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HLSC 222 - Pathophysiology Across the Lifespan > Chapter 14 - Pain and Temperature > Flashcards

Chapter 14 - Pain and Temperature Flashcards

1
Q

Pain Definition

A

dysfunction of general or specific senses

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2
Q

Pain is a ________ phenomenon

A

protective

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3
Q

Is pain subjective or objective? Why?

A

subjective, it is not measurable

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4
Q

The physical, cognitive, and emotional interactions of pain make it very ________

A

complex

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5
Q

How did McCaffery define pain?

A

“Whatever the experiencing person says it is, existing whenever they say it does.”

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6
Q

Variations in temperature can signal _________

A

disease

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7
Q

_______ is a common symptom of dysfunction

A

fever

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8
Q

What is often the first symptom of infectious or inflammatory conditions?

A

fever

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9
Q

Specific Pain Theory =

A

receptors

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10
Q

The specific pain theory says that injury activates specific pain ________ to the brain

A

receptors

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11
Q

The specific pain theory says that pain intensity is related to…

A

direct association with tissue injury ie. cutting hand with knife hurts more than finger prick

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12
Q

What is the problem with the specific pain theory?

A

it doesn’t account for emotional pain

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13
Q

Gate Control Theory =

A

spinal cord

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14
Q

The gate control pain theory explains _____________ aspects of pain

A

multidimensional

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15
Q

The gate control pain theory uses the spinal cord as a gate to control transmission to the _____

A

CNS (brain)

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16
Q

The Neuromatrix Theory =

A

brain

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17
Q

In the neuromatrix theory, stimuli trigger _______ of nerve impulses, but don’t produce them

A

patterns

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18
Q

Where are patterns of nerve impulses taken from?

A

genetic, psychological, or cognitive EXPERIENCES

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19
Q

What is an example of pain being felt without experience?

A

phantom limb

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20
Q

The afferent pathway brings the pain impulse from the _______ to the _______

A

epithelial receptors to the CNS

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21
Q

What part of the body interprets pain?

A

the brain and spinal cord

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22
Q

The efferent pathway brings the pain response from the _______ to the _________

A

CNS to the response organ (ie. muscle)

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23
Q

Nociception

A

processing of harmful stimuli through the nervous system

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24
Q

Nociceptors are _____ nerve endings in the ___________ PNS

A

free; afferent

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25
Q

What is larger: A delta or C fibres?

A

A Delta

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26
Q

Which of A delta or C fibres are myelinated?

A

A delta are myelinated, C fibres are not

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27
Q

_______ fibres access the large spinal cord tracts

A

A Delta

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28
Q

______ fibres access the small spinal cord tracts

A

C fibres

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29
Q

Which type of fibres produce the initial fast and sharp pain?

A

A delta

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30
Q

Which type of fibres produce the latter dull and throbbing pain?

A

C fibres

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31
Q

What is the “activation of nociceptors”?

A

transduction

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32
Q

What is the “conduction to dorsal horn and up the spinal cord”?

A

transmission

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33
Q

A transducer is…

A

a device that converts variations into an electrical signal

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34
Q

What does the sensory discriminative system do?

A

identify presence, location, and intensity of pain

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35
Q

What part of the brain is involved in sensory discrimination?

A

somatosensory cortex

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36
Q

What does the motivational-affective system do?

A

determines avoidance and emotional responses

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37
Q

What parts of the brain are involved in the motivational-affective system?

A

reticular formation and limbic system

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38
Q

The cognitive-evaluative system is involved with the ________ pain experience

A

learned

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39
Q

Pain Perception

A

conscious awareness of pain

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40
Q

The _______ and _______ systems are involved in pain perception

A

reticular and limbic

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41
Q

Pain Threshold

A

lowest recognizable intensity of pain

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42
Q

Pain Tolerance

A

highest intensity of pain a person can endure

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43
Q

**Pain tolerance ________ with repeated exposure

A

decreases

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44
Q

The concept of perceptual dominance says that intense pain at one location _______ the threshold at another location.

A

increases

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45
Q

What do pain modulation mechanisms do?

A

increase or decrease pain transmission

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46
Q

What are two triggers that initiate excitatory neurotransmitters?

A

tissue injury and chronic inflammation

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47
Q

What do excitatory neurotransmitters do?

A

reduce nociceptor activation threshold (increase their responsiveness)

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48
Q

Name 4 Examples of Excitatory Neurotransmitters

A

-substance P
-glutamate
-histamine
-prostaglandins

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49
Q

What do inhibitory neurotransmitters do?

A

reduce the transmission of a pain signal

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50
Q

Name 5 Examples of Inhibitory Neurotransmitters

A

-opioids
-GABA
-cannabinoids
-serotonin
-norepinephrine

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51
Q

What does the descending inhibitory pathway do?

A

releases endorphins to inhibit the pain signal

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52
Q

Endorphins (opiates) are a mixture of _______ and _________

A

endogenous and morphine

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53
Q

Where do endorphins bind?

A

opiate receptors

54
Q

Opiate receptors are G _________ coupled

A

protein

55
Q

Morphine-like neuropeptides are responsible for what sensation?

A

well-being

56
Q

What do morphine-like neuropeptides bind with? What do they do?

A

opioid receptors; inhibit pain impulses

57
Q

Cannabis produces a ________ containing cannabinoids

A

resin

58
Q

Cannabinoids are an analgesic meaning…

A

they relieve pain

59
Q

Cannabinoids have _________ and ___________ drawbacks

A

psychoactive and addictive

60
Q

When was Cannabis legalized in Canada?

A

2020

61
Q

Endocannabinoids are synthesized in the body from ___________ to modulate pain

A

phospholipids

62
Q

How does alcohol relieve pain?

A

depressing the CNS

63
Q

In 1200 to 1500 England a potion called ________ was used as an anesthetic.

A

dwale

64
Q

Dwale Ingredients

A

-alcohol base
-bile
-opium
-lettuce
-hemlock (highly toxic plant)
-vinegar

65
Q

When was Ether created?

A

1840

66
Q

When was the first pain free surgery performed? Where?

A

1846 in the amphitheatre at Mass Gen

67
Q

What is another name for acute pain?

A

Nociceptive pain

68
Q

Acute pain is a protective mechanism that…

A

alerts to harmful conditions and mobilizes person to relieve it

69
Q

How long does acute pain last?

A

minutes to weeks

70
Q

3 Types of Acute Pain:

A
  1. somatic
  2. visceral
  3. referred
71
Q

Where does somatic pain occur?

A

localized to skin, joints, muscles

72
Q

What fibres are responsible for sharp and localized somatic pain?

A

A delta

73
Q

What fibres are responsible for dull, throbbing somatic pain?

A

C fibres

74
Q

Where does visceral pain occur?

A

internal organs and body cavity lining

75
Q

Is visceral pain localized?

A

no, it is more achy

76
Q

Which fibres are responsible for visceral pain?

A

C fibres

77
Q

Where is referred pain felt?

A

distant to the point of origin

78
Q

Which receptors converge on the same ASCENDING neuron to provide referred pain?

A

cutaneous and visceral

79
Q

Why does referred pain happen?

A

the brain can’t distinguish which receptors are affected

80
Q

Why is referred pain often felt on the skin?

A

the skin has more receptors

81
Q

Persistent pain is aka __________ pain

A

intractable

82
Q

How long does persistent pain last?

A

3-6 months

83
Q

What is the purpose of persistent pain?

A

there isn’t one

84
Q

Persistent pain can be _________ or __________

A

-ongoing ie. back pain
-intermittent ie. migraine headaches

85
Q

Studies on persistent pain show a change in the _______ that show a _______ ability to cope with pain

A

brain; reduced

86
Q

Neuropathic pain is caused by a dysfunction of the _________ system

A

nervous

87
Q

Neuropathic pain results from ______ term changes in pain _________ and ________

A

long; pathway; processing

88
Q

Neuropathic pain ________ pain to a burning, shooting, tingling sensation

A

amplifies

89
Q

Neuropathic pain is characterized by an increased ____________ to stimuli, painful or not

A

sensitvity

90
Q

__________ (increased pain capacity) is a characteristic of neuropathic pain

A

hyperalgesia

91
Q

Hyperalgesia

A

increased capacity to feel pain

92
Q

Analgesia

A

absence of pain

93
Q

Fever Definition: the _________ resetting of __________ thermostat to higher levels in response to exogenous or endogenous pyrogens

A

temporary; hypothalamic

94
Q

Pyrogen

A

substance that produces fever when released into blood

95
Q

Pyro

A

related to fire

96
Q

Exogenous

A

growing from or on the outside

97
Q

Endogenous

A

growing/originating within

98
Q

Exogenous Pyrogens

A

pathogens

99
Q

Endogenous Pyrogens

A

TNF-a, IL-1, IL-6

100
Q

__________ pyrogens cause the release of __________ pyrogens

A

exogenous; endogenous

101
Q

How do pyrogens raise the thermal set point?

A

inducing hypothalamic synthesis of prostaglandin E2 (PGE2)

102
Q

How do prostaglandin’s increase temperature?

A

increased heat production and conservation

103
Q

Heat conservation through cutaneous ___________ and decreased sweating makes the individual feel ______

A

vasoconstriction; colder

104
Q

How long does the body maintain the increased temperature?

A

until the fever breaks and the original set point is reinstated

105
Q

Pathogen activates the release of m_________ that release ___________ and signal the temperature regulating centre to release ______ to raise the set point

A

macrophages; cytokines (TNF-a, IL-1, IL-6); PGE2

106
Q

How is heat generated after the set point is raised?

A

-increased muscle contraction
-shivering reflex
-increased metabolism

107
Q

Fever kills __________ and affects their growth an replication

A

microorganisms

108
Q

Fever decreases serum levels of ______ needed for bacterial growth

A

minerals

109
Q

Increased temperature causes ___________ breakdown which prevents…

A

lysosomal; viral replication

110
Q

Fever enhances ________ and antiviral _________

A

phagocytosis; interferon

111
Q

Hyperthermia

A

elevation of body temp without an increased hypothalamic set point

112
Q

What are 3 risks of hyperthermia?

A

-nerve damage
-protein coagulation
-death

113
Q

Heat cramps are severe________ (sporadic) cramps

A

spasmodic

114
Q

Heat cramps follow a) prolonged ________ and b) associated ______ loss

A

sweating; sodium

115
Q

How many mmol of sodium are in a L of sweat?

A

40-60

116
Q

Who is at risk for heat cramps?

A

-those not accustomed to heat
-those performing strenuous work in warm climates

117
Q

S&S of Heat Cramps

A

-↑ core temp
-rapid pulse
-↑ BP

118
Q

Heat exhaustion can result from high _____ or ___________ temperatures

A

core or environmental

119
Q

Heat Exhaustion: intense vasodilation and sweating leads to:

A

-dehydration
-hypotension (low BP)
-tachycardia (fast HR)

120
Q

Heat exhaustion manifests as: ______, _________, ________, and __________

A

dizziness, weakness, nausea, and confusion

121
Q

Heat stroke can be ________

A

lethal

122
Q

What body temperature does nerve damage and convulsions occur at?

A

41℃

123
Q

What body temperature does death occur?

A

43℃

124
Q

What is the normal core body temperature?

A

37℃

125
Q

Hypothermia occurs when the body temp is less than ____℃

A

35

126
Q

During hypothermia, what is produced inside cells that causes cellular rupture?

A

ice crystals

127
Q

Tissue hypothermia: ________ metabolic rate, ______ blood viscosity, ________ blood coagulation and vasoconstriction

A

slows; increases; facilitates

128
Q

When is therapeutic hypothermia used?

A

during surgery

129
Q

Why is therapeutic hypothermia used?

A

to slow metabolism and prevent ischemic tissue

130
Q

What is the risk of therapeutic hypothermia?

A

V fib or cardiac arrest

HLSC 222 - Pathophysiology Across the Lifespan (17 decks)

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