: Lithium is not metabolized and is excreted almost exclusively unchanged by the kidneys, with clearance closely
tracking glomerular filtration rate. Dehydration, sodium depletion, NSAIDs, ACE inhibitors, and thiazide diuretics all reduce
lithium clearance and increase toxicity risk. Hepatic metabolism (B) is irrelevant for lithium. Lithium is not protein-bound
(C), and enterohepatic recirculation (D) is not clinically significant.
Q11: A patient asks why oral clonazepam produces a slower onset of anxiolysis than sublingual alprazolam, even
though both are benzodiazepines. Which pharmacokinetic concept best explains this difference?
A. Sublingual administration bypasses first-pass hepatic metabolism, producing more rapid and complete
systemic availability [CORRECT]
B. Alprazolam has higher affinity for GABA-A receptors than clonazepam
C. Clonazepam is a partial agonist while alprazolam is a full agonist
D. Clonazepam is a CYP3A4 inducer, accelerating its own metabolism
Correct Answer: A
Rationale: Sublingual alprazolam is absorbed directly into systemic circulation via oral mucosa, bypassing intestinal and
hepatic first-pass metabolism and producing rapid peak concentrations (within 15 to 30 minutes). Oral clonazepam
undergoes first-pass effect, slowing onset. Receptor affinity (B) does not determine onset route. Both are full agonists (C).
Clonazepam is not a CYP inducer (D).
Page 4
