15/12/2025
✅Pathophysiology of fever✅
The process of fever begins when the body encounters foreign substances like bacteria or viruses, which are known as Exogenous Pyrogens. These pyrogens are detected by the body's immune cells, primarily macrophages, leading to their activation. The activated immune cells then release their own signaling molecules, called Endogenous Pyrogens or Cytokines (such as IL-1, IL-6, and TNF-alpha), into the bloodstream.
These cytokines travel to the brain and act on the thermoregulatory center in the hypothalamus. They stimulate the local production of Prostaglandin E2 (PGE2), which is the key molecule that "resets" the body's internal thermostat to a higher temperature.
With the set point now elevated, the body perceives itself as being too cold, initiating a phase called the Fever Ascent. To raise the core temperature to the new set point, the body conserves heat by constricting blood vessels in the skin (causing chills and paleness) and generates heat through shivering and increased metabolism. The fever then reaches a plateau, known as Fever Maintenance, where the temperature is held steady at the new, elevated level.
Finally, when the infection resolves or antipyretic medication is administered (which blocks PGE2 production), the hypothalamic set point drops back to normal. The body then rapidly sheds the excess heat through Defervescence, primarily by triggering peripheral vasodilation (flushing) and sweating.
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