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physiology and pharma > L14 - pain (also revise D&D lecture for this) > Flashcards

L14 - pain (also revise D&D lecture for this) Flashcards

1
Q

define pain

A

pain is a unique, unpleasant, sensory and emotional experience resembling actual /potential tissue damage

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2
Q

what are the sensory aspects of pain?

A

threshold of pain
intensity of pain
location of pain

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3
Q

what are the emotional aspects of pain

A

psychological aspects, eg
unpleasantness of stimulus and the emotions that evokes ( helplessness, fear)

which can escalate pain

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4
Q

describe the basic pain processing pathway

A

pain -> peripheral sensory nerves -> spinal cord -> cortex and limbic brain (pain perception) -> midbrain -> spinal cord (modification of pain we feel)

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5
Q

what brain region is associated with emotional aspect of pain processing

A

limbic brain

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6
Q

which brain region is associated with the sensory aspect of pain procesing

A

cortex

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7
Q

define nociception

A

the neural process of encoding noxious or potentially noxious stimuli

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8
Q

what are the 4 processes of nociception

A

transducton (stimulus to neurone)
transmission (peripheral neurones to brain)
modulation (descending inhibition)
perception

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9
Q

what sensory nerve fibres respond to noxious stimuli

A

(A delta) and C fibres

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10
Q

example of sensory nerve fibres do not normally respond to noxious stimuli

A

A beta

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11
Q

what are nociceptors

A

nerve endings in bodily tissues that can repsond to noxious stimuli and transduce them into receptor potentials

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12
Q

what inputs can nociceptors respond to?

A

mechanical
chemical
thermal

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13
Q

what is pain transduction

A

the coonversion of noxious stimuli to receptor potentials via nociceptors

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14
Q

describe process of pain transmission

A

process where pain message is carried from site of tissue injury to the brain (somatosensory cortex and limbic system) via axons of primary afferent nociceptor A∂ and C fibres

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15
Q

what is important to note about pain and transmission in the primary afferent fibre?

A

there can be pain percieved without transmisison in the PAF

there can be transmission in the PAF without pain being percieved

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16
Q

revise descending inhibition

A

x

17
Q

list the key nuclei in the descending inhibition pathway ( and where theyre located)

A

periaqueductal grey (midbrain)

Locus Coereleus and rostral ventralmedial medulla (brainstem)

18
Q

define acute pain

A

pain associated with tissue damage, shouldnt last longer than 3 months

serves a biological purpose - the pain prevents use of the damaged area, so it can heal effectively

19
Q

define chronic pain

A

chronic pain lasting more than 3 months and outlasting the normal healing time for the tissue

serves no biological purpose

20
Q

give examples of chronic pain

A

migranes

21
Q

list two causes of chronic pain

A

peripheral sensitisation

central sensitisation

22
Q

define peripheral sensitisation

A

increased sensitivity to afferent nerve stimulation

altered function of noicieptors

23
Q

describe the process of peripheral sensitisation

A

nociceptors produce many neuropeptides.

neuropeptides have many effects including hyperalgesia, upregulation of existing and new receptors) and more

this makes the sensory nerve endings more sensitive and responsive to the NTs, reducing the threshold for nociceptor firing leading to elevated pain state)

24
Q

give examples of neuropeptides released by nociceptors and the effects they have

A

substance P
histamine
5-HT

  • primary hyperalgesia (making a pain stimulus more painful)
  • allodynia (making a non painful stimulus painful)
  • upregulation of existing and new nociceptors
25
Q

define central sensitisation

A

amplification of pain by the CNS due to altered funcitoning of nociceptive neurones

26
Q

what type of molecules can cause central sensitisation and how?

A

kinases

they alter activation kinetics of NMDA and AMPA receptors, and their trafficking to the membrane

this:
increases spontaneous neuronal activity
reduces threshold for receptor activation

including in pathways that are not normally nociceptive (eg A beta fibres)

27
Q

what can central sensitisation lead to (sort of like symptoms)

A

pain when no pain stimulus is present

28
Q

difference between peripheral and Central sensitisation

A

peripheral is due to altered responsiveness of nociceptors, central is due to increased activity of nociceptive neurones

peripheral, the pain is limited to site of injury, central it isnt

29
Q

what are the types of pain

A

nociceptive (or inflammatory) -> from tissue damage
neuropathic -> from damage to pain system
other (central) -> due to neurological dysfunction (not damage)

30
Q

what are the main inflammatory pain enhancers?

A

PGE2

PGI2

31
Q

how do noxious factors activate nociceptors?

A

by increasing sensitivity and opening of VGNaC
by decreasing sensitivity and opening of VGKC
(in sensory neurones specifically)

leading to depolarisation and AP firing

32
Q

list some noxious factors

A 
prostaglandins 
bradykinins 
5-HT
ATP
H+
33
Q

describe process of neuropathy

A

a nerve lasceration, eg during surgery

damaged nerves cause firing and pain and nerves have a limited ability to heal themselves
so neuropathic pain often chronic

34
Q

explain how NSAIs treat pain

A
  1. block COX enzymes reducing production of prostaglandins (noxious stimuli) - anti-inflammatory
  2. possibly also work in CNS where PGs have role in pain processing
  3. anti-pyretic effects from actions in CNS
35
Q

what COX enzyme produces PGs

A

COX2

36
Q

what COX enzyme inhibited by NSAIDs

A

both COX1 and 2

37
Q

what effects does paracetamol have on symptoms

A

mild analgesic and anti-pyretic

38
Q

describe proposed mechanism of paracetamol action

A

not entirely known, but

peripherally -> weak COX-2 inhibitor
centrally -> possibly due to activation of descending inhibiton pathways, but likely due to inhibtion of PG synthesis

39
Q

how are analgesics used in neuropathy?

A

sometimes neuropathy can be due to dysfunction in channels of synapses / neurones (eg Na/K/Ca)

Ca2+ channels cannot be targeted as they are very widespread

Na channels can be targetted

physiology and pharma (18 decks)

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