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While ECT can be used in mania, especially when severe or refractory, it is not the most common indication. Pharmacologic stabilization with mood stabilizers and antipsychotics is typically first-line, and ECT is reserved for cases with poor response or life-threatening symptoms.

ECT is not routinely used for schizophrenia, particularly paranoid subtype. Antipsychotic medications are the mainstay of treatment. ECT may be considered in catatonic schizophrenia or when there is comorbid affective symptoms, but it is not the primary modality.

ECT is rarely indicated for OCD. First-line treatments include SSRIs and cognitive behavioral therapy. ECT may be considered only in extreme, treatment-resistant cases, and even then, its efficacy is limited compared to other conditions.

Monthly ECT is used in maintenance therapy, not during the acute phase. This schedule is insufficient for initial symptom resolution, as therapeutic effects require repeated stimulation over a short period.

Administering ECT three times weekly is correct, but a total of 20 to 30 sessions exceeds the typical acute course. This number may apply in chronic or refractory cases, but not as the average.

Daily ECT increases risk of cognitive impairment and is rarely used. It may be considered in life-threatening situations like catatonia or suicidality, but not as a standard regimen.

While ECT does activate the central nervous system via seizure induction, this is not the primary mechanism of its therapeutic effect. The benefit arises from downstream neurochemical and neuroplastic changes, not mere stimulation.

ECT does not decrease acetylcholine or monoamine oxidase. In fact, monoamine oxidase activity may remain unchanged or decrease slightly, but the therapeutic effect is due to increased monoamine levels, not reduction.

Altering sodium metabolism is not a recognized mechanism of ECT. While ionic shifts occur during seizures, they are transient and not linked to the antidepressant response. This choice confuses seizure physiology with therapeutic action.

Permanent brain damage and irreversible memory loss are rare and not typical. While retrograde amnesia may occur, especially with bilateral ECT, it is usually limited and improves over time. Modern techniques have significantly reduced these risks.

Fractures and dislocations were risks in early ECT before muscle relaxants were used. Today, succinylcholine prevents violent motor activity during seizures, making such injuries extremely rare.

Cardiac complications like myocardial infarction or arrest are uncommon. ECT is contraindicated in unstable cardiac conditions, and patients are pre-screened and monitored. When used appropriately, ECT poses minimal cardiovascular risk.

The risk for injury during ECT is minimal due to pre-procedure muscle relaxants and anesthesia. Sam is not currently undergoing ECT, and there is no evidence of physical instability or seizure-related complications at this time. The priority is psychological, not physical.

While Sam’s fear is influenced by media, the diagnosis of deficient knowledge alone does not capture the emotional component of his distress. Anxiety is the dominant issue, and focusing solely on knowledge deficit misses the urgency of his fear response.

There is no indication that Sam is experiencing cognitive disturbances or altered thought processes. He is expressing coherent concerns and referencing specific cultural imagery, which suggests intact cognition. This diagnosis would be premature and inaccurate.

Making guarantees is inappropriate and undermines the complexity of medical procedures. It dismisses Sam’s concerns and may create false expectations, which can erode trust if complications arise.

This statement is dismissive and paternalistic. It fails to validate Sam’s emotions and implies blind trust in authority rather than encouraging informed understanding and shared decision-making.

While emotionally supportive, this response lacks direction and does not address the underlying fear or knowledge deficit. It may comfort temporarily but does not empower Sam with the information he needs to make an informed choice.

While recording vital signs is important for baseline assessment, it is not the priority intervention. Vital signs are routinely taken before many procedures but do not address the legal and ethical prerequisites of ECT.

Having the patient void is a standard pre-procedure step to prevent incontinence during anesthesia, but it is secondary to confirming informed consent. It supports comfort and safety but does not impact the decision to proceed.

Succinylcholine is a muscle relaxant administered immediately before ECT to prevent injury during the induced seizure. However, it is given only after consent is confirmed and anesthesia is initiated. Administering it without consent would be a serious violation.

Atropine does not have anxiolytic properties. It does not act on GABAergic or serotonergic pathways involved in anxiety modulation. Benzodiazepines or other sedatives are used for anxiety, not anticholinergics.

Muscle relaxation during ECT is achieved using agents like succinylcholine, not atropine. Atropine does not affect nicotinic receptors at the neuromuscular junction and thus has no role in skeletal muscle relaxation.

Atropine is not an anesthetic. It does not induce unconsciousness or analgesia. Short-acting anesthetics like methohexital or thiopental are used in ECT to induce sedation before seizure induction.

Succinylcholine does not alleviate anxiety. It has no central nervous system activity and does not affect emotional or psychological states. Anxiolytics like benzodiazepines are used for anxiety management.

It does not reduce secretions. Anticholinergic agents like atropine are used to decrease salivary and respiratory secretions prior to ECT. Succinylcholine has no effect on glandular output.

Succinylcholine is not an anesthetic. It does not induce unconsciousness or analgesia. Anesthesia must be administered separately before succinylcholine to prevent awareness during paralysis.