Which client presenting in the clinic most likely reveals manifestation(s) of rheumatoid arthritis?

Choice A reason: Insulin lispro, a rapid-acting insulin, peaks 1-2 hours after administration (around 8:30-9:30 am for a 7:30 am dose). This peak coincides with maximum glucose-lowering effect, increasing hypoglycemia risk, especially if breakfast is inadequate or delayed. This time is the most likely for low blood sugar due to insulin’s pharmacodynamics.

Choice B reason: At 7:45 am, insulin lispro is just beginning to act (onset 15-30 minutes), and breakfast is likely being consumed, providing glucose to counter insulin’s effect. Hypoglycemia risk is lower than at peak action (1-2 hours), making this time less critical for hypoglycemia monitoring.

Choice C reason: By 12:30 pm, insulin lispro’s effect (duration 3-5 hours) is waning, and glucose from breakfast is metabolized. Hypoglycemia risk is lower unless additional insulin or activity occurs. This time is less likely for hypoglycemia compared to the peak action period around 8:30 am.

Choice D reason: Tomorrow at 6:30 am is beyond insulin lispro’s duration of action (3-5 hours). Hypoglycemia risk from the 7:30 am dose is negligible 23 hours later, as insulin is cleared. This time is irrelevant to the dose’s effect, making it the least likely for hypoglycemia.

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.