NR 546 Exam 1 V3 | NR 546 Advanced
Psychopharmacology | Chamberlain | Q&A
with Rationale (Chamberlain NR546 Exam
1)
1. A patient is prescribed a medication that is a known substrate of the CYP2D6 enzyme. If the
patient is also taking a potent CYP2D6 inhibitor like Paroxetine, what is the most likely clinical
outcome?
A. Decreased plasma levels of the substrate drug
B. Reduced effectiveness of the substrate drug
C. Increased rate of drug clearance from the body
D. Increased risk of toxicity due to elevated substrate levels
Answer: D
Rationale: When a CYP450 inhibitor is introduced, it blocks the metabolic pathway of the
substrate drug. This leads to an accumulation of the drug in the systemic circulation,
significantly increasing the risk of adverse effects or toxicity. The provider must either
reduce the dose of the substrate or choose an alternative medication to avoid this
interaction.
2. Which dopamine pathway is primarily responsible for the development of positive
symptoms in schizophrenia, such as hallucinations and delusions?
A. Mesolimbic pathway
,B. Mesocortical pathway
C. Nigrostriatal pathway
D. Tuberoinfundibular pathway
Answer: A
Rationale: The mesolimbic pathway projects from the ventral tegmental area to the
nucleus accumbens and is associated with reward and motivation. Overactivity or
hyperdopaminergic states in this specific pathway are linked to the ‘positive’ symptoms of
schizophrenia. Antipsychotic medications target this pathway by blocking D2 receptors to
reduce these symptoms.
3. A patient taking a Second-Generation Antipsychotic (SGA) exhibits significant weight gain
and increased fasting glucose. Which receptor is most likely implicated in these metabolic
side effects?
A. 5-HT2C and H1 receptors
B. D2 and Alpha-1 receptors
C. M1 and 5-HT1A receptors
D. D4 and NMDA receptors
Answer: A
Rationale: Blockade of the Histamine-1 (H1) and Serotonin 2C (5-HT2C) receptors is
strongly associated with increased appetite and weight gain. These metabolic changes can
,further lead to insulin resistance and type 2 diabetes. Monitoring weight, waist
circumference, and blood glucose is essential when managing patients on SGAs.
4. What is the primary mechanism of action of Fluoxetine in the treatment of Major
Depressive Disorder?
A. Inhibition of the Serotonin Transporter (SERT)
B. Antagonism of the 5-HT2A receptor
C. Blockade of the Norepinephrine Transporter (NET)
D. Inhibition of Monoamine Oxidase-A
Answer: A
Rationale: Fluoxetine is a Selective Serotonin Reuptake Inhibitor (SSRI) that works by
inhibiting the SERT protein. By blocking the reuptake of serotonin into the presynaptic
neuron, it increases the concentration of serotonin in the synaptic cleft. This prolonged
presence of serotonin allows for greater stimulation of postsynaptic receptors, which helps
alleviate depressive symptoms.
5. Which neurotransmitter is considered the brain’s primary inhibitory neurotransmitter and
is the target of benzodiazepines?
A. Glutamate
B. Gamma-Aminobutyric Acid (GABA)
C. Dopamine
, D. Acetylcholine
Answer: B
Rationale: GABA serves as the major inhibitory signal in the central nervous system,
balancing excitatory signals. Benzodiazepines act as positive allosteric modulators at the
GABA-A receptor, enhancing the effects of endogenous GABA. This leads to increased
chloride ion influx, hyperpolarization of the neuron, and an overall calming or anxiolytic
effect.
6. A patient starting Lamotrigine should be educated on the risk of a severe, life-threatening
rash known as:
A. Stevens-Johnson Syndrome (SJS)
B. Serotonin Syndrome
C. Akathisia
D. Tardive Dyskinesia
Answer: A
Rationale: Stevens-Johnson Syndrome is a rare but severe cutaneous reaction associated
with Lamotrigine therapy, particularly during the initiation phase. To minimize this risk,
providers must follow a very slow titration schedule to allow the body to adjust. Patients
must be instructed to discontinue the medication and seek immediate medical attention if
any skin rash or mucosal lesions appear.
Psychopharmacology | Chamberlain | Q&A
with Rationale (Chamberlain NR546 Exam
1)
1. A patient is prescribed a medication that is a known substrate of the CYP2D6 enzyme. If the
patient is also taking a potent CYP2D6 inhibitor like Paroxetine, what is the most likely clinical
outcome?
A. Decreased plasma levels of the substrate drug
B. Reduced effectiveness of the substrate drug
C. Increased rate of drug clearance from the body
D. Increased risk of toxicity due to elevated substrate levels
Answer: D
Rationale: When a CYP450 inhibitor is introduced, it blocks the metabolic pathway of the
substrate drug. This leads to an accumulation of the drug in the systemic circulation,
significantly increasing the risk of adverse effects or toxicity. The provider must either
reduce the dose of the substrate or choose an alternative medication to avoid this
interaction.
2. Which dopamine pathway is primarily responsible for the development of positive
symptoms in schizophrenia, such as hallucinations and delusions?
A. Mesolimbic pathway
,B. Mesocortical pathway
C. Nigrostriatal pathway
D. Tuberoinfundibular pathway
Answer: A
Rationale: The mesolimbic pathway projects from the ventral tegmental area to the
nucleus accumbens and is associated with reward and motivation. Overactivity or
hyperdopaminergic states in this specific pathway are linked to the ‘positive’ symptoms of
schizophrenia. Antipsychotic medications target this pathway by blocking D2 receptors to
reduce these symptoms.
3. A patient taking a Second-Generation Antipsychotic (SGA) exhibits significant weight gain
and increased fasting glucose. Which receptor is most likely implicated in these metabolic
side effects?
A. 5-HT2C and H1 receptors
B. D2 and Alpha-1 receptors
C. M1 and 5-HT1A receptors
D. D4 and NMDA receptors
Answer: A
Rationale: Blockade of the Histamine-1 (H1) and Serotonin 2C (5-HT2C) receptors is
strongly associated with increased appetite and weight gain. These metabolic changes can
,further lead to insulin resistance and type 2 diabetes. Monitoring weight, waist
circumference, and blood glucose is essential when managing patients on SGAs.
4. What is the primary mechanism of action of Fluoxetine in the treatment of Major
Depressive Disorder?
A. Inhibition of the Serotonin Transporter (SERT)
B. Antagonism of the 5-HT2A receptor
C. Blockade of the Norepinephrine Transporter (NET)
D. Inhibition of Monoamine Oxidase-A
Answer: A
Rationale: Fluoxetine is a Selective Serotonin Reuptake Inhibitor (SSRI) that works by
inhibiting the SERT protein. By blocking the reuptake of serotonin into the presynaptic
neuron, it increases the concentration of serotonin in the synaptic cleft. This prolonged
presence of serotonin allows for greater stimulation of postsynaptic receptors, which helps
alleviate depressive symptoms.
5. Which neurotransmitter is considered the brain’s primary inhibitory neurotransmitter and
is the target of benzodiazepines?
A. Glutamate
B. Gamma-Aminobutyric Acid (GABA)
C. Dopamine
, D. Acetylcholine
Answer: B
Rationale: GABA serves as the major inhibitory signal in the central nervous system,
balancing excitatory signals. Benzodiazepines act as positive allosteric modulators at the
GABA-A receptor, enhancing the effects of endogenous GABA. This leads to increased
chloride ion influx, hyperpolarization of the neuron, and an overall calming or anxiolytic
effect.
6. A patient starting Lamotrigine should be educated on the risk of a severe, life-threatening
rash known as:
A. Stevens-Johnson Syndrome (SJS)
B. Serotonin Syndrome
C. Akathisia
D. Tardive Dyskinesia
Answer: A
Rationale: Stevens-Johnson Syndrome is a rare but severe cutaneous reaction associated
with Lamotrigine therapy, particularly during the initiation phase. To minimize this risk,
providers must follow a very slow titration schedule to allow the body to adjust. Patients
must be instructed to discontinue the medication and seek immediate medical attention if
any skin rash or mucosal lesions appear.
