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PHSL232 Lectures 1-38 > Lecture 14 - Pain > Flashcards

Lecture 14 - Pain Flashcards

1
Q

what are pain receptors?

A

receptors with axon endings without obvious anatomical specialisations

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2
Q

where are pain receptors found?

A

found everywhere in the body except the brain

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3
Q

what do pain receptors respond to?

A

respond to strong mechanical stimuli and/or high temperatures and chemicals released in damaged tissues

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4
Q

what are the exogenous chemicals released that pain receptors respond to?

A

capsaicin and menthol

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5
Q

how do capsaicin and menthol chemicals activate pain receptors?

A

activate receptors directly by internalising receptors by over activating pain fibres till the receptors eventually stop responding

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6
Q

what are the 4 things pain is useful for?

A

to avoid injury
alert us to local infection
aid in recovery
indicate further disease

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7
Q

what are the 2 types of nerve fibres that carry pain?

A

“c” fibres and “A-delta” fibres

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8
Q

what are “c” pain nerve fibres?

A

smallest diameter fibres (in relation to A-delta fibres) myelinated axons

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9
Q

what is the conduction velocity of “c” pain nerve fibres?

A

slow conduction velocity

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10
Q

what do “c” pain nerve fibres signal to?

A

signal to sustained and ongoing damage (or potential damage)

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11
Q

what are “A-delta” pain nerve fibres?

A

a subtype of A fibres that are small diameter myelinated axons

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12
Q

what is the conduction velocity of “A-delta” pain nerve fibres?

A

fast conduction velocity

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13
Q

what do “A-delta”pain nerve fibres signal to?

A

signal the acute onset of a painful stimulus

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14
Q

what is hyperalgesia?

A

increasing sensitivity of pain pathways following an injury or an inflammatory disease (e.g arthritis)
–> the tenderness of an area

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15
Q

how does hyperalgesia occur?

A

occurs as the injury site and area around the injury become ‘tender’

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16
Q

why does the injury site and area around the injury become ‘tender’?

A

this is due to the sensation of sensory endings by locally released factors and changes at the CNS synapses

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17
Q

what are the local factors that might be released if we damage an area of the skin?

A

K+
bradykinins
5-HT (serotonin)
prostaglandins

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18
Q

what is the effect of the release of K+ in a damaged area of the skin?

A

an increase of K+ from the high concentration of K+ inside the cell will generate more AP’s in response to tissue damage

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19
Q

what is the function of prostaglandins?

A

platelet aggregation for cloating

activation of pain fibres

20
Q

what is the relationship between increasing sensitivity of a damaged area and the anterolateral pathway?

A

another way to increase sensitivity is to increase synapse efficiency in the anterolateral pathway in the spinal cord to the CNS

21
Q

what do pain fibres release once activated?

A

release substance P and CGRP

22
Q

what is the effect of the release of local factors?

A

local factors will activate mast cells to release histamine which will give positive feedback on to nerve terminals

23
Q

what is the effect of histamine?

A

histamine spreading out from mast cells recruits neighbouring axons to bring them closer to threshold

24
Q

what is the hyperalgesic area?

A

the area sensitised by neighbouring axons

25
Q

what causes the itch sensation?

A

histamine

26
Q

what is the function of asprin?

A

inhibitor of prostaglandin synthesis which are involved in blood clotting

27
Q

what is asprin?

A

both an anti-blood clotting agent and a pain reliever

28
Q

what is sensation in pain pathways modulated by?

A

modulated by descending pathways

29
Q

what is the inhibition of pain pathways?

A

the “gating” of pain impulses by non-painful stimuli of nearby nerves. Inputs from nearby non-pain nerves inhibits the response of ascending pain fibres which is a non-chemical innervation to pain relief)

30
Q

what are the methods of non-chemical innervation to pain relief?

A

methods include rubbing the affected area or trans-epidermal nerve stimulation (TENS) through an electronic skin rubber

31
Q

what is the function of endogenous opiates?

A

decrease the post synaptic excitability of axons taking pain information to the CNS

32
Q

where are endogenous opiates released?

A

released at synapses on pain-pathway neurons

33
Q

what are endogenous opiates?

A

the site of action to ‘centrally acting’ painkillers of morphine and codeine

34
Q

what is the function of endocannabinoids?

A

decrease long-term sensitivity to pain. They are involved in

  • arousal
  • placebo
  • anxiety
  • association
  • suggestion
35
Q

what is atonic modulation?

A

long term retrograde signalling thats released by the post synaptic neuron to effect the amount of neurotransmitter that the terminal releases on to it

36
Q

what is the relationship between the level of arousal and pain?

A

the level of arousal tunes out pain fibre sensation level of conciousness

37
Q

what are the symptoms of diabetic neuropathy?

A
  • tingling or burning (in toes, legs, fingers, hands or arms)
  • “pins and needles”
  • pain/cramping
  • loss of sensation
  • insensitivity to heat/cold
  • extreme sensitivity to light touch
  • muscle weakness in hands or feet
  • loss of coordination
  • multiple autonomic dysfunctions
38
Q

what do all of the symptoms of diabetic neuropathy result in?

A

result in loss of sensation, including loss of pain and this leads to tissue damage

39
Q

why does tingling occur?

A

because AP’s are not occurring in the correct sequence to be interpreted

40
Q

where does loss of sensation start?

A

starts way out in the periphery where the nerve endings are further away from the cell body in the spinal cord that is providing them their metabolic support

41
Q

why is dental pain poorly localised?

A

dental pain could be located in the mouth but could also be referred pain from a sinus/ear infection or migraine

42
Q

what is pulpitis?

A

a cavity in the tooth

43
Q

what is referred pain?

A

pain feelings from the viscera referred to a body surface

e.g heart pain to the neck and arm

44
Q

what causes referred pain?

A

the presumed “cross-talk” of visceral and somatic sensory pathways that is activated by stretch and ischemia

45
Q

what is neurogenic pain?

A

nerve compression that can cause pain to be felt in the region of nerve termination
e.g pain in the leg from the compression of a nerve in the back by a slipped disc (herniated intervertebral disc)

46
Q

what are the 2 causes of phantom limb pain?

A

1) ongoing activity in nerves that used to come from that limb
2) invasion of corticol representation for that part of intact body regions that cause spare neurons to invade regions that no longer exist
e. g cortex representation of amputated hand may become activated by inputs from the face

PHSL232 Lectures 1-38 (14 decks)

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