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Block 3 Up To Quiz 1 > Mechanisms Of Pain > Flashcards

Mechanisms Of Pain Flashcards

1
Q

pain definition

A

unpleasant sensory and emotional experiences associated with actual or potential tissue damge

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2
Q

pain is essential for

A

survival and health of animal

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3
Q

perception of pain is

A

subjective, affected by emotion and experience and environment

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4
Q

acute pain generally elicits

A

strong activation of autonomic reflexes with noticeable change in heart rate and blood pressure; vomiting also common with visceral pain

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5
Q

behavioral responses to pain

A

avoidance response or aggression towards subjects inflicting pain often observed

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6
Q

chronic pain can manifest as

A

changes in mood, appetite loss, depression

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7
Q

pain sensation is a

A
  • complex neurological process of both peripheral and central nervous systems, pain scale, and efficacy of analgesics vary from patient to patient
  • extent of pain experience dependent
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8
Q

pain classified into 3 different types based on mechanisms

A
  1. nociceptive pain
  2. inflammatory pain
    c. pathologic pain
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9
Q

nociception

A

one of somatosensory modalities; critical for detection and avoidance of noxious stimuli

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10
Q

nociception threshold

A

high threshold pain activated in presence of intense stimuli playing role in early warning physiological protective system

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11
Q

nociceptive pain clinically

A

easily localized not clinically a problem bc anesthetics and analgesics can reduce unpleasant feeling

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12
Q

nociceptive stimuli include

A
  • extreem heat
  • extreem cold
  • chemical irritants
  • intense mechanical force
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13
Q

nociceptive input is not

A

always perceived as pain even when noxious stimuli exist bc could be overwritten by other brain activities such as emotions or experience

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14
Q

inflammatory pain

A
  • upon tissue injury cells of innate immune system migrate toward site of injury and release proinflam cytokines and small moelecues
  • can be spontaneous pain
  • pain hypersensitivity
  • different inflammatory mediators= sensed by different receptors, inflammatory mediators= trigger for pain sensation
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15
Q

“inflammatory soup” fx

A

activate receptors on nociceptor neurons which either evoke action potentials to elicit pain signaling or modulates ion channel properties (often making nociceptors more excitable)

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16
Q

inflammatory pain fx

A

protect injured area (persistent warning system)

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17
Q

inflammatory pain threshold

A

low threshold pain

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18
Q

inflammatory pain treatment

A

NSAIDs often suppress it

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19
Q

chronic pain

A
  • unnecessarily-prolonged inflammatory pain can become debilitating chronic pain (ex rheumatoid arthritis, lower back pain, sever injury); this is v hard to treat
  • pathologic pain is debilitating type chronic pain
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20
Q

pathological pain function

A

there isn’t one it isn’t protective

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21
Q

pathological pain subclassifications

A
  • dysfuncitonal

- neuropathic pain

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22
Q

dysfunctional pain

A

substantial pain w/o noxious stimulus or peripheral inflammatory pathogens

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23
Q

dysfunctional pain conditions

A
  • fibromyalgia
  • IBS
  • tension type headache
  • TMJ dx
  • interstitial cystitis
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24
Q

neuropathic pain cause

A

neurons themselves are injured and pain hypersensitivity becomes persistant; generally caused by nerve injury
- (ex. back pain, neck pain, migraine, pain after limb amputation)

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25
Q

neuropathic pain can occur

A

spontaneously and duration and amplitude of its response to noxious stimuli are amplified and often irreversible (neuropathic pain = autonomous dx state of nervous system)

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26
Q

mechanism neuropathic pain

A

unclear

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27
Q

examples neuropathic pain vet species

A
  • pain from lumbosacral lesions
  • intervertebral disc herniation
  • other spinal cord injuries
  • discospondylitis
  • vertebral osteomyelitis
  • polyradiculoneuritis
  • feline orofacial pain syndrome
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28
Q

painpathway

A
  1. transduction
  2. transmission
  3. projeciton
  4. perception
  5. modulation
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29
Q

transduction

A

noxious stimuli recognized by nociceptors

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30
Q

transmission

A

nociceptive signals propagate as action potentials

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31
Q

projection

A

signals from nociceptors relayed to neurons in DH spinal cord -> transmitted to brainstem and thalamus

32
Q

perception

A

thalamic nuclei relay nociceptive info to cerebral cortex, perception pain regulated by non-nociceptive afferent fibers

33
Q

modulation

A

pain pathway plastic and modulated at many places in pain pathway can -> hypalgesia or analgesia

34
Q

nociceptors types

A
  • As= thinly myelinated (conduction speed 5-30m/s)

- C fibers- unmyelinated (conduction speed 1m/s)

35
Q

speed nociceptors

A

slower conduction than touch or proprioception

36
Q

nociceptor structure

A
  • free nerve endings in skin, muscle, jt, bone, viscera
  • cell bodies at DRG or trigeminal ganglia
  • pseudo unipolar
  • central and peripheral terminals emanate from common axonal stalk
37
Q

signal transduction direction nociceptor

A

bidirectional signal transduction made possible by majority of proteins synthesized in nociceptor neurons distributed to central and peripheral terminals

38
Q

types nociceptors

A
  • thermal nociceptors
  • mcechnaicla nociceptors
  • polymodal nociceptors
  • silent nociceptors
39
Q

thermal nociceptors

A
  • activated >45 C <5C

- As fibers

40
Q

mechanical nociceptors

A
  • intense pressure activated

- As

41
Q

polymodal nociceptors

A
  • activated by high intensity mechanical, chemical, or thermal stimuli
  • C fibers
42
Q

silent nociceptors

A
  • usually not responsive to noxious stimuli
  • responsive upon inflammation and various chemical agents in viscera
  • C fibers
43
Q

primary neurotransmitter of primary sensory neurons

A

glutamate

44
Q

cot transmitters of nociceptors

A

neuropeptides released as cotransmitters by many nociceptors

45
Q

neuropeptides vs neurotransmitters

A

no efficient mechanism peptide reuptake so neuropeptides diffuse greater distances than glutamate which can -> poorly localized character of many pain conditions

46
Q

molecular sensors detecting noxious stimuli location

A

expressed in peripheral terminals of nociceptors

47
Q

molecular sensors for detecting noxious stimuli are often

A

nonselective cation channels whose activation leads to membrane depolarization, a voltage change called “generator potential” or “receptor potential”

48
Q

steps molecular sensors for detecting noxious stimuli

A
  1. Nonselective cation channels activated -> membrane depolarization (voltage change called generator potential or receptor potential)
  2. Voltage-gated Na+ channels
  3. action potential
49
Q

each nociceptor tends to express

A

one class transduction receptors; segregation of diff molecular transducers into distinct subclasses sensory fibers allow peripheral nervous system to elicit specific types pain sensation = helps shape specific avoidance responses

50
Q

ion channels sense different

A

noxious stimuli

51
Q

what sense noxious stimuli

A
  1. Thermal sensors
  2. Chemical sensors
  3. Mechanical sensors
52
Q

Thermal sensors

A
  • thermal stimuli sensed by transient receptor potential (TRP) channels
  • open and close at different temperatures ranging from 0-60C
  • opening TRP allow cations to flow in -> action potential
53
Q

thermal sensors respond to

A
  • diff temperatuers
  • natural products (capsaicin, menthol)
  • membrane stretch
  • they are versatile sensors for all 3 types noxious stimuli)
54
Q

birds thermal sensors

A

relatively insensitive TRPV1 channels so more tolerant to high temperature and capsaicin

55
Q

chemical sensors

A

nociceptors can sense

  • pungent chemicals (methol capsaicin)
  • cellular components (ATP, signaling peptides like calcitonin gene-related peptide), or acid
  • chemical sensors are diff ligand gated channels that sense different stimuli
  • at peripheral nerve sites chemicals bind to receptors -> action potential; can have modulators modulate excitability of channel
56
Q

chemical sensors include

A
  • TRP channels
  • Acid-sensing ion channels (ASICs)
  • ionotropic purinergic receptors (P2X receptors)
  • receptor tyrosine kinases (ex. TrKA)
  • GPCRs
57
Q

activation TRP channels and ligand-gated ion channels

A

directly evokes generator potentials

58
Q

activation of receptor tyrosine kinases and GPCRs

A

do not directly trigger action potential but modulate ion channels in nociceptor neurons

59
Q

mechanical sensors

A
  • mechanosensing mechanisms poorly understood; some ion channels demonstrated to sense mechanical stimuli (not necisarrily painful stimuli) including:
  • TRP channels
  • candidate mechanosensors= 2 pore K+ channels (K2P), Mac-Like mechanosensitive channels, epithelial Na+ channels (ENaC/DEG), Piezo channels
60
Q

nociceptor input and central nociceptive pathways

A

nociceptor input can trigger prolonged increase in excitability and synaptic efficacy of neurons in central nociceptive pathways (pain sensitization including hyperalgesia, allodynia, and wind up)
- PNS and CNS cause pain sensation

61
Q

abnormal sensitization of pain can ->

A

maladaptive chronic pain

62
Q

hyperalgesia

A
  • increased pain sensitivity
  • primary hyperalgesia st site injury peripheral and central sensitization mechanisms involved
  • secondary hyperalgesia- area adjacent to or remote to site injury this is solely due to changes in central processing NOT sensitization nociceptive nerve endings
63
Q

allodynia

A
  • pain in response innocuous stimulis
  • occurs when pain pathway hijacked by other sensory pathway via nerve rewiring
  • generally pain evoked by AB fibers
64
Q

pain wind up

A
  • in response to repetitive stimulation primary afferent C-fibers
  • in absence of intention inflammation, trauma, nerve injury
  • underlying mechanism unclear
65
Q

peripheral sensitization

A
  • reduced threshold and increased responsiveness of nociceptor evoked by set of inflammatory mediators released from injured and inflammatory cells
  • broad range inducers (usually inflammatory get intracellular cascade of kinases that up regulate signals)
  • multiple intracellular signal transduction pathways are involved (mechanotropic receptors turn on intracell signals that indirectly up regulate channels)
  • usually inflammatory pain
66
Q

central sensitization

A
  • process that establishes state of hyper-excitability established in CNS -> enhanced processing nociceptive (pain) messages
  • C fiber -> interneuron -> brain -> pain
  • increase activity Ca2+ channels, increase neurotransmitter please
  • kinases can up regulate receptors
67
Q

mechanisms implicated in central sensitization

A
  1. alteration in glutamatergic neurotransmission/ NMDA receptor-mediated hypersensitivity
  2. Loss of tonic inhibitory controls (disinhibition)
  3. Glial-neuronal interactions
68
Q

nerve termini of sensitized nociceptors release

A

substance P and calcitonin gene-related peptide (CGRP) which triggers release of inducers from immune cells in peripheral sensitization

69
Q

can have unpleasant stimuli

A

that isn’t perceived as pain

70
Q

protective pain

A
  • acute nociceptive pain

- acute inflammatory pain

71
Q

debilitating pain

A
  • chronic inflammatory pain

- chronic pathologic pain (neuropathic/ dysfunctional)

72
Q

site of moduation

A

synapses; mainly glutaminergic in sensory system

73
Q

neuropathic pain main points

A
  • normally caused by nerve injury
  • low-threshold pain
  • pain hypersensiitivy
  • abnormal central processing
  • spontaneous pain
  • no appropriate treatments yet
  • chronic pain (debilitating and devastating)
74
Q

inflammatory pain main points

A
  • low threshold pain
  • pain hypersenstiivty
  • spontaneous pain
  • fairly effective treatments available (NSAIDs)
  • persistence warning system (protective) OR
  • chronic pain (debilatating)
75
Q

central sensitization inhibitory interneuron

A

can inhibit this then inhibition inhibited -> increase sensitization

76
Q

central sensitization microglial activation

A

have membrane proteins that release cytokines which activate receptors; multiple mechanisms can -> similar symptoms

77
Q

touch pathway in allodynia

A

goes through sensitized pain pathway and touch is then felt as pain

Block 3 Up To Quiz 1 (24 decks)

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