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HLSC 222 > Ch. 14 > Flashcards

Ch. 14 Flashcards

1
Q

Pain

A

Dysfunctions of general or spectifc senses

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2
Q

Pain characteristics

A

-Unpleasent but productive phenomnenon
-Can’t be defined, identified or measured by others

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3
Q

Complex characteristics of pain

A

interactions between, physical, cognative, and emotions

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4
Q

McCarffery Definition of pain

A

Whatever experiencethe person says it is, exhisting when they say it does

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5
Q

Temperature variations

A

-Signal disease

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6
Q

Manefestations of temperature functions

A

-Fever
-symptom of infectious or inflammatory conditions

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7
Q

Theories of pain

A

-Specificity theory
-Gate control theory
-Neuromatrix theory

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8
Q

Specific theory

A

-Injury activates specific pain receptors
-Intensity of pain is directly related to associated tissue injury

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9
Q

Example of specificity theory

A

-Pricking a finger: Minimal pain
-Cutting hand: Higher pain

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10
Q

Problem with specificity theory

A

Doesn’t account for persistant, emotional pain

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11
Q

Gate control theory

A

-Combines theories to explain multidimensionl aspects
-transmission altered by a balance of signals sent to s.cord: cells work as a “Gate”

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12
Q

Spinal gate

A

controls pai transmission to centers in the CNS

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13
Q

Neuromatrix theory

A

-Brain produces patterns of nerve impulses drawn from various inputs, including genetic, psychological, and cognitive experiences

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14
Q

Can pain be felt with out ecperiencing it?

A

Yes
-Phantom limb
-Neuromatrix theory

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15
Q

Neuromatrix theory stimuli

A

trigger patters but don’t make them

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16
Q

Pain pathway

A

3 parts of NS responsable for perception, sensation, and response
-Afferent pathways
-Interpretive pathways
-Efferent pathways

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17
Q

Nocioception

A

Processing of harmful (noxious) stimuli through NS

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18
Q

Nociocepters

A

Pain receptions
-Free nerve endings in afferent PNS

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19
Q

2 types of Nociocepters

A
  • A delta fibers
    -C fibers
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20
Q

A Delta fibers

A

-Large myelinated
-access large tracts in S.cord

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21
Q

C fibers

A

-Smaller unmylenatied
-Access smaller tracts in S.cord

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22
Q

Fast sharp pain is percieved by

A

A Delta fibers

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23
Q

Dull throbbing pain

A

C FIbers

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24
Q

Transduction

A

Activation of nociocepters

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25
Q

Transmission

A

Conduction to dorsal horn and up spinal cord

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26
Q

Transducer

A

Device that converts varations into an electric signal

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27
Q

Perception types

A

-Sensory-descriminative
-Motivational-affective
-Cognitive-evaluative

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28
Q

Sensory-discriminative

A

identifies presence, location, and intensity
(Somato sensory cortex)

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29
Q

Motivational-affective

A

determines avoidance and emotional responses
(Reticulat formation, limbic system)

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30
Q

Cognitive-Evaluative

A

Learned pain experience
(Can modulate perception of pain)

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31
Q

Pain perception

A

consoius awareness of pain (reticular and limbic system)

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32
Q

Pain threashold

A

lowest intensity of pain that a person can recognize

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33
Q

Pain tolerence

A

-Highest intensity of pain endurance
-Varies greatly among people and in same person over time
-Pain tolerence decreases with repeated exposure

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34
Q

Perceptual dominance

A

intense pain at one location may increase threashold in another location

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35
Q

Pain modulation

A

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

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36
Q

Perpheral triggoring mechanism

A

initiates exitatory neuro thransmitters include tissue injury and chrinic inflammation

37
Q

Excitatory NT

A

-Substance P, Glutamate, Histamine, Prostaglandins
-Reduce nocioceptior activation threashold

38
Q

What increases nocioceptor responsiveness

A

Exciatatory NT

39
Q

Inhibitory NT

A

-Opioides, GABA, Cannabinoids, serotonin, norepinepherine

40
Q

What inhibits/reduces transmission of pain signal

A

Inhibitory NT

41
Q

Decending pathway and endorphin response

A

-decending inhibitory impulses transmitted from brain to inhibit pain signal

42
Q

Endorphins

A

Combination of “endogeneous” and “morphine”

43
Q

Opiates receptors

A

Gprotein receptors coupled receptors for endorphins which are opiate neuropeptides

44
Q

Morphine-like neuropeptides

A

-Bind with opioid receptors throughout the body to inhibit pain impulese in periphery, s.cord, and brain

45
Q

Whats responsible for sensations of well being

A

Morphiene-like neuro peptides

46
Q

Cannabinoids

A

-Canabis (marajuana) produces resin containing cannabinoids

47
Q

Analgesic cannabinoids

A

relieve pain in humans

48
Q

Drawbacks to anagelisic cannabinoids

A

psychoactive and addictive properties
-Legalized in 2020

49
Q

Endocannabinoids

A

-synthesized in body from phospholipids
-modulate pain and other functions

50
Q

Alcohol pain reduction

A

functions by depressing CNS
-Slows down brain and NS
-Delivers some pain relief

51
Q

dwale

A

-potion anesthetic used from 1200-1500
-alcohol, bile, opium, lettuce, hemlock (toxic plant) and vinegar

52
Q

1840

A

ether created

53
Q

1846

A

first pain-free surgery performed in amphitheater of Massachusetts general hospital

54
Q

Acute pain

A

-nociceptive pain
-protective mechanism
-pain last minutes to weeks

55
Q

how is acute pain protective

A

alerts to harmful condition and mobilizes person to relieve it

56
Q

types of acute pain

A

-Somatic
-Visceral
-Referred

57
Q

Somatic pain

A

-skin, joints, muscles
-sharp and localized =delta fibers
-dull throbbing= C fibers

58
Q

Visceral

A

-internal organs and lining of body cavities
-poorly localized, aching, throbbing quality to pain
-C fibers

59
Q

Referred pain

A

-felt distant to place of origin
-cutaneous and visceral receptors converge on same ascending neuron
-brain can’t distinguish between the two
-skin has more receptors so pain is often referred to skin area

60
Q

Persistent pain

A

-intractable pain
-lasts more than 3-6 months
-serves no purpose/poorly understood
-ongoing(back pain) or intermittent(migraine headache)

61
Q

studies of persistent pain show

A

change in brain = reduced ability to cope with pain

62
Q

Neuropathic pain cause

A

dysfunction of nervous system = long term changes in pain pathway and abnormal processing

63
Q

neuropathic pain

A

-chronic/amplification of pain
-described as burning, shooting, or tingling

64
Q

neuropathic pain characterization

A

increased sensitivity to painful and nonpainful stimuli with hyperalgesia

65
Q

hyperalgesia

A

increased capacity to feel pain

66
Q

analgesia

A

absence of pain

67
Q

Fever

A

temporary resetting of hypothalamic thermostat to a higher level in response to exogeneous or endogenous pyrogens

68
Q

pyrogen

A

substance that produces fever when released into blood

69
Q

exogeneous pyrogens

A

(pathogens) cause release of endogenous pyrogens
(TNF-a, IL-1,IL-6)

70
Q

pyrogens job

A

raise thermal set point by inducing hypothalamic synthesis of prostaglandin E2 (PGE2)

71
Q

PGE2

A

prostaglandin E2

72
Q

prostaglandins effect

A

increase temperature through increased heat production and conservation

73
Q

How individuals feel from prostaglandins effects

A

-feel colder, fetal position to decrease surface area, go to bed to get warm

74
Q

cause of how individuals feels

A

heat conservation though cutaneous vasoconstriction

75
Q

how long is the increased fever temp maintained

A

until fever breaks and original set point is reinstated

76
Q

returning to original set point

A

individual feels warm, throws off covers, and stretches out

77
Q

fever benefits

A

-kills MO
-decreases minerals needed for bacterial replication
-breaks down lysosome, prevents viral replication
-facilitates immune response
-enhanced phagocytosis

78
Q

suppression of fever

A

can be effective but used with caution

79
Q

hyperthermia

A

-elevation of body temp w/o an increase in hypothalamic set
-can cause nerve damage, coagulation of cell proteins, and death

80
Q

Heat cramps

A

-Severe spasmodic cramps in abdomen and extremities
-follows prolonged sweating and associated Na loss(40-60mmol/L of swear)
-common in those not accustomed to heat or hard work in hot climates

81
Q

SS of heat cramps

A

increased core temperature, rapid pulse, and increased bp

82
Q

Heat exhaustion

A

-result of prolonged high core or environment temp
-profound vasodilation and profuse sweating = dehydration and tachycardia

83
Q

manifestations of heat exhaustion

A

dizziness, weakness, nausea, confusion

84
Q

Heat stroke

A

-potentially lethal
-41C (nerve damage, convulsions)
-43C (Death)

85
Q

Hypothermia

A

-body temp less then 35C
-produces ice crystals in cells= cells rupture

86
Q

Tissue hypothermia

A

-slows cellular metabolism rate
-increases blood viscosity
-facilitates blood coagulation and vasoconstriction

87
Q

therapeutic hypothermia

A

-used to slow metabolism= preserve ischemic tissue during surgery

88
Q
A

HLSC 222 (9 decks)

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