After assessing the patient and formulating the nursing diagnoses for a plan of care, what is the next action a nurse should take?
Determine the goals and outcome criteria
Design interventions to include in the plan of care
Implement the nursing plan of care
Complete the spiritual assessment
The Correct Answer is A
Choice A reason: After diagnosis, setting goals and outcomes guides care, addressing issues like serotonin-driven depression. Goals, like “improve mood stability,” align with neurobiological needs, ensuring measurable, patient-centered targets. This step precedes interventions, forming the foundation for effective psychiatric treatment planning.
Choice B reason: Designing interventions follows goal-setting. Interventions, like therapy for dopamine imbalances, are based on established outcomes. Acting prematurely without goals risks misaligned care, as neurobiological targets must be defined first, making this step incorrect as the immediate next action.
Choice C reason: Implementation occurs after goals and interventions are set. Acting before defining outcomes, like stabilizing GABA for anxiety, risks ineffective care. The nursing process requires sequential planning to address neurobiological deficits, making implementation premature and incorrect at this stage.
Choice D reason: Spiritual assessment, while valuable, is part of initial data collection, not the next step after diagnosis. Goals addressing neurobiological issues, like serotonin deficits, take precedence to ensure targeted care. This option is irrelevant to the immediate planning phase of the nursing process.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Histamine regulates wakefulness and allergic responses, not anxiety or fear. Its receptors in the brain promote alertness, but excessive histamine does not drive sympathetic activation like increased heart rate. This makes histamine an incorrect choice for the symptoms described, which align with autonomic arousal.
Choice B reason: Acetylcholine mediates parasympathetic responses, like slowing heart rate, not the sympathetic activation seen in anxiety. While it plays a role in attention, it does not primarily cause fear or tachycardia, making it an unsuitable choice compared to norepinephrine’s role in stress responses.
Choice C reason: GABA inhibits neural activity, reducing anxiety via GABA-A receptor activation. Low GABA levels may contribute to anxiety, but the symptoms described (tachycardia, fear) result from sympathetic activation, not GABA excess. This makes GABA incorrect for the neurotransmitter driving these symptoms.
Choice D reason: Norepinephrine, released during stress, activates the sympathetic nervous system, increasing heart rate and inducing fear via locus coeruleus activation. It heightens arousal in the amygdala, contributing to anxiety symptoms. This aligns with the fight-or-flight response, making norepinephrine the correct neurotransmitter for these symptoms.
Correct Answer is B
Explanation
Choice A reason: Histamine blockade, as in antipsychotics like olanzapine, promotes sedation, not weight loss. Weight gain is common due to histamine’s role in appetite regulation via hypothalamic signaling. Weight loss is not a typical side effect, making this response inaccurate for histamine-blocking medications.
Choice B reason: Histamine receptor blockade, common in medications like quetiapine, reduces wakefulness by inhibiting histamine’s alerting effects in the cortex. This causes drowsiness, a frequent side effect in psychiatric treatments, aligning with the pharmacological mechanism and making this the correct response.
Choice C reason: Insomnia is not typical with histamine blockade, which promotes sedation. Histamine enhances alertness; blocking it, as in antihistaminic antipsychotics, induces sleepiness, not wakefulness. This response contradicts the neuropharmacological effect, making it incorrect for expected side effects.
Choice D reason: Blood pressure increase is unrelated to histamine blockade. Histamine affects wakefulness and appetite, not vascular tone directly. Antihistaminic drugs may cause orthostatic hypotension via other receptors, not hypertension, making this response inaccurate for histamine-blocking medication effects.
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