A patient asks the nurse, “Why did my health care provider prescribe buspirone (Buspar) for my anxiety instead of diazepam (Valium)?” The nurse’s reply is based on the knowledge of which characteristic of buspirone?
It can be administered as needed
It is faster acting than diazepam
It may produce blood dyscrasias
It is not known to cause dependence
The Correct Answer is D
Choice A reason: Buspirone is not used as needed; it requires weeks for serotonin modulation to reduce anxiety. Diazepam’s rapid GABA enhancement suits acute use. Buspirone’s chronic dosing schedule makes this characteristic incorrect for explaining its preference over diazepam for long-term anxiety management.
Choice B reason: Buspirone is slower-acting, taking weeks to enhance serotonin activity, unlike diazepam’s rapid GABA-mediated effects. For anxiety driven by amygdala hyperactivity, diazepam acts faster, making buspirone’s slower onset an incorrect reason for its prescription over diazepam in this context.
Choice C reason: Blood dyscrasias are not a known side effect of buspirone, which primarily affects serotonin receptors. This is unrelated to its preference over diazepam, which carries dependence risks. This characteristic is inaccurate and irrelevant to the rationale for choosing buspirone.
Choice D reason: Buspirone’s lack of dependence risk, unlike diazepam’s GABA-mediated addiction potential, makes it safer for long-term anxiety management. By enhancing serotonin in the prefrontal cortex, it reduces chronic anxiety without habit-forming effects, aligning with its preference for sustained treatment, making this the correct reason.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A reason: Decreasing dopamine is used for disorders like schizophrenia, where excess mesolimbic dopamine causes hallucinations. Memory difficulties, often linked to Alzheimer’s, involve cholinergic deficits, not dopamine excess. Reducing dopamine could worsen cognition by disrupting reward and attention pathways, making this approach scientifically inappropriate for memory issues.
Choice B reason: Inhibiting GABA production is irrelevant for memory. GABA regulates neural inhibition, and its reduction could increase excitability, worsening conditions like seizures. Memory deficits, particularly in dementia, stem from reduced acetylcholine in the hippocampus, not GABA, making this option misaligned with the neurobiology of memory impairment.
Choice C reason: Preventing acetylcholine destruction, via cholinesterase inhibitors, enhances cholinergic activity in the hippocampus and cortex, critical for memory in conditions like Alzheimer’s. Low acetylcholine levels impair neural signaling, causing memory deficits. This approach directly addresses the neurochemical basis of memory difficulties, making it scientifically appropriate for treatment.
Choice D reason: Increasing dopamine sensitivity is relevant for disorders like Parkinson’s, not memory deficits. Dopamine affects motivation and movement, not memory, which relies on acetylcholine in the hippocampus. Enhancing dopamine could disrupt cognitive balance, worsening memory without addressing the cholinergic deficits central to memory impairment.
Correct Answer is A
Explanation
Choice A reason: Venlafaxine inhibits serotonin and norepinephrine reuptake, enhancing synaptic levels of these neurotransmitters in the prefrontal cortex and amygdala, improving mood and anxiety. This mechanism aligns with SNRIs, making it the correct choice for treating conditions like depression or anxiety with dual neurotransmitter modulation.
Choice B reason: Propranolol is a beta-blocker, reducing sympathetic activity by blocking norepinephrine at beta receptors, not reuptake. It treats physical anxiety symptoms, not mood via serotonin-norepinephrine pathways. This makes it incorrect for an SNRI, as it lacks reuptake inhibition properties.
Choice C reason: Amitriptyline, a tricyclic antidepressant, inhibits serotonin and norepinephrine reuptake but also affects other receptors, causing significant side effects. It is not classified as an SNRI due to its broader mechanism, making it an incorrect choice compared to venlafaxine’s specific SNRI action.
Choice D reason: Fluoxetine is an SSRI, selectively inhibiting serotonin reuptake, not norepinephrine. It enhances serotonin in mood-regulating areas like the hippocampus but lacks norepinephrine modulation, making it incorrect for an SNRI, which requires dual reuptake inhibition for broader neurotransmitter effects.
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