MSN 671 : Psychopathopharmacology I -Module 4 quiz 4
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Free MSN 671 : Psychopathopharmacology I -Module 4 quiz 4 Questions
Which statement is true regarding delusions and auditory hallucinations?
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Excessive glutamate release into the ventral tegmental area causes hyperactivity of the mesolimbic dopamine pathway, resulting in delusions and auditory hallucinations
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Excessive glutamate release into the ventral tegmental area causes decreased dopamine activity in the nigrostriatal pathway, resulting in delusions and auditory hallucinations
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Diminished glutamate released into the ventral tegmental area causes increased dopamine levels in the tuberoinfundibular pathway, resulting in delusions and auditory hallucinations
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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 mood stabilizer is known for the risk of Stevens-Johnson Syndrome, especially with rapid dose titration?
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Lithium
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Lamotrigine
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Valproate
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Carbamazepine
Explanation
Correct Answer:
B. Lamotrigine
Explanation:
Lamotrigine carries a well-known risk of Stevens-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN), particularly if the dose is increased too quickly. To minimize this risk, lamotrigine must be titrated slowly over several weeks. Despite this risk, it is valued as a mood stabilizer, especially for preventing bipolar depression episodes.
Why Other Options Are Wrong:
A. Lithium
This is incorrect because lithium is associated with renal and thyroid toxicity, not Stevens-Johnson Syndrome.
C. Valproate
This is incorrect because valproate’s main risks include hepatotoxicity, pancreatitis, teratogenicity (neural tube defects), and weight gain, not SJS.
D. Carbamazepine
This is incorrect because carbamazepine can also cause Stevens-Johnson Syndrome, particularly in individuals with the HLA-B*1502 allele (common in Asian populations), but lamotrigine is the classic mood stabilizer most strongly associated with SJS risk during rapid titration.
The dysfunction of what 2 pathways are hypothetically associated with positive and negative symptoms of schizophrenia?
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Mesolimbic and Nigrostriatal pathways
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Nigrostriatal and Tuberoinfundibular pathways
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Mesocortical and Mesolimbic pathways
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Tuberoinfundibular and Mesocortical pathways
Explanation
Correct Answer:
C. Mesocortical and Mesolimbic pathways
Explanation:
Positive and negative symptoms of schizophrenia are explained by dysfunction in two major dopamine pathways. Hyperactivity in the mesolimbic pathway (increased dopamine signaling to the nucleus accumbens) produces positive symptoms such as hallucinations and delusions. Hypoactivity in the mesocortical pathway (reduced dopamine to the prefrontal cortex) contributes to negative symptoms like apathy, reduced motivation, and impaired cognition. These two pathways together form the core of the dopamine hypothesis of schizophrenia.
Why Other Options Are Wrong:
A. Mesolimbic and Nigrostriatal pathways
This is incorrect because the nigrostriatal pathway is involved in movement regulation, and its dysfunction causes extrapyramidal side effects, not schizophrenia’s positive or negative symptoms.
B. Nigrostriatal and Tuberoinfundibular pathways
This is incorrect because these two pathways are not linked to schizophrenia symptoms. The nigrostriatal pathway governs motor control, while the tuberoinfundibular pathway regulates prolactin release.
D. Tuberoinfundibular and Mesocortical pathways
This is incorrect because the tuberoinfundibular pathway is not related to psychotic symptoms. Only the mesocortical pathway among these is relevant, as it contributes to negative and cognitive symptoms.
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.
Positive and negative symptoms of schizophrenia are hypothetically linked to dysfunction in which two pathways?
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Nigrostriatal and tuberoinfundibular
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Mesolimbic and nigrostriatal
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Tuberoinfundibular and mesocortical
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Mesocortical and mesolimbic
Explanation
Correct Answer:
D. Mesocortical and mesolimbic
Explanation:
Positive and negative symptoms of schizophrenia arise from dysfunction in two dopamine pathways. Mesolimbic hyperactivity is linked to positive symptoms such as hallucinations and delusions. In contrast, mesocortical hypoactivity contributes to negative symptoms such as apathy, flat affect, and impaired executive function. This dual dysfunction underpins the modern dopamine hypothesis of schizophrenia.
Why Other Options Are Wrong:
A. Nigrostriatal and tuberoinfundibular
This is incorrect because the nigrostriatal pathway regulates movement (EPS side effects), and the tuberoinfundibular pathway regulates prolactin secretion. Neither produces schizophrenia symptoms.
B. Mesolimbic and nigrostriatal
This is incorrect because while mesolimbic hyperactivity explains positive symptoms, the nigrostriatal pathway is not involved in schizophrenia symptoms—it is associated with movement control.
C. Tuberoinfundibular and mesocortical
This is incorrect because although mesocortical hypofunction contributes to negative symptoms, the tuberoinfundibular pathway only regulates prolactin levels, not psychotic symptoms.
Parkinson's disease psychosis (PDP) is conceptualized as an imbalance in ______ with upregulation of 5HT2A receptors and treatable with 5HT2A antagonists.
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Serotonin and Dopamine
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Dopamine and Epinephrine
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Serotonin and Norepinephrine
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Glutamate and Norepinephrine
Explanation
Correct Answer:
A. Serotonin and Dopamine
Explanation:
Parkinson’s disease psychosis is thought to arise from an imbalance between serotonin and dopamine systems. In PDP, there is upregulation and overactivity of 5HT2A receptors in cortical and limbic areas. This disrupts the dopamine-serotonin balance and contributes to hallucinations and delusions. Treatment with selective 5HT2A antagonists (like pimavanserin) restores balance and reduces psychotic symptoms without worsening motor symptoms.
Why Other Options Are Wrong:
B. Dopamine and Epinephrine
This is incorrect because epinephrine does not play a central role in PDP pathophysiology.
C. Serotonin and Norepinephrine
This is incorrect because norepinephrine imbalance is not the primary mechanism of psychosis in Parkinson’s disease.
D. Glutamate and Norepinephrine
This is incorrect because while glutamate dysfunction is linked to other psychiatric disorders, it is not the main factor in PDP.
_____ is the major excitatory neurotransmitter in the central nervous system and is sometimes considered the "master switch" of the brain, since it can excite and turn on virtually all central nervous system neurons.
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Norepinephrine
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Epinephrine
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Glutamate
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Dopamine
Explanation
Correct Answer:
C. Glutamate
Explanation:
Glutamate is the brain’s major excitatory neurotransmitter and is often referred to as the “master switch” because nearly all neurons in the central nervous system can be activated by glutamatergic signaling. It plays a critical role in synaptic plasticity, learning, and memory. Through receptors like NMDA, AMPA, and kainate, glutamate enables fast excitatory neurotransmission and is central to both normal cognition and pathological processes such as excitotoxicity.
Why Other Options Are Wrong:
A. Norepinephrine
This is incorrect because norepinephrine acts as a neuromodulator involved in alertness, arousal, and the fight-or-flight response, but it is not the primary excitatory neurotransmitter.
B. Epinephrine
This is incorrect because epinephrine functions mainly as a hormone in the periphery and has limited neurotransmitter roles in the CNS.
D. Dopamine
This is incorrect because dopamine is a modulatory neurotransmitter involved in reward, motivation, and motor control, but it is not the brain’s major excitatory neurotransmitter.
N-methyl-D-aspartate (NMDA) receptor activation necessitates the following:
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Glutamate only
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Glutamate and glycine
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Glutamate, glycine and magnesium
Explanation
Correct Answer:
B. Glutamate and glycine
Explanation:
NMDA receptors are ionotropic glutamate receptors that require co-activation by two ligands: glutamate, the primary excitatory neurotransmitter, and glycine (or D-serine), which acts as a co-agonist at a separate binding site. Both must be present for the channel to open. Additionally, at resting membrane potential, the channel pore is blocked by magnesium ions. Depolarization is required to expel magnesium, allowing calcium and sodium influx, but magnesium is not a ligand needed for activation.
Why Other Options Are Wrong:
A. Glutamate only
This is incorrect because glutamate binding alone is insufficient to open NMDA receptors—glycine (or D-serine) must also bind.
C. Glutamate, glycine and magnesium
This is incorrect because magnesium does not activate the receptor. In fact, magnesium blocks the channel until the membrane depolarizes; its role is inhibitory, not activating.
A patient with Parkinson’s develops hallucinations due to psychosis. This is linked to what imbalance?
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Dopamine hyperactivity and serotonin downregulation
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Dopamine-serotonin imbalance with 5HT2A upregulation
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Glutamate and norepinephrine imbalance
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GABA and acetylcholine imbalance
Explanation
Correct Answer:
B. Dopamine-serotonin imbalance with 5HT2A upregulation
Explanation:
Parkinson’s disease psychosis is thought to arise from an imbalance between dopamine and serotonin systems. Long-term dopaminergic therapy may overstimulate pathways, while cortical 5HT2A receptor upregulation contributes to hallucinations and delusions. This is why pimavanserin, a selective 5HT2A antagonist, is effective for treating Parkinson’s psychosis without worsening motor symptoms.
Why Other Options Are Wrong:
A. Dopamine hyperactivity and serotonin downregulation
This is incorrect because serotonin is not downregulated; in fact, 5HT2A overactivity contributes to psychosis.
C. Glutamate and norepinephrine imbalance
This is incorrect because neither glutamate nor norepinephrine plays the central role in Parkinson’s psychosis.
D. GABA and acetylcholine imbalance
This is incorrect because while GABA and acetylcholine are relevant in Parkinson’s motor symptoms, they are not the main drivers of psychosis.
Hallucinogens such as LSD act primarily on which receptor?
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D2 receptor
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5HT2A receptor
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GABA-A receptor
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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.
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