MSN 671 : Psychopathopharmacology I -Module 4 quiz 4
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Free MSN 671 : Psychopathopharmacology I -Module 4 quiz 4 Questions
Which class of drugs is being studied as an adjunctive treatment for schizophrenia by enhancing NMDA receptor function?
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GABA-A modulators
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Glycine-site agonists
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D2 receptor antagonists
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5HT1A receptor antagonists
Explanation
Correct Answer:
B. Glycine-site agonists
Explanation:
The glutamate hypothesis of schizophrenia suggests that NMDA receptor hypofunction contributes to negative and cognitive symptoms. Drugs that act as glycine-site agonists (or co-agonists such as D-serine and glycine transporter inhibitors) enhance NMDA receptor function, thereby improving synaptic signaling and potentially alleviating symptoms that dopamine-based antipsychotics do not fully address. This adjunctive approach is under active investigation.
Why Other Options Are Wrong:
A. GABA-A modulators
This is incorrect because while GABA-A dysfunction may influence psychosis, these modulators are not the primary focus for enhancing NMDA receptor function in schizophrenia.
C. D2 receptor antagonists
This is incorrect because D2 antagonists form the core of current antipsychotic treatment, but they do not address NMDA hypofunction.
D. 5HT1A receptor antagonists
This is incorrect because 5HT1A modulation affects anxiety and mood, but it does not directly enhance NMDA receptor function.
Which neurotransmitter is the major excitatory “master switch” of the brain?
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Dopamine
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Norepinephrine
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Glutamate
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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.
Which statement is true regarding delusions and auditory hallucinations?
-
Excessive glutamate release into the ventral tegmental area causes hyperactivity of the mesolimbic dopamine pathway, resulting in delusions and auditory hallucinations
-
Excessive glutamate release into the ventral tegmental area causes decreased dopamine activity in the nigrostriatal pathway, resulting in delusions and auditory hallucinations
-
Diminished glutamate released into the ventral tegmental area causes increased dopamine levels in the tuberoinfundibular pathway, resulting in delusions and auditory hallucinations
-
Diminished glutamate released into the ventral tegmental area causes decreased dopaminergic levels in the mesocortical pathway, resulting in delusions and auditory hallucinations
Explanation
Correct Answer:
A. Excessive glutamate release into the ventral tegmental area causes hyperactivity of the mesolimbic dopamine pathway, resulting in delusions and auditory hallucinations
Explanation:
Delusions and auditory hallucinations are classified as positive symptoms of schizophrenia. They are strongly linked to hyperactivity of dopamine at D2 receptors in the mesolimbic pathway. One major driver of this hyperactivity is excessive glutamatergic stimulation of the ventral tegmental area (VTA). Overactivation of VTA dopaminergic neurons leads to increased dopamine release in the nucleus accumbens, causing aberrant salience attribution, which manifests as delusions and hallucinations.
Why Other Options Are Wrong:
B. Excessive glutamate release into the ventral tegmental area causes decreased dopamine activity in the nigrostriatal pathway, resulting in delusions and auditory hallucinations
This is incorrect because the nigrostriatal pathway regulates movement, not psychotic symptoms. Excessive glutamate to the VTA does not reduce dopamine here; instead, it increases dopamine activity in the mesolimbic system.
C. Diminished glutamate released into the ventral tegmental area causes increased dopamine levels in the tuberoinfundibular pathway, resulting in delusions and auditory hallucinations
This is incorrect because the tuberoinfundibular pathway controls prolactin release, not psychosis. Alterations in this pathway lead to endocrine changes but not delusions or hallucinations.
D. Diminished glutamate released into the ventral tegmental area causes decreased dopaminergic levels in the mesocortical pathway, resulting in delusions and auditory hallucinations
This is incorrect because reduced dopamine in the mesocortical pathway is linked to negative symptoms and cognitive deficits, not the positive symptoms of hallucinations and delusions.
Which opioid receptor subtype is primarily responsible for euphoria and reinforcement?
-
Kappa
-
Mu
-
Delta
-
Sigma
Explanation
Correct Answer:
B. Mu
Explanation:
The mu-opioid receptor is the primary receptor responsible for the euphoric and reinforcing effects of opioids. Activation of mu receptors in the mesolimbic dopamine pathway (particularly in the nucleus accumbens) increases dopamine release, producing the rewarding effects that contribute to opioid abuse and dependence. Mu receptors are also responsible for analgesia, respiratory depression, and constipation.
Why Other Options Are Wrong:
A. Kappa
This is incorrect because kappa receptor activation produces dysphoria and hallucinations, not euphoria.
C. Delta
This is incorrect because delta receptors are involved in mood regulation and analgesia but do not primarily mediate euphoria or reinforcement.
D. Sigma
This is incorrect because sigma receptors are not true opioid receptors; they are associated with psychotomimetic effects, not the rewarding effects of opioids.
The PMHNP performs a neuropsychological assessment of selective attention for a patient with ADHD. The PMHNP requires the patient to name the color in which a word is written, instead of saying the word itself. For example, the word "blue" is written in red. What is the name of this test?
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NICHQ Vanderbilt Assessment Scale
-
Wender Utah Rating Scale for ADHD
-
ADHD Rating Scale
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Stroop Task
Explanation
Correct Answer:
D. Stroop Task
Explanation:
The Stroop Task is a classic neuropsychological test used to assess selective attention, cognitive flexibility, and inhibitory control. In this task, individuals must name the color of the ink in which a word is printed, rather than reading the word itself. This creates a conflict between automatic word reading and controlled processing, making it a sensitive measure of executive dysfunction commonly observed in ADHD.
Why Other Options Are Wrong:
A. NICHQ Vanderbilt Assessment Scale
This is incorrect because the Vanderbilt scale is a behavioral rating tool completed by parents and teachers, not a direct neuropsychological test.
B. Wender Utah Rating Scale for ADHD
This is incorrect because the Wender Utah Rating Scale is a retrospective self-report questionnaire used to assess ADHD symptoms that began in childhood.
C. ADHD Rating Scale
This is incorrect because the ADHD Rating Scale is a symptom checklist aligned with DSM criteria, not a cognitive performance task.
Which antipsychotic would be most appropriate in a patient with schizophrenia and comorbid hyperprolactinemia?
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Risperidone
-
Haloperidol
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Aripiprazole
-
Paliperidone
Explanation
Correct Answer:
C. Aripiprazole
Explanation:
Aripiprazole is a partial D2 agonist that acts as a dopamine system stabilizer. Unlike full D2 antagonists, it can reduce antipsychotic-induced hyperprolactinemia by providing partial stimulation of D2 receptors in the tuberoinfundibular pathway, thereby restoring dopamine’s inhibitory control on prolactin release. This makes it especially useful in patients with schizophrenia who also suffer from hyperprolactinemia.
Why Other Options Are Wrong:
A. Risperidone
This is incorrect because risperidone strongly blocks D2 receptors and is well known to cause hyperprolactinemia.
B. Haloperidol
This is incorrect because haloperidol, a high-potency typical antipsychotic, is strongly associated with hyperprolactinemia due to potent D2 antagonism.
D. Paliperidone
This is incorrect because paliperidone, the active metabolite of risperidone, also carries a high risk of hyperprolactinemia.
Which mood stabilizer is associated with neural tube defects if used during pregnancy?
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Lithium
-
Valproic acid
-
Carbamazepine
-
Lamotrigine
Explanation
Correct Answer:
B. Valproic acid
Explanation:
Valproic acid is strongly associated with teratogenic effects, particularly neural tube defects (e.g., spina bifida), when used during pregnancy. It interferes with folate metabolism, increasing the risk of fetal malformations. For this reason, valproic acid is generally avoided in women of childbearing potential unless no suitable alternatives are available.
Why Other Options Are Wrong:
A. Lithium
This is incorrect because lithium is linked to Ebstein’s anomaly (a congenital heart defect), not neural tube defects.
C. Carbamazepine
This is incorrect because carbamazepine also carries teratogenic risks, including neural tube defects, but the risk is lower than with valproic acid.
D. Lamotrigine
This is incorrect because lamotrigine is considered one of the safer mood stabilizers in pregnancy, though it may increase the risk of oral clefts, not neural tube defects.
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.
Hallucinogens such as LSD act primarily on which receptor?
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D2 receptor
-
5HT2A receptor
-
GABA-A receptor
-
5HT1A receptor
Explanation
Correct Answer:
B. 5HT2A receptor
Explanation:
Classical hallucinogens such as LSD, psilocybin, and mescaline exert their effects primarily through agonism at the serotonin 5HT2A receptor. This receptor is abundant in the cerebral cortex, where its overstimulation alters sensory perception, cognition, and mood, leading to hallucinations and psychotic-like experiences.
Why Other Options Are Wrong:
A. D2 receptor
This is incorrect because D2 receptor hyperactivity is implicated in schizophrenia’s positive symptoms, but it is not the primary mechanism of LSD’s hallucinogenic effects.
C. GABA-A receptor
This is incorrect because GABA-A receptors mediate inhibitory neurotransmission and are the target of benzodiazepines and alcohol, not hallucinogens.
D. 5HT1A receptor
This is incorrect because 5HT1A receptors are involved in anxiety and mood regulation (and targeted by buspirone), but they do not mediate the hallucinogenic effects of LSD.
Which receptor mechanism explains the ability of aripiprazole to act as both a dopamine stabilizer and antipsychotic?
-
Full agonist at D2 receptors
-
Partial agonist at D2 receptors
-
Antagonist at 5HT1A receptors
-
Inverse agonist at NMDA receptors
Explanation
Correct Answer:
B. Partial agonist at D2 receptors
Explanation:
Aripiprazole is a partial agonist at dopamine D2 receptors, which allows it to act as a dopamine system stabilizer. In states of excess dopamine (such as the mesolimbic pathway), it reduces signaling by competing with dopamine but producing only partial activation. In states of low dopamine (such as the mesocortical pathway), it provides some receptor activation, preventing underactivity. This dual action explains its effectiveness as an antipsychotic while causing fewer EPS and prolactin-related side effects.
Why Other Options Are Wrong:
A. Full agonist at D2 receptors
This is incorrect because a full agonist would overstimulate dopamine receptors and worsen psychosis rather than stabilize it.
C. Antagonist at 5HT1A receptors
This is incorrect because aripiprazole is actually a partial agonist at 5HT1A receptors, which contributes to its anxiolytic and antidepressant effects, not its dopamine-stabilizing properties.
D. Inverse agonist at NMDA receptors
This is incorrect because NMDA receptors are glutamate receptors, not dopamine receptors, and inverse agonism here would not explain aripiprazole’s mechanism.
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