Physiology Pain Flashcards by Louise Emerson

what is pain

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

How well did you know this?

Not at all

Perfectly

what is nocieptive pain

adaptive- an immediate protective response, short lived

How well did you know this?

Not at all

Perfectly

what is inflammatory pain

adaptive- assists healing, persists over days, possibly weeks

How well did you know this?

Not at all

Perfectly

what is pathological pain

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

How well did you know this?

Not at all

Perfectly

how is acute mild pain managed

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

How well did you know this?

Not at all

Perfectly

what types of drug manage chronic pain

antidepressants
anticonvulsants
local anaesthetics

How well did you know this?

Not at all

Perfectly

what are nociceptors

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

How well did you know this?

Not at all

Perfectly

where are the central terminals on nociceptors

in CNS

How well did you know this?

Not at all

Perfectly

what transmitter does nociceptors release

glutamate

How well did you know this?

Not at all

Perfectly

what is the peripheral end of a nociceptor like

free nerve ending

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

what causes secondary pain

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

How well did you know this?

Not at all

Perfectly

what happens when a stimuli activates a nociceptor nerve ending

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

How well did you know this?

Not at all

Perfectly

what are the thermal stimuli receptors

transient receptor potential A1, C3, V1

How well did you know this?

Not at all

Perfectly

when is TRPV1 sensitised

in inflammation- means in is active at body temperature

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

where is the soma of a nociceptor

within dorsal root ganglion (or trigeminal ganglion)

How well did you know this?

Not at all

Perfectly

what is the nociceptive pathway in the spinal cord

enter dorsal horn
cross segmentally
ascend in spinothalamic or spinoreticulithalamic tracts

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what can long term noxious stimulation cause

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

How well did you know this?

Not at all

Perfectly

what do glutamate and peptides do

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

How well did you know this?

Not at all

Perfectly

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

peptides: substance P and CGRP

How well did you know this?

Not at all

Perfectly

what does substance P cause

Study These Flashcards

(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

what cells receive input from Abeta fibres

proprioceptive

what do wide dynamic range neurones receive input from

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

what does visceral arise from and what causes it

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

what does visceral pain feel like

poorly localised, dull, aching, throbbing character perceived at a distance from the affected organ associated with autonomic features (sweating, nausea, vomiting, pallor)

what is the path of visceral afferents from nociceptors

follow sympathetic pathways before entering the dorsal horn

what causes referred pain

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

where do terminals of visceral nociceptors terminate

in laminae I and V not II

what can happen to the segemental dermatome in referred pain

may show signs of hyperalgesia

what is the segmental dermatome for the heart

T1-5

what is the segmental dermatome for the gallbladder

what does viscerosomatic pain feel like

sharp and well localised

what causes viscerosomatic pain

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

where is referred gall bladder pain

shoulder

where is referred diaphragm pain

shoulder

where is referred liver pain

neck

where is stomach/ pancreas referred pain

centre of chest below nipple line

where is the REFERRED pain from appendix felt

umbilicus

are pain and nociception the same thing

no can have pain with no nociception | pain is awareness of suffering

what is the gate control theory

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

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 ...?

substantia gelatinosa

what allows the gate control theory to work

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

what are the two major ascending nociceptive tracts

spinothalamic tract | spinoreticular tract

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

posterior nucleus of the thalamus

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

in the posterior ventroposterior nucleus of the thalamus

what does the spinoreticular tract mainly transmit

slow C fibre pain

what does the spinoreticular tract connect with in the brain

reticular nuclei in brain stem and parabrachial nucleus

what does the spinoreticular tract do

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

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

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

are all thermoreceptors the same

no have warm and cold sensitive neurones

Physiology Pain Flashcards

(59 cards)