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31 Cards in this Set
- Front
- Back
Opioids |
Drug with a morphine like action acts on opioid receptors |
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Opiates |
drug with morphine like structure |
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Opium |
extract from the juice of the oriental poppy Papaver somniferum Produce euphoria, analgesia, sleep, combating diarrhoea
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2 groups of opioid |
morphine analogues: morphine, codeine, diamorphine, naloxone Synthetic opioids: pethidine, fetanyl, methadone, pentacozine |
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Opioids receptors |
mu, kappa, delta -Gi GPCR -> inhibit AC -> decrease cAMP -> open K channel, close Ca channel -> hyperpolarisation of neurones -> neurotransmitter can't be released
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Where is mu receptors? |
Mostly in the brain, spinal cord, periphery |
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Where is delta receptors |
Periphery (increase expression in inflammation) |
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Where is kappa receptor? |
mainly in the spinal cord |
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Opioid effects on the CNS |
Analgesia: antinociceptive, decrease the affective component of pain Euphoria: mainly mu mediated, offset by k mediated dysphoria Respiratory depression: less sensitive of respiratory center to pCO2, all analgesics (can be fatal) Cough suppression: antitussive, limited evidence N&V Pupillary constriction: central mediated |
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Opioid effects on peripheral |
Decrease GI tone, motility -> constipation, decrease drug absorption Histamine release from mast cell -> itching, urticaria, hypotension, bronchospasm
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Endogenous opioid peptides |
Endophins, enkedophins, dorphins, endomorphins |
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NSAIDS |
Degree of inflammation: varies with drug: indomethacin > ibu > para Inhibition of PGs, TXA formation from AA by COX
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COX-1 |
Constitutive Products involved in signalling and homeostasis
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COX-2 |
Inducible A part of inflammatory response |
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Where do PGs act? |
On EP receptor At the sensory nerves, PGs: not direct pain producers but potentiate the action of other agents at their receptors
PGs enhance the function of kinin receptors, TRPV1, P2X...
PGs decreases temperature required to open TRPV1 by phosphorylating channel proteins |
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Unwanted side effects of NSAIDS |
GIT disturbance, skin reactions, renal damage, analgesic neuropathy, brochospasm With COX 2, increase stroke, CV risk |
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Sites of action of opioids and NSAIDs |
Opioids: descending inhibitory pathway (5HT, NA) -> negative excitation of transmission neuron) Opioids: negative neuropeptide release ->( transmission of C fibre -> excitation ) NSAIDS: inhibit inflammation -> (mediatators released -> noxious stimulus to C fibre)
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NICE/WHO pain ladder |
Stage 1: non-opioids Step 2: weak opioids Step 3: strong opioids |
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TRVP1 channels |
highly expressed in sensory nerves Activated by inflammatory conditions (temp, heat, chemical modification) Gated cations -> depolarisation of sensory nerves and excitatory mediator release Stimulated by vanilloids (capsaicin) Agonist: rapidly sensitise the channels -> burning sensation -> analgesia
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Cannabinoids |
Major active component: THC, act via CB1, CB2, mimic action of endocannabinoids anandamide, 2AG Inhibits neurotransmitter release -> decrease excitation in pain pathway
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Where is CB1? |
spinal cord, brain, sensory nerve |
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Where is CB2? |
immune cells, also inflammatory effects |
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Tramadol |
Weak mu opioids receptor agonist, 5HT releaser, NA reuptake inhibitor Metabolised to 0-desmethyltramadol -> much more potent than any opioids Descending monoamine control of pain transmission effect Not CD in UK Antagonist at NMDA receptors, 5HT, NAChr, MAChr, TRPV1 receptor Treatment of chronic pain, immediate pain Risk of seizures (if overdose) Long half life: decrease abuse potential |
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Tapentadol |
Centrally acting analgesics with a dual mode of action: agonist at mu opioid receptor, NA reuptake inhibitor Descending pain control: potentiated Same effects to other opioids but have better SEs profile Caution in seizure prone patient Not CD in UK
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Clonidine |
alpha 2 AR agonist act on pre-synaptic receptors: decrease neurotransmitter release Analgesic effect: reduce excitatory transmitter release in brain, spinal cord pathways but lack of selectivity -> not use clinically Except migraine prevention
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Neuropathic pain |
damage to neural tissue bc of trauma, herpes, infection, diabetes, chemo, central pain, HIV, alcoholism Accompanied by allodynia Caused by peripheral, central sensitisation of pathways More difficult to treat than other forms of pain Common therapy: tricyclic antidepressants, anti-epileptic |
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Anti depressants |
Amitriptyline, TCAs. enhance descending monoaminergic pain control Dose less than for anti-depression |
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Anti-epileptic drugs |
Pregabatin, gabapentin: 1st line treatment for diabetic neuropathy GABA agonist, interact with voltage sensitive Ca channel, pre synaptic NMDA receptor, enhance descending NA pain control
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Anti-convulsants |
Carbamazepine effective in treating trigeminal neuralgia Acts on voltage gated Na channel Lamotrigine: post-stroke pain, HIV/AIDS neuropathy in patient who received antiretroviral therapy Efficacy of opioids, tramadol, morphine, oxycodone if other meds fail |
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Capsaicin |
same evidence for relief with topical capsaicin (TRVP1 agonist) Intense burning, pre treatment with EMLA cream necessary
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Acupuncture |
Placebo effect 70% report significant effect, 60% report with sham acupuncture (inappropriate needle placement)
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