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Flashcards in Physiology Pain Deck (59)
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what is pain

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


what is nocieptive pain

adaptive- an immediate protective response, short lived


what is inflammatory pain

adaptive- assists healing, persists over days, possibly weeks


what is pathological pain

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


how is acute mild pain managed

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


what types of drug manage chronic pain

local anaesthetics


what are nociceptors

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


where are the central terminals on nociceptors

in CNS


what transmitter does nociceptors release



what is the peripheral end of a nociceptor like

free nerve ending


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)


what causes secondary pain

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


what happens when a stimuli activates a nociceptor nerve ending

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


what are the thermal stimuli receptors

transient receptor potential A1, C3, V1


when is TRPV1 sensitised

in inflammation- means in is active at body temperature


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


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


where is the soma of a nociceptor

within dorsal root ganglion (or trigeminal ganglion)


what is the nociceptive pathway in the spinal cord

enter dorsal horn
cross segmentally
ascend in spinothalamic or spinoreticulithalamic tracts


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


what can long term noxious stimulation cause

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


what do glutamate and peptides do

glutamate= mediates fast synaptic response
peptides= mediates slow synaptic response


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

peptides: substance P and CGRP


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


what does CGRP cause

induces vasodilation


what is the end result of neurogenic inflammation

Primary and secondary hyperalgesia and allodynia


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


where are the cell bodies of the primary afferent neurones

dorsal root ganglia


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


what do nociceptive specific cells synapse with

only C and Asimga fibres