Analgesia And Effects Of Manual Therapy Flashcards
What are the goals of pharmacological pain treatment?
- increase inhibitory neurotransmitter => analgesia from decoupling response of nocioception and pain
- prevent development of peripheral or central sensitisation
- restore normal responsiveness of nociceptive pathway
What are the different classes of analgesics?
- non-opioid analgesic e.g. paracetamol + NSAIDs
- non-steroidal anti-inflammatory it’s e.g. non-prescription aspirin, ibuprofen, naproxen, topical, prescription (Diclofenac, indomethacin), coxibs (COX-2 selective)
- opioid analgesics e.g. codeine, tramadol (x.1), morphine (x1), oxycodone (x1.5), buprenorphine (x50)
What additional (adjuvant) medications that may be given to patients for analgesic purposes?
- antidepressants e.g. tricyclic antidepressants (re-uptake of noradrenaline to increase descending inhibition) e.g. amitriptyline
- anticonvulsants e.g. gabapentin (inhibits ca-channels on pre-synaptic neurone)
- NMDA receptor antagonists e.g. ketamine
- cannabinoids
- capsaicin
Describe the WHO pain ladder stages:
- stage 1 = non-opioid +/- adjuvant
- stage 2 = opioid for mild to moderate pain +/- non-opioid +/- adjuvant
- stage 3 = opioid for moderate to severe pain +/- non-opioid +/- adjuvant
What is the difference between COX-1 and COX-2?
- both come from arachidonic acid
- cox-1 = expressed constantly throughout body, primary organs are kidneys, stomach + platelets
- cox-2 = only expressed when cells are injured (inflammatory, pain + fever)
What are the side-effects of NSAIDs on COX-1 in the GI mucosa?
- cox-1 increases mucus secretion, bicarbonate + mucosal blood flow
- cox-1 inhibition can lead to peptic ulcers + GI bleeding
What are the side-effects of NSAIDs on COX-1 in the kidney?
- cox-1+2 increase GFR + increase sodium + water excretion
- cox-1+2 inhibition => sodium + water retention, hypertension, hémodynamique acute kidney injury
What are the side-effects of NSAIDs on COX-1 in the cardiovascular system?
- cox-1 increase platelet aggregation + vasoconstriction
- cox-2 increase vasodilation, inhibit platelet aggregation
- cox-2 > cox1 inhibition => stroke + myocardial infarction
*low dose aspirin irreversibly inhibits platelet COX-1
What happens when taking NSAIDs 72 hours after injury?
- leads to blocking of resolvins => failure of complete tissue healing
What do anti-convulsants do e.g. gabapentin?
- effect voltage dependent calcium ion channels @ post-synaptic dorsal horns
- relieve neuropathic pain
- reduces allodynia and hyperalgesia in animals
- fewer side effects than amitriptyline
How are timelines of pain defined?
- acute = 0-6 weeks
- subacute = 6-12 weeks
- chronic = 12+ weeks
What is the issue with defining pain as chronic?
- based on duration only
- may miss patients with poor prognosis
- ignores speed of sensitisation e.g. mins/hours/days
- implies condition worsens with time
What changes might you see in the brain activity of early/acute/subacute back pain groups?
- brain activity is limited to regions involved in acute pain
What changes might you see in the brain activity of chronic back pain groups?
- activity is confined to emotion-related circuitry (medial prefrontal cortex + amygdala)
What happens with chronic pain in the first year?
- brain creates a chronic pain state
- first year is critical for treatment
