L4 - pain Flashcards
pain meaning
bad experience associated with tissue damage
-combo of sensory and emotional components
nocieption meaning
sensory component of pain without emotional component
how is pain detected
sensory receptors in the skin - nerve endings
- activated by intense stimuli that is enough to cause tissue damage
- AP generated
two kinds fo nociceptor
-mechanical
o
-polymodal
what is mechanicalnocieptor
activated by strong force in skin like cut
-leads to sharp pain
what is polymodal nocieptor
respond to many stimuli
- EPSP is generated but once it reaches the threshold, the AP is generated and there is a dull, throbbing pain
- pain causes by the chemical released by the damaged tissue
what fibre does mechanical nociceptor send the signal to
delta fibres - very fast
what fibres does the polymodel send the signal to
C fibres - unmyelinated, much slower
transmission of what sensory afferent nerves of sharp and dull pain
first - the sharp pain is transmitted through the delta fibres
second - then dull pain comes along when polymodal nociceptor is also activated
pathway of the primary afferent fibres into CNS
the signal is transmitted through the C fibres then spilt up into B fibres into substantia gelatinosa and C fibres into the brain
what section of the dorsal horn does the input from AB fibres go to
III-V sections
what section of the dorsal horn does the input from ASand C fibres go to
cutaneous I-II
viscera I, V X
what makes up the vast majority of the dorsal horn neurons
interneurons
are majority of interneurons are inhibitory or excitatory
inhibtiory so when the pain signal arrive here in the dorsal horn, it has to overcome in hibition to be sent to brain
- refer to gate their of the pain
what is the gate theory of pain
there is a gatekeeping neurone which prevents the signal from going to the brain
- but there is an inhibitory neurone that can be activated. Then it stops action of the gatekeeping neurone
- so the “gate” is open and sent to the brain
how to close the gate for the pain signal
stimulating mechanoreceptors like rubbing the injuired area.
- this activates the AB fibres
- send the signal to the spinal cord to the gate keeping neurone
- -the gate is now closed, so the pain signal cant go to the brain
- so relieving the pain
pathway through the spinal cord for pain
spinothalamic pathway
- perceived at subcortical level
- localised at cortical level
descending pathway for pain down the spinal cord
through the brainstem
- releases chemicals like Nadr, ankephalin
- to close the spinal gate -
what happens during normal physio pain
sensation of pain is equal to the afferent input
what happends during persistent pain
increases sensitivity to pain when oen is injuired
- peripheral and central sensitisation
peripheral mechanism for increased sensitivity to pain
-area injuried so AP generated
- releases substance P and CGRP from nerve ending >
redness, swelling, >
immune cell migration and activation > release prostagladins, H+, cytokines> increases sensitivity and the area heats up >
activates ploymodal receptor
why is it more painful to touch the injured
increases sensitivity due to lower threshold for AP to reacg
what is primary hyperalgesia
increased pain sensitivity directly in damaged tissue
eg of peripheral sensitisation
what is secondary hyper glasia
increased pain sensitivity distant from site of injury
- eg of central sensitisation
