MSN 671 : Psychopathopharmacology I -Module 4 quiz 4

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Free MSN 671 : Psychopathopharmacology I -Module 4 quiz 4 Questions

1.

A patient taking risperidone develops muscle rigidity, fever, autonomic instability, and altered mental status. What is the most likely diagnosis?

  • Tardive dyskinesia

  • Neuroleptic malignant syndrome

  • Serotonin syndrome

  • Acute dystonia

Explanation

Correct Answer:

B. Neuroleptic malignant syndrome

Explanation:

Neuroleptic malignant syndrome (NMS) is a rare but life-threatening reaction to antipsychotics such as risperidone. It is characterized by the classic tetrad of severe muscle rigidity, hyperthermia (fever), autonomic instability, and altered mental status. It is caused by sudden, severe dopamine blockade in the central nervous system. Treatment includes immediate discontinuation of the antipsychotic, supportive care, and agents such as dantrolene or bromocriptine.

Why Other Options Are Wrong:

A. Tardive dyskinesia

This is incorrect because tardive dyskinesia involves chronic, involuntary movements (lip smacking, tongue protrusion) after long-term antipsychotic use, not fever and autonomic instability.

C. Serotonin syndrome


This is incorrect because serotonin syndrome presents with hyperreflexia, clonus, tremor, and GI symptoms, usually after serotonergic drug use. Muscle rigidity and “lead-pipe” stiffness are more characteristic of NMS.

D. Acute dystonia


This is incorrect because acute dystonia occurs within hours to days of starting an antipsychotic and involves painful muscle spasms (e.g., torticollis, oculogyric crisis), but it does not include fever or altered mental status.


2.

Which neurotransmitter is the major excitatory “master switch” of the brain?

  • Dopamine

  • Norepinephrine

  • Glutamate

  • Serotonin

Explanation

Correct Answer:

C. Glutamate

Explanation:

Glutamate is the primary excitatory neurotransmitter in the central nervous system and is often called the brain’s “master switch.” It activates nearly all neurons and is critical for learning, memory, and synaptic plasticity through receptors such as NMDA, AMPA, and kainate. Dysregulation of glutamate transmission is implicated in conditions such as schizophrenia, epilepsy, and excitotoxicity.

Why Other Options Are Wrong:

A. Dopamine

This is incorrect because dopamine primarily modulates reward, motivation, and motor pathways but is not the brain’s main excitatory neurotransmitter.

B. Norepinephrine

This is incorrect because norepinephrine functions mainly as a neuromodulator involved in arousal and the stress response, not as the central excitatory switch.

D. Serotonin

This is incorrect because serotonin regulates mood, sleep, and appetite, but it is not the primary excitatory neurotransmitter.


3.

There are neurodevelopmental delays in the prefrontal cortical synaptic connections that are associated with ADHD causing subsequent inefficient "tuning" of information processing in prefrontal circuits. There are 2 neurotransmitters that regulate processing in the prefrontal circuits. What are they?

  • Dopamine and norepinephrine

  • Serotonin and norepinephrine

  • Serotonin and dopamine

  • Dopamine and glutamate

Explanation

Correct Answer:

A. Dopamine and norepinephrine

Explanation:

The prefrontal cortex, which regulates attention, working memory, and executive function, relies heavily on the balance of dopamine and norepinephrine signaling. In ADHD, disruptions in these neurotransmitters impair the fine-tuning of prefrontal cortical circuits, leading to difficulties in sustaining attention, impulse control, and organization. Medications such as stimulants (e.g., methylphenidate, amphetamines) work by enhancing dopamine and norepinephrine activity in the prefrontal cortex, improving symptoms.

Why Other Options Are Wrong:

B. Serotonin and norepinephrine

This is incorrect because serotonin modulates mood and anxiety more than attention regulation in prefrontal circuits.

C. Serotonin and dopamine

This is incorrect because while dopamine is critical, serotonin is not the second key neurotransmitter for prefrontal cortical tuning in ADHD.

D. Dopamine and glutamate

This is incorrect because glutamate is the major excitatory neurotransmitter, but prefrontal "tuning" deficits in ADHD are more directly linked to dopamine and norepinephrine dysregulation.


4.

There are several known dopamine pathways in the brain. Which of the following pathways contributes to an increase in prolactin levels, resulting in galactorrhea or amenorrhea, when a patient is treated with an antipsychotic drug that blocks D2 receptors?

  • Thalamic Dopamine Pathway

  • Nigrostriatal Dopamine Pathway

  • Tuberoinfundibular Dopamine Pathway

  • Mesolimbic Dopamine Pathway

  • Mesocortical Dopamine Pathway

Explanation

Correct Answer:

C. Tuberoinfundibular Dopamine Pathway

Explanation:

The tuberoinfundibular pathway projects from the hypothalamus to the pituitary gland and regulates the secretion of prolactin. Normally, dopamine inhibits prolactin release via D2 receptor stimulation. When antipsychotic drugs block D2 receptors in this pathway, dopamine’s inhibitory control is lost, leading to elevated prolactin levels (hyperprolactinemia). Clinically, this can result in galactorrhea, amenorrhea, gynecomastia, and sexual dysfunction in patients receiving antipsychotic therapy.

Why Other Options Are Wrong:

A. Thalamic Dopamine Pathway

This is incorrect because there is no well-defined thalamic dopamine pathway associated with prolactin regulation.

B. Nigrostriatal Dopamine Pathway


This is incorrect because the nigrostriatal pathway is involved in motor control, and its D2 blockade causes extrapyramidal side effects, not hyperprolactinemia.

D. Mesolimbic Dopamine Pathway


This is incorrect because the mesolimbic pathway regulates reward and emotion. D2 blockade here reduces positive symptoms of schizophrenia but does not affect prolactin.

E. Mesocortical Dopamine Pathway


This is incorrect because the mesocortical pathway influences cognition and negative symptoms. Its dysfunction is linked to apathy and impaired executive function, not prolactin regulation.


5.

Which anxiolytic acts as a 5HT1A partial agonist and has no risk of dependence?

  • Lorazepam

  • Hydroxyzine

  • Buspirone

  • Clonazepam

Explanation

Correct Answer:

C. Buspirone

Explanation:

Buspirone is an anxiolytic that works as a partial agonist at 5HT1A receptors. Unlike benzodiazepines, it does not act on GABA-A receptors and therefore carries no risk of dependence, tolerance, or withdrawal. It is especially useful in treating generalized anxiety disorder (GAD), though it takes several weeks for therapeutic effects to appear.

Why Other Options Are Wrong:

A. Lorazepam

This is incorrect because lorazepam is a benzodiazepine that enhances GABA-A receptor activity and carries a risk of dependence.

B. Hydroxyzine

This is incorrect because hydroxyzine is an antihistamine (H1 antagonist) used for anxiety and sedation, but it does not act as a 5HT1A partial agonist.

D. Clonazepam

This is incorrect because clonazepam is another benzodiazepine, associated with dependence and withdrawal risks, not 5HT1A receptor activity.


6.

Which of the following antipsychotics carries the highest risk of agranulocytosis, requiring regular blood monitoring?

  • Olanzapine

  • Risperidone

  • Clozapine

  • Aripiprazole

Explanation

Correct Answer:

C. Clozapine

Explanation:

Clozapine is the antipsychotic most strongly associated with agranulocytosis, a potentially life-threatening drop in white blood cells (neutropenia). Because of this risk, patients must undergo regular CBC (complete blood count) monitoring. Despite this, clozapine is highly effective for treatment-resistant schizophrenia and reduces the risk of suicide in psychotic patients.

Why Other Options Are Wrong:

A. Olanzapine

This is incorrect because olanzapine can cause weight gain, sedation, and metabolic syndrome, but it is not linked to agranulocytosis.

B. Risperidone

This is incorrect because risperidone commonly causes hyperprolactinemia and EPS at higher doses but not agranulocytosis.

D. Aripiprazole

This is incorrect because aripiprazole is a partial D2 agonist with fewer metabolic and EPS risks, and it is not associated with agranulocytosis.


7.

A patient treated with haloperidol develops galactorrhea. Which pathway’s dopamine blockade explains this?

  • Mesolimbic

  • Mesocortical

  • Tuberoinfundibular

  • Nigrostriatal

Explanation

Correct Answer:

C. Tuberoinfundibular

Explanation:

The tuberoinfundibular pathway connects the hypothalamus to the pituitary gland and regulates prolactin secretion. Dopamine normally inhibits prolactin release via D2 receptors. When haloperidol (a D2 antagonist) blocks these receptors, the inhibitory effect is lost, causing hyperprolactinemia, which can manifest as galactorrhea, amenorrhea, or gynecomastia.

Why Other Options Are Wrong:

A. Mesolimbic

This is incorrect because dopamine blockade here reduces positive symptoms of schizophrenia but does not affect prolactin levels.

B. Mesocortical


This is incorrect because blockade in this pathway worsens negative and cognitive symptoms, not prolactin regulation.

D. Nigrostriatal


This is incorrect because blockade here causes extrapyramidal side effects (EPS) and movement disorders, not galactorrhea.


8.

Which neurobiological mechanism best explains negative symptoms of schizophrenia?

  • Hyperdopaminergic activity in the mesolimbic pathway

  • Hypodopaminergic activity in the mesocortical pathway

  • Hypodopaminergic activity in the nigrostriatal pathway

  • Hyperdopaminergic activity in the tuberoinfundibular pathway

Explanation

Correct Answer:

B. Hypodopaminergic activity in the mesocortical pathway

Explanation:

Negative symptoms of schizophrenia—such as apathy, flat affect, social withdrawal, and impaired executive function—are linked to reduced dopamine activity in the mesocortical pathway. This pathway projects from the ventral tegmental area (VTA) to the prefrontal cortex. Insufficient dopamine signaling here leads to deficits in motivation, cognition, and emotional regulation.

Why Other Options Are Wrong:

A. Hyperdopaminergic activity in the mesolimbic pathway

This is incorrect because mesolimbic hyperactivity explains positive symptoms like hallucinations and delusions, not negative symptoms.

C. Hypodopaminergic activity in the nigrostriatal pathway

This is incorrect because dopamine deficiency here causes motor symptoms and extrapyramidal side effects, not schizophrenia’s negative symptoms.

D. Hyperdopaminergic activity in the tuberoinfundibular pathway

This is incorrect because this pathway regulates prolactin release. Hyperactivity here is not associated with schizophrenia but with endocrine imbalance.


9.

Which atypical antipsychotic is unique for its high risk of QT interval prolongation and requires EKG monitoring?

  • Quetiapine

  • Ziprasidone

  • Lurasidone

  • Clozapine

Explanation

Correct Answer:

B. Ziprasidone

Explanation:

Ziprasidone is the atypical antipsychotic most associated with QT interval prolongation, which can increase the risk of torsades de pointes and sudden cardiac death. Because of this, baseline and periodic EKG monitoring is recommended, especially in patients with preexisting cardiac conditions or those taking other QT-prolonging medications.

Why Other Options Are Wrong:

A. Quetiapine

This is incorrect because quetiapine can cause sedation and moderate metabolic effects but does not carry the highest risk for QT prolongation.

C. Lurasidone

This is incorrect because lurasidone has a relatively favorable cardiac profile and is not primarily associated with QT prolongation.

D. Clozapine

This is incorrect because clozapine carries risks of agranulocytosis, seizures, myocarditis, and metabolic syndrome, but not a high risk of QT prolongation.


10.

The positive symptoms of schizophrenia are most strongly linked to which pathway dysfunction?

  • Nigrostriatal pathway

  • Mesolimbic pathway

  • Mesocortical pathway

  • Tuberoinfundibular pathway

Explanation

Correct Answer:

B. Mesolimbic pathway

Explanation:

Positive symptoms of schizophrenia, including delusions and hallucinations, are strongly associated with dopamine hyperactivity in the mesolimbic pathway. This pathway projects from the ventral tegmental area (VTA) to the nucleus accumbens and other limbic structures, and its overactivation produces the abnormal salience attribution that drives psychosis.

Why Other Options Are Wrong:

A. Nigrostriatal pathway

This is incorrect because the nigrostriatal pathway is primarily involved in motor control. D2 blockade here causes extrapyramidal side effects, not psychotic symptoms.

C. Mesocortical pathway


This is incorrect because mesocortical dopamine hypofunction is associated with negative symptoms (apathy, flat affect) and cognitive impairment, not positive symptoms.

D. Tuberoinfundibular pathway


This is incorrect because this pathway regulates prolactin secretion. D2 blockade here leads to hyperprolactinemia, not hallucinations or delusions.


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