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NSB > Physiology of Pain > Flashcards

Physiology of Pain Flashcards

1
Q

Pain is accompanied by an

A

emotional reaction

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2
Q

Why do we feel pain?

A
  • helps us learn to avoid harmful/dangerous
    situations
  • prevents further injury or death
  • tells us to rest and heal following
    injury
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3
Q

Types of Pain:

A

insert flowchart

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4
Q

Adaptive Pain:

A

insert flowchart

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5
Q

Pathological Pain:

A

insert slide

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6
Q

Sensations of Pain:

A
  • sharp stab
  • deep ache
  • burning
  • freezing
  • itch
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7
Q

What are nociceptors?

A
  • primary sensory afferent neurons
  • detect noxious stimuli
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8
Q

Nociceptors

A

insert diagram

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9
Q

Nocicpetors have —– ——- —— in the periphery.

A

free nerve endings

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10
Q

Afferent Nerve Endings:

A

insert diagram

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11
Q

Afferent Nerve Fiber Classification:

A

insert diagram

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12
Q

When Aδ fiber nociceptor are activated, what type of pain is experienced?

A

sharp pricking pain

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13
Q

When C fiber nociceptors are activated, what type of pain is experienced?

A
  • slow dull ache
  • burning
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14
Q

Timing of nociceptors:

A

insert diagram

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15
Q

Pain transduction occurs in

A

two waves; first pain which is fast and sharp and the second pain which dull and slow

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16
Q

Pain Transduction

A
  • fast and sharp = A delta
  • then c fibers which last longer
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17
Q

What activates nociceptors (4)?

A
  • pressure
  • temperature
  • chemical
  • tissue damage/inflammation
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18
Q

Which modality do c-fiber nociceptors respond to?

A
  • most are polymodal
  • respond to pressure, temp and
    chemical
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19
Q

Nociceptors: Pressure Transduction:

A
  • mechanically sensitive ion
    channels respond to pressure
  • precise channels and ions not
    identified
  • polymodal (respond to many
    stimuli)
  • possible acid sensing
  • possible transient receptor
    potential channels
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20
Q

Nociceptors: Temperature Transduction:

A
  • transient receptor potential family
    of channels transduce different
    temperatures
  • TRPV1 = hot = chilli is agonist
  • TRPM = cold = menthol
  • TRPA1 = v vold = cinnamon
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21
Q

What chemicals are released as part of tissue injury and inflammation?

A
  • ATP
  • H+
  • serotonin from platelets
  • histamine from mast cells
  • bradykinin
  • prostaglandins
  • nerve growth factors
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22
Q

Prostaglandins are produced from

A

the conversion of arachidonic acid by COX enzymes

23
Q

What is the effect of chemical released during tissue injury and inflammation on nociceptors?

A

excitatory effect
(begins the pain pathway)

24
Q

Activation of nociceptors by inflammation:

  • ATP binds to
  • H+ binds to
  • Serotonin binds to
A
  • P2X
  • acid sensing ion channels
  • 5-HT3

binding of the above excites nociceptors

25
Q

Neurogenic inflammation is

A

inflammation arising due to activity of neurons

26
Q

Neurogenic Inflammation: Process:

A
  • activation of one branch of a
    nociceptor by inflammation,
    triggers the release of substance P
    and CGRP from another branch
  • this causes vasodilation
  • and activation of mast cells
  • which results in the release of
    histamine
  • leading to increased inflammation
  • contributes to the
    pathophysiology of inflammatory
    diseases
27
Q

Hyperalgesia

A

noxious stimuli produce an exaggerated pain response

28
Q

Allodynia

A

non-noxious stimuli produce a painful response

29
Q

Nociceptors are modulated by

A

inflammation and can cause hypersensitivity

30
Q

What is the purpose of pain hypersensitivity?

A

Pain hypersensitivity after an injury promotes healing by ensuring that there is minimum contact with the injured tissue until repair is complete

31
Q

Hyperalgesia alone leads to —– sensitisation

A

peripheral

32
Q

Continued peripheral sensitisation due to hyperalgesia leads to

A

central sensitisation
due to barrage of information reaching spinal cord

allodynia + hyperalgesia

33
Q

Hypersensitivity:

A

insert slide

34
Q

Is peripheral or central sensitisation a major mechanism in neuropathic pain?

A

Central sensitisation

35
Q

Peripheral sensitisation is an increase in the responsiveness of

A

the peripheral ends of nociceptors

36
Q

Peripheral sensitisation is driven by

A

tissue injury or inflammation

37
Q

What chemicals are involved in peripheral sensitisation (3)?

A
  • bradykinin
  • neuron growth factor
  • prostaglandins
38
Q

Peripheral Sensitisation: Role of Bradykinin:

A

to reduce the threshold of heat activated channels (TRPV1)

39
Q

Peripheral Sensitisation: Role of Neuron Growth Factors:

A

to reduce the threshold of heat activated channels (TRPV1)

40
Q

Peripheral Sensitisation: Role of Prostaglandins:

A

to reduce the threshold of Na+ channels, allowing influx of Na+ to depolarise neuron leading to action potential firing

41
Q

How does bradykinin act on TRPV1?

A
  • indirectly
  • bradykinin binds to a
    metabotropic GPCR
  • leading to the activation of protein
    kinase
  • leading to the phosphorylation of
    TRPV1
  • phosphorylation of TRPV1 reduces
    its threshold, hence more action
    potentials are fired
42
Q

Nociceptive information ascends via which spinal tract?

A

the spinothalamic tract

43
Q

What is the path of the first order neuron in the pain pathway?

A
  • first order neurons are
    nociceptors
  • enter the dorsal horn of grey
  • synapse in the substantia
    gelatinosa
  • collateral branch up and
    downwards form the tract of
    Lissauer
  • excites the second order neuron
44
Q

Spinothalamic Tract: pathway:

A

insert diagram

45
Q

What is the path of the second order neuron in the pain pathway?

A
  • crosses in dorsal horn at each
    level (decussates just above entry level)
  • ascend in the anterolateral column
    to the thalamus
46
Q

Spinothalamic Tract: Second-order Neuron:

A

insert diagram

47
Q

Why is pain sometimes referred to different areas? eg: visceral pain as cutaneous

A

convergence of visceral and cutaneousq nociceptors on same second order neurons resulting in the brain perceiving visceral pain as cutaneous

48
Q

What is the path of the third order neuron in the pain pathway?

A
  • third order neurons ascend to the
    primary somatosensory cortex
  • the third order neurons project ot the
    insular cortex

In the primary somatosensory cortex the sensory component is encoded:
- tell us where it hurts and the modality

In the insular cortex the emotional component of pain is encoded:
- unpleasantness
- negative effect

49
Q

Regulation of Pain in the Descending Pathway:

A
  • higher cortical regions project to the
    periaqueductal grey matter
  • pag projects to the rostral ventromedial
    medulla
  • rvm projects to the dorsal horn of grey

pathway can be excitatory to increase the pain or inhibitory to decrease the pain

PAG neurons excite serotonergic neurons

those serotonergic 5HT neurons project to the dorsal horn

the release of serotonin in the dorsal horn activates inhibitory interneurons in the dorsal horn

inhibitory interneurons will release enkephalins, endorphins and dynorphins which will act on opiod receptors

results in inhibition of the second order neuron in ascending pathway

reducing the activity of second order neuron, reduces the pain information that reaches the brain, hence analgesia at this point

RVM will release noradrenaline which will be parallel and achieve the same result

50
Q

The endogenous opiod system plays an important role in the pain pathway; to

A

inhibit pain

51
Q

The endogenous opiod system can be activated by:

A
  • the spinothalamic tract:
    spinomesecephalic fibers
  • higher cortical regions: limbic structures,
    primary somatosensory cortex
52
Q

Endogenous Opiod System:

A

insert diagram

53
Q

Pain Treatment:

A

insert flowchart

NSB (50 decks)

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