pain Flashcards
what are the 2 different sensor fibres
type c and delta fibres
what are type c fibres
- small, non-myelinated fibres
- slower passing of pain information
what type of pain do type c fibres detect
dull and aching
what type of pain do delta fibres detect
hit and sharp pain
how do sensors work under the skin
- there are free nerve ending receptors on the end of the fibres
- different receptors will respond to different stimuli eg heat, mechanical manipulation
how to TRP receptors work for sensation
- they are receptors used to detect painful stimuli
- they change shape to let different ions in when stimulated
- this creates and action potential
stages of pain pathway to the brain
- receptors detect stimulus which travels through the spinothalamic tract to the thalamus
- information processed in the cortex
- pain information goes to the reticular formation
- pain is relayed to the limbic system from the reticular formation - where decision on what to do occurs
what happens with a broken cell membrane
- platelet activation
- phospholipase are free ready to degrade the phospholipids in an orderly fashion
- leads to the arachidonic acid pathway
what are the stages of the arachidonic acid pathway
- tissue injury
- injury to phospholipid membrane
- arachidonic acid released
- Cyclooxygenase pathway and lipoxygenase pathway
what are the stages of the COX pathway
- COX pathway tiggered
- prostaglandin G2
- prostaglandin H2
- prostacyclin, prostaglandin, thromboxane
what is the lipoxygenase pathway broken into
leukotrienes - causing bronchoconstriction and smooth muscle contraction
what does prostaglandin production cause
pain and inflammation
what does thromboxane production cause
platelet aggregation
what is in cellular content
- potassium ions from intracellular fluid
- hydrogen ions needed for energy,
how are hydrogen ion part of pain sensitisation
they affect pain perception and are released from cells when damaged which cause pain
what molecules are involved in platelet activation
- bradykinin - produced from the clotting cascade
- 5HT (serotonin) - produced from activation of platelets and in the CNS its a neurotransmitter
is peripheral sensitization from cell injury and platelet activation what compounds accumulate
- potassium
- hydrogen
- prostaglandins
- bradykinin
- 5HT
how to increase nociceptor sensitization
- increase the number of channels
- need a lower threshold for the channels to respond to
hyperalgesia
bigger response to sensitization
allodynia
hyperalgesia to something that wasn’t painful
stages of pain sensitsiation
- lesion to the cells
- releases H+, K+, Prostaglandin, 5-HT, bradykinin
- these sensitise the nerves which produce substance p
- substance p tiggers the mast cells to release histamine which acts of the nociceptors to send the pain signal
- substance p is also a vasodilator creating redness and warmth in injury
what are the2 ways that bradykinin works in pain sensitisation
it both activates and causes pain in the pathway
why do we get referred pain
- there are non specific/ individualised nociceptors for organs so pain is directed to where there is better nociception eg the skin
- the skin and organ also synapse at the same dermatome
what do sensory neurones do
detect the pain
what does the motor neurone do
responds to the pain and where withdrawal from the pain (reflex to spine)
what is the pain gate
- inside the dorsal horn
- touch sense receptors from Abeta fibres which synapse onto our pain system
stages of the pain gate working
- touch sensation enters
- stimulates the inhibitory interneuron in the dorsal horn
- A beta fibres fire
- these synapse on the inhibitory neurones
- reduced or weak activation of pain
how does pain change with out the A beta fibres
the inhibitory neurone is not activated so the touch sensation travels in on the c fibre to the projection neurone causing strong activation
what do projection neurons do
it is where the pain extends through to go to the brain stem and the reticular activation system
what is the reticular activation system
contains grey matter in the brain - periaqueductal grey
what is periaqueductal grey
the start of the descending pain pathway
what are the stage of the descending pain pathway
- periaqueductal grey - this descends from the same level of the spine as where the pain started
- it releases encephalins and endorphines when it gets a pain trigger
- these synapse onto 2 lower neurone on the brain stem
- serotonergic and noradrenergic neurones secrete serotonin and noradrenaline
- these 4 inhibit the projection neurons in the descending pain pathway
what are SSRI and SNRI
- SSRI - selective serotonin reuptake inhibitor
- SNRI - selective noradrenergic reuptake inhibitor
how to the 2 serotonin descending pathways work
one inhibits and one facilitates pain modulation
how does morphine work as pain management
it stimulated the release or serotonergic and noradrenergic neurones to inhibit pain
how does aspirin work as as pain management treatment
- decrease the production of prostaglandins
- decreases nociceptor sensitivity
how does local anaesthetic work as as pain management treatment
- sodium channel blocker
- stops pain as action potentials can’t travel
how does spinal opioids/ ket work as as pain management treatment
bind to the dorsal horn and affect the serotonin pathway
how do alpha 2 agonists work as as pain management treatment
have a greater activity on the descending inhibitory pain pathway
how does inflammation change pain and central sensitisation
- it makes the nociceptors to become more sensitive (COX2 inhibitor treatment)
- damaged neurones can also become perpetually stimulated
what occurs in central sensitisation
- the CNS is more sensitive
- projection neurones become more and more active
- causes glutamate secretion to NMDA receptors
why is there an increased response in central sensitisation
there is increased NMDA receptors causing long term potentiation and a decrease in inhibitory interneurons
