Which statement best describes how physiologic doses of glucocorticoids are used?
Physiologic doses of glucocorticoids balance the feedback loop in clients with adrenal insufficiency
Physiologic doses of glucocorticoids have the greatest impact on fluid and electrolyte balance
Physiologic doses of glucocorticoids treat inflammatory disease in the body like rheumatoid arthritis
Physiologic doses of glucocorticoids lower blood glucose in place of insulin
The Correct Answer is A
Choice A reason: Physiologic doses of glucocorticoids, like hydrocortisone, mimic normal cortisol production (20-30 mg/day) in adrenal insufficiency, restoring hypothalamic-pituitary-adrenal axis feedback. This maintains metabolism, stress response, and immune function without excess. This statement is accurate, as these doses replace deficient cortisol to stabilize endocrine function.
Choice B reason: Physiologic doses have minimal impact on fluid and electrolyte balance compared to pharmacologic doses, which cause sodium retention via mineralocorticoid effects. In adrenal insufficiency, physiologic doses normalize cortisol without significant fluid shifts. This statement is inaccurate, as electrolyte effects are secondary and less pronounced.
Choice C reason: Physiologic doses replace cortisol in adrenal insufficiency, not treat inflammation. Pharmacologic (higher) doses suppress inflammation in diseases like rheumatoid arthritis by inhibiting cytokine production. This statement is inaccurate, as physiologic doses are insufficient for anti-inflammatory effects required in such conditions.
Choice D reason: Glucocorticoids increase, not lower, blood glucose by promoting gluconeogenesis and insulin resistance. Physiologic doses maintain normal glucose metabolism in adrenal insufficiency but do not replace insulin’s role. This statement is inaccurate, as glucocorticoids oppose insulin’s glucose-lowering effects, even at physiologic levels.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
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.
Correct Answer is B
Explanation
Choice A reason: Prednisone causes hyperglycemia by increasing gluconeogenesis and insulin resistance, similar to other corticosteroids. Its lower mineralocorticoid activity does not significantly reduce this effect compared to other steroids. This statement is inaccurate, as prednisone’s glycemic impact is comparable, not less extreme, than other corticosteroids.
Choice B reason: Prednisone has minimal mineralocorticoid activity compared to steroids like hydrocortisone, resulting in less sodium and water retention. Mineralocorticoids promote renal sodium reabsorption, causing fluid retention. Prednisone’s glucocorticoid dominance reduces these effects, making this statement accurate for expected nursing observations during administration.
Choice C reason: Prednisone’s low mineralocorticoid activity leads to less, not more, sodium retention. It does not disproportionately affect water retention independently of sodium. This statement is inaccurate, as prednisone’s profile minimizes both sodium and water retention compared to steroids with higher mineralocorticoid effects.
Choice D reason: Prednisone causes hyperglycemia, but its effect is not more extreme than other corticosteroids like dexamethasone. Its glucocorticoid activity drives gluconeogenesis similarly across the class. This statement is inaccurate, as prednisone’s hyperglycemic effects are standard, not uniquely severe, among oral corticosteroids.
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