Hyperthermia vs fever

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Fever vs. Hyperthermia - The Core Conflict

FeatureFever (Pyrexia)Hyperthermia
Hypothalamic Set-PointIncreased (regulated)Normal (unregulated)
MechanismPyrogens (IL-1, TNF) → ↑ $PGE_2$Uncontrolled heat production or failed dissipation
SkinInitially cold/clammy, then warmHot, dry
Response to AntipyreticsYes (resets set-point)No

⭐ The failure of high body temperature to respond to antipyretics (e.g., NSAIDs) is a key sign pointing to hyperthermia, necessitating immediate physical cooling instead.

Pathophysiology - How It Gets Hot

  • Fever: Hypothalamic set-point is elevated.

    • Exogenous pyrogens (e.g., LPS) → stimulate immune cells.
    • Endogenous pyrogens (e.g., IL-1, IL-6, TNF-α) → travel to hypothalamus.
    • Cause release of Prostaglandin E₂ ($PGE₂$) via COX-2 enzyme.
    • $PGE₂$ raises the thermoregulatory set-point in the anterior hypothalamus.
    • Body activates heat conservation/production (shivering, vasoconstriction) to match the new, higher set-point.
  • Hyperthermia: Hypothalamic set-point remains normal.

    • Heat gain overwhelms the body's ability to dissipate heat.
    • Caused by exogenous heat exposure (heat stroke) or endogenous heat production (malignant hyperthermia, strenuous exercise).

⭐ NSAIDs (e.g., ibuprofen) and acetaminophen reduce fever by inhibiting COX enzymes, thereby blocking $PGE₂$ synthesis and resetting the hypothalamic set-point downwards.

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Clinical Clues - Spot the Difference

FeatureHyperthermiaFever
MechanismUncontrolled heat gainHypothalamus ↑ set-point
Set-PointNormalElevated
SkinHot, dry (no sweating)Hot, moist (sweating)
Diurnal VariationAbsentPresent
AntipyreticsNo responseResponse (resets set-point)
CausesHeat stroke, drugs (MDMA), malignant hyperthermiaInfection, inflammation, malignancy

Management - Cooling Down

ManagementFeverHyperthermia (e.g., Heat Stroke)
Primary GoalLower the hypothalamic set-pointDissipate heat; core temp is high despite a normal set-point
AntipyreticsEffective. Inhibit prostaglandin E₂ synthesis, resetting the thermostat.Ineffective. The hypothalamic set-point is already normal.
Physical CoolingAdjunctive, for comfort.Primary treatment. Use evaporative or ice-water immersion for rapid cooling.

High‑Yield Points - ⚡ Biggest Takeaways

  • In fever, the hypothalamic set-point is elevated due to pyrogens; the body correctly thermoregulates to a higher temperature.
  • In hyperthermia, the hypothalamic set-point remains normal; heat-dissipating mechanisms are simply overwhelmed or fail.
  • Antipyretics (e.g., NSAIDs) are effective in fever by lowering the set-point but are ineffective in hyperthermia.
  • Key causes of hyperthermia include heat stroke, malignant hyperthermia, and drug-induced states.

Practice Questions: Hyperthermia vs fever

Test your understanding with these related questions

A 15-year-old boy is brought to the emergency department by his father 10 minutes after falling into a frozen lake during ice fishing. He was in the water for less than 1 minute before his father managed to pull him out. On arrival, his clothes are still wet and he appears scared. His body temperature is 36.2°C (97.1°F), pulse is 102/min, blood pressure is 133/88 mm Hg. Which of the following mechanisms contributes most to maintaining this patient's core body temperature?

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Flashcards: Hyperthermia vs fever

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Which interleukin is primarily responsible for fever and acute inflammation?_____

TAP TO REVEAL ANSWER

Which interleukin is primarily responsible for fever and acute inflammation?_____

IL-1

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