Chronic pain Flashcards
(26 cards)
describe chronic pain prevalence
3.24million aussies
53.8% are women
restricts activitis for 56%, 68.3% are working age
prevalence will inc 5.23 2050
what is pain definition + chronic pain
unpleasant, sensory, emotional associated with or resembling that associated with actual tissue damage
chronic pain persists or recurs for longer than 3 months
why do we need pain
info about potential damage, actual damage, recovery process
describe chronic nociceptive, neuropathic, nociplastic pain
nociceptive = inflam/tissue damange (osteoarthitis)
neuropathic = damage pns/cns (migraine, MS)
nociplastic = pain arising altered function pain-related sensory pathways in pns/cns (fibromyalgia, lower back pain)
what is primary pain + egs
chronic pain in 1+ areas that persists 3+ months + emotional distress, functional disability
chronic widespread pain, regional pain, headache + orofacial, primary visceral + musculoskeletal
difference between pain and nociception
nociception detects potential/actual harm NOT measure pain
dorsal root ganglion -> spinal cord -> brain neurons for conscious awareness
Is there only 1 type of nociceptor?
NO
eg there is mechanical allodynia (P2X3)
thermal hyperalgesia (TrpV1)
what has to be activated to elicit pain
small unmyelinated + lightly myelinated nociceptors
what type of threshold do nociceptors have
super high, high intensity stimuli
many potential stimuli
describe the structure of nociceptors
eg why redness when scratch
not just afferent for modulation/processing, but also releases things as neurogenic inflammation upon stimulation eg sub P, ATP
different types of nociceptive neurons
A & C fibres
can be polymodal, CMH, AM, silent
can be peptidergic, non-peptidergic (lab animals)
where do sensory inputs/motor outputs go
sensory input = dorsal horn
motor outputs = ventral horn
where do nociceptive fibres terminate
defined areas of the spinal cord
lamina I + 2 (upper section, grey matter)
can you modulate nociceptive processing in the spinal cord?
yes
grabbing area of pain activated skin mechanoreceptors
act on inhibitory interneurons to weaken signal sent to thalamus
describe pain signalling in brain
1st neurons DRG neurons
end and synapse on neurons on the dorsal horn (2nd neuron)
projection neurons of neuron 2 cross to other side
travels via spinothalamic tract (3rd neuron)
describe ascending fibres
spinothalamic tract - sensory discriminative = 1st pain
fibres ending in PBN - affective emotional 2nd pain
describe descending fibres
important for placebo effect, pain inhibition after severe injury
release serotonin and noradrenalin
how to stop chronic pain?
multimodal:
change in lifestyle eg exercise, sleep, weight reduction
pharmacological therapies
physio
psychotherapy (cognitive behavioural therapy)
what drugs can be used for chronic neuropathic pain
anti-epileptic (gabapentine, pregabaline)
analgesic antidepressants (tricyclic antidepressants (amitriptyline)), serotonin reuptake inhibitors (duloxetine)
describe chronic non-neuropathic pain drugs
NSAIDs
opiods
what’s the problem with opioids
dont work after 20 days
need higher sensitivity
big side effects with increased dosage
describe the receptors that opioids act on
mu-opiate = beta endorphin endogenous ligand (euphoria, sedation, addiction)
delta = enkephalin endogenous ligand (supra +spinal analgesia)
kappa = dynorphin A endogenous ligand (supra + spinal analgesia, diuresis respiratory depression)
where do we find the opioid receptors
everywhere there is pain signalling at DRG
peri aquaductal grey
processing areas in cortex/cortical areas
how to treat non-neuropathic chronic pain
non-steroidal anti-inflam drugs = NSAIDs
ibuprofen, aspirin (acetylsalicylic acid), paracetamol (acetaminophren)
block cyclooxygenases, block prostaglandin synthesis, activate endogenous cannabinoid system
