Test 3: 37 pain Flashcards

1
Q

nociception

A

the sensory nervous system’s response to a harmful or potentially
harmful stimuli

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2
Q

pain vs nociception

A

Nociception– the sensory nervous system’s response to a harmful or potentially harmful stimuli

Pain – nociception + perception (needs consciousness)

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3
Q

acute pain

A

last less than 3 – 6 months, and/or is directly related to tissue damage. Short duration and gradually resolves as injured tissues heal.

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4
Q

chronic pain

A

extends beyond the expected period of healing (long duration), is not related to resolving injury, has no useful purpose, and is refractory to treatment.

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5
Q

abnormally increase in sensitivity to pain (“what hurts, now hurts a lot more”)

A

Hyperalgesia

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6
Q

triggering of a pain response from a stimuli that do not normally provoke pain (“what should not hurt, now hurts”)

A

allodynia

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7
Q

tranduction of pain

A

change of noxious stimuli into electrical impulse

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8
Q

transmission of pain

A
  • Propagation of impulse through the nervous system
  • A-delta fibers – myelinated, fast speed, sharp pain
  • C fibers – unmyelinated, slow speed, longer-lasting, dull, diffuse pain
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9
Q

what kind of pain fibers for dull, diffuse pain

A

C fibers: unmyelinated, slow speed, longer-lasting, dull, diffuse pain

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10
Q

what find of pain fibers for sharp pain

A

A-delta fibers: myelinated, fast speeds, sharp pain

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11
Q

how does modulation of pain work

A

in spinal cord- will change the pain tranmission

activate descending analgesic systems: opioids, serotonin, NE

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12
Q

perception of pain is by

A

Integration of thalamocortical, reticular, and limbic function to produce final conscious subjective and emotional experience

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13
Q

3 neuron pain pathway simply is

A

First Order
* Originates in the periphery and projects to the spinal cord- primary afferent fiber

Second order
* Ascends to the spinal cord

Third order
* Projects into the cerebral cortex and other supraspinal structures

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14
Q

how do TRP work

A

Transient receptor potential (TRP) vanilloid / capsaicin (TRPV1)

  • TRP are activated and allow calcium influx into the 1st order neuron, activating an action potential
  • Acute pain – receptor turns off as soon as the stimulus is gone
  • Chronic pain – receptors don’t turn off, and activating substances persist : Substance P, Calcitonin gene-related peptide, Potassium ions and Inflammatory mediators
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15
Q

lamina V contain — neurons that are able to respond to both — and —

A

wide dynamic range

noxious and non noxious stilumi

can be involed in wind up pain and the development of chronic pain

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16
Q

what does plasticity in the dorsal horn mean

A

can modify the pain stimuli depending on the type and strength of signal input

17
Q

gate control theory

A

“Trick the nervous system to block painful stimuli transmission by sending non- painful stimuli”

when you hurt an area, you rub it, that rubbing will decrease painful signal

18
Q

antinociceptive system of the brain tries to decrease pain by —

A

releasing
* Endorphins (endorphin, enkephalin, and dynorphin)
* Serotonin
* norepinephrine

inhibits transmission in spinal cord pain pathway at the dorsal horn

19
Q

how does limbic system effect pain

A

limbic system will assign an negative emotional value to a painful experience

  • pain hurts, avoid it
20
Q

why is acute pain important

A

occurs when there is tissue damage and resolves when healed

  • Serves to alter animal behavior in order to avoid or minimize damage
  • Protective mechanism
21
Q

two types of acute pain

A

nociceptive pain: radicular, somatic, visceral

inflammatory pain

22
Q

what types of nociceptive acute pain

A

Caused by the detection of (potential) harmful stimuli around the body by
nociceptors

  • Radicular pain – from nerve root irritation
  • Somatic pain – from tissues such as muscle, bone, or skin
  • Visceral pain – from internal (hollow) organs
23
Q

Pain originated from an insult to the integrity of tissues at the cellular level

A

inflammatory pain
type of acute pain caused by release of inflammatory mediators and recruitment of inflammatory cells

24
Q

neuroplasticity

A
  • Continuous process of short-, medium, and long-term remodeling of the neurosynaptic organization of the spinal
    cord and brain
  • Ability to adapt to change
  • Can be positive or negative changes for the wellbeing
25
Q

what is central sensitization

A

wind up

in responce to chronic pain, body will lower the threshold needed to cause pain

↑ activation of NMDA (glutamate) channels= ↑ excitability

Recruitment of silent nociceptors → hyperreactivity of 2nd order neurons in the spinal cord → recruitment of WDR neurons to function as pain transmitters (very difficult to turn off once activated)

results in hyperalgesia and allodynia

26
Q

central sensitization will cause the recruitment of —

A

silent nociceptors

27
Q

central sensitization results in — and —

A

Hyperalgesia – abnormally increase in sensitivity to pain (“what hurts, now hurts a lot more”)

Allodynia – triggering of a pain response from a stimuli that do not normally provoke pain (“what should not hurt, now hurts”)

28
Q

what are some simple pain scores

A

visual analogic scale (VAS): line with dash at pain scale
numeric rate: 1 out of 10
simple categorical scores: 1-3 mild, 4-6 moderate

29
Q

mulidimensional pain scores include

A

physiologic and behavior signs