A patient diagnosed with major depressive disorder tells the nurse, "Bad things that happen are always my fault." To support the patient to reframe this overgeneralization, the nurse's best response is:
I really doubt that one person can be blamed for all the bad things that happen.
Let's look at one bad thing that happened to see if another explanation exists.
How does your belief in fate relate to your cultural heritage?
You are being exceptionally hard on yourself when you say those things.
The Correct Answer is B
Choice A reason: This response dismisses the patient’s cognitive distortion without engaging in therapeutic exploration. Major depressive disorder involves negative cognitive biases due to altered serotonin and dopamine signaling in the prefrontal cortex, impairing rational attribution of causality. This choice fails to facilitate cognitive restructuring, missing the opportunity to address neurocognitive mechanisms underlying overgeneralization.
Choice B reason: This response uses cognitive-behavioral techniques to challenge overgeneralization, a distortion linked to dysfunctional prefrontal cortex activity and low serotonin levels in depression. Examining a specific event encourages re-evaluation of faulty attributions, promoting neuroplasticity through cognitive restructuring, which can enhance rational thinking and reduce depressive symptoms by altering maladaptive neural pathways.
Choice C reason: This response shifts focus to cultural beliefs, irrelevant to the patient’s cognitive distortion. Depression involves altered amygdala-prefrontal cortex interactions, leading to negative self-attribution. Exploring cultural heritage does not address serotonin deficiency or facilitate cognitive reframing, making it ineffective for correcting overgeneralized thinking driven by neurochemical imbalances.
Choice D reason: This response acknowledges self-criticism but fails to engage in active cognitive restructuring. Depression involves hyperactive amygdala responses and reduced prefrontal inhibition, perpetuating negative self-perceptions. Without guiding the patient to explore alternative explanations, this choice misses the chance to alter maladaptive neural pathways, limiting its therapeutic impact on distorted thinking.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: In PTSD, glutamate drives excitatory signaling in the amygdala, enhancing fear memory consolidation, while norepinephrine heightens arousal via locus coeruleus activation, strengthening traumatic memory encoding. This hyperactive glutamatergic-noradrenergic interaction sustains fear responses, contributing to PTSD’s persistent hyperarousal and intrusive memories.
Choice B reason: GABA inhibits neural activity, counteracting excitation, but its role in PTSD is secondary, modulating rather than driving fear memory formation. Glutamate is critical for memory consolidation in the amygdala, but pairing with GABA does not fully explain PTSD’s hyperarousal and fear encoding mechanisms.
Choice C reason: Histamine regulates wakefulness and arousal but is not directly involved in PTSD’s fear memory encoding. GABA modulates inhibition but does not drive the excitatory processes in the amygdala critical for trauma-related memory consolidation, making this pair irrelevant to PTSD’s core neurochemistry.
Choice D reason: Acetylcholine modulates attention and memory but is not a primary driver of PTSD’s fear responses. Serotonin influences mood but plays a secondary role in trauma memory encoding compared to glutamate and norepinephrine, which directly mediate amygdala hyperactivity in PTSD.
Correct Answer is A
Explanation
Choice A reason: Bipolar II involves hypomania, which is less severe than bipolar I’s mania, causing milder dopamine-driven limbic hyperactivity. Hypomania impairs functioning less, as it lacks psychosis and severe impulsivity, allowing better prefrontal cortex regulation compared to bipolar I’s intense manic episodes.
Choice B reason: Bipolar II is less often recognized than bipolar I due to hypomania’s subtlety, often mistaken for normal mood. Bipolar I’s severe mania, driven by dopamine excess, is more noticeable, leading to earlier diagnosis, making this statement factually incorrect.
Choice C reason: Bipolar I includes severe mania, not just depression, driven by dopamine and norepinephrine surges in the limbic system. Bipolar II involves hypomania and depression, so this statement inaccurately describes bipolar I’s clinical features, which include prominent manic episodes.
Choice D reason: Bipolar I and II differ in mania severity, not just suicide risk. Bipolar I’s severe mania increases impulsivity via dopamine dysregulation, but both have suicide risks. This statement oversimplifies the disorders’ neurochemical and clinical distinctions, making it incorrect.
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