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Negative thoughts are more aligned with cognitive theories of mood disorders. While they may exacerbate symptoms, they do not explain the biological etiology of bipolar disorder.

Blaming a parent reflects misunderstanding of genetic predisposition. Biological theory emphasizes inherited risk, not fault or intentional transmission.

Learning through family interactions aligns with behavioral or social learning theories. It does not demonstrate understanding of the biological mechanisms underlying bipolar disorder.

While accountability is important, insisting on responsibility before understanding the behavior may hinder rapport. Insight and change often follow empathetic exploration, not confrontation.

Increasing self-esteem may reduce manipulative behaviors, but this statement oversimplifies the complex psychological function of grandiosity. It does not address the nurse’s role in understanding motivation.

Reinforcement strategies are useful in behavior modification but do not directly address the emotional or cognitive roots of grandiosity. This approach is more applicable to structured behavioral interventions.

While psychosocial theories offer valuable insights, their credibility has not necessarily “strengthened” in isolation. Modern understanding favors integrative models rather than elevating psychosocial theory alone.

Describing bipolar disorder as purely genetic oversimplifies its etiology. Although heritability is high, environmental and psychological factors significantly influence onset and progression.

Manic episodes following substance use reflect substance/medication-induced mood disorders, not psychosocial theory. This explanation aligns more with pharmacologic or biological models.

Family studies demonstrate genetic risk, not biochemical changes. While heritability is important, this statement aligns with genetic theory rather than biochemical mechanisms.

MRI findings indicate structural brain changes, such as ventricular enlargement and white matter abnormalities. These support neuroanatomical theories, not biochemical ones.

Twin studies highlight genetic concordance, showing heritable patterns of bipolar disorder. This evidence supports genetic predisposition, not biochemical dysfunction.

ECT is not primarily used to prevent depressive episodes. While it can treat bipolar depression, its role is therapeutic rather than prophylactic. Preventive strategies typically involve long-term pharmacologic maintenance.

ECT may be used in schizophrenia, but chronic undifferentiated schizophrenia is not a common dual indication with bipolar disorder. This statement inaccurately generalizes ECT use across unrelated diagnoses.

Disordered eating is not a primary indication for ECT. While mania may involve poor impulse control, ECT is reserved for severe mood symptoms, not behavioral patterns like eating disturbances.

Suggesting the client is seeking attention reinforces stigma and dismisses the seriousness of the illness. It lacks empathy and undermines the therapeutic environment.

While promoting respectful language is important, this response does not address the misunderstanding about the client’s behavior or provide insight into the condition.

Saying the client has the “right” to be difficult to assess is vague and non-informative. It neither educates nor fosters empathy, and may confuse the assistant further.