What is the physiologic mechanism behind the development of pyrexia?
Release of pyrogens resetting the hypothalamic thermostat
Increased peripheral vasoconstriction reducing heat loss
Decreased metabolic rate increasing heat production
Inhibition of prostaglandin synthesis in the hypothalamus
The Correct Answer is A
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.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Chronic kidney disease (CKD) does not primarily cause anemia by leaking red blood cells (RBCs) into urine. While hematuria may occur in some renal conditions, anemia in CKD results mainly from reduced erythropoietin production, not RBC loss. This statement is inaccurate, as it misrepresents the primary mechanism of anemia in CKD.
Choice B reason: Inflammation in CKD may contribute to anemia by suppressing erythropoiesis through cytokine release, but it does not directly attack RBCs. The primary cause is erythropoietin deficiency due to impaired renal function. This statement is inaccurate, as it overstates inflammation’s role and ignores the key hormonal mechanism in CKD-related anemia.
Choice C reason: High vascular pressure in CKD can damage kidneys but does not directly cause RBCs to burst (hemolysis). Anemia in CKD stems from reduced erythropoietin, not mechanical RBC destruction. This statement is inaccurate, as it incorrectly links hypertension’s renal effects to direct RBC damage, misrepresenting the anemia’s cause.
Choice D reason: CKD causes anemia due to reduced erythropoietin synthesis by damaged kidneys. Erythropoietin stimulates RBC production in bone marrow. In CKD, impaired renal function decreases erythropoietin, leading to anemia. This statement is accurate, as it correctly identifies the hormonal deficiency as the primary cause of low RBC counts in CKD.
Correct Answer is A
Explanation
Choice A reason: SGLT-2 inhibitors, like empagliflozin, block sodium-glucose cotransporter 2 in the proximal tubule, preventing glucose reabsorption. This increases urinary glucose excretion, lowering blood sugar in type 2 diabetes. The mechanism is insulin-independent, reducing hyperglycemia and promoting weight loss, making this statement accurate for their primary action.
Choice B reason: SGLT-2 inhibitors do not interact with transcription factors to improve insulin sensitivity. This describes metformin’s action via AMPK activation in liver and muscle. SGLT-2 inhibitors act renally, not on transcription factors, making this statement inaccurate as it misattributes their mechanism to a different drug class.
Choice C reason: Inhibiting hepatic glucose production and increasing insulin sensitivity is metformin’s mechanism, not SGLT-2 inhibitors. SGLT-2 inhibitors work renally to excrete glucose, not by altering hepatic gluconeogenesis or peripheral insulin sensitivity. This statement is inaccurate, as it describes a different antidiabetic drug’s action.
Choice D reason: Blocking ATP-sensitive K+ channels is the mechanism of sulfonylureas, like glipizide, which stimulate insulin secretion from beta cells. SGLT-2 inhibitors act on renal glucose reabsorption, not beta cell channels. This statement is inaccurate, as it incorrectly assigns a sulfonylurea mechanism to SGLT-2 inhibitors.
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