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Phys3 Thermoregulate

Effects of temperature in the body 1.Folding of proteins. 2.membrane fluidity. 3.rates of chemical reactions. 4.rates of enzymatic reactions. 5.osmolarity.
What is Tset and what are the major influences of it? Tset is the reference point that determines threshold for initiation of thermoregulatory responses. Ifluenced by: 1.Age. 2.Health. 3.Exercise. 4.time of day.
how is heat transfered from tissue/organ to the skin 1.conduction (dissipation of heat directly across tissues to skin. 2.convection (from tissue to BL).
How is heat transfered from skin to environment? 1.radiation (b/w skin and objects in environment). 2.evaporation (vaporization of sweat). 3.convection (heat transfer via liquid or gas). 4.conduction (heat transfer by contact with solid or liquid of lesser temp).
What is shivering a result of? A loss of negative regulatory input to the posterior hypothalamus from the preoptic area. The former then sends signals to the motor neurons.
what is normal body temp 98.6 deg F, 37deg C
What is the controller of the Tset? Hypothalamus.
Risk factors associated with dysregulation 1.Age. 2.Medications. 3.Health. 4.environment.
What affects convection of heat from tissue to the Blood? 1.Rate of heat production by the tissues. 2.Temp of tissue Vs. temp of BL. 3.Rate of BF through the tissue.
Important Thermoreceptors 1.Hypothalamus. 2.Heart. 3.Skin. 4.Pulmonary vessels. 5.Spinal cord.
Eccrine sweat glands SNS innervation, very numerous, fatigue with continued exposure to heat, increase efficiency with training.
SNS affects on Apical skin 1.NE causes vasoconstriction of glomulus bodies (Vascular anastamoses have myoepithelial layers innervated by SNS). 2.Lack of NE to glomulus bodies causes passive vasodilation.
Where are glomulus bodies found? 1.Ears, 2.pads of fingers, 3.pads of toes, 4.nail beds.
SNS affects on Nonapical skin 1.NE causes vasoconstriction. 2.ACh causes eccrine gland secretion. 3.ACh causes vasodilation.
Where are warm receptors located? Dermis.
Where are cold receptors located? Epidermis.
how do the warm and cold receptor's signals travel to the Anterior hypothalamus? up the spinal cord, through the medulla and pons on the spinothalamic tract.
What is the posterior hypothalamus in charge of? Shivering. Recieves signals from the Preoptic area located in the anterior hypothalamus.
Pyrogens affect on Tset? Raise it
Acclinmatizations affect on Tset? Lowers it
What is compared to Tset to generate error signals? core temperature (Tc). The error signal is integrated with skin temperature (Tsk) to produce effector signals.
What could cause a change in temperature set point? FEVER, Tset is higher than Tc so there is a negative error signal. **This causes the Tc to rise to return the error signal to 0.
Does exercise change the temperature set point? NO, only increases the core temperature (Tc) which becomes greater than Tset. **This produces an error signal equal to the load error.
External Pyrogens causing fever Microbial source cause an INC in PGE2 which alters the Tset. **Immune response leads to IL-1 which Inc PGE2
Endogenous Pyrogens causing fever Cytokines: alter the Tset. **Examples: IL-1, Interferon y, TNF
Cardiovascular strain due to heat stress 1.Vasodilation leads to pooling of BL in the periphery. 2.This decreases the central BV. 3.Liver and splanchnic circulation is then decreased to compensate.
Acclimatization to Heat 1.Reduction in heart rate required to sustain activity. 2.Reduction in threshold for cutaneous vasodilation. 3.Changes in sweat gland function. 4.Core temp triggering sweating and VD decreases.
What changes in sweat glad function are seen with heat acclimatization? 1.Inc sensitivity to cholinergic (ACh) stimulation. 2.Inc sweat secretion by glands in limbs. 3.Dec Na+ secretion from sweat glands in response to aldosterone (dec volume loss).
Acclimatization to Cold 1.Dec conductance of core to skin heat loss. 2.could Inc or Dec metabolic rate. 3.Cold induced vasodilation. **Lewis hunting response: cycle b/w VD and VC
Heat related illness: Exposure to environmental heat Impedes dissipation of heat.
Heat related illness: Physical exercise Increased heat production
Pathophysiology behind heat-related illnesses 1.Inc body temp leads to Inc BF to skin. 2.BL pools in vessels, fluid & heat are lost via sweat. 3.This reduces perfusion of viscera (causing ischemia, endotoxemia, oxidative stress)
3 types of Mild heat-related illnesses 1.Miliaria Rubra (heat rash from occlusion of eccrine sweat gland ducts). 2.Heat Syncope (fainting due to pooling of BL in periphery). 3.Heat cramps (Inc Na loss in sweat).
2 types of Severe heat-related illnesses 1.Heat exhaustion 101-104 deg: (most common type) Dec CO leads to collapse, maybe due to dehydration. 2.Heat Stroke >104 deg: elevated core temperature can cause stroke, organ failure, death (2 types: Classical seen in sick, Exertional seen in fitness)
Malignant hyperthermia Genetic mutation of RYRs inhibition protein, leads to fever and severe muscle cramps in response to general anaesthesia.
Peripheral cold injuries: non freezing 1.Chilblain: localized inflammatory lesions on skin. 2.Trench foot: cold-wet exposure leads to skin breakdown and never damage.
Peripheral cold injury: freezing 1.Frostbite: cold damage to the skin & underlying tissues. Usually ocuring in hands, nose feet, and ears. **Initially feels like pins and needles followed by numbness then blisters.
Hypothermia severities (types) 1.Mild(32-35deg C): w/ shivering & CNS depression. 2.Moderate(28-32degC): Progressive CNS symptoms. 3.Severe(<28degC):voluntary muscle movement & reflex loss, unconciousness.
When is someone officially dead? When they are WARM and dead, revival has occured from core temps as low as 17degC that appeared clinically dead thanks to our good lord savior and superior medicine... and Big Papa
Created by: WeeG



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