Flashcards in Physiology Pain Deck (59)
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1
what is pain
unpleasant sensory and emotional experience, associated with actual tissue damage or described in terms of such damage
2
what is nocieptive pain
adaptive- an immediate protective response, short lived
3
what is inflammatory pain
adaptive- assists healing, persists over days, possibly weeks
4
what is pathological pain
maladaptive- no physiological purpose, persists over months, years, lifetime
5
how is acute mild pain managed
NSAIDs, paracetamol (doesnt resolve inflammation), opiods (in moderate/ severe cases)
6
what types of drug manage chronic pain
antidepressants
anticonvulsants
local anaesthetics
7
what are nociceptors
specific peripheral sensory afferent neurones normally activated preferentially by intense stimuli that are noxious
8
where are the central terminals on nociceptors
in CNS
9
what transmitter does nociceptors release
glutamate
10
what is the peripheral end of a nociceptor like
free nerve ending
11
what are the two types of nociceptor and what do they do
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)
12
what causes secondary pain
Secondary pain results from a developing inflammation response- the chemicals in this inflammation activate the C fibres
13
what happens when a stimuli activates a nociceptor nerve ending
Na/Ca2+ influx
depolarised membrane
volatge gates Na+ channel activation
action potential to CNS
14
what are the thermal stimuli receptors
transient receptor potential A1, C3, V1
15
when is TRPV1 sensitised
in inflammation- means in is active at body temperature
16
what is the receptors for a noxious chemical stimuli
H+ activates acid sensing ion channels (ASICs), ATP activates P2X and P2Y receptors, bradykinin activates B2 receptors
17
what is the difference between the two types of Adelta fibres
type I and II
type I activates at a higher temp than type II
18
where is the soma of a nociceptor
within dorsal root ganglion (or trigeminal ganglion)
19
what is the nociceptive pathway in the spinal cord
enter dorsal horn
cross segmentally
ascend in spinothalamic or spinoreticulithalamic tracts
20
Peptidergic polymodal nociceptors are a type of C fibre, what is their function
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
21
what can long term noxious stimulation cause
increased spinal excitability= hyperalgesia, allodynia (pain when no stimuli)
22
what do glutamate and peptides do
glutamate= mediates fast synaptic response
peptides= mediates slow synaptic response
23
what is released from free nerve ending of peptidergic nociceptor due to tissue damage, or inflammatory mediators
peptides: substance P and CGRP
24
what does substance P cause
(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
what does CGRP cause
induces vasodilation
26
what is the end result of neurogenic inflammation
Primary and secondary hyperalgesia and allodynia
27
how does neurotransmission occur between the primary afferent and second order neurones in the dorsal horn
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
where are the cell bodies of the primary afferent neurones
dorsal root ganglia
29
where do axons from the primary afferent cell bodies terminate
in dorsal horn of spinal cord in various laminae of rexed
C and A delta fibres terminate superficially in laminae I and II
30