Chapter 14- Pain and Temperature Flashcards

1
Q

What is pain?

A

Dysfunctions of general or specific senses that cannot be defined, identified or measured by an observer

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2
Q

What kind of phenomenon is pain?

A

Unpleasant but a protective phenomenon

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3
Q

Pain: Complex?

A

Interactions between physical, cognitive , emotional etc

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4
Q

How did McCaffrey define pain?

A

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

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5
Q

What can pain and variations in temperature signal?

A

Disease

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6
Q

What is a common manifestation of temperature dysfunction?

A

Fever

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7
Q

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

A

Temperature changes

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8
Q

What are the 3 Theories of Pain?

A
  1. Specificity theory
  2. Gate Control theory
  3. Neuromatrix theory
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9
Q

What is the specificity theory?

A

Injury activates specific pain receptors in the brain. Intensity of pain is directly related to associated tissue injury.
-Pricking one’s finger = minimal pain
-Cutting hand with a knife = more pain

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10
Q

What is the problem with the specificity theory?

A

Does not account for persistent, emotional pain

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11
Q

What is the Gate control Theory?

A

Combines and builds upon theories to explain multidimensional aspects of pain.
Pain transmission is altered by a balance of signals sent to spinal cord where cells work as a “gate”
Spinal gate controls pain transmission to higher centres in CNS

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12
Q

What is the Neuromatrix theory?

A

Brain produces patterns of nerve impulses draw from various inputs (genetic, psychological, cognitive). However pain can be felt without them, like phantom limb. Therefore stimuli may trigger the patterns but do not produce them.

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13
Q

What are the 3 portions of the nervous system responsible for (in relation to pain)?

A

Pain perception, sensation and response

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14
Q

What are the 3 portions of the nervous system involved in perceiving pain?

A
  1. Afferent pathway
  2. Interpretive centres CNS
  3. Efferent pathways
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15
Q

What is Nociception?

A

processing of harmful (noxious) stimuli through nervous system

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16
Q

What are Nociceptors?

A

Pain receptors

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17
Q

What kind of nerve endings do Nociceptors have?

A

Free nerve endings in afferent PNS

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18
Q

What are the 2 types of nociceptors?

A

A delta fibers
C fibers

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19
Q

What are A delta fibres?

A

Large, myelinated that access large tracts in spinal cord

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20
Q

What are C fibers?

A

Smaller, unmyelinated that access smaller tracts in spinal cord

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21
Q

What pain is perceived by A delta fibres?

A

Fast sharp pain

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22
Q

What pain is perceived by C fibres?

A

Dull, throbbing pain

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23
Q

What kind of pain is perceived first? And what pain follows it?

A

Fast sharp pain is perceived first, followed by dull, throbbing pain

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24
Q

What is a transducer?

A

Device that converts variations into an electrical signal

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25
Q

What is Transduction?

A

Activation of nociceptors

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26
Q

What is Transmission?

A

Conduction to dorsal horn and up in spinal cord

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27
Q

What are the 3 systems of pain perception?

A
  1. Sensory-discriminative system
  2. Motivational-affective system
  3. Cognitive-evaluative system
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28
Q

What is the sensory-discriminative system?

A

Identifies presence, location and intensity (somatosensory cortex)

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29
Q

What is the Motivational-affective system?

A

Determines avoidance and emotional responses (reticular formation, limbic system)

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30
Q

What is the Cognitive-evaluative system?

A

Learned pain experience (can therefore modulate perception of pain)

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31
Q

What is pain perception?

A

Conscious awareness of pain
-Reticular and limbic system

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32
Q

What is Pain threshold?

A

Lowest intensity of pain that a person can recognise

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33
Q

What is Pain tolerance?

A

Highest intensity of pain a person can endure.
-Varies among people and in same person over time

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34
Q

How does pain tolerance decrease?

A

Decreases with repeated exposure

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35
Q

What is perceptual dominance?

A

Intense pain at one location may increase threshold (lower pain perception) in another location

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36
Q

What is pain modulation?

A

Different mechanisms act to increase or decrease pain transmission through nervous system

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37
Q

What peripheral triggering mechanism initiates excitatory neurotransmitters?

A

Tissue injury
Chronic inflammation

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38
Q

What are examples excitatory neurotransmitters?

A

Substance P
Glutamate
Histamine
Prostaglandins

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39
Q

What do excitatory neurotransmitters do to nociceptors?

A

Reduce nociceptors activation threshold, increasing the nociceptors’ responsiveness

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40
Q

What are examples of inhibitory neurotransmitters?

A

Opioids
GABA
Cannabinoids
Serotonin
Norepinephrine

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41
Q

What do inhibitory neurotransmitters do to pain?

A

Inhibit/reduce transmission of pain signal

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42
Q

What are endorphins?

A

Combination of “endogenous” and “morphine”
-Opiod neuropeptides

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43
Q

What is transmitted from the brain to inhibit pain signal?

A

Descending inhibitory impulse

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44
Q

What kind of receptors are Opiate receptors?

A

G protein coupled receptors

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45
Q

What do morphine-like neuropeptides bind with throughout the body?

A

Opiod receptors

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46
Q

What happens when opioid receptors bind with morphine-like neuropeptides?

A

Pain impulses in periphery, spinal cord and brain are inhibited

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47
Q

What are morphine-like neuropeptides responsible for?

A

Well-being

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48
Q

What does cannabis produce?

A

Resin containing cannabinoids

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49
Q

Cannabinoids are ________ in humans

A

Analgesic (relieve pain)

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50
Q

What are the drawbacks of cannabinoids?

A

Psychoactive
Addictive

51
Q

When were cannabinoids legalised in Canada?

A

2020

52
Q

What are Endocannabinoids?

A

Synthesised in body from phospholipids that modulate pain

53
Q

How does alcohol reduce pain?

A

Alcohol depresses CNS, slowing down the brain and NS which delivers some pain relief

54
Q

What was the method of pain relief in 1200-1500 England?

A

-Potion called “Dwale” for anesthetic
Ingredients; Alcohol-based, bile, opium, lettuce, hemlock (toxic plant) and vinegar

55
Q

What was created in 1840 for pain relief?

A

Ether

56
Q

What happened in 1846 in amphitheatre of Massachusetts General Hospital?

A

First pain-free surgery was preformed

57
Q

What kind of pain is Acute pain?

A

Nociceptive

58
Q

What is acute pain?

A

Protective mechanism that alerts to harmful condition and mobilises person to relieve it.

59
Q

How long does acute last?

A

Minutes to weeks

60
Q

What 3 areas does acute pain arise from?

A
  1. Somatic
  2. Visceral
  3. Reffered
61
Q

What parts of body is somatic acute pain?

A

Skin
Joints
Muscles

62
Q

Is somatic acute pain localised?

A

Very localised

63
Q

What fibres are involved in somatic acute pain?

A

A delta = Sharp, well localised
C fibers = Dull throbbing

64
Q

What parts of body is visceral acute pain?

A

Internal organs
Lining of body cavities

65
Q

Is visceral acute pain localised?

A

No. It’s poorly localised

66
Q

What fibres are involved in visceral acute pain?

A

C fibers: Aching, throbbing pain

67
Q

What is referred acute pain?

A

Pain is felt distant from point of origin

68
Q

What receptors are involved in referred acute pain?

A

Cutaneous
Visceral

69
Q

Where do referred acute pain receptors converge and what is the result of this?

A

On same ascending neuron
-Brain can’t distinguish between the two receptors

70
Q

Where is pain often referred to ?(referred acute pain)

A

Skin area

71
Q

Why is pain often referred to the skin?

A

Because skin has more receptors

72
Q

What kind of pain is persistent pain?

A

Intractable pain

73
Q

What is persistent pain?

A

Pain that lasts more than 3-6 months (beyond expected healing time)

74
Q

What is the purpose of persistent pain?

A

Serves NO purpose
-Poorly understood too

75
Q

What are the kinds of persistent pain?

A

Ongoing e.g back pain
Intermittent e.g migraines

76
Q

How does a change in the brain affect persistent pain?

A

Change in brain = reduced ability to cope with pain

77
Q

What causes neuropathic pain?

A

Dysfunction of nervous system caused by long term changes in pain pathway and abnormal processing

78
Q

What kind of pain is neuropathic pain?

A

Chronic/ amplification of pain

79
Q

How is neuropathic pain described?

A

As burning, shooting, shock-like or tingling

80
Q

What is neuropathic pain characterised by?

A

Increased sensitivity to painful and NON-painful stimuli with hyperalgesia

81
Q

What is hyperalgesia?

A

Increased capacity to feel pain

82
Q

What is analgesia?

A

Absence of pain

83
Q

What is a fever?

A

Temporary resetting of hypothalamic thermostat to a higher level in response to exogenous or endogenous pyrogens

84
Q

Pyrogens

A

Substance hat produces fever when released into blood

85
Q

What are exogenous pyrogens?

A

Pathogens

86
Q

What do exogenous pyrogens cause the release of?

A

Endogenous pyrogens

87
Q

What are endogenous pyrogens?

A

TNF-a
IL-1
IL-6

88
Q

How do pyrogens raise the thermal set point?

A

By inducing hypothalamus synthesis of prostaglandin E2 (PGE2)

89
Q

What does Pyro mean?

A

Related to fire

90
Q

What is Prostaglandins effect on temperature/fever?

A

Increase temperature through increased heat production and conservation

91
Q

When prostaglandins are in effect during a fever, how does the individual feel?

A

Feels colder, curls up to decrease body surface area, goes to bed to get warm

92
Q

How is heat conserved during a fever to make the individual feel cold?

A

Cutaneous vasoconstriction

93
Q

The increased body temperature is maintained until the fever ______?

A

Breaks and original set point is reinstated

94
Q

When the original set point is reinstated during a fever, how does the individual feel?

A

Feels warm, throws off covers and stretches out

95
Q

How does the ANS react to production of PGE2 raising the thermostatic set point?

A

Heat conservation or heat generation aka fever

96
Q

What does the ANS do to conserve heat?

A

Cutaneous vasoconstriction
Decreased sweating

97
Q

What does the ANS do to generate heat?

A

Increased muscle contraction
Shivering reflex
Increased metabolism

98
Q

What does the raised temperature produced by a fever do to microorganisms?

A

Kills many of them and adversely affects their growth and replication

99
Q

What does the raised temperature produced by a fever do to bacterial replication?

A

Decreases serum levels of minerals e.g Iron needed for bacterial replication

100
Q

What does the raised temperature produced by a fever do to viral replication in infected cells?

A

Prevents viral replication by causing lysosomal breakdown

101
Q

What does the raised temperature produced by a fever do to immune response?

A

It facilitates immune response

102
Q

What does the raised temperature produced by a fever do to phagocytosis and interferon?

A

Phagocytosis is enhanced and antiviral interferon is augmented

103
Q

Can suppression of fever be effective?

A

Yes, but should be used with caution

104
Q

What are some disorders of temperature regulation?

A
  1. Hyperthermia
  2. Heat cramps
  3. Heat exhaustion
  4. Heat stroke
  5. Hypothermia
  6. Tissue hypothermia
    7.Therapeutic hypothermia
105
Q

What is hyperthermia?

A

Elevation of body temp without an increase in hypothalamic set point

106
Q

What can hyperthermia produce?

A

Nerve damage
Coagulation of cell proteins
Death

107
Q

What are heat cramps?

A

Severe spasmodic cramps in the abdomen and extremities

108
Q

What do heat cramps follow?

A

Prolonged sweating and associated sodium loss (40-60mmol of sodium/litre of sweat)

109
Q

Heat cramps are common in which individuals?

A

Individuals not accustomed to heat or performing strenuous work in warm climates

110
Q

Signs/symptoms of heat cramps?

A

Increased core temp
Rapid pulse
Increased blood pressure

111
Q

What is heat exhaustion?

A

The result of prolonged high core or environmental temperatures

112
Q

What does heat exhaustion lead to?

A

Profound vasodilation and profuse sweating which causes dehydration, hypotension and tachycardia

113
Q

How does heat exhaustion manifest?

A

Dizziness
Weakness
Nausea
Confusion

114
Q

Heat stroke is potentially ______?

A

Lethal

115
Q

What occurs if someone with heat stroke reaches 41°C?

A

Nerve damage and convulsions

116
Q

What occurs if someone with heat stroke reaches 43°C

A

Death

117
Q

What is the normal core body temperature?

A

37°C

118
Q

What is the core body temperature of someone who is hypothermic?

A

Less than 35°C

119
Q

What happens to the cells of someone with Hypothermia?

A

Ice crystals are produced inside cells causing cellular rupture

120
Q

What is tissue hypothermia?

A

Slows cellular metabolism rate
Increases blood viscosity
Facilitates blood coagulation and vasoconstriction

121
Q

What is therapeutic hypothermia?

A

Used to slow metabolism to preserve ischemic tissue during surgery

122
Q

What is the risk associated with therapeutic hypothermia?

A

May lead to ventricular fibrillation and cardiac arrest

123
Q

What are the pain facilitators?

A

Glutamate
Substance P
Histamine
Prostaglandin
Bradykinin

124
Q

What are the pain inhibitors?

A

Opioids
GABA
Cannabinoids
Serotonin
Norepinephrine