Physiology Pain Flashcards

1
Q

what is pain

A

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

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2
Q

what is nocieptive pain

A

adaptive- an immediate protective response, short lived

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3
Q

what is inflammatory pain

A

adaptive- assists healing, persists over days, possibly weeks

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4
Q

what is pathological pain

A

maladaptive- no physiological purpose, persists over months, years, lifetime

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5
Q

how is acute mild pain managed

A

NSAIDs, paracetamol (doesnt resolve inflammation), opiods (in moderate/ severe cases)

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6
Q

what types of drug manage chronic pain

A

antidepressants
anticonvulsants
local anaesthetics

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7
Q

what are nociceptors

A

specific peripheral sensory afferent neurones normally activated preferentially by intense stimuli that are noxious

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8
Q

where are the central terminals on nociceptors

A

in CNS

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9
Q

what transmitter does nociceptors release

A

glutamate

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10
Q

what is the peripheral end of a nociceptor like

A

free nerve ending

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11
Q

what are the two types of nociceptor and what do they do

A

Adelta- are mechanical/thermal nociceptors that are thinly myelinated, respond to noxious mechanical and thermal stimuli. Mediate ‘first’, or fast, pain

C fibres- unmyelinated, collectively respond to all noxious stimuli (e.g. they are polymodal). Mediate ‘second’, or slow, pain (burning, throbbing, cramping, aching)

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12
Q

what causes secondary pain

A

Secondary pain results from a developing inflammation response- the chemicals in this inflammation activate the C fibres

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13
Q

what happens when a stimuli activates a nociceptor nerve ending

A

Na/Ca2+ influx
depolarised membrane
volatge gates Na+ channel activation
action potential to CNS

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14
Q

what are the thermal stimuli receptors

A

transient receptor potential A1, C3, V1

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15
Q

when is TRPV1 sensitised

A

in inflammation- means in is active at body temperature

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16
Q

what is the receptors for a noxious chemical stimuli

A

H+ activates acid sensing ion channels (ASICs), ATP activates P2X and P2Y receptors, bradykinin activates B2 receptors

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17
Q

what is the difference between the two types of Adelta fibres

A

type I and II

type I activates at a higher temp than type II

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18
Q

where is the soma of a nociceptor

A

within dorsal root ganglion (or trigeminal ganglion)

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19
Q

what is the nociceptive pathway in the spinal cord

A

enter dorsal horn
cross segmentally
ascend in spinothalamic or spinoreticulithalamic tracts

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20
Q

Peptidergic polymodal nociceptors are a type of C fibre, what is their function

A

have afferent and efferent functions:
-afferent: transmit nociceptive info to CNS via release of glutamate and peptides (substance P and neurokini A) within dorsal horn

-efferent: release pro inflam mediators (CGRP, substance P) from peripheral terminal which contributes to neurogenic inflammation

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21
Q

what can long term noxious stimulation cause

A

increased spinal excitability= hyperalgesia, allodynia (pain when no stimuli)

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22
Q

what do glutamate and peptides do

A
glutamate= mediates fast synaptic response 
peptides= mediates slow synaptic response
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23
Q

what is released from free nerve ending of peptidergic nociceptor due to tissue damage, or inflammatory mediators

A

peptides: substance P and CGRP

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24
Q

what does substance P cause

A

(i) local vasodilation and extravasation of plasma proteins (promotes formation of bradykinin and prostaglandins)
(ii) release of histamine from mast cells
(iii) sensitizes surrounding nociceptors

25
Q

what does CGRP cause

A

induces vasodilation

26
Q

what is the end result of neurogenic inflammation

A

Primary and secondary hyperalgesia and allodynia

27
Q

how does neurotransmission occur between the primary afferent and second order neurones in the dorsal horn

A

Action potential arrives at central terminal and opens ca channels, calcium influx, exocytosis, glutamate release
Glutamate diffuses across synaptic cleft and causes a fast excitatory postsynaptic potential
Activates glutamate receptors (primarily postsynaptic AMPA receptors with NMDA receptor participation (when afferent input is intense) )
(Normally NDMA receptors are silent as usually blocked by magnesium ion (pos charge). When the cells become depolarised by AMPA then magnesium pops out as membrane becomes more negative and the receptor can then contribute to transmission)

Peptides (substance P and CGRP) also participate (particularly during high frequency stimulation) causing a slow and prolonged e.p.s.p. that facilitates activation of NMDA receptors by relieving voltage-dependent block by Mg2+
sensitivity of post synaptic cell to glutamate is increase

28
Q

where are the cell bodies of the primary afferent neurones

A

dorsal root ganglia

29
Q

where do axons from the primary afferent cell bodies terminate

A

in dorsal horn of spinal cord in various laminae of rexed

C and A delta fibres terminate superficially in laminae I and II

30
Q

what do nociceptive specific cells synapse with

A

only C and Asimga fibres

31
Q

what cells receive input from Abeta fibres

A

proprioceptive

32
Q

what do wide dynamic range neurones receive input from

A

all three types of pain fibres and thus a wide range of stimuli (Abeta, A delta and C)

33
Q

what does visceral arise from and what causes it

A

nociceptors covering tissues (e.g. peritoneum, pleura), or walls of hollow organs.
Originates from stretching, twisting, inflammation and ischaemia – but not cutting, or burning

34
Q

what does visceral pain feel like

A

poorly localised, dull, aching, throbbing character

perceived at a distance from the affected organ
associated with autonomic features (sweating, nausea, vomiting, pallor)

35
Q

what is the path of visceral afferents from nociceptors

A

follow sympathetic pathways before entering the dorsal horn

36
Q

what causes referred pain

A

some visceral and skin afferents converge upon the same spinothalamic neurones (all cells with a visceral receptive field also have a separate cutaneous RF)

The brain ‘interprets’ the nociceptive information arising from the viscera as originating from an area of skin that may be distant to the internal organ

37
Q

where do terminals of visceral nociceptors terminate

A

in laminae I and V not II

38
Q

what can happen to the segemental dermatome in referred pain

A

may show signs of hyperalgesia

39
Q

what is the segmental dermatome for the heart

A

T1-5

40
Q

what is the segmental dermatome for the gallbladder

A

C4

41
Q

what does viscerosomatic pain feel like

A

sharp and well localised

42
Q

what causes viscerosomatic pain

A

when inflammatory exudate from a diseased organ contacts a somatic (body wall) structure (e.g. parietal peritoneum)

43
Q

where is referred gall bladder pain

A

shoulder

44
Q

where is referred diaphragm pain

A

shoulder

45
Q

where is referred liver pain

A

neck

46
Q

where is stomach/ pancreas referred pain

A

centre of chest below nipple line

47
Q

where is the REFERRED pain from appendix felt

A

umbilicus

48
Q

are pain and nociception the same thing

A

no can have pain with no nociception

pain is awareness of suffering

49
Q

what is the gate control theory

A

Pain evoked by activity in nociceptors (C- and Aδ- fibres) can be reduced by simultaneous activity in low threshold mechanoreceptors (Aβ-fibres)

50
Q

Innocuous and nociceptive signals conduct to the spinal cord via Aβ- and C/Aδ- fibres respectively and are in part processed by neuronal circuits of the …?

A

substantia gelatinosa

51
Q

what allows the gate control theory to work

A

Certain projection neurones (P) within the substantial gelatinosa project to the spinothalamic tract and are postulated to be excited by both large diameter (Aβ) sensory axons and unmyelinated (C/Aδ) nociceptive axons

The projection neurone (P) inputs are inhibited by an interneurone (I) and the interneurone is excited by the large sensory axon and inhibited by the nociceptive axon

Thus, activity in the nociceptive axon alone maximally excites the projection neurone, allowing nociceptive signals to arise to the brain

52
Q

what are the two major ascending nociceptive tracts

A

spinothalamic tract

spinoreticular tract

53
Q

where do projection neurones from lamina I (fast fibre Adelta pain) terminate

A

posterior nucleus of the thalamus

54
Q

where do projection neurones from lamina V (WDR neurones) terminate

A

in the posterior ventroposterior nucleus of the thalamus

55
Q

what does the spinoreticular tract mainly transmit

A

slow C fibre pain

56
Q

what does the spinoreticular tract connect with in the brain

A

reticular nuclei in brain stem and parabrachial nucleus

57
Q

what does the spinoreticular tract do

A

autonomic response to pain, arousal, emotional responses, fear of pain

58
Q

what in the spinothalamic needs to BOTH be stimulated in order to feel pain

A

fibres in lamina 1 (delta) and 5 (WDR neurones)

59
Q

are all thermoreceptors the same

A

no have warm and cold sensitive neurones