MSN 671 : Psychopathopharmacology I -Module 4 quiz 4

Correct Answer:

B. Lorazepam

Explanation:

Lorazepam is metabolized primarily through glucuronidation (conjugation) rather than hepatic oxidation. Because glucuronidation is less affected by liver dysfunction, lorazepam is safer in patients with hepatic impairment, including those with cirrhosis. This is why lorazepam is often preferred for managing alcohol withdrawal or acute anxiety in patients with compromised liver function.

Why Other Options Are Wrong:

A. Diazepam

This is incorrect because diazepam undergoes extensive hepatic oxidation and has active metabolites, leading to prolonged effects in liver disease.

C. Clonazepam

This is incorrect because clonazepam is metabolized by hepatic oxidation and is not ideal for patients with liver impairment.

D. Chlordiazepoxide

This is incorrect because chlordiazepoxide also requires hepatic oxidation and has active metabolites, making it unsafe in severe liver disease.

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.

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.

Correct Answer:

A. Paroxetine

Explanation:

Paroxetine has one of the shortest half-lives among SSRIs, leading to a high risk of discontinuation syndrome if stopped suddenly. Symptoms include dizziness, nausea, fatigue, irritability, insomnia, and “electric shock” sensations. To avoid this, paroxetine should be tapered gradually.

Why Other Options Are Wrong:

B. Fluoxetine

This is incorrect because fluoxetine has the longest half-life among SSRIs (and an active metabolite, norfluoxetine), making discontinuation symptoms much less likely.

C. Sertraline

This is incorrect because sertraline has an intermediate half-life and can cause discontinuation symptoms, but the risk is lower compared to paroxetine.

D. Escitalopram

This is incorrect because escitalopram also has an intermediate half-life and carries some risk, but not as high as paroxetine.

Correct Answer:

C. Citalopram

Explanation:

Among SSRIs, citalopram is most strongly associated with QT interval prolongation, especially at higher doses (>40 mg/day). This increases the risk of torsades de pointes and sudden cardiac death. Because of this risk, the FDA has issued dosing limits and recommends EKG monitoring in patients with cardiac risk factors.

Why Other Options Are Wrong:

A. Paroxetine

This is incorrect because paroxetine is not associated with significant QT prolongation; its main concerns are weight gain and withdrawal symptoms.

B. Fluoxetine

This is incorrect because fluoxetine has a long half-life and drug–drug interactions but is not strongly linked to QT prolongation.

D. Fluvoxamine

This is incorrect because fluvoxamine is more associated with drug interactions due to CYP inhibition, not QT interval prolongation.

Correct Answer:

C. Excessive DA release in the NA and reduced DA release in the PFC

Explanation:

NMDA receptor hypofunction on GABAergic interneurons leads to disinhibition of glutamatergic output in the ventral tegmental area (VTA). This excessive glutamate drive increases dopamine release in the mesolimbic pathway (nucleus accumbens), which contributes to positive symptoms such as hallucinations and delusions. At the same time, it disrupts mesocortical projections, causing reduced dopamine in the prefrontal cortex, which contributes to negative symptoms (apathy, flat affect) and cognitive dysfunction.

Why Other Options Are Wrong:

A. Excessive DA release in NA and excessive DA release in PFC

This is incorrect because while dopamine increases in the NA, dopamine is actually reduced in the PFC.

B. Reduced DA release in NA and reduced DA release in PFC

This is incorrect because dopamine is not reduced in the NA; it is excessive there and drives positive symptoms.

D. Reduced DA release in NA and excessive DA release in PFC

This is incorrect because this is the opposite of what occurs—positive symptoms require increased dopamine in the NA, and negative symptoms result from decreased dopamine in the PFC.

Correct Answer:

B. Mirtazapine

Explanation:

Mirtazapine is well known for its strong antagonism of histamine H1 receptors, which causes pronounced sedation and weight gain. These side effects can be beneficial in patients with depression who also have insomnia or low appetite. Mirtazapine also works as an α2-adrenergic antagonist and enhances norepinephrine and serotonin release, contributing to its antidepressant effects.

Why Other Options Are Wrong:

A. Bupropion

This is incorrect because bupropion is generally weight-neutral or associated with weight loss and does not cause sedation; it is activating.

C. Escitalopram

This is incorrect because escitalopram, an SSRI, may cause mild weight gain or sexual dysfunction but does not strongly block H1 receptors, so sedation and weight gain are not prominent.

D. Sertraline

This is incorrect because sertraline, another SSRI, is usually weight-neutral to mildly weight gaining and does not produce the marked sedation and appetite increase seen with mirtazapine.

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.

Correct Answer:

D. Midazolam

Explanation:

Midazolam is a short-acting benzodiazepine with the shortest half-life among the listed options. It is primarily used in medical settings for acute sedation, procedural anesthesia, and rapid anxiolysis. Because of its rapid onset and short duration, it is less commonly prescribed for outpatient panic attacks but is considered the shortest-acting option here.

Why Other Options Are Wrong:

A. Diazepam

This is incorrect because diazepam has a long half-life and active metabolites, making it less suitable for rapid, short-term relief.

B. Alprazolam

This is incorrect because alprazolam has an intermediate half-life and is commonly prescribed for panic attacks, but it is not the shortest-acting benzodiazepine.

C. Lorazepam

This is incorrect because lorazepam also has an intermediate duration of action and is useful for acute anxiety, but it lasts longer than midazolam.