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Organ Systems > Thermoregulation > Flashcards

Thermoregulation Flashcards

1
Q

What is normal body temperature?

A

Traditionally 37 C or 98.6 F

36.8 C or 98.2 F is now average with a -/+ 1 C difference

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2
Q

When does body temperature peak?

A

Between 4-6 pm

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3
Q

What is thermoregulation?

A

The balance between heat production and heat loss to maintain a steady body temperature

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4
Q

What are the four types of heat dissipation?

A

Radiation
Conduction
Convection
Evaporation

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5
Q

How do we produce heat?

A

Through metabolism!

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6
Q

What generally does the BMR do?

A

(Basal metabolic rate) is the metabolic heat needed to compensate for heat loss/gain through skin or respiration

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7
Q

What hormones can increase metabolic rate?

A

Epinephrine and thyroid hormones

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8
Q

What is DIT?

A

Dietary induced thermogenesis, result of increased metabolism

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9
Q

How is BMR measured?

A

Amount of heat given off per unit of time; at rest it depends on proportionality of body surface area

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10
Q

What determines the rate at which the body loses heat?

A

The surface to volume ratio (Surface/Volume)

- greater surface area ratio implies and increase in heat conduction from body core to the air

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11
Q

What is the effect of evaporation?

A

Cools the body

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12
Q

What is heat radiation?

A

Objects exchanging heat with the air; warmer objects loose heat to colder objects

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13
Q

What is conduction?

A

Direct transfer of heat when objects of different temperatures come into contact

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14
Q

What is convection?

A

The contact of fluid or air around a surface, facilitating conduction and evaporation

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15
Q

Mathematically explain conduction

A

(efficiency of heat movement)
J = k(Tc-Tsk)/L
J=conduction; Tc=temp core; Tsk=temp skin

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16
Q

What is the benefit of having low and high conductivity tissues and what are examples of each?

A

Low conductivity: insulates (ex: muscle and fat)

High conductivity: facilitates convection from core to skin to air (blood and sweat)

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17
Q

How does air convection improve heat conduction?

A

Convection thins the surface layer of poorly conducting air, improving the conduction of skin to air.

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18
Q

What are the three skin layers?

A

Epidermis, dermis, and hypodermis

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19
Q

What is circulatory convection?

A

Constriction/dilation of vessel layers in dermis determine the degree of convection to epidermis
- regulates dry release of conductive, convective, and radiation heat

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20
Q

What vessels regulate blood convection in retention or loss of heat?

A

A-V (arterio-venous) anastomoses among subpapillary and cutaneous blood vessels

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21
Q

What is the role of A-V anastomoses?

A

To shunt blood from arterioles to veins

  • Dilation: blood shunted away from superficial capillary bed (retaining heat)
  • Constriction: blood enters superficial capillaries and slows (permits conductive, convective, and radiation of heat)
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22
Q

What controls the look and color of the skin?

A

Sympathetic activity

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23
Q

How does circulatory convection respond to a cool environment?

A
  • vasoconstriction and dilation of A-V anastomoses (reduce convection)
  • Cooling outer shell (less heat gradient, less heat loss)
  • low S/V ratio in inner core and low heat conduction from interior (conserving heat)
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24
Q

How does circulatory convection respond to a warm environment?

A
  • vasodilation and constriction of A-V anastomoses (increase convection)
  • warming outer shell (greater thermal gradient b/w skin and air: more heat loss)
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25
Q

How do venae comitantes aid in heat control?

A
  • countercurrent temp. regulation to minimize heat loss

- when cold, heat is transfered from arteries to veins, warming the returning venous blood

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26
Q

How do superficial veins aid in heat control?

A
  • dilate to release excess heat

- constrict with excess cold and shunt blood to venue comitantes via perforating branches

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27
Q

What are the effects of cold on vascular convection?

A

induces vasoconstriction of arterioles and veins, dilates AV shunts, reducing heat loss thru skin

  • stimulates alpha-2 receptors producing vasoconstriction
  • stimulates cold receptors to do sympathetic constriction from hypothalamus and brain stem
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28
Q

What is CIVD?

A

(Cold induced vasodilation)
- 15-30 min cold inhibits vasoconstriction to improve perfusion; persistent cycles of vasodilation and constriction are called the Lewis Hunting Response

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29
Q

What is Raynaud’s Disease?

A

Increased cold sensitivity of the alpha-2 receptors, causing vasoconstriction, ischemia and pain

30
Q

What are the effects of heat on vascular convection?

A
  • reduced thermal gradient which reduces heat loss

- a need to bring core heat to the surface (forced gradient) enhancing heat dissipation

31
Q

How does heat stimulate sensory pathways for vasodilation of arterioles?

A
  • Sympathetic withdrawal (alpha-2 receptor inhibition)

- sympathetic cholinergic vasodilation reflex (ACh, NO, VIP, histamine, prostanoids, substance P)

32
Q

Explain the process of evaporation

A
  • Eccrine glands secrete water
  • Water is highly conductive, and its heat becomes latent heat of evaporation
  • evaporation depends on pressure gradient, not temperature gradient
33
Q

How does humidity effect evaporation?

A

the pressure gradient b/w skin and humid air is low, limiting evaporation
sweat drips without heat loss or evaporation

34
Q

What are the types of sweat glands?

A

Eccrine (merocrine) and Apocrine sweat glands

- both are tubular, but apocrine is larger in mass and luminally

35
Q

Describe the secretory portion of sweat glands

A

cuboidal or low columnar epithelia, coiled into a sphere at lower border of dermis

36
Q

_______ constrict to facilitate release of sweat. These cells are between _______ and _________.

A

Myoepithelial cells…..epithelium…basement membrane

37
Q

Eccrine sweat glands

A

(merocrine)
- all over body
- do merocrine exocytosis of vesicles
- hypotonic sweat, pH neutral (contains water, Na, K, Cl, urea, ammonia, lactic and uric acid)
- duct reabsorbs water and solutes via aldosterone

38
Q

What innervations do eccrine glands have? in response to what?

A
  • cholinergic responding to heat

- adrenergic sympathetic responding to emotion

39
Q

What regulates the sympathetic control of eccrine sweat glands?

A

Anterior (preoptic) hypothalamus and medullary, also pontine nuclei in brain stem

40
Q

How do sympathetic neural pathways stimulate most eccrine glands?

A
  • muscarinic cholinergic receptors
41
Q

How does adrenal medullary epinephrine stimulate eccrine glands and where?

A
  • adrenergically in hands and soles (early stress response)
42
Q

Sweating is controlled primarily and secondarily by what?

A

Primarily by brain temperature

Secondarily by skin temperature

43
Q

Apocrine Sweat Glands

A
  • located in axilla, external genitalia, anus
  • excretion into upper hair follicle, not skin surface
  • sympathetic innervation; adrenergic when responding to emotional and sensory stimuli (not heat)
44
Q

Explain apocrine secretion

A
  • apical part and contents secrete into lumen
  • milky, proteinaceous, odorless
  • the smell comes from bacteria breaking down the the sweat from armpits
  • only activated by puberty, influenced by sex steroids
45
Q

How is body temperature controlled homeostatically and by what?

A

(by hypothalamus)

  • anterior (preoptic) and posterior nuclei regulatee autonomic control of sweating, blood flow to skin, and metabolic activity related to heat generation
  • posterior hypothalamus to brain stem to preganglionic sympathetic neurons in spinal chord
46
Q

What are integration sites?

A

anterior and preoptic regions of hypothalamus that integrate thermal/non-thermal input

47
Q

What are effectors?

A
  • posterior regions of hypothalamus that generate thermoregulatory responses
  • each is stimulated at a different threshold of core temp.
48
Q

Explain temperature autoregulation

A
  • maintained internal homeostasis despite changes in ambient temperature
49
Q

Short term homeostatic control is maintained by what types of mechanisms?

A

hypothalamic mechanisms

- specific threshold temperatures indicate when each specific effector should initiate a response

50
Q

How is long term thermoregulation maintained?

A

By endocrines (thyroid hormone, estrogen, etc)

51
Q

Explain sweating as a heat defense

A
  • starts at a higher threshold than vasodilation
  • second line of defense to increased blood flow
  • higher threshold b/c water is precious and saved for greater stresses
52
Q

Explain shivering as a cold defense

A

Only at a lower threshold than vasoconstriction

53
Q

What is the interthreshold zone?

A

Temp range where only vascular changes regulate core temperature

  • vascular responses are less noticeable here
  • autonomic sweating or shivering responses can be activated here
  • can be thermally or non-thermally regulated
54
Q

What is Cold Uresis?

A

Cold inhibits ADH release and vasoconstricts peripheral vessels to increase core volume
- triggers pressure natriuresis

55
Q

How do we induce increased heat production?

A
  • shivering

- neuroendocrine thermogenesis: NE, EPI, and thyroid hormone enhance metabolic generation of heat

56
Q

What is hypothermia?

A

Cold depressing neuronal metabolic activity, inhibiting hypothalamic heat production responses

57
Q

What are the responses to heat?

A
  • sweating, vasodilation, decrease in heat production
58
Q

What is heat syncope?

A

Systemic vasodilation causing lightheadedness, pooling of venous blood, lowered CO and decreased perfusion

59
Q

What is heat stroke?

A

Therrmoregulatory responses are depressed causing dizziness, nausea, vomiting, and delirium

60
Q

Explain the negative feedback of temperature control

A
  • typical type when responding to core temp change

- when ambient conditions change core temp, the latter elicits thermoregulatory responses in hypothalamus

61
Q

Explain feedforward temperature control

A
  • ambient conditions alter hypothalamic integrator activity, producing responses prior to changes in core temp
  • resetting of thresholds for generating heat loss/retention
62
Q

How does skin temperature alter thermoregulatory equilibrium?

A

Cutaneous temp receptors provide feedforward signals that coordinate heat loss/conservation responses
- brief exposure changes temp eq point, but not core temp

63
Q

How do non-therman stimuli alter thermoregulatory thresholds?

A
  • Motor activity increases core temp, which increases sweating
  • Glucose receptors (some) can detect hypoglycemia, minimizing motor activity and causing shivering
64
Q

How does hypoglycemia affect temp threshold?

A

Shifts for shivering at a lower temp level

65
Q

How does dehydration affect temp threshold?

A

(detected by baroreceptors, osmoreceptors) raising temp threshold for sweating to preserve water

66
Q

What is the effect of motion sickness at low temp?

A

increases vasodilation

67
Q

What is fever?

A

Pyrogens elevating temp eq. point

  • exogenous pyrogen release endogenous pyrogens, cytokines, from leukocytes and macrophages
  • trigger PGE release from hypothalamic neurons
68
Q

What initiates fever?

A
  • cytokines and PGE increase eq. point

- shivering increases core temp to match eq.

69
Q

What is the steady state of fever?

A

(plateau)
- no sense of hot or cold
- higher body temp enhances metabolic rate and immune response

70
Q

What is the defervescence of fever?

A

(crisis)
- decreased eq. point after reduction in pyrogens
- sweating and vasodilation return core temp to normal

71
Q

What effect do neuroendocrine changes in the brain have?

A
  • altering of the threshold zone

- changes in ambient temp elicit a non-vasculatory thermo-response

72
Q

What are hot flashes?

A
  • sweating, peripheral vasodilation, heat perception
  • triggered with slight increases in body temp reaching upper side of narrowed threshold zone
  • zone is narrowed due to high NE release in cerebral cortex or decreased estrogen levels (reversed by clonidine and HRT, respectively)

Organ Systems (20 decks)

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