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 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 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.
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