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Patho > Ch 14- Pain and Temperature > Flashcards

Ch 14- Pain and Temperature Flashcards

1
Q

what is pain?

A

dysfunctions of general or specific senses

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2
Q

what are some characteristics of pain?

A
  • unpleasant but protective phenomenon
  • cannot be defined, identified, or measured by an observer
  • complex: interaction between physical, cognitive, and emotional
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3
Q

how is temperature like main?

A

variations in temperature can signal disease
- fever is a common manifestation of dysfunction
- often first symptom of infectious or inflammatory conditions

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4
Q

what is the specificity theory?

A
  • injury activates specific pain receptors to brain
  • intensity of pain is directly related to associated tissue injury
  • problem: does not account for persistent, emotional pain
  • pricking ones finger=minimal pain, cutting hand with knife= more pain
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5
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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6
Q

what is the neuromatrix theory?

A
  • brain produces patterns of nerve impulses drawn from various inputs including genetic, psychological and cognitive experiences
  • pain can be felt without experiencing it, meaning stimuli may trigger the patterns but do not produce them
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7
Q

what are the 3 portions of the nervous system that are responsible for pain perception, sensation, and response?

A
  1. afferent pathway
  2. interpretive centers (CNS)
  3. efferent pathways
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8
Q

what does nociception mean?

A

processing of harmful (noxious) stimuli through nervous system

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9
Q

what are nociceptors?

A

pain receptors
- free nerve endings in afferent PNS

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10
Q

what are the 2 types of nociceptors?

A
  • A-delta fibers: large, myelinated, and access large tracts in spinal cord
  • C fibers: smaller, unmyelinated, and access smaller tracts in spinal cord
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11
Q

what is received first? A delta or C fibers?

A

fast sharp pain is perceived first (A delta fibers) followed by a dull, throbbing pain (C fibers)

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12
Q

what does transduction mean?

A

activation of nociceptors

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13
Q

what does transmission mean?

A

conduction to dorsal horn and up spinal cord

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14
Q

what does sensory-discriminative system identify?

A

presence, location, and intensity

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15
Q

what does the motivational-affective system determine?

A

avoidance and emotional responses

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16
Q

what does the cognitive-evaluative system do?

A

learned pain experience (can therefore modulate perception of pain)

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17
Q

what is a transducer?

A

device that converts variations into an electrical signal

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18
Q

what does pain perception mean?

A

conscious awareness of pain (reticular and limbic system)

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19
Q

what does pain threshold mean?

A

lowest intensity of pain that a person can recognize

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20
Q

what does pain tolerance mean?

A
  • highest intensity of pain a person can endure
  • varies greatly among people and in same person over time
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21
Q

what is perceptual dominance?

A

intense pain at 1 location may increase threshold (lower pain perception) in another location

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22
Q

what does pain modulation mean?

A

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

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23
Q

what are excitatory neurotransmitters? (tell the brain there is pain)

A
  • Substance P
  • Glutamate
  • Histamine
  • Prostaglandins
  • Reduce nociceptors activation threshold= increased responsiveness of nociceptors
24
Q

what are inhibitory neurotransmitters?

A
  • opioids
  • GABA
  • cannabinoids
  • serotonin
  • norepinephrine
  • inhibit/reduce transmission of pain signal
25
Q

what peripheral triggering mechanism initiate excitatory neurotransmitters?

A

tissue injury and chronic inflammation

26
Q

what is the descending pathway and endorphin response?

A

descending inhibitory impulse transmitted from brain to inhibit pain signal

27
Q

what are endorphins?

A

combination of endogenous and morphine

28
Q

what are opiate receptors?

A

G protein coupled receptors for endorphins which are opioid neuropeptides

29
Q

what do prphine-like neuropeptides bind with and what do they do?

A

they bind with opioid receptors throughout body to inhibit pain impulses in periphery, spinal cord, and brain
- responsible for sensations of well- being

30
Q

what are cannabinoids?

A
  • cannabis produces a resin containing cannabinoids
  • analgesic (relieve pain) in humans
  • drawbacks: psychoactive (affects the mind) and addictive properties
  • 2020 legalized in Canada
31
Q

what are endocannabinoids?

A

synthesized in body from phospholipids/ modulate pain and other functions

32
Q

how does alcohol pain reduction work?

A
  • functions by depressing central nervous system
  • it slows down brain and nervous system/ delivers a certain amount of pain relief
33
Q

what is the 1200-1500 England method of pain relief?

A
  • potion called “dwale” used as an anesthetic
  • alcohol-based, bile, opium, lettuce, hemlock (highly toxic plant), and vinegar
34
Q

what was the 1840 pain method?

A

ether created

35
Q

what are the 1846 pain method?

A

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

36
Q

what is acute pain (nociceptive pain)?

A
  • protective mechanism that alerts to harmful condition and mobilizes person to relieve it
  • pain lasting minutes to several weeks, you recover from it
37
Q

what areas does acute pain arise from?

A
  1. Somatic:
    - skin, joints, muscles, very localized
    - sharp and well localized= A delta fibers
    - dull throbbing= C fibers
  2. Visceral:
    - internal organs and lining of body cavities
    - poorly localized, aching, throbbing quality to pain
    - C fibers
  3. Referred:
    - felt distant from point of origin
    - cutaneous (skin) and visceral receptors converge on same ascending neuron
    - brain cannot distinguish between the 2 because skin has more receptors often is referred to a skin area
38
Q

what is persistent pain (intractable pain)?

A
  • pain that lasts more than 3-6 months (pain lasting well beyond expected healing time)
  • serves no purpose/ poorly understood
  • ongoing (back pain) or intermittent (migraine headache)
  • studies: change in brain= reduced ability to cope with pain
39
Q

what is neuropathic pain?

A
  • cause: dysfunction of nervous system= long term changes in pain pathway and abnormal processing
  • chronic/amplification of pain
  • described as burning, shooting, shock-like, or tingling
  • characterized by increased sensitivity to painful and non painful stimuli with hyperalgesia ( hyper=increased/algesia=capacity to feel pain)
40
Q

what does analgesia mean?

A

absence of pain

41
Q

what is pyrogen?

A

substance that produces fever when released into blood

42
Q

what is a fever?

A

temporary resetting of hypothalamic thermostat to a higher levels in response to exogenous or endogenous pyrogens

43
Q

what cause the release of endogenous pyrogenes? (TNF-a, IL-1, IL-6) ?

A

exogenous pyrogens (pathogens)

44
Q

what do pyrogens do?

A

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

45
Q

what is the prostaglandins effect?

A

increase temperature through increased heat production and conservation

46
Q

what happens during the prostaglandins effect takes place?

A

the individual feels colder, curls up to decrease body surface area, goes to bed to get warm
- cause: heat conservation through cutaneous vasoconstriction

47
Q

when does increased body temperature come back down?

A

when fever breaks and original set point is reinstated
- individual feels warm, throws off covers, and stretches out

48
Q

what are the benefits of a fever?

A
  • kills microorganisms affecting their growth and replication
  • decreases serum levels of minerals needed for bacterial replication in infected cells
  • causes lysosomal breakdown, preventing viral replication in infected cells
  • hat facilitates immune response
  • phagocytosis enhaced and antiviral interferon is augmented
  • suppression of fever can be effective but should be used with caution
49
Q

what are heat cramps?

A
  • severe spasmodic cramps in abdomen and extremities
  • follows prolonged sweating and associated sodium loss (40-60 mmol of sweat)
  • common in individuals not accustomed to heat or performing strenuous work in warm climates
  • si/sy: increased core temp, rapid pulse, and increased blood pressure
49
Q

what is hyperthermia?

A
  • elevation of body temperature without an increase in hypothalamic set point
  • can produce nerve damage, coagulation of cell proteins and death
50
Q

what is heat exhaustion?

A
  • result of prolonged high core or environmental temperatures
  • profound vasodilation and profuse sweating= dehydration, hypotension, tachycardia
  • manifestations: dizziness, weakness, nausea, confusion
51
Q

what is a heat stroke?

A
  • potentially lethal
  • 41 C (nerve damage, convulsions)
  • 43 C (death)
52
Q

what is hypothermia?

A
  • normal: 37 C
  • hypothermia: less than 35 C
  • produces ice crystals inside cells= cellular rupture
53
Q

what is tissue hypothermia?

A
  • slows cellular metabolism rate
  • increases blood viscosity
  • facilitates blood coagulation and vasocontriction
54
Q

what is therapeutic hypothermia?

A
  • used to slow metabolism= preserve ischemic tissue during surgery
  • risk: may lead to ventricular fibrillation and cardiac arrest

Patho (7 decks)

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