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PMCOL 412 > PAIN I > Flashcards

PAIN I Flashcards

1
Q

Nociception

A

The neural encoding of a noxious stimulus

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2
Q

What is meant when we say that nociception is neurophysiological

A

The stronger the stimulus the higher the frequency of action potentials

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3
Q

Pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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4
Q

the 2 Properties of pain

A

Salience and valence; applied to nociceptive signal to give us pain

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5
Q

Salience

A

Level of importance or ability to be noticed, ability to interrupt ongoing activity and behaviour

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6
Q

Valence

A

How pleasant or unpleasant it is perceived to be

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7
Q

Acute (first) pain is ___ (good or bad)

A

`Good pain’ serves biological purpose (protection from tissue injury)–to notice and remove yourself from painful stimuli

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8
Q

Bad pain

A

If Injury leads to inflammation causes chronic pain, carried by C-fibers (second pain)

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9
Q

Acute pain is carried by

A

A-delta fibers to the CNS (‘first’ pain)

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10
Q

First pain is ___ to stimulus

A

proportional

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11
Q

Acute pain

A

Nociceptive stimulus, e.g. stepping on a nail, causes acute pain via activation of nociceptive pathways

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12
Q

Chronic Pain Timeline

A

No set time for chronic pain–could be 1 month or a year

Is any stimulus-independent pain

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13
Q

Chronic pain is better described as

A

Stimulus independent pain

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14
Q

Subtypes of Chronic pain

A
  • Mild, musculoskeletal pain
  • Deep pain
  • Neuropathic Pain
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15
Q

Mild, musculoskeletal pain –cause

A

Ongoing pain caused by release of bradykinin, histamine, acid metabolites and prostaglandins

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16
Q

Mild, musculoskeletal pain is ____ to stimulus intensity

A

not proportional

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17
Q

Is Mild, musculoskeletal pain protective?

A

Yes, allow healing

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18
Q

Mild, musculoskeletal pain–treatments

A

Treated with NSAIDs (non-steroidal anti-inflammatory drugs)

ex. aspirin (acetylsalicylic acid) or ibuprofen

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19
Q

Deep Pain–treatments

A

Treated with major analgesics (opioids) such as morphine

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20
Q

Deep pain–localization and def

A

Deep aching pain, deep to body surface, poorly localized

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21
Q

Deep Pain causes

A

Pain associated with major trauma, traffic accident, childbirth, some forms of post operative pain or disease such as heart attack or cancer

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22
Q

Is deep pain beneficial

A

Yes, still ‘good pain’ as it is protective. Allows healing process to progress

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23
Q

Neuropathic Pain-definition

A

pain induced by injury to or disease of the somatosensory system

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24
Q

Neuropathic pain results froom

A

injury to the nervous system

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25
Q

Examples of neuropathic pain

A

Herpes Zoster –> postherpetic neuralgia (shingles)
Phantom limb pain, trigeminal neuralgia, postherpetic, diabetic and HIV-related neuropathies, post-stroke pain, fibromyalgia

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26
Q

Timeline of neuropathic pain

A

Outlasts initial injury, slow onset (develops long after initial acute pain)

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27
Q

Is neuropathic pain beneficial

A

NO, has no obvious protective role

It is “bad pain”

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28
Q

Neuropathic pain is characterized by

A

Spontaneous shooting pain
Causalgia
Hyperalgesia
Allodynia

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29
Q

Hyperalgesia–definition

A

heightened pain sensitivity, same stimulus mode

increased sensitivity to painful stimuli

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30
Q

Allodynia–definition

A

painful response to innocuous stimulus, different stimulus mode, can be touch, cold or warmth
(pain to innocuous stimuli)

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31
Q

Pain perception has 2 components

A

Somatosensory component and Affective component

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32
Q

Somatosensory Component of pain

A

Specific pain pathways allow the localization, intensity and quality of pain–how pain is felt (how strong, where, what)

33
Q

Affective component of pain

A
  • Production of negative emotion
  • Arousal
  • Initiation of stress responses
  • Interruption of ongoing procedures (i.e. waking due to pain)
  • Learning (associating stimuli to pain)
  • Stress, anxiety, anticipation make pain worse
34
Q

Free nerve endings–what are they

A

primarily afferent nociceptors;

cutaneous nociceptors

35
Q

Free nerve endings–role

A

Transduce mechanical, thermal, chemical or tissue damaging stimuli into trains of a.p.’s

36
Q

Free nerve endings stronger stimulus…

A

stronger stimulus more a.p’s

37
Q

Where are the cell bodies of free nerve endings

A

Cell bodies in DRG

38
Q

Pathway of free nerve endings

A

receptors in the skin , cell bodies in DRG –> project to substantia gelatinosa, marginal zone and wide dynamic range neurons in dorsal horn of SC –> brainstem –> thalamus –> somatosensory cortex

39
Q

Primary Afferent fibres

A

A-alpha and A-beta fibres
A-delta fibres
C-fibres

40
Q

Properties of A-alpha and A-beta fibres

A

fast conducting (40-50 m/s)
thickly myelinated fibers
proprioception
touch sensors

41
Q

A-delta fibers

A 
myelinated
slower conducting (~ 20m/s) 
high threshold mechanoreceptors--need strong stim (ex. pain stim) for stimulation
42
Q

C-fibres

A 
unmyelinated
 slow conducting (< 2m/s)
43
Q

2 subtypes of C-fibres

A

Polymodal nociceptors (peptidergic) and non-peptidergic

44
Q

Polymodal nociceptors

A

contain neuropeptides (SP and CGRP) and express TRPV1 channels

45
Q

Non-peptidergic

A

“itch” fibres

bind isolectin B4 (IB4)

46
Q

Damaged tissue or inflammation releases:

A 
• NGF (nerve growth factor)
• bradykinin (painful when applied)
• ATP (leaked from damaged cells)
• histamine (inflammatory)
• Prostaglandin (from cell memb breakdown)
• H+,K+
• 5-HT
• Cytokines (IL-6 and IL-1b, TNF-alpha)
CAUSES activation of C-fibres
47
Q

TRPV1 Receptors

A

aka Vanilloid receptors

Ligand gated ion channels activated by: warmth etc.

48
Q

TRPV1 Receptors activated by

A
  • Capsaicin (why u sweat when u eat spicy food)
  • Resiniferatoxin
  • Moderate thermal stimuli (43 degrees C)
  • H+
49
Q

TRPA1 Receptor activated by

A

Noxious heat (> 52 degrees C) on A-delta cells

50
Q

TRPM-8 receptor activated by

A 
Noxious cold (8-28 degrees C)
Menthol and icilin
51
Q

Number of TRP channels

A

> 30

52
Q

Are hot and cold channels on the same cells

A

sometimes!

different channels but can be expressed on same cells

53
Q

Ionotropic Receptors

A
  • 5HT3 Receptors
  • P2X3
  • ASIC
54
Q

P2X3 receptors

A

iontropic receptor that is ATP-sensitive and found on sensory neurons

55
Q

ASIC receptor

A

iontropic receptor that is acid sensitive

activated by H+

56
Q

Metabotropic Receptors

A
  • B2 bradykinin
  • Eicosanoid (activated by prostaglandins)
  • Histamine (mainly Hist 1)
  • 5HT1 and 5HT2
  • NK1 (atcivated by substance P)
57
Q

Tyrosine kinase receptors

A

TrkA, TrkB, cytokine

58
Q

Sensitization

A

Release of prostaglandins, interleukins, bradykinin, acid metabolites, nerve growth factor sensitize nociceptors beyond site of injury

59
Q

Hyperalgesia is due to _____

A

sensitization; enhanced response to pain

60
Q

Neurogenic inflammation cause

A

Axon reflex

C-fibre excitation causes release of substance P and calcitonin gene related peptide (CGRP) –> excite other C-fibres

61
Q

Axon reflex

A

When C-fibres are activated –> CGRP release –> excites other C-fibres
Axon reflex b/c don’t need to be connected (use chemical messager–CGRP, substance P)

62
Q

Signs of inflammation

A

Redness (rubor), swelling (tumor), heat (Calor), pain (dolor)

63
Q

Neurogenic inflammation causes

A

Vasodilation –> rednesss
Extravasation of plasma proteins
Edema (as fluid follows proteins)–> swelling

64
Q

In dorsal horn, pain fibers project to

A 
Lamina II (substantia gelatinosa) 
Lamina I (marginal zone) 
Lamina IV
65
Q

Lamina I projection neurons project to

A

brainstem, parabrachial nucleus (in hypothalamus), hypothalamus and thalamus

66
Q

Local circuit interneurons allow

A

local withdrawal and autonomic reflexes

67
Q

Pain fibres contact to ___ neurons in the lamina __ and __

A

The dendrites of Wide dynamic range neurons (WDR); lamina IV and V

68
Q

WDR deferential firing to diff fibres

A

fire slowly with Ab fibre input (tactile stim= weak)

strongly with Ad fibre input (pain stim = strong)

69
Q

Descending inputs

A

NA/5HT from rostroventral medulla, LC and raphe nucleus

Modulatory–how mood, etc. can alter pain

70
Q

Primary afferent fibers release

A

Glutamate;

glut –> acts on NMDAR/AMPAR –> EPSCs

71
Q

Release of P, CGRP and Neurokinin A

A

Generates slow EPSPs in dorsal horn cells

72
Q

5HT release in dorsal horn

A

predominantly excitatory

73
Q

NA release in dorsal horn

A

predominantly inhibitory

74
Q

Transmission in the dorsal horn is modulated

A

GABA / glycine inhibitory interneurons

75
Q

Sensitization of cutaneous nociceptors and repetitive discharge leads to

A

sensitization of dorsal horn neurons

76
Q

Sensitization of dorsal horn neurons and plasticity has led to

A

the pre- emptive use of local anaesthetics (in addition to general anaesthetics) in surgery–to keep sensory nerves quiet to they don’t become sensitized and cause pain after surgery

77
Q

Types of Pain

A

Acute (first) and chronic (second) pain

2nd pain types: Musculoskeletal, Deep pain, Neuropathic Pain

78
Q

Peripheral Mechanisms

A

Vanilloid and other receptors role of inflammatory mediators in generating pain
Neurogenic inflammation/axon reflex

79
Q

Dorsal Horn in pain

A
  • Integration in substantia gelatinosa
  • Inputs to laminae I, IV and V
  • Descending modulation via 5-HT and NA pathways

PMCOL 412 (35 decks)

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