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NR 546 Exam 1 V2 | NR 546 Advanced Psychopharmacology | Chamberlain | Q&A with Rationale (Chamberlain NR546 Exam 1)

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NR 546 Exam 1 V2 | NR 546 Advanced Psychopharmacology | Chamberlain | Q&A with Rationale (Chamberlain NR546 Exam 1)

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NR 546 Exam 1 V2 | NR 546 Advanced
Psychopharmacology | Chamberlain | Q&A
with Rationale (Chamberlain NR546 Exam
1)
1. A patient is prescribed a medication that acts as a full agonist at the D2 receptor. How does

a full agonist affect the signal transduction compared to the natural neurotransmitter?

A. It blocks the receptor, preventing any signal transduction.


B. It produces a submaximal response compared to the natural neurotransmitter.


C. It mimics the natural neurotransmitter and elicits a maximum biological response.


D. It induces the opposite biological effect of the natural neurotransmitter.


Answer: C


Rationale: A full agonist binds to a receptor and mimics the action of the endogenous

neurotransmitter to produce the maximum possible response. This is distinct from partial

agonists, which only provide a moderate response regardless of concentration.

Understanding these mechanisms is crucial for PMHNPs when determining the efficacy of

various psychotropic drugs.


2. The PMHNP is considering prescribing a drug that is a substrate of CYP2D6. The patient is

also taking fluoxetine. What is the primary concern regarding this drug combination?

A. Fluoxetine is a potent inhibitor of CYP2D6, leading to increased drug levels and potential

toxicity.

,B. Fluoxetine is an inducer of CYP2D6, leading to decreased drug levels.


C. The combination will cause immediate renal failure due to competitive binding.


D. There is no significant interaction between fluoxetine and CYP2D6 substrates.


Answer: A


Rationale: Fluoxetine and paroxetine are well-known potent inhibitors of the CYP2D6

enzyme system. When an inhibitor is present, it prevents the metabolism of other drugs

that are substrates of that enzyme, causing their plasma concentrations to rise. This

increases the risk of side effects and toxicity, requiring the provider to adjust dosages

accordingly.


3. Which neurotransmitter is considered the primary inhibitory neurotransmitter in the

central nervous system?

A. Glutamate


B. Dopamine


C. Norepinephrine


D. Gamma-aminobutyric acid (GABA)


Answer: D


Rationale: GABA is the major inhibitory neurotransmitter in the brain, functioning to

reduce neuronal excitability. It works in opposition to glutamate, which is the primary

, excitatory neurotransmitter. Many anxiolytics and sedatives work by enhancing GABAergic

activity to produce a calming effect.


4. When assessing a patient for symptoms of schizophrenia, the PMHNP understands that

positive symptoms like hallucinations are primarily associated with overactivity in which

dopamine pathway?

A. Nigrostriatal pathway


B. Tuberoinfundibular pathway


C. Mesocortical pathway


D. Mesolimbic pathway


Answer: D


Rationale: The mesolimbic pathway projects from the ventral tegmental area to the

nucleus accumbens and is involved in reward and emotion. Excessive dopamine in this

pathway is thought to be responsible for the positive symptoms of schizophrenia, such as

delusions and hallucinations. Conversely, negative symptoms are often linked to dopamine

deficits in the mesocortical pathway.


5. A patient experiences significant weight gain and sedation after starting an atypical

antipsychotic. Blockade of which receptor is most likely responsible for these side effects?

A. Histamine H1 receptors


B. Alpha-1 adrenergic receptors


C. D2 receptors

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