A patient presents with anxiety, increased heart rate, and fear. The nurse suspects the activation of which neurotransmitter?
Histamine
Acetylcholine
GABA
Norepinephrine
The Correct Answer is D
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
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.
Correct Answer is D
Explanation
Choice A reason: Canceling discharge overrides patient autonomy and recovery progress. Stabilized schizophrenia, managed with antipsychotics targeting dopamine, supports discharge with adherence. This action disregards the patient’s rights and neurobiological stabilization, making it an inappropriate advocacy response.
Choice B reason: Notifying security dismisses family concerns and escalates unnecessarily. Schizophrenia management relies on medication adherence, not coercion. This approach ignores patient rights and family education needs, failing to address neurobiological treatment principles, making it incorrect for advocacy.
Choice C reason: Transferring to long-term care assumes ongoing instability, ignoring current stabilization. Antipsychotics correct dopamine imbalances, supporting outpatient management. This undermines patient autonomy and recovery potential, making it an inappropriate advocacy action for a stabilized patient.
Choice D reason: Explaining medication adherence promotes patient autonomy and recovery. Antipsychotics reduce dopamine-driven hallucinations, ensuring symptom control. Educating the family empowers support for adherence, aligning with patient rights and neurobiological treatment principles, making this the correct advocacy response.
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