The client with type 2 diabetes mellitus is prescribed semaglutide. The client knows that this medication is used for diabetes but that it is also popular for weight loss. What is the mechanism of action of this drug?

Choice A reason: Metformin is safe for kidneys in patients with normal renal function but is excreted renally, requiring monitoring in chronic kidney disease (CKD). Reduced glomerular filtration rate (GFR) can lead to metformin accumulation, increasing lactic acidosis risk. Regular renal function tests (e.g., creatinine, GFR) are needed, making this statement accurate.

Choice B reason: Metformin is not nephrotoxic; it does not directly damage kidneys. Its primary risk in renal impairment is lactic acidosis due to reduced clearance, not direct toxicity. This statement is inaccurate, as metformin is generally renal-safe when monitored appropriately in patients with adequate kidney function.

Choice C reason: Metformin does not increase kidney stone risk. It lowers blood glucose by reducing hepatic gluconeogenesis and improving insulin sensitivity, without altering urinary composition linked to stones. Kidney stones are more associated with conditions like hyperuricemia or dehydration, making this statement inaccurate for metformin’s effects.

Choice D reason: Metformin requires renal function monitoring, as it is cleared by the kidneys. In renal impairment, accumulation can cause lactic acidosis, a rare but serious complication. This statement is inaccurate, as monitoring (e.g., eGFR) is essential to ensure safe use, especially in patients with kidney disease risk.

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.