Pain Flashcards

(23 cards)

1
Q

pain is defined as

A

an unpleasant sensory or emotional experience associated with actual or potential tissue damage

(discriminative + emotional)

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2
Q

mechanical nociceptors (a delta)

A

activated by strong shearing force in the skin - cut/ strong blow/
-sharp pain

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3
Q

polymodal nociceptors (c fibres)

  • both excitatory - Glu
A

respond to sharp blows, damaging heat > 46 deg
chemicals such as histamine, PG, bradykinin
- dull burning pain

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4
Q

a delta fibres

A

fast transmission = sharp pain/ myelinated

1-3

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5
Q

C fibres

A

slower transmission= dull, burning pain

  • afferent CV explains 2 different types of pain
  • 1,5,10 - viscera / diffuse pain
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6
Q

The gate theory

A

pain signals must overcome inhibition to reach the brain

  • ensure only feel pain when appropriate
  • inhibitory interneurons /projections, modulate response
  • stimulated by excitatory afferents (ad/c)
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7
Q

the substantia gelatinosa

A
  • laminar 2
  • houses inhibitory interneurones
  • direct/ indirect contact from afferents
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8
Q

During a non- noxious stimuli

A
  • a-beta fibres- mechanoR activated
  • excitatory synapse on the ascending projection
  • excitatory synapse on an inhibitory IN
  • causes an IPSP at the projecting N
  • does not reach vT- no Pain experienced
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9
Q

during a noxious stimuli

A
  • inhibition is switched off and ascending fibres fire APs
  • excitatory afferents from c fibres
  • synapse with another population of inhibitory IN within the SG
  • these synapse with the gatekeeper N
  • causes an IPSP at the GKN
  • alleviates inhibitory signal from GKN and allows excitatory C fibre to excite ascending projection towards the brain (separate synapse)
  • feel pain
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10
Q

closing the gate to prevent pain signal

A
  • rubbing the injured area -n activation of a `beta fibres
  • TENS - childbirth - activation of a beta fibres (excite GKNs)
  • acupuncture
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11
Q

cortical level of the pathway

A

localisation of pain

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12
Q

subcortical level

A

perceive the stimulus as pain

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13
Q

limbic system

A

effective component

- emotional and affection aspects

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14
Q

The descending pathway (modulation of pain via brain)

A
  • brainstem nuclei rich in opioids
  • release of 5-HT, Nad, enkephalin (endogenous O)
  • close the spinal gate
  • intrinsic analgesia system
  • swearing is an example
  • very powerful
  • inhibits ascending signals
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15
Q

normal physiological pain

A
  • amount of pain experienced directly equal to the afferent input duration and intensity
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16
Q

persistent/ chronic pain

A
  • increased sensitivity to pain
  • promotes guarding and protection of an injured limb
  • feel more pain to prevent aggregation of injury and further damage
    • Process of peripheral and central sensitisation , modification of neurotransmission plasticity - feel more pain after a previous injury
  • requires far less pressure to stimulate sensation of pain after a previous injury
  • stimulus that was previously innocuous is now noxious
17
Q

allodynia

A

level of stimulus wasn’t generating pain (innocuous) now generates pain

18
Q

hyperalgesia

A

stimulus generates even more pain due to injury (was noxious)

19
Q

neurogenic Inflammation

A

axon reflex - antidromic AP conduction

  • peripheral release of substance P, CGRP from nerve ending
  • induces swelling, plasma extravasation, immune cell migration and activation
  • inflam soup
  • Nerve ending expresses R of which these mediators bind to (cks etc)
  • sensitisation of polymodal NC
  • low stimulus intensity generates AP (lowered vT)
  • idea of HA/ AD
20
Q

secondary hyperalgesia

A
  • promotes protection of secondary injury sites (indirectly injured sites)
  • increased pain sensitivity distal from site of injury
  • mechanisms in dorsal horn
21
Q

primary hyperalgesia

A
  • increased pain sensitivity that occurs directly in damaged tissue
22
Q

low stimulus

A
  • release of GLu from afferent
  • binds to AMPAr present on SON
  • single AP fired
  • intensity and duration related to afferent input
23
Q

facilitated pain

A
  • neurogenic inflammation leads to more frequent firing of afferents
  • SP released (only at high freq)
  • preferential release
  • increased AMPA stimulation activates NK-1
  • change in conformation of NMDA r blocked by mg
  • membrane sufficiently depolarised to relieve block
  • NMDA involved in EPSP
  • ca influx
  • post SNN more responsive to input
  • amplification of signal frequency sent to brain