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PFM: Biweekly Exam 3 > Thermoregulation > Flashcards

Thermoregulation Flashcards

1
Q

fever in a cyclical pattern (on and off for days to weeks)

A

Pel-Ebstein fever

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2
Q

disease that has Pel-Ebstein fever

A

Hodgkin lymphoma

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3
Q

in patients with typhoid, do they experience tachycardia or bradycardia

A

bradycardia

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4
Q

intermittent fever example (gaps between temperatures, but it does reach normal temp.)

A

Sepsis

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5
Q

2 specific types of non-infectious fevers

A

vascular (ischemia, hemorrhage)
aseptic inflammation (not involved w. infection)

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6
Q

what is the normal mid morning ORAL temperature

A

36.5-37.5 C
(97.7-99.5 F)

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7
Q

2 things that having optimum body temperature facilitates:

A
  1. integrity of membrane lipids
  2. enzyme activity
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8
Q

what balances heat production and heat dissipation

A

hypothalamus

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9
Q

the hypothalamic neurons will read the change in temperature in the body and do what

A

increase or decrease neuronal firing to increase or decrease heat production/cooling

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10
Q

2 things that will first sense change in temperature before sending information to hypothalamus

A

blood and skin

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11
Q

core body temperature sensor

A

blood

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12
Q

cold receptor on the skin

A

CMR1

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13
Q

heat receptor on the skin

A

TRPVR1

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14
Q

what happens after hypothalamus receives message about a change in body temperature

A

sends signals to organs

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15
Q

skin arterioles receive message from hypothalamus and can either _____ or ______

A

constrict: to conserve heat (traps it)
dilate: to lose heat

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16
Q

sweat glands receive message from hypothalamus and can do what

A

release sweat: lose heat

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17
Q

the liver receives message from hypothalamus and activates what

A

non-shivering thermogenesis

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18
Q

brown fat receives message from the hypothalamus and activates what

A

non-shivering thermogenesis

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19
Q

muscles receive message from hypothalamus and activates what

A

shivering thermogenesis

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20
Q

what happens when the set point is raised

A

need to heat the body to match the set point

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21
Q

what happens when the set point is lowered

A

need to cool the body to match the set point

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22
Q

first step to raise temperature to set point: (we get a fever)

A
  1. prevent heat loss (vasoconstriction), skin cools to ambient temp., cold receptors activated, pt. feels cold and wraps in blanket
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23
Q

second step to raise temperature to set point:(we get a fever)

A
  1. shivering (generate heat from muscle)
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24
Q

third step to raise temperature to set point: (we get a fever)

A
  1. non-shivering (generate heat from liver)
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25
Q

what happens when body temp. matches the raised set point

A

hypothalamus maintains fever (balancing act)

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26
Q

first step to lower temperature to set point: (when the fever quits)

A
  1. increase heat loss (skin vasodilation), skin heats up to core fever temp, heat receptors activated, pt. feels hot
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27
Q

second step to lower temperature to set point: (when the fever quits)

A
  1. lose heat by evaporation of sweat
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28
Q

what happens once body temp. matches the lowered set point

A

hypothalamus maintains normal body temp. (balancing act)

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29
Q

what does shivering do

A

traps heat

30
Q

what does sweating do

A

releases heat

31
Q

a fever of >41.5 C (>106.7F); increased temperature set point

A

hyperpyrexia (fever)

32
Q

overheated body exceeding heat loss capacity; normal temperature set point

A

hyperthermia (no fever)

33
Q

when skin temperature is >30C, what happens

A

preoptic warm-sensitive neuron is fired from hypothalamus and leads to heat loss

34
Q

when skin temperature is <24C, what happens

A

preoptic cold-sensitive neuron is fired from hypothalamus and leads to heat retention and generation

35
Q

what kind of cytokines produce fever

36
Q

pyrogenic cytokines (4 main ones)

A

IL-1, IL-6, and TNF-alpha, INF-gamma

37
Q

what induces the synthesis of PGE2

A

pyrogenic cytokines

38
Q

an increase in PGE2 in the periphery leads to what

A

muscle and joint pain w/ fever

39
Q

myalgia

A

muscle pain

40
Q

arthralgia

A

joint pain

41
Q

an increase in PGE2 in the hypothalamus leads to what

42
Q

humoral control of increased set point: 4 steps

A
  1. macrophages in blood vessel produces IL-1 (pyrogenic cytokine)
  2. IL-1 induces PGE2 to be made and binds to EP3 on astrocyte
  3. EP3 decreases production of cAMP leading to decreased firing of preoptic warm-sensitive neuron
  4. decreased firing leads to increased set point
43
Q

these molecules are against raising the temperature

A

antipyretics

44
Q

what 2 things have very tight junctions

A

brain (think blood-brain barrier) and retina

45
Q

what organ has fenestrated capillaries that deals with lots of exchange

46
Q

what 2 things have sinusoidal capillaries (whole cells can pass through)

A

liver, bone marrow

47
Q

what causes polarity of cells

A

tight junctions

48
Q

sensory organ in the hypothalamus that is circumventricular (allows cytokines to pass through)

49
Q

this hypothalamic nucleus contains warm-sensitive neurons and allows access to pyrogens (deals with non-shivering)

A

preoptic nucleus

50
Q

this hypothalamic nucleus receives information from pyrogens (deals with shivering)

A

posterior nucleus

51
Q

this specific anastomoses in the skin causes vasoconstriction and vasodilation

A

glomus bodies

52
Q

this happens when acetylcholine binds to M3 on sweat gland

53
Q

this happens when norepinephrine binds to alpha1 in vascular smooth muscle

A

vasoconstriction

54
Q

this happens when norepinephrine binds to beta2 in vascular smooth muscle

A

vasodilation

55
Q

what neuron causes the main big muscle to contract

56
Q

what neuron takes over when alpha neuron caused big muscle to contract

57
Q

gamma neuron causes what to contract

A

muscle spindle

58
Q

4 steps to host defense response to inflammation and infection:

A
  1. macrophages produce pyrogenic cytokines (IL-1, IL-6, TNF-alpha)
  2. immune response: activation of neutrophils, macrophages, and lymphocytes
  3. acute phase response: liver produces fibrinogen, CRP (helps w/ phagocytosis)
  4. fever
59
Q

used to treat fever by blocking activation of PGE2

A

NSAIDs (acetaminophen)

60
Q

what drug is contraindicated in thyrotoxic storm by leading to increase of free T4

61
Q

leads to increase in Na/K ATPase and increase expression of uncouplers (UCPS) of protein gradient

A

increase in T3

62
Q

an increase in T3 ultimately leads to what loss

A

energy lost as heat

63
Q

does not involve increase in the set point; NSAIDs don’t work to treat this

A

hyperthermia

64
Q

released/absorbed heat produces this if heat dissipation mechanisms are overwhelmed

A

hyperthermia

65
Q

activity of ATPases and UCPs increase what process

A

thermogenesis

66
Q

2 main CAUSES of hyperthermia

A

heat stroke (decreased sweating)
malignant hyperthermia (RyR mutation)

67
Q

what do you not treat hyperthermia with

A

aspirin (exacerbate bleeding) or acetaminophen (metabolizing by deranged liver)

68
Q

stages of hyperthermia (3)

A

heat stress
heat exhaustion
heat stroke

69
Q

3 main signs of heat stroke

A

CVS collapse
CNS abnormalities
temp. >40C

70
Q

receptor mutation leading to malignant hyperthermia

71
Q

what drug is used to inhibit mutated RyR (ryanodine receptor) to alleviate burden of SERCA and stop hyperthermia from happening

A

Dantrolene

PFM: Biweekly Exam 3 (20 decks)

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