Which medication would be considered a first-line medication therapy for generalized anxiety disorder (GAD)?
Paroxetine (Paxil)
Imipramine (Tofranil)
Hydroxyzine (Vistaril)
Alprazolam (Xanax)
The Correct Answer is A
Choice A reason: Paroxetine, an SSRI, is first-line for GAD, enhancing serotonin in the amygdala and prefrontal cortex, reducing excessive worry. Its efficacy and tolerability, with minimal dependence risk, align with evidence-based guidelines for long-term anxiety management, making it the preferred choice.
Choice B reason: Imipramine, a tricyclic antidepressant, affects serotonin and norepinephrine but has significant anticholinergic side effects, reducing tolerability. It is not first-line for GAD due to slower onset and side effect profile compared to SSRIs, which better target anxiety’s neurobiological basis.
Choice C reason: Hydroxyzine, an antihistamine, reduces anxiety via histamine receptor blockade, causing sedation. It is used as needed, not for chronic GAD management. SSRIs, like paroxetine, offer sustained serotonin modulation, making hydroxyzine a less effective, non-first-line option for long-term treatment.
Choice D reason: Alprazolam, a benzodiazepine, enhances GABA activity, providing rapid anxiety relief but carries high dependence risk. It is not first-line for GAD, as SSRIs offer safer, long-term serotonin-based treatment, making alprazolam unsuitable for chronic management due to addiction potential.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: Muscarinic receptor blockers inhibit parasympathetic activity, reducing salivary gland secretion via acetylcholine pathways. This causes dry mouth, as muscarinic receptors in salivary glands are blocked, decreasing saliva production. This anticholinergic effect is common in drugs like benztropine, requiring assessment to manage discomfort and prevent oral health issues.
Choice B reason: Orthostatic hypotension is linked to alpha-1 adrenergic blockade, not muscarinic receptors. Muscarinic blockers affect cholinergic pathways, not vascular tone regulated by norepinephrine. While autonomic effects occur, hypotension is not a primary consequence, making this side effect unrelated to muscarinic receptor antagonism.
Choice C reason: Pseudoparkinsonism results from dopamine receptor blockade, common in antipsychotics, not muscarinic blockers. Muscarinic receptors regulate parasympathetic functions like salivation, not motor control. Blocking muscarinic receptors may alleviate parkinsonism by balancing cholinergic-dopaminergic activity, making this an incorrect side effect for assessment.
Choice D reason: Gynecomastia is associated with hormonal imbalances or dopamine blockade, not muscarinic receptors. Muscarinic blockers affect cholinergic systems, not prolactin or estrogen pathways. This side effect is unrelated to muscarinic antagonism, which primarily causes anticholinergic effects like dry mouth, not endocrine changes.
Correct Answer is A
Explanation
Choice A reason: Blocking norepinephrine at alpha-1 receptors inhibits vasoconstriction, reducing vascular tone. This disrupts baroreceptor-mediated blood pressure regulation, causing orthostatic hypotension when standing. The autonomic nervous system fails to compensate for positional changes, leading to dizziness and fainting, a common side effect of alpha-1 blockers like prazosin.
Choice B reason: Increased psychotic symptoms are linked to dopamine dysregulation, not alpha-1 receptor blockade. Norepinephrine blockade affects autonomic functions, not psychosis, which involves mesolimbic dopamine hyperactivity. This side effect is unrelated to alpha-1 receptors, making this option scientifically inaccurate for the described mechanism.
Choice C reason: Appetite disturbance is typically associated with serotonin or histamine receptor effects, not alpha-1 norepinephrine blockade. Norepinephrine at alpha-1 receptors regulates vascular tone, not appetite control, which involves hypothalamic signaling. This side effect is not a direct consequence of alpha-1 blockade, rendering this option incorrect.
Choice D reason: Hypertensive crisis results from excessive norepinephrine activity, often due to monoamine oxidase inhibitors, not alpha-1 receptor blockade. Blocking alpha-1 receptors causes vasodilation, lowering blood pressure, not raising it. This makes hypertensive crisis an unlikely side effect, contrary to the pharmacological mechanism of alpha-1 blockers.
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