---

Body Temperature Physiology - 10 Marks

---

1. Normal Body Temperature

• Core temperature (deep tissues - liver, brain, heart): maintained within a very narrow range of 36°C - 37.5°C (96.8°F - 99.5°F). Oral measurement averages 98.0-98.6°F; rectal is ~1°F higher.
• Skin temperature: varies freely with the environment and is important for heat transfer to surroundings.

---

2. Heat Balance Equation

Body temperature = Heat Production - Heat Loss

---

3. Heat Production

• Guyton and Hall Textbook of Medical Physiology, p. 892

---

4. Heat Loss Mechanisms

A. Radiation (~60%)

B. Conduction (~3%)

C. Convection

D. Evaporation (~22-25%)

• Insensible perspiration: 600-700 mL/day evaporates from lungs and skin continuously. Cannot be controlled.
• Sweating (sensible perspiration): Controlled by the hypothalamus via sympathetic cholinergic fibers to eccrine sweat glands. At maximum activity, sweat rate can reach 1.5 L/hour. Each gram of water evaporated loses ~0.58 kcal of heat.
• Evaporation is the only effective mechanism when ambient temperature exceeds body temperature.

E. Role of Skin Blood Flow

• Guyton and Hall Textbook of Medical Physiology, pp. 892-895

---

5. Thermoregulatory Center - The Hypothalamus

• Contains warm-sensitive neurons (fire when temperature rises → activate heat dissipation)
• Contains cold-sensitive neurons (fire when temperature falls → activate heat conservation)
• Receives input from: peripheral cutaneous receptors (especially cold receptors in skin), spinal cord thermoreceptors, deep tissue receptors, and intrinsic hypothalamic receptors - each contributing approximately 20% of the integrated signal (Ganong)

• Sweating and vasodilation: 37°C
• Vasoconstriction: 36.8°C
• Non-shivering thermogenesis: 36°C
• Shivering: 35.5°C
• Ganong's Review of Medical Physiology, 26th Ed., p. 324

---

6. Responses to Cold (Heat Conservation & Production)

1. Cutaneous vasoconstriction - sympathetic adrenergic activation constricts skin arterioles and AV anastomoses; diverts blood away from skin
2. Shivering - involuntary rhythmic muscle contractions; can increase heat production 3-5 times above basal
3. Non-shivering thermogenesis - epinephrine/norepinephrine increase cellular metabolism; important in neonates via brown adipose tissue (BAT)
4. Thyroid hormone release - increases basal metabolic rate (longer-term adaptation)
5. Countercurrent heat exchange - in limbs, warm arterial blood transfers heat to cold venous blood (venae comitantes), conserving core temperature
6. Behavioral responses - huddling, adding clothing, seeking warmth

---

7. Responses to Heat (Heat Dissipation)

1. Cutaneous vasodilation - decreased sympathetic tone; skin blood flow rises dramatically
2. Sweating - sympathetic cholinergic fibers activate eccrine glands; primary heat-loss mechanism in hot conditions
3. Behavioral responses - seeking shade, removing clothing, reducing activity
4. Inhibition of shivering and non-shivering thermogenesis

---

8. Fever

Mechanism:

• IL-1β (the most important - also called leukocyte pyrogen)
• IL-6, TNF-α, IFN-β, IFN-γ

Course of Fever:

1. Chill phase: new set-point is higher than current temperature → hypothalamus activates heat-conservation (vasoconstriction) and heat-production (shivering) → patient feels cold, shivers
2. Plateau phase: body temperature reaches new set-point; balance between production and loss
3. Defervescence (crisis/lysis): pyrogens removed → set-point returns to normal → body temperature now "too high" → hypothalamus activates sweating and vasodilation to dissipate heat

Antipyretics (e.g., Aspirin, NSAIDs):

• Costanzo Physiology 7th Ed., p. [block 2]; Guyton & Hall, p. 900

---

9. Clinical Disturbances of Thermoregulation

---

Summary Table

---

---

Body Temperature Physiology - MBBS 1st Year PYQ Answers (10 Marks Each)

---

⭐ PYQ 1 - Most Repeated (Almost Every Year)

"Describe the regulation of body temperature. Add a note on fever." [10 marks]

---

Definition & Normal Values

• Core temperature: 36°C - 37.5°C (oral avg = 98.6°F / 37°C; rectal = 0.5°C higher)
• Skin temperature: varies with environment
• Diurnal variation: lowest at 6 AM (~36°C), highest at 6 PM (~37.5°C)
• Core temperature = Heat produced - Heat lost

---

I. HEAT PRODUCTION (Sources)

---

II. HEAT LOSS MECHANISMS

Key point: When ambient temperature > body temperature, evaporation is the ONLY effective mechanism. This is why humidity impairs heat loss.

---

III. THERMOREGULATORY CENTER - HYPOTHALAMUS

1. Peripheral cutaneous cold/warm receptors (skin)
2. Spinal cord thermoreceptors
3. Deep tissue receptors
4. Extrahypothalamic brain receptors
5. Intrinsic hypothalamic thermosensitive neurons

• Vasodilation + sweating onset: 37°C
• Vasoconstriction onset: 36.8°C
• Non-shivering thermogenesis: 36°C
• Shivering onset: 35.5°C

---

IV. RESPONSES TO COLD (Heat Conservation)

1. Cutaneous vasoconstriction - sympathetic adrenergic activation; diverts blood from skin to core
2. Shivering - involuntary rhythmic skeletal muscle contractions; increases heat production 3-5x; controlled by posterior hypothalamus
3. Non-shivering thermogenesis - epinephrine/NE release → uncoupling of oxidative phosphorylation, especially in BAT (important in neonates)
4. Thyroid hormone release - long-term increase in BMR (acclimatization)
5. Countercurrent heat exchange - deep veins (venae comitantes) run alongside arteries in limbs; warm arterial blood transfers heat to cold venous blood, conserving core temperature
6. Behavioral - seeking warmth, adding clothing, curling up

---

V. RESPONSES TO HEAT (Heat Dissipation)

1. Cutaneous vasodilation - decreased sympathetic tone; AV anastomoses open; skin blood flow → up to 30% cardiac output
2. Sweating - sympathetic cholinergic fibers → eccrine sweat glands; max rate ~1.5 L/hour; each gram evaporated = 0.58 kcal heat lost
3. Inhibition of shivering and thermogenesis
4. Behavioral - removing clothing, reducing activity, seeking shade

---

VI. FEVER

Infection/Tissue damage
        ↓
Exogenous pyrogens (endotoxins, LPS, viral antigens)
        ↓
Phagocytosis by Macrophages, Monocytes, Kupffer cells
        ↓
Release of Endogenous Pyrogens (Cytokines):
  • IL-1β (most important - "leukocyte pyrogen")
  • IL-6
  • TNF-α
  • IFN-β, IFN-γ
        ↓
Act on OVLT (Organum Vasculosum of Lamina Terminalis)
[circumventricular organ - lacks BBB]
        ↓
Stimulate Preoptic Hypothalamus
        ↓
↑ Arachidonic acid → ↑ COX → ↑ Prostaglandin E2 (PGE2)
        ↓
SET-POINT RAISED above 37°C

---

⭐ PYQ 2 - Frequently Asked

"Describe the mechanisms of heat loss from the body." [10 marks]

• Skin: ~300-400 mL/day (diffusion, cannot be controlled)
• Lungs: ~300-400 mL/day (expired air is saturated at 37°C)
• Total insensible loss: 600-700 mL/day

---

⭐ PYQ 3 - Common Short/Long Note

"Write a note on Heat Stroke and Heat Exhaustion." [10 marks]

Heat Illnesses Classification (Park's Textbook)

Heat Stroke - Details

• Classic heat stroke: Elderly, sedentary, during heat waves; not due to exertion
• Exertional heat stroke: Young athletes/military; vigorous exercise in hot humid conditions

• Extreme rise in temp → positive feedback loop begins at ~41°C
• Hypothalamus itself damaged by heat → thermoregulation fails
• Multiorgan dysfunction: rhabdomyolysis, DIC, renal failure, hepatic failure

• Rapidly cool body in ice-water bath until rectal temp falls below 38.9°C (102°F)
• Monitor rectal temperature continuously
• Supportive: treat hypovolemia, hyperkalemia, rhabdomyolysis, hypocalcemia

Heat Exhaustion - Details

• Prolonged heat + sweating → loss of water and electrolytes → ECF/blood volume ↓ → BP ↓ → cardiovascular failure
• Heat-dissipating mechanisms (sweating) are still functional
• Spontaneously resolves if the victim can rehydrate

Heat Cramps

• Painful spasmodic contractions of skeletal muscles during heavy work in heat
• Cause: Loss of sodium and chloride in sweat
• Treatment: Salt and water replacement

---

⭐ PYQ 4 - Frequently Asked (5-10 marks)

"Write a note on Hypothermia." [5-10 marks]

• Direct effects: Crystallization of intra/extracellular water → disruption of plasma membranes
• Indirect effects: Slow chilling → vasoconstriction + increased capillary permeability → edema → nerve damage → gangrene. Rapid chilling → vascular injury + increased blood viscosity → ischemia → infarction

---

⭐ PYQ 5 - Explain Why / Short Note

"Why does sweating not cool the body in humid conditions?" / "Role of humidity in heat regulation"

• Heat loss by evaporation depends on the vapor pressure gradient between sweat on skin and surrounding air
• In high humidity, air is already saturated with water vapor → vapor pressure gradient is minimal → sweat cannot evaporate efficiently
• Sweat drips off instead of evaporating → no cooling effect
• Body continues to sweat → progressive dehydration without effective temperature control
• This is why humid heat is more dangerous than dry heat at the same temperature

---

⭐ PYQ 6 - Short Note

"Write a note on Acclimatization to heat." [5 marks]

• Mechanism: aldosterone (from adrenal cortex) is secreted in response to Na⁺ loss in sweat → increases reabsorption of Na⁺ in sweat ducts
• Unacclimatized persons need extra salt in first 10 days only

---

Quick Revision Table - All Key Points

---