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Pain definition Unpleasant sensory/emotional experience associated w/ or resembling actual/potential tissue damage
Nociception definition Neural process of encoding noxious stimuli
Nociceptor fibres Thinly myelinated A-delta fibres (sharp stabbing pain), unmyelinated C fibres (dull burning pain)
Nociception transduction Ion channels -> receptor potnetial reaches sufficient depolarisation -> open VGNaC -> AP propagation to spinal cord presynaptic terminals -> VGCaC -> Ca2+ influx -> nt release to postsynaptic terminals in spinal cord
Heat receptors TRPV1, TRPM3, anoctamin-1, TRPA1
Cold receptors TRPM8, TRPA1
Proton receptors ASICs, TRPV1, TASK-1 (K+ efflux ion channel blocked by H+)
ATP receptors P2X3 (ionotropic)
Mechanical stimuli receptors Piezo1/2, TRPV4, ASICs
Nociceptor classes Polymodal -> respond to many different stimuli, unimodal (only respond to particular type of stimuli), silent (only sensitised/recruited by cytokines during inflammation)
Nociceptor sensitisation If stimulus is sufficient to cause tissue damage, there is increased response to subsequent stimuli -> hyperalgesic (same stimulus = more painful), allodynic (previously innocuous -> painful)
What pain stimuli are released during tissue damage? Intracellular factors from damaged/overstressed cells -> excitatory agents/ATP, bradykinin -> formed by kallikrein cleaving kininogen, acid -> released by anoxic anaerobic/overloaded metabolism
What are sensitising agents? Don't directly activate nociceptors but enhance the responses to excitatory agents -> PG, NGF
What is released when nociceptors are stimulated? CGRP (calcitonin gene-related peptide -> potent vasodilator), substance P (vasodilator/inflammatory mediator - mast cell degranulation)
Erenumab CGRP mAb antagonist -> prevents vasodilation -> prophylactic relief in migraines
Arachidonic acid pain pathway Metabolised to prostanoids via COX-1/2 -> AA cyclised and oxygenated to form PGG2 (endoperoxide) -> hydroperoxyl reduced to form PGH2 -> converted to PGE2 by PGE synthase
PGE2 effect on nociceptors Sensitising agent for 4 PGE2 receptors -> Gs -> increase AC -> increase cAMP -> PKA activation -> Na+ channel phosphorylation (opening) -> Na+ influx -> reduce activation threshold -> smaller depolarisation evokes AP firing
Neuropathic pain definition Pain outlasting initial nerve injury due to phangom limb, infectious disease (HIV, leprosy, hepatitis), diabetic neuropathy, trigeminal neuralgia, postherpetic neuralgia
Analgesics definition and examples Inhibit nociceptor sensitisation by decreasing neuronal excitability -> NSAIDs, opioids, antidepressants, GABA analogues, Nav inhibitor, Cav inhibitor
NSAIDs Inhibit COX enzymes -> inhibit PG production -> less nociception sensitisation > enter hydrophobic channel on PGE synthase enzyme -> form H-bonds w/ Arg120 -> prevent AA entrance into catalytic domain -> xcp aspirin
Aspirin NSAID -> enters PGE synthase active site -> acetylates Ser530 -> irreversible acetylation/inactivation of COX -> long-lasting aspiring action -> weakly COX-1 selective -> cardiovascular protection (prevent platelet derived thromboxane) and treat migraines
COX-1 vs COX-2 COX-1 is constitutive (inhibition has unwanted side effects), COX-2 is only induced in activated inflammatory cells via TNF-alpha (inhibition has anti-inflammatory/analgesic effects)
NSAID examples Ibuprofen -> weakly COX-1 selective (RA/gout/soft tissue disorder symptomatic relief), paracetamol -> analgeisc/antipyretic (poor anti-inflammatory - not NSAID), ectoricoxib -> COX-2 selective (osteoarthritis/RA)
NSAID side effects Inhibition of constitutive COX-1 activity -> GI bleeding (PGs inhibit gastric acid secretion/stimulate mucin release), renal insufficiency (PGE/I2 maintain RBF), stroke/MI (inhibit PG vasodilation), bronchospasm
Naloxone Opioid receptor antagonist
Opioids Substance producing morphine-like effects -> mu, kappa, delta, ORL1 receptors -> Gi/o coupled -> betagamma subunit opens GIRK (hyperpolarisation - less likely AP), inhibit Ca2+ channel opening -> decreased Ca2+ influx -> decreased nt release
Opioid peripheral inhibitory action Peripheral -> AC inhibition counteracts PG nociceptor sensitising effects
Opioid central inhibitory action Spinal cord dorsal horn -> presynaptic nociceptor inhibition decreases nt release, postsynaptic nociceptor inhibition decreases dorsal horn excitability, supraspinal -> PAG evokes endogenous inhibitory systems and reduce affective pain (mu-mediated)
Opioid examples Morphine, diamorphine, codeine, buprenorphine, etorphine
Morphine and diamorphine Opioids -> morphine -> acute/chronic pain, diamorphine (heroin) -> prodrug metabolised to 6-monoacetyl/morphine -> higher lipid solubility than morphine when IV administered -> BBB penetration -> subsequent deacetylation gives analgesic effects
Codeine Opioid -> oral absorption (less analgesic effects) -> prodrugs combined w/ NSAID for mild pain
Buprenorphine Opioid -> partial opioid receptor agonist -> patch administration -> slow dissociation + combined high affinity/low efficacy -> antagonises other opioids -> more effective than full agonists as gives moderate analgesia w/ less respiratory depression
Etorphine Opioid -> 1000x more potent than morphine (large animals)
Additive analgesia Drugs inducing analgesia via different mechanisms -> less of each drug needs to be given -> will reduce side effects -> co-codamol = paracetamol (NSAID) + codeine (opioid)
Opioid side effects mu-mediated respiratory depression (inhibit respiratory rhythm/central chemoreceptors), nausea/vomiting (delta/mu-mediated), constipation (mu/delta/kappa-mediated)
Antidepressants 5-HT selective reuptake inhibitors (SSRI) -> largely inefficacious, 5-HT/NA reuptake inhibitors (SNRI) and tricyclic antidepressants (TCAs)
Fluoxetine Antidepressant - SSRI -> largely inefficacious
Duloxetine Antidepressant - SNRI -> relief in neuropathic pain -> descending inhibitory pain modulation from locus ceoruleus w/ NA
Amitriptyline Tricyclic antidepressant
GABA analogue mechanisms Decrease cell surface localisation of Ca2+ channel alpha2 delta1 subunit -> decrease in Ca2+ channel current density -> prevent neuropathic pain/reduce nt release
Gabapentin/pregabalin GABA analogue -> epilepsy treatment -> no effect on acute pain
Nav inhibitor mechanism/examples Prevent Na+ influx -> reduce depolarisation -> raise threshold for AP -> lidocaine (Ib - LA -> prevents spontaneous peripheral neuron discharge for neuropathic pain), carbamazepine -> anti-epileptic/treat neuropathic pain via trigeminal neuralgia
Cav inhibitor mechanism/examples Prevent Ca2+ influx -> reduce nt release -> ziconotide -> synthetic analogue administered intrathecally to prevent widespread, deleterious side effects -> expensive and invasive
Pain ladder Step 1 -> non-opioid NSAID + adjuvant, step 2 -> weak opioid (codeine) +- non-opioid/adjuvant, step 3 -> strong opioid (morphine) +- non-opioid/adjuvant
Pain ladder dis/advantages Developed for cancer pain -> works well for post-operative pain but less well for neuropathic pain
Created by: vykleung
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