,NR 546 / NR546 Midterm Exam (Latest ) – 2 Exam
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PMHNP
1. A patient with schizophrenia shows poor response to typical
antipsychotics. Which receptor profile is most associated with
treatment-resistant symptoms?
• A) High D2 occupancy only
• B) Low 5-HT2A and high D2
• C) High D2 and low 5-HT2A
• D) Low D2 and high 5-HT1A
• Answer: A – High D2 occupancy alone fails to address
negative/cognitive symptoms; treatment resistance often
involves glutamate/NMDA dysfunction.
Question 2
2. Which brain region's hypofunction is most linked to
negative symptoms of schizophrenia?
• A) Nucleus accumbens
• B) Prefrontal cortex
• C) VTA
• D) Hypothalamus
, • Answer: B – Hypofrontality correlates with negative
symptoms (avolition, anhedonia).
Question 3
3. A patient develops EPS after haloperidol. Which pathway is
primarily affected?
• A) Mesolimbic
• B) Mesocortical
• C) Nigrostriatal
• D) Tuberoinfundibular
• Answer: C – Nigrostriatal D2 blockade causes EPS.
Question 4
4. Scenario: A 45-year-old male on risperidone reports
galactorrhea. Which receptor action explains this?
• A) 5-HT2A antagonism
• B) D2 blockade in tuberoinfundibular pathway
• C) H1 blockade
• D) M1 antagonism
• Answer: B – D2 blockade in tuberoinfundibular pathway
leads to increased prolactin.
Question 5
, 5. Which neurotransmitter is primarily degraded by MAO-B?
• A) Norepinephrine
• B) Serotonin
• C) Dopamine
• D) Acetylcholine
• Answer: C – MAO-B prefers dopamine.
6. The therapeutic lag of SSRIs is best explained by:
• A) Rapid receptor desensitization
• B) Downregulation and desensitization of somatodendritic
5-HT1A autoreceptors leading to increased net neuronal
firing and sustained neurotransmitter release
• C) Immediate depletion of synaptic vesicle monoamines
• D) Permanent blockade of acetylcholinesterase enzymes
• Answer: B
• Rationale: The delay in therapeutic response (therapeutic
lag) of SSRIs is attributed to the time required for chronic
increases in synaptic serotonin to desensitize inhibitory
somatodendritic 5-HT1A autoreceptors, which ultimately
disinhibits serotonergic neurons and increases serotonin
neurotransmission.
Question 7
Versions (A & B) with Questions & Verified Answers | 100%
Guaranteed Pass | Complete A+ Guide for Chamberlain
PMHNP
1. A patient with schizophrenia shows poor response to typical
antipsychotics. Which receptor profile is most associated with
treatment-resistant symptoms?
• A) High D2 occupancy only
• B) Low 5-HT2A and high D2
• C) High D2 and low 5-HT2A
• D) Low D2 and high 5-HT1A
• Answer: A – High D2 occupancy alone fails to address
negative/cognitive symptoms; treatment resistance often
involves glutamate/NMDA dysfunction.
Question 2
2. Which brain region's hypofunction is most linked to
negative symptoms of schizophrenia?
• A) Nucleus accumbens
• B) Prefrontal cortex
• C) VTA
• D) Hypothalamus
, • Answer: B – Hypofrontality correlates with negative
symptoms (avolition, anhedonia).
Question 3
3. A patient develops EPS after haloperidol. Which pathway is
primarily affected?
• A) Mesolimbic
• B) Mesocortical
• C) Nigrostriatal
• D) Tuberoinfundibular
• Answer: C – Nigrostriatal D2 blockade causes EPS.
Question 4
4. Scenario: A 45-year-old male on risperidone reports
galactorrhea. Which receptor action explains this?
• A) 5-HT2A antagonism
• B) D2 blockade in tuberoinfundibular pathway
• C) H1 blockade
• D) M1 antagonism
• Answer: B – D2 blockade in tuberoinfundibular pathway
leads to increased prolactin.
Question 5
, 5. Which neurotransmitter is primarily degraded by MAO-B?
• A) Norepinephrine
• B) Serotonin
• C) Dopamine
• D) Acetylcholine
• Answer: C – MAO-B prefers dopamine.
6. The therapeutic lag of SSRIs is best explained by:
• A) Rapid receptor desensitization
• B) Downregulation and desensitization of somatodendritic
5-HT1A autoreceptors leading to increased net neuronal
firing and sustained neurotransmitter release
• C) Immediate depletion of synaptic vesicle monoamines
• D) Permanent blockade of acetylcholinesterase enzymes
• Answer: B
• Rationale: The delay in therapeutic response (therapeutic
lag) of SSRIs is attributed to the time required for chronic
increases in synaptic serotonin to desensitize inhibitory
somatodendritic 5-HT1A autoreceptors, which ultimately
disinhibits serotonergic neurons and increases serotonin
neurotransmission.
Question 7
