Pain Flashcards
Outline the biopsychosocial model of pain perception
Biological: pain
Psychological: attitudes and beliefs about health, psychological distress, illness behaviour
Social: being withdrawn
Describe the MOA of NSAIDs and which drugs selectively target a COX enzyme?
Inhibit cyclooxyrgenase enzymes which usually breakdown arachidonic acid to prostaglandins, therefore inhibiting prostaglandin production, which usually cause voltage gated Na+ channel depolarisation (pain transmission) by prostaglandin binding to prostaglandin GPCR receptor
Celecoxib + Etoricoxib target COX-2
Outline the nociceptive pathway involved in the perception of pain
C or Aδ fibres activated by nociceptor activation
Synapse onto 2nd order neurone where they decussate in SG of DH
Axons ascend to VPL (or if facial then VPM via trigeminothalamic tract) to somatosensory cortex
What are the main types of pain seen clinically?
Nociceptive
Neuropathic
Referred
Headaches
What are typical symptoms of neuropathic pain?
Parasthesias, shooting/burning pain, tingling, numbness
What’s the typical presentation of different types of headache?
Migraine - unilateral
Cluster - localised, unilateral, sympathetic involvement
Tension - frontal bilateral
Sinus - ‘butterfly shape’
Medication overuse - will stop with cessation of drug
What are some techniques and interventions used to treat pain?
Nerve ablation Nerve block Physiotherapy/acupuncture/exercise TENS Neuromodulator implants
What drugs are typically used for the treatment of neuropathic pain?
TCAs and antiepileptic drugs
Carbamezapine for trigeminal neuralgia
Gabapentin + Amitriptyline
How might higher pain centres modulate pain at the spinal level?
Brainstem/cortical nuclei can send projections to override ascending pain signals at the level of SG
Descending inhibition via dorsolateral funiculus
Gate control theory - cutaneous fibres excite projection neurones and encephalinergic neurones to inhibit pain pathway
Outline how the pain pathway is altered in chronic pain and why might this persistent pain/increased sensitivity occur?
Continued pain input -> DH continuously sensitised -> channels to brain stem activated increases and descending inhibition reduced
Brainstem -> limbic system -> chronic pain behaviour
Brainstem -> CVS/RS -> increased risk of hypertension and CVS issues
Badly managed acute pain, emotionally sensitive patient, poor coping skills, previous bad pain experiences, surgical complications, genetic predispositions
What’re the differences between nociceptive and neuropathic pain?
Nociceptive:
Caused by physical damage or inflammation activating free nerve endings (Adelta, Ac fibres)
Causing physiological/acute responses to pain
Responds to analgesics
Neuropathic:
Caused by damage/changes in pain neurones themselves
Usually chronic and difficult to treat as doesn’t respond to conventional analgesics (use TCAs, AEDs)
What types of pain do nociceptive and neuropathic include?
Nociceptive: visceral pain (endometriosis/pancreatitis), arthritis, low back pain, myofascial pain
Neuropathic: phantom limb, trigeminal neuralgia, post stroke pain, complex regional pain syndrome
Define referred pain
Sensory info from ANS travels to spinal cord alongside sympathetic and parasympathetic neurones, entering at the same level = pain sensation is perceived in the cutaneous region where it enters
What’s the Gate Control Theory of pain?
Input from pain fibres activates 2nd order cells in the SG which inhibit local inhibitory interneurones so that pan can be transmitted to the thalamus
Non painful input (AB mechanical input) activates the inhibitory interneurones, which reduces pain transmission by inhibiting the 2nd order cells
What are the 3 main outputs of descending inhibition? In which pathway to they travel?
PAG, Hypothalamus, Brainstem (nucleus raphe magnus and locus coeruleus)
Descend to inhibit cells in spinal lamina in the dorsolateral funiculus
