A client with type 1 diabetes is receiving insulin therapy. The nurse observes the patient experiencing symptoms such as sweating, trembling, and confusion. What is the nurse’s first action?

Choice A reason: Sweating, trembling, and confusion indicate hypoglycemia in type 1 diabetes, likely from excess insulin. Administering fast-acting carbohydrates (e.g., glucose tablets, juice) rapidly raises blood glucose by providing readily absorbable sugars, reversing neuroglycopenic symptoms. This is the first action to prevent seizures or coma, ensuring immediate stabilization.

Choice B reason: Administering insulin during hypoglycemia would further lower blood glucose, exacerbating symptoms and risking severe outcomes like unconsciousness. Insulin drives glucose into cells, worsening the deficit. This action is contraindicated and dangerous, as it directly opposes the need to raise blood sugar immediately.

Choice C reason: Complex carbohydrates and proteins digest slowly, providing delayed glucose release, unsuitable for acute hypoglycemia requiring rapid correction. While appropriate for long-term glucose stability, this is not the first action, as it fails to address the urgent need for fast-acting sugars to reverse symptoms.

Choice D reason: Calling the healthcare provider delays treatment of hypoglycemia, which requires immediate carbohydrate administration to prevent neurological damage. While provider consultation may follow for insulin adjustment, it is not the first action. This choice is inappropriate, as it postpones critical intervention needed for symptom resolution.

Choice A reason: GABA, an inhibitory neurotransmitter, is not the primary target of antidepressants like SSRIs or tricyclics. These drugs focus on monoamines (serotonin, norepinephrine). GABAergic drugs, like benzodiazepines, treat anxiety, not depression. This statement is inaccurate, as antidepressants do not enhance GABA efficacy in the limbic system or cortex.

Choice B reason: SSRIs and tricyclics block reuptake of serotonin and/or norepinephrine in the synaptic cleft, increasing their availability to stimulate postsynaptic receptors. This enhances monoamine signaling, alleviating depressive symptoms. This statement is accurate, as reuptake inhibition is the shared mechanism across these antidepressant classes, targeting mood-regulating neurotransmitters.

Choice C reason: Dopamine receptor antagonism is not a mechanism of antidepressants but is associated with antipsychotics like haloperidol. While some antidepressants indirectly affect dopamine, it is not their primary action. This statement is inaccurate, as SSRIs and tricyclics focus on serotonin and norepinephrine, not dopamine receptor blockade.

Choice D reason: Antagonizing serotonin receptors would reduce serotonin signaling, counteracting antidepressant effects. SSRIs and tricyclics increase serotonin availability via reuptake inhibition, not receptor blockade. This statement is inaccurate, as blocking serotonin receptors is not a mechanism of action for these depression treatments.