What is the physiologic mechanism behind the development of pyrexia?

Choice A reason: Pyrexia (fever) occurs when pyrogens, like cytokines (IL-1, IL-6), released during infection or inflammation, act on the hypothalamus to raise the body’s temperature set point. This triggers heat production via shivering and vasoconstriction, conserving heat to create a fever, enhancing immune response. This statement accurately describes the primary mechanism of pyrexia.

Choice B reason: Peripheral vasoconstriction occurs during fever to conserve heat but is a response, not the cause, of pyrexia. It results from hypothalamic signaling after pyrogens reset the thermostat. This statement is inaccurate, as vasoconstriction is a secondary effect, not the initiating physiologic mechanism of fever development.

Choice C reason: Fever increases, not decreases, metabolic rate to generate heat via thermogenesis. Pyrogens elevate the hypothalamic set point, prompting energy expenditure through shivering and muscle activity. This statement is inaccurate, as reduced metabolism would lower body temperature, counteracting the fever response triggered by infection or inflammation.

Choice D reason: Prostaglandin synthesis, particularly PGE2, in the hypothalamus is stimulated by pyrogens, raising the temperature set point to cause fever. Inhibiting prostaglandin synthesis (e.g., by NSAIDs) reduces fever, not causes it. This statement is inaccurate, as prostaglandin inhibition opposes the physiologic mechanism of pyrexia.

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.