Insulin forces which electrolyte out of the plasma and into the cells?

Choice A reason: Allopurinol does not directly target inflammation or pain in acute gout attacks; it lowers uric acid levels to prevent future attacks. Anti-inflammatories like NSAIDs or colchicine manage acute symptoms. This statement is inaccurate, as allopurinol’s role is preventive, not for acute symptom relief.

Choice B reason: Allopurinol inhibits xanthine oxidase, reducing uric acid production, which prevents urate crystal formation and gout attacks. It is used for long-term management of hyperuricemia. This statement is accurate, as decreased uric acid production is the primary mechanism, critical for patient education on its purpose.

Choice C reason: Kidney function tests are necessary with allopurinol, as it is renally excreted, and impaired renal function can increase toxicity risk (e.g., rash, interstitial nephritis). Monitoring ensures safe use, especially in gout patients with potential renal issues, making this statement inaccurate for discharge instructions.

Choice D reason: Limiting fluid intake to 1000cc daily is inappropriate; high fluid intake (2-3L/day) is recommended with allopurinol to prevent urate kidney stones by diluting urine. This statement is inaccurate, as it contradicts the need for hydration to support uric acid excretion and prevent complications.

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.