pian lectures Flashcards
why are the 4 main steps for pain pathways
- noxious activity is transducted into the nerve cavities
- nerve activity transmitted along nociceptive pathways to the central nervous system
- modulation of nerve activity in cns
- pereception of pain
what is transduction
the conversion of noxious mechanical, thermal and chemical stimuli into nerve impulses, this is mediated by nociceptirs and these are the pain receptors at the nerve endings
these are activated by inflammatory mediators from damaged tissues
once activated the nerves impulses are transmitted along primary afferent fibres to the spinal cord
what are the 3 primary afferent fibres
a delta fibres
- thinly myelinated- small diameter
- faster transduction
- respond to thermal and mechanical stimuli
- rapid and sharp pain
- responsible for initial reflex to pain
c fibres
- not myelinated so smallest diameter
- slowest conduction
- high threshold fibres
- activated by ll noxious stimuli
- transmit dull aching stimuli
- poorly localised pain
ab fibres
- highly myelinated, large diameter
- rapid signal conduction
- low activation threshold
-respond to light touch and transmit non noxious stimuli
come back
ascending pathway
descending pathway
perception of pain
the areas activated in the brain once pain is felt is the primary and secondary somatosensory (s1 and s2) insular
anterior cingulate cortex and prefrontal cortex and thalamus
difference between acute and chronic pain
acute
- pain resolved as healing occurs
- drug prognosis is good
chronic
- multiple underlying mechanisms contribute to chronic pain
- pain presents when injury is resolved
- changes in both the peripheral and cns processing
- drug prognosis is poor
types of pain
nociceptive pain
- responded to noxious peripheral stimuli
- clear cause
- split into somatic - involves superficial tissues like skin and then visceral which involves internal organs and this is defined as referred pain (because the source of the pain is not close to where pain is felt)
inflammatory pain
- responds to inflammatory stimuli,
- this is just chronic nociceptive
- activation and sensitisation of nociceptors
neuropathic pain
- response to stimuli from nerve ending
- aberrant sensory perception associated with changes in excitability of neurones in central or peripheral nervous system
- pain typically allodynamic or hyperalgesic
what are the 3 main opioid receptors
MOPr
DOPr
KOPr
these are activated by the inhibition of neuronal signalling by increasing the k+ channel which will therefore decrease the ca2+ channel
this activation produces analgesia by inhibiting excitatory neurotransmission
what process will occur when each of these receptors are activated
insert table
opioids mode of action
they boost the descending inhibitory activity
suppress neuronal activity in dorset horns of spinal cord
- block nociceptive transduction in peripheral neurones
how are the opioids metabolised
there are two main types of
- CYP450 - this si the main method
metabolise, CODEINE, FENTANYL, METHADONE, OXYCODONE, OXYMORPHINE - UGT’s - secondary method of metabolism, responsible for the formation of glucermides
metabolise, HYDROMORPHINE, MORPHINE, OXYMORPHONE.
role of nsaid
the block the production of the chemical mediators prostaglandins and thromboxanes and are used to treat pain. they block at the cox 1 and cox 2 in the arachidonic process
they decrease vasodilation and oedemas
what are the side effects of nsaids and why
gastric bleeding
ulcerations
diarrhoea
dyspepsia
renal failure
this si because they block the production of pg which is essential for protecting the mucus and other things
