Thermoregulate Flashcards

1
Q

What is the range of temperatures to support mammalian life?

A

27-45 C (below 27-29 cardiac fibrillation and death occur, above 45 can cause fatal brain lesions. Below 34C mammals lose the ability to regulate their temperature)

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2
Q

How do homeotherms maintain a constant temperature despite the environmental temp?

A

Requires a higher metabolic rate and therefore higher energy intake

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3
Q

Core vs. Peripheral temperature. What is rectal temp compared to core? What changes the range of temperatures that an animal can tolerate?

A

Usually a bit lower. Animals in temperate climates have a narrower range than animals in more extreme climates.

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4
Q

How much does shivering increase the basal metabolic rate?

A

up to 4 x basal metabolic rate for short periods

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5
Q

What increases the basal metabolic rate in the body?

A

Thyroxine and the effect of catecholamines on fat. Newborn mammals have brown fat (specialized vascular mitochondrial rich fat located between the scapulae; more sensitive to catecholamine induced metabolism; these cells are largely uncoupled and mainly produce heat and very little ATP)

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6
Q

What are the sources of heat in the body?

A

remote from the skin. Liver, heart, brain, limb muscles.
Body tissues are poor conductors (especially fat)- hence the effectiveness of blubber as an insulator. The main type of heat transfer from these tissues is by convection to the circulation.

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7
Q

Circulatory convection, what is it? How else can the body cool?

A

Mechanism allows preferential redistro of heat to conserve core temperature. This can protect the brain and major viscera. Alternatively heat can be preferentially directed to the skin to promote coolings by:

1) dilation of arterioles of the skin vascular beds
2) opening the artiovenous anastamoses in the limbs, ears, and muzzle

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8
Q

Countercurrent exchanges

A

When environmental temp is high, superficial veins are used for venous return. When it is cold, deep veins are used.

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9
Q

Carotid rete?

A

Cartoid artery forms a rete (An interwoven network of nerves, blood vessels or passageways) bathed in a venous sinus that drains the nasal cavity. This cools the blood going to the brain and is especially important during exercise.

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10
Q

What is another method of countercurrent exchange in horses?

A

Air filled guttural pouches of horses surround the internal carotid artery and are believed to have similar function to carotid rete.

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11
Q

What are the mechanisms of heat loss?

A

1) convection- body warms surrounding air or water (rate of loss by convection can be increased by forced convection- where the limbs are moved to move air or water over the skin surface- a breeze or current does this– especially bad for juveniles or small animals)
2) conduction- body warms a surface in direct contact with it (not a major form of heat loss except where poor husbandry or prolonged anaesthesia on a stainless steel table or cage)
3) radiation- body radiated infrared radiation (if ambient temperature approaches body temperature, evaporation is the only effective mechanism for heat loss- this depends on air humidity)
4) evaporation- of respiratory secretions, sweat, saliva

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12
Q

How can rate of loss of convection be reduced?

A

Piloerection (goose bumps)
thickness of hair coat
reducing the exposed SA by curling in a ball or huddling together

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13
Q

What controls reabsorption of Na and Cl?

A

Aldosterone

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14
Q

What is sweating under control of?

A

Sympathetic cholinergic fibres

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15
Q

What is panting?

A

Movement of small tidal volumes over the respiratory dead space. Animals doing this also engorge respiratory and oral mucosa and increase salivation. Because only ventilating dead space, hyperventilation and resp alkalosis largely avoided.

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16
Q

How does horses and cattle lose heat?

A

Sweat is the major form

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17
Q

Dogs lose heat?

A

Pant

18
Q

Sheep lose heat?

A

sweat and pant

19
Q

Lagomorphs, rabbits?

A

Smear saliva or water on their fur

20
Q

Where are the central receeptors located?

A

Hypothalamus. Sensors area lso located throughout the body which feed back to the hypothalamus

21
Q

What sensors predominate?

A

Cold sensors and central receptors over peripheral sensors. (a rise in core temp increase cooling mechanisms much more than a similar rise in peripheral receptors)

22
Q

How are small changes of set point handled?

A

Vaso-motor mechanisms

23
Q

How are large changes to set point handled?

A

Evaporative cooling or thermogenesis

24
Q

What does chronic cold do?

A

Increase thyroxine production

25
Q

Causes of temperature derangements

A

Fever (acute phase response), heat stroke, exercise induced hyperthermia, Malignant Hyperthermia (Pathologic and Pharmacologic Hyperthermia)

26
Q

How is fever initiated?

A

Initiated by exogenous pyrogens that activate endogenous pyrogens. The pyrogens enter the hypothalamus and cause the endothelial cells to produce additional prostaglandins E2 and other arachidonic acid metabolites that reset the body’s setpoint.

27
Q

Why fever?

A

Fish and reptiles seek higher temps to raise their body temp, fever enhances leucocyte activity, reduces morbidity and mortality from many infectious diseases, many viruses are heat sensitive and cannot replicate in high temps

28
Q

Exogenous pyrogens

A

Infectious agents: bacterial, fungi, viruses, etc.

Nonmicrobial agents: soluble antigen-antibody complexes, bile acids, pharmacological agents, etc.

29
Q

Endogenous pyrogens

A

Cytokines released from the immune system, some neoplastic cells also release cytokines

30
Q

Heat stroke

A

Hyperthermia associated with systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates. In other words the hallmark of heat stroke is severe CNS derrangement (comatose, poorly responsive, disorientated, depends on the stage- if you have this and high temp- then you have to assume heat stroke)

31
Q

What is heat stroke a result of?

A

Inadequate heat dissipation, larger breed dogs, obesity, brachycephalic breeds predisposed, may occur rapidly in a closed environment

32
Q

Heat stroke consequences?

A

Once temperature exceeds 41.5C to 42.5C cellular function is seriously impaired and organ damage occurs. there is an exaggerated acute phase response and alteration of heat shock proteins. This leads to the inflammatory cascade, multi-organ failure and death.
* oxygen consumption exceeds oxygen delivery
* cellular energy production cannot keep up with need
* cellular function and integrity deteriorate
** Renal failure (acute, uremia)
**Hepatic failure (hypoglycemia, hyperbilirubinemia)
**GI failure (epithelial desquamation, endotoxin absorption, haemorrhage)
** DIC (thrombosis and bleeding)
(hypoxemia, metabolic acidosis, hyperkalemia, myocardial failure, skeletal muscle cytolysis (break down), tachycardia and hypotension, tachypnoea and hyperventilation, cerebral oedema- waste products and vasodilation of the brain- also getting blood vessel volume to go down)

33
Q

How do you treat heat stroke?

A

Total body cooling (owner calls- hose the animal down- allows for evaporation), does not respond to anti-pyretic agents, appropriate supportive care is also required for successful treatment
** coagulation problems- one way to test how severe

34
Q

What is the pathway of exercise induced hyperthermia?

A

Similar pathway to heat stroke, causes include inappropriate amounts of exercise and secondary to seizures including seizures from eclampsia (seizure because of low calcium). How high is the temp? Do I need to do active cooling now?

35
Q

Active cooling

A

Quick variations aren’t great. Rectal temp lags behind core temperature. Temp at 42C- cool it do 40C instead of regular temp because core temp is lagging behind.

36
Q

Malignant hyperthermia

A

Rare. Rapid and relentless progressive increase in body temp. Has to do with intracellular calcium metabolism. Pigs and people- dogs, cats, and horses (grey hounds). Hard to treat. Can be triggered by drugs. Pathological lesions affecting hypothalamus can also cause hyperthermia. These include neoplasia curshing the hypothalamus

37
Q

Hypothermia

A

Heat loss exceeds production. Primary hypothermia- caused by excessive exposure to low env. temp. Secondary hypothermia- result of disease, trauma, surgery, or drug-induced (happens sooner than primary)

38
Q

Secondary hypothermia

A

<32C is critical (i.e. in surgery)

39
Q

Hypothermia CV and resp effects

A

Initially increased HR and BP from catecholamine release. Vasodilation leading to hypotension and low CO. Oxygen curve shifts left- Hb does not give up O2 as easily- hypoxia. Slower HR eventually because the heart is cold and not depolarizing properly. Lower stimulus to breathe and shallowered. Pulmonary oedema. Bronchopneumonia. Mucociliary action decreased.

40
Q

Hypothermia neurological

A

decreased mentation, unconsciousness, cerebral metabolism decreases,

41
Q

Hypothermia metabolic effects

A

Peripheral vasoconstriction, body perceives increased BV, decreases production of ADH and leads to diuresis. Can cause dehydration and azotemia. If this continues- renal blood flow decreases, glomerular filtration decreases and along with ischemia, acute renal failure can occur.

  • decrease liver activity- if patient is cold during surgery, can mean that patient wont’ get rid of anaesthetic agents as quickly so post op recovery is prolonged.
  • Acidosis from respiratory depression (hypoventilation) and tissue hypoxia and increased muscle activity from shivering
  • primary immune functions are impaired through in animals mild hypothermia has not been found to be a risk factor in post op infection
  • Coagulation stops working properly- this can be bad in surgery- looks like they are bleeding from a lot of places- likely not to do with clotting factors- likely the patient is just cold.
  • DIC can occur from impairment of inhibitors of fibrinolysis
42
Q

Hypothermia treatment

A

Rewarm them slowly. Don’t heat extremities (vasodilation and then lose heat that way).