Western Governors University
MRAHP · 543D
W
College of Health Professions
EST. 1997
A NEW KIND OF U
WGU D345 Master Set — Psychopharmacology
P H A R M ACO DY N A M I CS , P H A R M ACO K I N E T I CS , A N T I D E P R E SS A N TS & A N T I PSYC H OT I CS
INSTITUTION Western Governors University COURSE CODE D345
PROGRAM Psychiatric Mental Health Nurse ACADEMIC YEAR
Practitioner
EXAM TITLE WGU D345 Master Set — TOTAL QUESTIONS 85 Questions
Psychopharmacology
COURSE TITLE Advanced Psychopharmacology for the FORMAT Multiple Choice — Select the Single Best
PMHNP Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Pharmacodynamics, pharmacokinetics (ADME), receptor theory, neurotransmitter systems, dopamine pathways, and
psychotropic drug classes are all testable content.
▸ SSRIs, SNRIs, bupropion, mirtazapine, trazodone, TCAs, MAOIs, FGAs, and SGAs are emphasized with mechanisms, side
effects, and clinical pearls.
▸ Correct answers and detailed rationales incorporating Stahl and Carlat pearls appear below each question.
▸ All content reflects current PMHNP board examination standards.
, SECTION I — D345 PSYCHOPHARMACOLOGY: FOUNDATIONS
Questions 1 – 85
THROUGH ANTIPSYCHOTICS
1. What is pharmacodynamics?
A. The study of what the body does to drugs through absorption, distribution, metabolism, and excretion
B. The study of what drugs do to the body, including receptor interactions and mechanisms of action
C. The study of genetic influences on medication response
D. The study of how drugs are formulated and manufactured
CORRECT ANSWER B — The study of what drugs do to the body, including receptor interactions and
mechanisms of action
RATIONALE Pharmacodynamics (PD) explains therapeutic and adverse effects by describing how drugs
interact with receptors, ion channels, enzymes, and other molecular targets. The D345
mnemonic is "Drug → Body." Stahl emphasizes that most psychotropics alter neurotransmitter
signaling. Carlat notes that understanding mechanisms helps clinicians anticipate side effects.
Pharmacodynamics answers "What does the drug do?" — agonists activate receptors,
antagonists block them, partial agonists produce submaximal activation. This is distinct from
pharmacokinetics (Choice A — "Body → Drug"), pharmacogenomics (Choice C), and
pharmaceutics (Choice D).
2. What is an agonist?
A. A drug that binds to a receptor and blocks activation
B. A drug that binds to and activates a receptor, mimicking endogenous neurotransmitters
C. A drug that produces a smaller effect than a full agonist
D. A drug that reduces receptor activity below baseline
CORRECT ANSWER B — A drug that binds to and activates a receptor, mimicking endogenous
neurotransmitters
RATIONALE An agonist binds to a receptor and activates it — Stahl describes this as turning receptors "on."
Agonists mimic endogenous neurotransmitters and produce predictable physiologic effects.
Examples: morphine (mu-opioid agonist), albuterol (beta-2 agonist). Antagonists (Choice A)
block receptors. Partial agonists (Choice C) activate but produce submaximal effects — Carlat
notes aripiprazole is the classic example, acting as a "dimmer switch." Inverse agonists (Choice
D) reduce activity below baseline. The agonist-antagonist spectrum is fundamental
pharmacology — it predicts both therapeutic and adverse effects across all drug classes.
,3. What is pharmacokinetics?
A. The study of what drugs do to the body
B. The study of what the body does to drugs through absorption, distribution, metabolism, and excretion
C. The study of drug-receptor interactions
D. The study of genetic variations in drug response
CORRECT ANSWER B — The study of what the body does to drugs through absorption, distribution,
metabolism, and excretion
RATIONALE Pharmacokinetics (PK) describes the body's handling of drugs — ADME (Absorption,
Distribution, Metabolism, Excretion). The D345 mnemonic is "Body → Drug." Stahl emphasizes
thinking in ADME terms. Carlat notes that pharmacokinetics explains why dosing schedules
differ between medications. PK determines drug levels, onset, duration, and clearance. Key
concepts include half-life (time for 50% reduction), steady state (achieved after 4–5 half-lives),
bioavailability, first-pass metabolism, volume of distribution, and protein binding.
Pharmacodynamics (Choice A) is "Drug → Body." Receptor interactions (Choice C) are PD.
Genetic variations (Choice D) are pharmacogenomics.
4. Which CYP enzyme is inhibited by fluoxetine and paroxetine?
A. CYP3A4
B. CYP2D6
C. CYP1A2
D. CYP2C19
CORRECT ANSWER B — CYP2D6
RATIONALE CYP2D6 is strongly inhibited by fluoxetine and paroxetine — this is a major source of
psychotropic drug-drug interactions. When these SSRIs are co-prescribed with CYP2D6
substrates (many antipsychotics, TCAs, beta-blockers), substrate levels can rise significantly,
causing toxicity. CYP3A4 (Choice A) metabolizes many psychiatric medications but is not
primarily inhibited by fluoxetine/paroxetine. CYP1A2 (Choice C) metabolizes clozapine and
olanzapine and is induced by smoking. CYP2C19 (Choice D) metabolizes citalopram and
escitalopram. Carlat emphasizes watching for CYP2D6 interactions, and Stahl notes that
escitalopram has the fewest CYP interactions, making it preferred in medically complex patients.
, 5. Which SSRI has the longest half-life?
A. Paroxetine
B. Sertraline
C. Fluoxetine
D. Citalopram
CORRECT ANSWER C — Fluoxetine
RATIONALE Fluoxetine has the longest half-life among SSRIs due to its active metabolite norfluoxetine,
which prolongs pharmacological activity. D345 Tip: Think "self-tapering." Carlat notes fluoxetine
has the lowest discontinuation risk because the long half-life provides a natural taper. In
contrast, paroxetine (Choice A) has the shortest half-life and is associated with significant
discontinuation symptoms — avoid abrupt cessation. Sertraline (Choice B) and citalopram
(Choice D) have intermediate half-lives. The FINISH mnemonic describes discontinuation
symptoms: Flu-like symptoms, Insomnia, Nausea, Imbalance, Sensory disturbances,
Hyperarousal. Fluoxetine's long half-life is a clinical advantage when adherence is uncertain.
6. What is an antagonist?
A. A drug that binds to and activates a receptor
B. A drug that binds to a receptor and blocks activation
C. A drug that produces a submaximal response
D. A drug that increases receptor activity above baseline
CORRECT ANSWER B — A drug that binds to a receptor and blocks activation
RATIONALE An antagonist occupies receptors without activating them — it prevents endogenous
neurotransmitters or agonist drugs from binding and producing effects. Stahl describes
antagonists as "occupying receptors without turning them on." Carlat notes many
antipsychotics work this way (D2 antagonism). Examples: naloxone (opioid antagonist),
propranolol (beta-blocker), haloperidol (D2 antagonist). Agonists (Choice A) activate receptors.
Partial agonists (Choice C) produce submaximal activation — aripiprazole is the classic example,
acting as a "dimmer switch." Understanding antagonist mechanisms explains how drugs can
reduce symptoms by blocking overactive neurotransmitter systems.
MRAHP · 543D
W
College of Health Professions
EST. 1997
A NEW KIND OF U
WGU D345 Master Set — Psychopharmacology
P H A R M ACO DY N A M I CS , P H A R M ACO K I N E T I CS , A N T I D E P R E SS A N TS & A N T I PSYC H OT I CS
INSTITUTION Western Governors University COURSE CODE D345
PROGRAM Psychiatric Mental Health Nurse ACADEMIC YEAR
Practitioner
EXAM TITLE WGU D345 Master Set — TOTAL QUESTIONS 85 Questions
Psychopharmacology
COURSE TITLE Advanced Psychopharmacology for the FORMAT Multiple Choice — Select the Single Best
PMHNP Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Pharmacodynamics, pharmacokinetics (ADME), receptor theory, neurotransmitter systems, dopamine pathways, and
psychotropic drug classes are all testable content.
▸ SSRIs, SNRIs, bupropion, mirtazapine, trazodone, TCAs, MAOIs, FGAs, and SGAs are emphasized with mechanisms, side
effects, and clinical pearls.
▸ Correct answers and detailed rationales incorporating Stahl and Carlat pearls appear below each question.
▸ All content reflects current PMHNP board examination standards.
, SECTION I — D345 PSYCHOPHARMACOLOGY: FOUNDATIONS
Questions 1 – 85
THROUGH ANTIPSYCHOTICS
1. What is pharmacodynamics?
A. The study of what the body does to drugs through absorption, distribution, metabolism, and excretion
B. The study of what drugs do to the body, including receptor interactions and mechanisms of action
C. The study of genetic influences on medication response
D. The study of how drugs are formulated and manufactured
CORRECT ANSWER B — The study of what drugs do to the body, including receptor interactions and
mechanisms of action
RATIONALE Pharmacodynamics (PD) explains therapeutic and adverse effects by describing how drugs
interact with receptors, ion channels, enzymes, and other molecular targets. The D345
mnemonic is "Drug → Body." Stahl emphasizes that most psychotropics alter neurotransmitter
signaling. Carlat notes that understanding mechanisms helps clinicians anticipate side effects.
Pharmacodynamics answers "What does the drug do?" — agonists activate receptors,
antagonists block them, partial agonists produce submaximal activation. This is distinct from
pharmacokinetics (Choice A — "Body → Drug"), pharmacogenomics (Choice C), and
pharmaceutics (Choice D).
2. What is an agonist?
A. A drug that binds to a receptor and blocks activation
B. A drug that binds to and activates a receptor, mimicking endogenous neurotransmitters
C. A drug that produces a smaller effect than a full agonist
D. A drug that reduces receptor activity below baseline
CORRECT ANSWER B — A drug that binds to and activates a receptor, mimicking endogenous
neurotransmitters
RATIONALE An agonist binds to a receptor and activates it — Stahl describes this as turning receptors "on."
Agonists mimic endogenous neurotransmitters and produce predictable physiologic effects.
Examples: morphine (mu-opioid agonist), albuterol (beta-2 agonist). Antagonists (Choice A)
block receptors. Partial agonists (Choice C) activate but produce submaximal effects — Carlat
notes aripiprazole is the classic example, acting as a "dimmer switch." Inverse agonists (Choice
D) reduce activity below baseline. The agonist-antagonist spectrum is fundamental
pharmacology — it predicts both therapeutic and adverse effects across all drug classes.
,3. What is pharmacokinetics?
A. The study of what drugs do to the body
B. The study of what the body does to drugs through absorption, distribution, metabolism, and excretion
C. The study of drug-receptor interactions
D. The study of genetic variations in drug response
CORRECT ANSWER B — The study of what the body does to drugs through absorption, distribution,
metabolism, and excretion
RATIONALE Pharmacokinetics (PK) describes the body's handling of drugs — ADME (Absorption,
Distribution, Metabolism, Excretion). The D345 mnemonic is "Body → Drug." Stahl emphasizes
thinking in ADME terms. Carlat notes that pharmacokinetics explains why dosing schedules
differ between medications. PK determines drug levels, onset, duration, and clearance. Key
concepts include half-life (time for 50% reduction), steady state (achieved after 4–5 half-lives),
bioavailability, first-pass metabolism, volume of distribution, and protein binding.
Pharmacodynamics (Choice A) is "Drug → Body." Receptor interactions (Choice C) are PD.
Genetic variations (Choice D) are pharmacogenomics.
4. Which CYP enzyme is inhibited by fluoxetine and paroxetine?
A. CYP3A4
B. CYP2D6
C. CYP1A2
D. CYP2C19
CORRECT ANSWER B — CYP2D6
RATIONALE CYP2D6 is strongly inhibited by fluoxetine and paroxetine — this is a major source of
psychotropic drug-drug interactions. When these SSRIs are co-prescribed with CYP2D6
substrates (many antipsychotics, TCAs, beta-blockers), substrate levels can rise significantly,
causing toxicity. CYP3A4 (Choice A) metabolizes many psychiatric medications but is not
primarily inhibited by fluoxetine/paroxetine. CYP1A2 (Choice C) metabolizes clozapine and
olanzapine and is induced by smoking. CYP2C19 (Choice D) metabolizes citalopram and
escitalopram. Carlat emphasizes watching for CYP2D6 interactions, and Stahl notes that
escitalopram has the fewest CYP interactions, making it preferred in medically complex patients.
, 5. Which SSRI has the longest half-life?
A. Paroxetine
B. Sertraline
C. Fluoxetine
D. Citalopram
CORRECT ANSWER C — Fluoxetine
RATIONALE Fluoxetine has the longest half-life among SSRIs due to its active metabolite norfluoxetine,
which prolongs pharmacological activity. D345 Tip: Think "self-tapering." Carlat notes fluoxetine
has the lowest discontinuation risk because the long half-life provides a natural taper. In
contrast, paroxetine (Choice A) has the shortest half-life and is associated with significant
discontinuation symptoms — avoid abrupt cessation. Sertraline (Choice B) and citalopram
(Choice D) have intermediate half-lives. The FINISH mnemonic describes discontinuation
symptoms: Flu-like symptoms, Insomnia, Nausea, Imbalance, Sensory disturbances,
Hyperarousal. Fluoxetine's long half-life is a clinical advantage when adherence is uncertain.
6. What is an antagonist?
A. A drug that binds to and activates a receptor
B. A drug that binds to a receptor and blocks activation
C. A drug that produces a submaximal response
D. A drug that increases receptor activity above baseline
CORRECT ANSWER B — A drug that binds to a receptor and blocks activation
RATIONALE An antagonist occupies receptors without activating them — it prevents endogenous
neurotransmitters or agonist drugs from binding and producing effects. Stahl describes
antagonists as "occupying receptors without turning them on." Carlat notes many
antipsychotics work this way (D2 antagonism). Examples: naloxone (opioid antagonist),
propranolol (beta-blocker), haloperidol (D2 antagonist). Agonists (Choice A) activate receptors.
Partial agonists (Choice C) produce submaximal activation — aripiprazole is the classic example,
acting as a "dimmer switch." Understanding antagonist mechanisms explains how drugs can
reduce symptoms by blocking overactive neurotransmitter systems.
