NURS 660/NURS660 EXAM 1 (LATEST
2026/2027): PSYCHOPHARMACOLOGY AND
ADVANCED MENTAL HEALTH | QUESTIONS
AND VERIFIED ANSWERS | GRADE A -
MARYVILLE
NURS 660/NURS660
PSYCHOPHARMACOLOGY AND ADVANCED
MENTAL HEALTH
NURS 660/NURS 660 Exam 1, AT MARYVILLE
Psychopharmacology & Advanced Mental Health
Latest 2026/2027 | Grade A Standard | Verified Answers
1. How does aripiprazole work?
Answer:
Aripiprazole acts primarily as a partial agonist at dopamine D2 receptors, allowing it to
stabilize dopamine activity rather than fully blocking it. When dopamine levels are
high, it reduces dopamine signaling, improving positive symptoms such as
hallucinations and delusions. When dopamine levels are low, it increases dopaminergic
activity, which helps improve negative symptoms, cognition, and mood. Additionally, it
has activity at dopamine D3 receptors and antagonizes serotonin 5-HT2A receptors,
which enhances dopamine release in certain brain regions.
2. How long does it take aripiprazole to work?
Answer:
Aripiprazole may begin producing noticeable symptom improvement within one week,
particularly for agitation or psychotic symptoms. However, full therapeutic efficacy
typically requires four to six weeks of consistent dosing. This delayed response is
,related to gradual neurochemical adaptations in dopamine and serotonin pathways.
Patients should be counseled to continue therapy even if early improvement is
modest.
3. How does aripiprazole cause side effects?
Answer:
Aripiprazole blocks alpha-1 adrenergic receptors, which can result in dizziness,
sedation, and orthostatic hypotension. Its partial agonism at dopamine D2 receptors in
the striatum can lead to extrapyramidal symptoms, particularly akathisia. Dopamine
modulation in the gastrointestinal and central nervous systems contributes to nausea,
vomiting, and activating effects such as restlessness or insomnia.
4. What are the notable side effects of aripiprazole?
Answer:
Common side effects include dizziness, insomnia, akathisia, and activation or
restlessness. Gastrointestinal effects such as nausea, vomiting, and constipation may
occur. Patients may also experience headaches, muscle weakness (asthenia), and
orthostatic hypotension. Although rare, there is a theoretical risk of tardive dyskinesia
with long-term use.
5. What are the life-threatening adverse effects of aripiprazole?
Answer:
Serious adverse effects include neuroleptic malignant syndrome, which presents with
hyperthermia, muscle rigidity, and autonomic instability. Aripiprazole has been
associated with impulse control problems such as compulsive gambling and
hypersexuality. Seizures and cerebrovascular events may occur, especially in elderly
patients with dementia. Overdose typically causes sedation and vomiting but is rarely
fatal.
6. What is the recommended dosage of aripiprazole for
schizophrenia?
Answer:
The usual therapeutic dosage for schizophrenia ranges from 15 to 30 mg once daily.
Treatment is often initiated at 10 to 15 mg to assess tolerability. Dose adjustments
,should be made based on clinical response and side effects. Aripiprazole does not
typically require slow titration compared to other antipsychotics.
7. What is brexpiprazole (Rexulti)?
Answer:
Brexpiprazole is an atypical, third-generation antipsychotic similar to aripiprazole. It
functions as a dopamine D2 partial agonist and serotonin 5-HT1A agonist while
antagonizing 5-HT2A receptors. Compared to aripiprazole, it has lower intrinsic
dopamine activity, resulting in less akathisia. It is approved for schizophrenia and
adjunctive treatment of major depressive disorder.
8. What distinguishes third-generation antipsychotics from first-
and second-generation agents?
Answer:
Third-generation antipsychotics primarily act as dopamine partial agonists rather than
pure antagonists. This mechanism allows stabilization of dopamine activity instead of
complete blockade. As a result, they tend to cause fewer extrapyramidal symptoms
and less prolactin elevation. They also offer improved efficacy for negative and
cognitive symptoms.
9. What neurotransmitter pathways are primarily targeted by
antipsychotic medications?
Answer:
Antipsychotics primarily target dopamine pathways, especially the mesolimbic and
mesocortical systems. Blockade or modulation of dopamine in the mesolimbic
pathway reduces positive symptoms of psychosis. Effects on the mesocortical pathway
influence negative and cognitive symptoms. Serotonin pathways are also targeted,
particularly by atypical antipsychotics.
10. How do first-generation antipsychotics reduce psychotic
symptoms?
Answer:
First-generation antipsychotics reduce psychotic symptoms by strongly antagonizing
dopamine D2 receptors. This decreases excessive dopamine activity in the mesolimbic
pathway. While effective for positive symptoms, they often worsen negative
, symptoms and cognition. Their non-selective dopamine blockade contributes to
significant extrapyramidal side effects.
11. Why do antipsychotics cause extrapyramidal symptoms?
Answer:
Extrapyramidal symptoms occur due to dopamine D2 receptor blockade in the
nigrostriatal pathway. This pathway is responsible for motor control, and reduced
dopamine disrupts normal movement regulation. The severity of symptoms depends
on dopamine binding affinity and receptor occupancy. High-potency antipsychotics
carry the greatest risk.
12. What is akathisia and how is it managed?
Answer:
Akathisia is a subjective feeling of inner restlessness accompanied by an inability to
stay still. It commonly occurs with antipsychotics that have strong dopamine activity.
Management includes dose reduction, switching agents, or adding medications such
as beta-blockers or benzodiazepines. Early recognition is critical to prevent
nonadherence.
13. What is neuroleptic malignant syndrome?
Answer:
Neuroleptic malignant syndrome is a rare but life-threatening reaction to dopamine
blockade. It presents with hyperthermia, muscle rigidity, altered mental status, and
autonomic instability. Laboratory findings often include elevated creatine kinase and
leukocytosis. Immediate discontinuation of the offending agent and supportive care
are required.
14. What role does serotonin play in atypical antipsychotic efficacy?
Answer:
Atypical antipsychotics block serotonin 5-HT2A receptors, which increases dopamine
release in the nigrostriatal and mesocortical pathways. This reduces extrapyramidal
symptoms and improves negative symptoms. Serotonin modulation also enhances
mood and cognition. This dual mechanism distinguishes atypicals from first-generation
agents.
2026/2027): PSYCHOPHARMACOLOGY AND
ADVANCED MENTAL HEALTH | QUESTIONS
AND VERIFIED ANSWERS | GRADE A -
MARYVILLE
NURS 660/NURS660
PSYCHOPHARMACOLOGY AND ADVANCED
MENTAL HEALTH
NURS 660/NURS 660 Exam 1, AT MARYVILLE
Psychopharmacology & Advanced Mental Health
Latest 2026/2027 | Grade A Standard | Verified Answers
1. How does aripiprazole work?
Answer:
Aripiprazole acts primarily as a partial agonist at dopamine D2 receptors, allowing it to
stabilize dopamine activity rather than fully blocking it. When dopamine levels are
high, it reduces dopamine signaling, improving positive symptoms such as
hallucinations and delusions. When dopamine levels are low, it increases dopaminergic
activity, which helps improve negative symptoms, cognition, and mood. Additionally, it
has activity at dopamine D3 receptors and antagonizes serotonin 5-HT2A receptors,
which enhances dopamine release in certain brain regions.
2. How long does it take aripiprazole to work?
Answer:
Aripiprazole may begin producing noticeable symptom improvement within one week,
particularly for agitation or psychotic symptoms. However, full therapeutic efficacy
typically requires four to six weeks of consistent dosing. This delayed response is
,related to gradual neurochemical adaptations in dopamine and serotonin pathways.
Patients should be counseled to continue therapy even if early improvement is
modest.
3. How does aripiprazole cause side effects?
Answer:
Aripiprazole blocks alpha-1 adrenergic receptors, which can result in dizziness,
sedation, and orthostatic hypotension. Its partial agonism at dopamine D2 receptors in
the striatum can lead to extrapyramidal symptoms, particularly akathisia. Dopamine
modulation in the gastrointestinal and central nervous systems contributes to nausea,
vomiting, and activating effects such as restlessness or insomnia.
4. What are the notable side effects of aripiprazole?
Answer:
Common side effects include dizziness, insomnia, akathisia, and activation or
restlessness. Gastrointestinal effects such as nausea, vomiting, and constipation may
occur. Patients may also experience headaches, muscle weakness (asthenia), and
orthostatic hypotension. Although rare, there is a theoretical risk of tardive dyskinesia
with long-term use.
5. What are the life-threatening adverse effects of aripiprazole?
Answer:
Serious adverse effects include neuroleptic malignant syndrome, which presents with
hyperthermia, muscle rigidity, and autonomic instability. Aripiprazole has been
associated with impulse control problems such as compulsive gambling and
hypersexuality. Seizures and cerebrovascular events may occur, especially in elderly
patients with dementia. Overdose typically causes sedation and vomiting but is rarely
fatal.
6. What is the recommended dosage of aripiprazole for
schizophrenia?
Answer:
The usual therapeutic dosage for schizophrenia ranges from 15 to 30 mg once daily.
Treatment is often initiated at 10 to 15 mg to assess tolerability. Dose adjustments
,should be made based on clinical response and side effects. Aripiprazole does not
typically require slow titration compared to other antipsychotics.
7. What is brexpiprazole (Rexulti)?
Answer:
Brexpiprazole is an atypical, third-generation antipsychotic similar to aripiprazole. It
functions as a dopamine D2 partial agonist and serotonin 5-HT1A agonist while
antagonizing 5-HT2A receptors. Compared to aripiprazole, it has lower intrinsic
dopamine activity, resulting in less akathisia. It is approved for schizophrenia and
adjunctive treatment of major depressive disorder.
8. What distinguishes third-generation antipsychotics from first-
and second-generation agents?
Answer:
Third-generation antipsychotics primarily act as dopamine partial agonists rather than
pure antagonists. This mechanism allows stabilization of dopamine activity instead of
complete blockade. As a result, they tend to cause fewer extrapyramidal symptoms
and less prolactin elevation. They also offer improved efficacy for negative and
cognitive symptoms.
9. What neurotransmitter pathways are primarily targeted by
antipsychotic medications?
Answer:
Antipsychotics primarily target dopamine pathways, especially the mesolimbic and
mesocortical systems. Blockade or modulation of dopamine in the mesolimbic
pathway reduces positive symptoms of psychosis. Effects on the mesocortical pathway
influence negative and cognitive symptoms. Serotonin pathways are also targeted,
particularly by atypical antipsychotics.
10. How do first-generation antipsychotics reduce psychotic
symptoms?
Answer:
First-generation antipsychotics reduce psychotic symptoms by strongly antagonizing
dopamine D2 receptors. This decreases excessive dopamine activity in the mesolimbic
pathway. While effective for positive symptoms, they often worsen negative
, symptoms and cognition. Their non-selective dopamine blockade contributes to
significant extrapyramidal side effects.
11. Why do antipsychotics cause extrapyramidal symptoms?
Answer:
Extrapyramidal symptoms occur due to dopamine D2 receptor blockade in the
nigrostriatal pathway. This pathway is responsible for motor control, and reduced
dopamine disrupts normal movement regulation. The severity of symptoms depends
on dopamine binding affinity and receptor occupancy. High-potency antipsychotics
carry the greatest risk.
12. What is akathisia and how is it managed?
Answer:
Akathisia is a subjective feeling of inner restlessness accompanied by an inability to
stay still. It commonly occurs with antipsychotics that have strong dopamine activity.
Management includes dose reduction, switching agents, or adding medications such
as beta-blockers or benzodiazepines. Early recognition is critical to prevent
nonadherence.
13. What is neuroleptic malignant syndrome?
Answer:
Neuroleptic malignant syndrome is a rare but life-threatening reaction to dopamine
blockade. It presents with hyperthermia, muscle rigidity, altered mental status, and
autonomic instability. Laboratory findings often include elevated creatine kinase and
leukocytosis. Immediate discontinuation of the offending agent and supportive care
are required.
14. What role does serotonin play in atypical antipsychotic efficacy?
Answer:
Atypical antipsychotics block serotonin 5-HT2A receptors, which increases dopamine
release in the nigrostriatal and mesocortical pathways. This reduces extrapyramidal
symptoms and improves negative symptoms. Serotonin modulation also enhances
mood and cognition. This dual mechanism distinguishes atypicals from first-generation
agents.
