CNS22 Temperature Regulation and Fever PDF
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Uploaded by EasierGothicArt
Universiti Putra Malaysia
2023
Nurul Hayati Mohamad Zainal
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Summary
These are lecture notes on temperature regulation and fever, focusing on the mechanisms and regulation of body temperature. The notes cover topics such as normal body temperature, heat production, and thermoregulation, alongside discussions about disorders related to temperature regulation such as fever, heat exhaustion, and hypothermia. The notes are from Universiti Putra Malaysia session 2023/2024.
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LEARNING OBJECTIVES To list range of normal body temperature and its significance. To describe temperature regulating mechanism. To correctly identify the relevant temperature regulating mechanism in various common conditions. CONTENTS 1.0 NORMAL BODY TE...
LEARNING OBJECTIVES To list range of normal body temperature and its significance. To describe temperature regulating mechanism. To correctly identify the relevant temperature regulating mechanism in various common conditions. CONTENTS 1.0 NORMAL BODY TEMPERATURE 2.0 HEAT PRODUCTION IN MEN 3.0 TEMPERATURE-REGULATING MECHANISMS 4.0 DISORDERS OF THERMOREGULATION 5.0 REFERENCES 1.0 NORMAL BODY TEMPERATURE Core Shell temperature temperature The T˚ within the inner The T˚of the superficial core, which consists of parts of the body, the abdominal and essentially the skin and Storing glycogen, thoracic organs, CNS and fats, iron, copper, vitamins subcutaneous fat skeletal muscles. Not regulated but Kept constant, fluctuates considerably homeostatically in the same direction as maintained at 37.8˚C the ambient temperature surrounding 1.0 NORMAL BODY TEMPERATURE Normal T˚: denatured 35.5˚C to 37.7˚C ~ 36.7˚C · 741 c = - - enzyme T˚ regulation is important because body enzymes have optimum T˚ at which the rate of chemical reactions they catalyze is Storing maximum glycogen, fats, iron, copper, vitamins Metabolic processes slow down as the body T˚. Enzymes will be denatured at T˚. medium of blood acts as the vehicle of(heat exchange( Human1 between the core of the body and its shell. 1.1 Sites and Locations for Body T˚ Measurement superficial skin subcutaneous fat ↑ , Shell temperature Oral (widely used clinically, convenience for measuring) Axillary, forehead. & O 1.1 Sites and Locations for Body T˚ Measurement inner core > - thoracic and abd-organ , CNS , sheletal m/s ~ Core temperature Tympanic membrane, rectal, oesophagal, stomach, heart, liver, brain and blood * most accurate Rectal (highest, best index of core T˚). Highest shell I shell T Rectal T˚ > 0.6˚C Oral T˚ > 0.6˚C Axillary T˚ 1.2 Factors Affecting Variation of Body T˚ * 1) Individual variation. on-going / biologically recurring 24/7 > + X day time changes 2) Diurnal variation of core T˚ (circadian rhythm) Lowest in the early morning (3-4 am, 35.5˚C), highest in the evening (5–7 pm, 37.7˚C) Due to cyclic resetting of the hypothalamic thermostat The difference ~ 1˚C. 3) Sex Women – in reproductive age have basal body T˚ by 0.5˚C in the postovulatory period, T˚ persists and falls with decreased steroid level just before the onset of menstruation If pregnant, this T˚ elevation is sustained until delivery Men – scrotal T˚ is 2 to 4˚C lower than the core T˚. ↓ located outside body 1.2 Factors Affecting Variation of Body T˚ 4) Physical activity – lowest during sleep and higher during exercise (heat production by muscles, 40˚C). - - 5) Emotional excitement – may account for some unexplained fever due to unconscious tensing of muscles. happy sangat > - deman ! + 6) In extremely cold or hot weather, fall or rise 1˚C. Storing glycogen, 7) Thermoregulatory fats, iron, copper, mechanisms vitamins (coordinated by the hypothalamus). body thermosat 2.0 HEAT PRODUCTION IN MEN 2.1 Thermal Balance Heat loss from the body = heat gain from the surrounding. Heat loss > Heat gain (body T˚ falls) Heat gain > Heat loss (body T˚ rises) The individual in a state of thermal balance at which body T˚ is kept constant. Heat input: gain from external environment + internal heat production. Heat output: heat loss from exposed body surface to external environment. 2.0 HEAT PRODUCTION IN MEN 2.1 Thermal Balance Heat gain mechanisms Heat loss mechanisms Reduction of heat loss Reduction > of heat gain of appetite - lack > lack of interest 1. Skin vasoconstriction 1. Anorexia, apathy, inertia > tendency to do nothing - - orremain 2. Piloerection (vestigial in humans) 2. Decreased metabolic heat production unchange ↳part of body Crudimentary) 3. Behaviour that become atrophic and (cold intolerance in hypothyroidism) clothing functionless 3. Behaviour curling up reduction of clothing artificial heating (heat gain). cooler environment. Y heater When heat loss is reduced, body T˚. So, reduction of heat loss is considered as heat gain mechanism. When heat gain is reduced, body T˚. So, reduction of heat gain is considered as heat loss mechanism. 2.11 Mechanisms of heat transfer from the bod When environmental T˚ is in the hot season, sweating followed by evaporation is the only mean of heat loss. Vaporization of sweat involves loss of heat from nearby surrounding tissues (2.42 kJ for every gram of water evaporated). Evaporation does not need a thermal gradient. - Evaporation influenced by environment humidity. A More humid the environment: less evaporation. Very hot humid environments are incompatible with life because sweat cannot evaporate. 2.11 Mechanisms of heat transfer from the bod ** * electromagnetic * direct contact waves * liquid > - gaseous / * air movement current Ref: Human Physiology, Lauralee Sherwood, 4th Edition 2012 page 488 3.0 TEMPERATURE-REGULATING MECHANISMS 3.1 Thermoregulation Balance between heat gain and heat loss. Controlled by: Nervous system Endocrine (reflexes & 2 (secondary semireflexes) importance) 3.0 TEMPERATURE-REGULATING MECHANISMS 3.1 Thermoregulation Nervous system (thermoregulatory reflex) 3. Integrating 4. Effector pathways and 2. Afferent 1. Receptor pathways center effector organs 1) Peripheral Pathway to Hypothalamus a) Somatic nervous system thermoreceptors hypothalamus TWO centers for Pyramidal tract – voluntary muscular (located in dermis of thermoregulation activity skin: cold receptors & warm receptors and a) Anterior Lateral tectospinal tract – shivering detect ). hypothalamus (heat loss center) b) ANS – sympathetic division 2) Central – activated when Sympathetic noradrenergic nerve: - thermoreceptors - skin (cutaneous) vasoconstriction or (located in anterior (warmth). vasodilatation, hypothalamus and - piloerection – pilomotor mechanism detect ). b) Posterior (in hairy animals), hypothalamus - brown fat thermogenesis, (heat production - heat generation (in newborn center) – activated mammals). Sympathetic cholinergic nerve: (cold). sweating (sudomotor mechanism) 3.0 TEMPERATURE-REGULATING MECHANISMS 3.1 Thermoregulation Nervous system (thermoregulatory reflex) ant -- heat los cent - When body temp ↑ Hypothalamus > 94 -. - post + heat production in. > act -. when body ↓ Body’s thermostat Detect changes in blood T˚ as small as 0.01˚ C In increasing heat loss Hypothalamic control can override CVS control of these vessels In extreme hot weather, BP can due to extensive vasodilation. In increasing heat production Shivering (reflex) – muscle tone, rhythmic, skeletal muscles contraction, rapid: 10-20/sec but not in newborns (lack ability to shiver) – effective: heat production 2-5 times Augment by heat producing actions: bouncing, clapping hands. 3.0 TEMPERATURE-REGULATING MECHANISMS 3.1 Thermoregulation 3.0 TEMPERATURE-REGULATING MECHANISMS 3.1 Thermoregulation Endocrine (secondary importance) # not doesn't play a role Endocrine control is not important in day-to-day control of T˚. * comes into action when 7 Becomes important on prolonged exposure to cold. Hormones which increase heat production (calorigenic hormones): thyroid, catecholamines and glucagon. Non-shivering thermogenesis (semireflex) by epinephrine, thyroid hormones – stimulate fat metabolism. 3.0 TEMPERATURE-REGULATING MECHANISMS 3.1 Thermoregulation Endocrine (secondary importance) Hormones in prolonged exposure to cold: * calorigenic hormones 1) Hypothalamo –hypophyseal –thyroidal axis: release of thyroid and heat production is increased by stimulating O2 consumption of almost all metabolically active tissues. 2) Sympathoadrenal axis: NA & Adrenaline potentiate the calorigenic effect of the thyroid and NA reduces heat loss by causing skin vasoconstriction. 3) Hypothalamo –hypophyseal –adrenocortical axis: release of glucocorticoid for permissive action. ↑ heat gain 3.0 TEMPERATURE-REGULATING MECHANISMS 3.2 Response to Heat and Cold in Men Includes: Physiological Behavioural response response (thermoregulation) Because of these responses, man can survive and work in hot or cold climates. 3.0 TEMPERATURE-REGULATING MECHANISMS 3.2 Response to Heat and Cold in Men Physiological VS Behavioural Man has 2 million sweat glands for evaporative (heat loss). heat conserve But the naked human body has little hair as insulation. Thus, men are structurally and functionally fitted to live in a hot environment. Physiological responses are more important on exposure to heat. Behavioral responses are more important on exposure to cold. 3.0 TEMPERATURE-REGULATING MECHANISMS 3.2 Response to Heat and Cold in Men 3.0 TEMPERATURE-REGULATING MECHANISMS 3.2 Response to Heat and Cold in Men Heat conservative responses: 1) Piloerection (in hairy animals): hairs pull upright and increases the layer of air trapped on skin surface and reduces heat loss. 2) Increase metabolic rate: by brown fat thermogenesis (in newborns) by actions of calorigenic hormones (prolonged exposure to cold). 3.0 TEMPERATURE-REGULATING MECHANISMS 3.3 Response to Cold (in cold weather) are activated to for - 3.0 TEMPERATURE-REGULATING MECHANISMS 3.3 Response to Cold 45 3.0 TEMPERATURE-REGULATING MECHANISMS 3.3 Response to Cold Adaptive changes include: 1) An increase in metabolic rate (calorigenic hormones) 2) Generalized vasoconstriction except in hand, foot, face and ears where cold vasodilatation occurs. Because of high blood flow, the hands remain warm and do not become numb. If behavioral responses are effective, physiological adaptation does not occur. 3.0 TEMPERATURE-REGULATING MECHANISMS 3.4 Response to Heat or in hot weather (heat Peripheral and are activated for 3.0 TEMPERATURE-REGULATING MECHANISMS 3.5 Adaptation to Heat Improvement in heat tolerance after a few days of exposure to a hot environment is associated with: 1) Sweating starts at a lower T˚ 2) Diminished loss of Na+ and Cl- in sweat and urine due to increased secretion of aldosterone. 4.0 DISORDERS OF THERMOREGULATION Heat Heatstroke Heat Cramps Exhaustion Hyperthermia Frostbite Hypothermia E.g., fever 4.0 DISORDERS OF THERMOREGULATION 4.1 Heat Exhaustion - A state of collapse (fainting), caused by BP due to overtaxing heat-loss mechanisms. - load Extensive sweating - CO by depleting plasma volume + pronounced skin vasodilation = TPR = BP. Result of overactivity heat-loss mechanisms. Body T˚ only mildly elevated. * Less severe than heatstroke. dizziness Warning symptoms: headache, giddiness, nausea, cramps, irritability and= fainting. Signs: tachycardia, hypotension and cold clammy skin (cold moist man). ↓ BP - ↓ w ↳ ↓ TPR ↑ excessive reat. loss mech 4.0 DISORDERS OF THERMOREGULATION 4.2 Heatstroke (heat hyperpyrexia) body can't evaporate well > - In prolonged exposure to a hot and humid environmental T˚. - Extremely dangerous, rapidly fatal if untreated, especially in elderly. Can caused – irreversible protein denaturation. & /7 humid environment No sweating despite high body T˚ due to unable to initiate heat-loss mechanism. * Complete breakdown of hypothalamic thermoregulation. Harmful positive feedback (body T˚ high – increase chemical reaction – increase metabolism rate – produce more heat). Predisposing factors that interfere with evaporation of sweat e.g., unsuitable clothing, poor ventilation & prolonged exposure in high T˚ and humidity. can't and sweat I evaporate , Sign: dry burning skin (hot dry man). 4.0 DISORDERS OF THERMOREGULATION Heat Exhaustion and Heatstroke 4.0 DISORDERS OF THERMOREGULATION 4.3 Heat Cramps Due to acute hypotonicity in people sweating in high rates and replacing sweat only by drinking water. ↳ not replacing the electrolyte Due to loss of sodium in sweat. ↑ H20 electrolyte => hypotonic. 4.0 DISORDERS OF THERMOREGULATION 4.4 Hyperthermia > Definition: elevation in T˚ above the normally accepted range. - All other imbalances between heat gain and heat loss that T˚. Has a variety of causes, either normal or pathological. 4.0 DISORDERS OF THERMOREGULATION 4.4 Hyperthermia Exercise induced Inormal hyperthermia Sustained exercise O Elevation in core temp - maintained at a higher level while continuing exercise. Pathological Excess heat production due to thyroid & epinephrine due to dysfunctions of the gland (thyroid, adrenal medulla) Elevate core temp (by increasing metabolic activity) Malfunction hypothalamic control centers E.g., fever. 4.0 DISORDERS OF THERMOREGULATION 4.41 Fever Definition = elevation in T˚ caused by endogenous pyrogen resetting the hypothalamic set point during infection or inflammation. An increase in core T˚ in response to bacterial, viral, protozoal infection and disease process of tissue breakdown. The T˚ set point (thermostat) has been reset to a new set point above 37.8˚ C. * So, receptors detect this condition as fall in T˚ and heat - gain mechanisms (responses to cold) are activated - causing fever. When the fever breaks, the original set point has been reestablished and the T˚ is brought back to normal. 4.0 DISORDERS OF THERMOREGULATION Mechanism of Fever * Release Infection or Macrophages endogenous inflammation pyrogen Initiation of resetting Hypothalamic “cold Prostaglandin set point response” above" 37 8 %. receptor detect fall of To , heat-gain mech activated Body D Heat temperature to production; new set point heat loss = Fever 4.0 DISORDERS OF THERMOREGULATION ** A Pathogenesis of Fever 4.0 DISORDERS OF THERMOREGULATION 4.5 Frostbite Definition: excessive cooling of a particular part of the body to the point where tissue in that area is damaged. If exposed tissues actually freeze, tissue damage results from cell disruption by formation of ice crystal or by lack of liquid water. = irreversible damage/necrosis 4.0 DISORDERS OF THERMOREGULATION 4.5 Frostbite ice formation - crystal water - lack of liquid 4.0 DISORDERS OF THERMOREGULATION 4.6 Hypothermia Definition: A fall in body T˚ when generalized cooling 3) of the body exceeds the ability of the normal heat- producing and heat-conserving regulatory mechanism to match the excessive heat loss. Rate of metabolic processes slow down. Sign/symptoms: altered cerebral functions Loss of judgement, apathy, disorientation, tiredness Later respiratory centre depressed – slow + weak breathing CVS activity – heart slow, CO – cardiac rhythm disturbed – VF – death. 4.0 DISORDERS OF THERMOREGULATION 4.6 Hypothermia Induced hypothermia used extensively in surgery > - in transplant (heart) benefit – circulation becomes slow because oxygen need is reduced, BP is low, and bleeding is minimal. Accidental hypothermia due to prolonged exposure to cold I not matured enough infants & elderly Y are old at high risk too social factors (poverty, inadequate clothing, under- nutrition) are risk factors. 5.0 REFERENCES Anatomy & Physiology, 8th Edition, 2008, Seeley, Stephens, Tate, McGraw Hill. Fundamentals of Human Physiology, Lauralee Sherwood, 4th Edition, 2010,CENGAGE Learning. Ganong’s Review of Medical Physiology 24th edition, Barrett et al, 2012. Human Physiology (From cells to system) 8th edition, Sherwood L, 2013. Lippincott’s Illustrated Reviews Physiology, Preston RR & Wilson TE, 2013.