After several therapeutic encounters with a patient who recently attempted suicide, which occurrence should cause the nurse to consider the possibility of countertransference?
The nurse develops a trusting relationship with the patient
The patient states, “Talking to you feels like talking to my parents.”
The patient’s reactions toward the nurse seem realistic and appropriate
The nurse feels extremely happy when the patient’s mood begins to lift
The Correct Answer is D
Choice A reason: A trusting relationship is the goal of therapeutic alliances, not countertransference. It reflects effective communication, calming amygdala-driven distress in suicidal patients. This is a normal outcome, not an emotional overreaction, making it an incorrect indicator of countertransference in psychiatric care.
Choice B reason: The patient comparing the nurse to parents suggests transference, not countertransference. Transference involves patient projections, often tied to past emotional patterns, not nurse emotions. This is unrelated to the nurse’s feelings, making it an incorrect choice for countertransference concerns.
Choice C reason: Realistic patient reactions indicate a healthy therapeutic dynamic, not countertransference. Appropriate responses align with stabilizing neurobiological states, like serotonin balance in depression. This reflects effective care, not nurse emotional overinvolvement, making it an incorrect indicator of countertransference in this context.
Choice D reason: Extreme happiness tied to the patient’s mood improvement suggests countertransference, where the nurse’s emotions, possibly influenced by mirror neuron activation, overly align with the patient’s state. This indicates personal overinvolvement, risking bias in care for suicidal patients with serotonin imbalances, making it the correct choice.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Buspirone enhances serotonin activity, taking weeks to reduce anxiety. Panic attacks, driven by acute norepinephrine surges in the amygdala, require rapid intervention. Buspirone’s delayed onset makes it ineffective for acute symptom relief, unlike fast-acting options targeting immediate neurochemical imbalances.
Choice B reason: Venlafaxine, an SNRI, increases serotonin and norepinephrine over weeks, unsuitable for acute panic attacks. Panic involves rapid sympathetic activation, requiring immediate GABA enhancement or similar fast-acting mechanisms, not gradual reuptake inhibition, making venlafaxine incorrect for rapid relief.
Choice C reason: Imipramine, a tricyclic, modulates serotonin and norepinephrine but takes weeks to act. Acute panic, driven by locus coeruleus norepinephrine spikes, needs immediate relief. Imipramine’s slow onset and side effects make it inappropriate for rapid intervention in acute anxiety episodes.
Choice D reason: Alprazolam, a benzodiazepine, enhances GABA-A receptor activity, rapidly inhibiting excessive neural firing in the amygdala during panic attacks. This provides quick relief from acute anxiety symptoms, like tachycardia, within minutes, making it the correct choice for immediate neurobiological stabilization in panic episodes.
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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