Physiology of Heat and Cold Practice Test

Fever caused by pyrogens is driven by prostaglandin E2 acting in the hypothalamus to raise the body's temperature set point. Pyrogens trigger cytokines like IL-1 and TNF-α, which increase COX-2 activity and boost PGE2 production. PGE2 then binds receptors in the hypothalamic preoptic area, signaling that heat should be conserved and produced, which leads to fever through mechanisms like shivering and vasoconstriction. Drugs that reduce fever (NSAIDs) work by blocking COX and lowering PGE2 synthesis in the hypothalamus. Other prostaglandins have different primary roles (for example, TXA2 in platelet function and vasoconstriction, PGD2 in sleep and vasodilation, PGE1 in various vascular effects) and are not the main mediators of fever.