Control Of Body Temperature PDF

Control Of Body Temperature The thermoregulatory system is composed of: A. Sensory receptors (Thermoreceptors). B. Central integrator (Centre). C. Effector organs. A. Thermoreceptors 1. Peripheral Thermoreceptors: Site: § Skin contain both cold and warmth receptors...

Control Of Body Temperature The thermoregulatory system is composed of: A. Sensory receptors (Thermoreceptors). B. Central integrator (Centre). C. Effector organs. A. Thermoreceptors 1. Peripheral Thermoreceptors: Site: § Skin contain both cold and warmth receptors with more cold receptors. § Deep body temperature receptors are present in abdominal viscera and spinal cord to detect body core temperature. Pathway: § The peripheral thermoreceptors discharge impulses via the lateral spinothalamic tract to the thalamus and somatosensory cortex with collateral from the thalamus pass to activate the heat regulatory center in hypothalamus. 2. Central Thermoreceptors: § The anterior hypothalamus and the preoptic area contain large number of heat and cold sensitive neurons. § These receptors are sensitive to core temperature (brain and blood temperature). B. Thermoregulatory center (thermostat) § It is present in the hypothalamus. § It receives impulses from the thermo receptors and compares it with its specific standard reference temperature (set-point) which almost 37.1 oc body core temperature. § If body temperature > set point → stimulation of anterior hypothalamus → ­ heat loss. § If body temperature < set point → stimulation of posterior hypothalamus → ­ heat production and ¯ heat loss.  C. The effectors organs § Skin (blood vessels and sweat gland). § Skeletal muscle. § Endocrine glands. Effects of Exposure to Cold § Exposure to cold stimulates the which regulate the heat balance by: 1. Decrease in heat loss: A. Vasoconstriction of skin blood vessels: § The posterior hypothalamus stimulates the vasoconstrictor centre in the medulla → sympathetic adrenergic fibres → VC. § so the skin becomes cold as the weather with no heat loss occurs. § Also, sympathetic stimulation to skin causes piloerection which act as insulator layer around skin (little effect in human). B. Counter-current heat exchanger: § As vasoconstriction of cutaneous blood vessels directs blood to deep veins which run parallel to the arteries. § Heat is conducted from the warm arterial blood to the cold venous blood → warm venous blood return to the heart and cold arterial blood to skin. C. Behavioral responses: § Putting on heavy clothes. § Curling the body to decrease surface area. § Erection of hair as an insulator for cold (sympathetic effect). 2. Increase in heat production: A. Shivering: § It is involuntary rhythmic contractions of the skeletal muscle to produce large amount of heat. § Its center is present in posterior hypothalamus in area called the primary motor center for shivering (this area is normally inhibited by  impulses from heat center in the anterior hypothalamic preoptic area). § This center stimulates the extrapyramidal tracts → AHCs to increase muscle tone to high level → shivering. § Shivering can be prevented by curare (neuromuscular blocker). B. Hormonal thermogenesis: Adrenaline: 1. Hypothalamus stimulates the adrenaline secreting center in medulla which stimulate suprarenal medulla → adrenaline → Increase metabolic rate. 2. Cutaneous vasoconstriction. 3. Stimulate glycogenolysis. 4. Stimulate lipolysis (of depot fat {fat stores} which is rich in children). Thyroxin: § Hypothalamus stimulates the Thyrotropin Releasing Hormone (TRH) → stimulate anterior pituitary gland to secrete Thyroid Stimulating Hormone (TSH) → stimulate thyroid gland to secrete thyroxin hormone → ­ BMR slowly (in cold climate there is high incidence of toxic goiters). Cortisol: § Hypothalamus stimulates the Corticotrophin Releasing Factor (CRF) → stimulates Anterior Pituitary → ACTH → stimulate adrenal cortex →­ cortisol →­ blood gulcose and metabolic rate. C. Behavioral responses: § Increase appetite to increase SDA.  Effect of exposure to heat § Exposure to heat stimulates the which regulate body heat balance by: 1. Decrease heat gain: § By strong inhibition of mechanisms that cause heat production and by behavioural responses as apathy (decreased activity) and anorexia (decrease appetite). 2. Increased heat loss: A. Vasodilatation of skin blood vessels: causes: 1. Inhibition of the sympathetic centers in posterior Hypothalamus → VD →­ heat transfer to skin then lost to surrounding. 2. Direct effect of heat on skin. 3. Release of bradykinin from sweat glands. B. Sweating: Sweat is: § Hypotonic secretion of NaCl. Center: § Its center is the preoptic nuclei in the anterior hypothalamus. Supply: § The eccrine sweat glands are supplied by sympathetic cholinergic fibers (blocked by atropine). Sweat secretion: § Is an active process in which the acini secrete isotonic sweat (primary sweat) as plasma, but NaCl is gradually reabsorbed by the ducts so the sweat becomes hypotonic (secondary sweat) (this change depends on the rate of sweating as increase rate of sweating doesn’t give time of modification of the primary sweat, also depends on aldostrone level which increase NaCl reabsorption).  Cooling effect of sweat: § Each 1ml evaporated sweat removes 0.6 K Cal. § Sweat start at environmental temperature of 32 oc. § Dribbling alone without evaporation → no loss. Acclimatization of Sweating: § In acute exposure to hot weather ® a person sweat 700 ml/h + loss of 15-30 gm Nacl/day. § After exposure to hot weather for 6 weeks ® he sweat 2000 ml/h and Nacl loss 3-5 gm/day (due to increase sweating capability of the sweat glands also due to ­ aldostrone secretion by the associated decrease in NaCl level in the body) Cold sweat: § It is an emotional sweating even with cold and vasoconstriction. Disorders of temperature regulation Fever (pyrexia) § Definition: § It is hyperthermia caused by resetting of the setpoint of the hypothalamus to a higher level. § Mechanism of fever: § Toxins of bacteria + degenerated tissue → exogenous pyrogens which act on the monocytes and macrophages which release interleukin (IL-1) and Tumor Necrosing Factor (TNF) which are called endogenous pyrogens. § The endogenous pyrogens (IL-1) reach the hypothalamic thermosensitive neurons cause fever within 10 minutes by formation of prostaglandin E2 (PGE2) which activates resetting of the central thermostat (­ set-point) by synthesis of cAMP. § Because body temperature is still less than the set-point, the person has false feeling of cold and mechanisms of elevation of body temperature occur → VC → cold skin and shivers (chills) which continue till the body temperature is elevated to the level of set-point → fever. § The Crisis (Flush): § If the factor that causes fever is removed (treated), the set-point returns to the normal level and the body temperature is still more than the set-point → sensation of hotness → ­ mechanism of heat loss → VD → flushed skin and intense sweating → return the body temperature to normal level. § Control of fever: 1. PGE2 has negative feedback on interleukin I. 2. ­ interleukin I → down regulation of its receptors. 3. Glucocorticoids as cortisol → ¯ interleukin I. 4. Aspirin as antipyretic drugs → ¯ synthesis of PGE2 from arachidonic acid → ¯ set point level →­ heat loss by sweating (aspirin doesn’t lower body temperature of a normal person because normal person doesn’t have any interleukin-1) Also, aspirin stimulates the heat losing center. Heat stroke § Cause: § This occurs due to exposure to hot humid weather or to high fever. § Mechanism: § ­ body temperature → excessive sweating → dehydration and salt loss → depression of heat regulating centre → ¯ sweating and dry hot skin →­ body temperature at 43 oc → irreversible denaturation of tissue proteins → depression of the centre (vicious circle) → death. § Clinical Picture: 1. Dizziness. 2. Loss of fluids and sweat may lead to circulatory shock and tissue degeneration. § Treated by: 1. Immediate cooling of the body by immersion in ice cold water. 2. Sponge with alcohol. 3. Antipyretic drugs as aspirin.  Sun stroke § Beside sweating and dehydration damage of brain tissue by direct sun rays → severe fever. § It is treated by immersion in ice bath and drinking saline. Physiological changes associated with hyperthermia 1. Central Nervous System: § At first, hyperthermia stimulates the CNS leading to tremors and convulsions. § But at body temperature above 41oc ® malfunction of CNS occurs leading to loss of reflexes and coma. 2. Cardio Vascular System: § Increase heart rate by 10 beats/min for each 1oc. § Increase in body temperature due to direct stimulation of SAN or cardio- accelerator centre. § Increase cardiac output due to vasodilatation of peripheral arterioles with increase in venous return. § Increase systolic blood pressure (by increase C.O.P) and decrease diastolic blood pressure (by peripheral vasodilatation) but on exposure to hot humid atmosphere, excessive sweating and vasodilatation will lead to dehydration and hypotension, a condition known as (heat exhaustion). 3. Respiration: § Increased respiratory rate by stimulation of the central and peripheral chemoreceptors.  Hypothermia § It is a drop of body temperature to low level with slow metabolic and physiologic processes (respiration and heart rate). Causes: 1. Exposure of the body to extreme cold water (ice water) for 20 minutes: → ¯ body temperature → heart stop. § The ability of the hypothalamus to regulate body temperature is greatly impaired with sleepiness and even coma occur. 2. Frost bite: § Exposure of the body to extreme cold weather → freezing in lobes of ears and digits of hands and feet (frost – bite) may lead to gangrene. 3. Artificial hypothermia: § By strong sedative which depress heat regulating centers or cooling the patient with ice. § This is used to stop the heart artificially for many minutes during cardiac surgery.