Pain control (pharmacologic and non pharmacologic) Flashcards
LO: Pathophysiology of pain and pain pathways:
What fibres carry pain perception?
- Pain perception mediated by small diameter myelinated A-delta fibres –> Sharp and Immediate Pain
- non myelinated C fibres -> Diffuse and Prolonged Pain
LO: Pathophysiology of pain and pain pathways:
Describe the pain pathways from the body
Pain carried by the Spinothalamic Tract
- STT –> pain, temp, simple touch
- sensory neurone enters spinal cord via dorsal spinal roots, travels 1-2 levels in the tract of lissauer in dorsal grey matter
- synapses in dorsal horn with 2nd order neurone
- 2nd order neurone decussates via anterior white commisure
- Ascends in spinothalamic tract, to the VPL of thalamus
- Synapses with 3rd order neurone, travels to the primary somatosensory cortex
LO: Pathophysiology of pain and pain pathways:
Describe pain pathway from the face
Pain pathway from the face carried by the Trigeminothalamic tract
- Activation of free nerve ending carrying pain and temperature sensation
- 1st order neurone Travels via V1/V2/V3
- travels to the spinal trigeminal nucleus in the brainstem where it synapses with 2nd order neurone
- This neurone decussates and travels with other trigeminal nerves in the trigeminal lemniscus to the VPM of the thalamus
- synapses here with 3rd order neurone, travels to the primary somatosensory cortex
LO: Pathophysiology of pain and pain pathways:
Revision from yr 1: Two types of pain and their characteristics
1) nociceptive pain –> caused by physical damage or response to the inflammatory soup, involves activation of free nerve endings, responds to analgesics, responds to mechanical/chemical/temp/ pressure
2) neuropathic pain –> Chronic and highly debilitating, caused by damage to the neurone itself, leads to hyperexcitability/sensitivity, involves: shooting, tingling, numbness, stabbing, electric shock like, pins and needles type sensations
LO: Pathophysiology of pain and pain pathways:
Causes of Neuropathic pain
- Peripheral nerve injury –>
- e.g. neuropathy in diabetes/HIV/Chemotherapy
- nerve compression (carpal tunnel, meralgia paraesthetica)
- post herpetic neuralgia
- vasculitic nerve lesion (diabteic femoral neuropathy)
- nerve trauma (phatom limb)
- trigeminal neuralgia
- Radiculopathy due to IV disc prolapse
- Plexopathy (inflammatory or neoplastic infiltrative)
- CNS disorder:
- MS (pain common in progressive form)
- post stroke
- spinal cord lesion
- Parkinsons
LO: LO: Pathophysiology of pain and pain pathways:
What is the Gate control theory of pain?
-
Pain modulation at the level of the spinal cord:
- Transmission of afferent nociceptive pain is regualted in spinal cord dorsal horn by afferent impulses from non nociceptive large diameter sensory fibres and
- descending pw’s from PAG and other brainstem regions
- Collateral or large diameter sensory fibres activate inhibitory interneurones which inhibit pain transmission at level of spinal cord (at point of synapse in spinal cord)
LO: Describe WHO pain ladder
- First level of pain –> Non Opiod analgesic –> Paracetamol and NSAIDS
- Second level of pain –> Weak opiod analgesics –> Codeine, codeine and paracetamol (Co-codamol).
- Third level of pain –> Strong opiod analgesics –> Morphine and related compounds e.g. fentanyl, methadone
LO: Describe Non pharamcological interventions for pain relief and explain their MOA
- Physiotherpay –> e.g. posture correction, stretching exercises, range of motion exercises in myofascial pain, pool hydrotherapy and weight reduction in MSK pain
- Occupational therapy -> pain management training and work modifications
- pain management psychology –> relaxation techniques, stress management, CBT
- Alternative therapies: massage, acupuncture, PET therapy
- Transcutaneous electrical nerve stimualation –> Spinal cord stimulation or peripheral nerve simulation (works via gate control theory of pain).
- Invasive tx –> nerve block or ablation, implants, neuromodulators (alteration of nerve activity directly through chemical or electric stimulation)
LO: Revise drug classes commonly used in management of pain, MOA and side effects
1) Drugs for nociceptive pain
NO Pain:
NSAIDS
Opiates
Paracetamol
LO: Revise drug classes commonly used in management of pain, MOA and side effects
Drugs for neuropathic pain
- TCA’s –> notriptyline, amitryptiline
- Antiepileptics –> Pregabalin (VGCC block) , carbmazapine (Na+ channel block) , gabapentin (increase GABA, inhibits VDCC)
LO: Revise drug classes commonly used in management of pain, MOA and side effects:
Name the NSAIDS (non selective and selective)
NSAID
Naproxen
Selective –> celexicoxib, etoricoxib
Aspirin
Ibuprofen/ Indomethacin
Diclofenac
LO: Revise drug classes commonly used in management of pain, MOA and side effects:
MOA of NSAIDS
- inhibits cyclooxygenase enzyme from converting AA –> prostaglandin
- COX2 inhibition useful as associated with inflammation specifically rather than ubiquitously expressed
- 3 actions:
- 1) Antiinflammatory –> inhibits PG mediated vasodilation and oedema
- 2) Antipyretic –> inibits PG mediated increase in temp point in hypoT
- 3) Analgesic –> inhibits PG mediated sensitisation of nociceptive fibres
- Analgesia MOA: Neuronal level:
- normally PG activate PROSTANOID receptor (GPCR on neuronal cell membrane, activates VG Na+ channel, leads to depol and pain sensation
- COX inhibition –> less PG, less prostanoid activation, less nociceptive neuronal firing
LO: Revise drug classes commonly used in management of pain, MOA and side effects:
SE’s NSAIDS
- GI disturbance:
- nausea/ vomiting
- Diarrhoea
- heartburn
- ulceration/ bleeding
- Cardiovascular events:
- Renal impairment (Block COX2 in renin-secreting macula densa)
- Hypertension
- Thrombosis
- MI/ Stroke
- Hypersensitivity reactions:
- Bronchospasm
skin reactions- rashes, angiooedema
photosensitivity
- Psychological/ head:
- Headache
- Depression
- Anxiety
- Insomnia
- Balance/ Hearing:
- Tinnitus
- Vertigo
- Dizziness
LO: Revise drug classes commonly used in management of pain, MOA and side effects:
Paracetamol MOA
SE’s
- MOA: Not entirely known, theories that it Inhibits COX1/COX2, inhibits prostaglandin synthesis, theory that it inhibits COX3, antipyretic effects from direct action on heat regulating centres in the brain resulting in peripheral vasodilation, sweating.
- SE’s: nausea, vomiting, constipation, rash, pruritus dysponea, headache
LO: Revise drug classes commonly used in management of pain, MOA and side effects:
Opiates: Name the opiates used in pain management
What is the MOA?
what are their main SE’s?
What are their uses?
Weak opiods –> Codeine and Dihydrocodeine (stimulation of opiod receptors), constipation and nausea
USE: mild- moderate pain
Strong opiods –> Morphine, diamorphine, fentanyl, pethidine –> stimulate analgesic opiod receptors, constipation and nausea
USE: severe pain
Partial/ mixed agonist opiod analgesics –> Buprenorphine, pentazocine, modulation of analgesic opiod receptors (mu and kappa), again constipation and nausea.
USE: moderate - severe pain
