Pain control (pharmacologic and non pharmacologic) Flashcards Preview

CCE1: Specialities Block > Pain control (pharmacologic and non pharmacologic) > Flashcards

Flashcards in Pain control (pharmacologic and non pharmacologic) Deck (22)
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1

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 

2

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 

3

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 

4

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 

5

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 

6

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) 

7

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 

8

LO: Describe Non pharamcological interventions for pain relief and explain their MOA 

  1. Physiotherpay --> e.g. posture correction, stretching exercises, range of motion exercises in myofascial pain, pool hydrotherapy and weight reduction in MSK pain 
  2. Occupational therapy -> pain management training and work modifications 
  3. pain management psychology --> relaxation techniques, stress management, CBT 
  4. Alternative therapies: massage, acupuncture, PET therapy 
  5. Transcutaneous electrical nerve stimualation --> Spinal cord stimulation or peripheral nerve simulation (works via gate control theory of pain). 
  6. Invasive tx --> nerve block or ablation, implants, neuromodulators (alteration of nerve activity directly through chemical or electric stimulation)

9

LO: Revise drug classes commonly used in management of pain, MOA and side effects 

1) Drugs for nociceptive pain 

NO Pain:

NSAIDS 

Opiates 

Paracetamol

10

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) 

11

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 

12

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 

13

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 

14

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

15

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  

16

LO: Revise drug classes commonly used in management of pain, MOA and side effects: 

What is the MOA of the opiates at the neuronal level? 

  • Activation of opiod receptor leads to intracellular signalling pathways that modulate the activity of certain ion channels, reducing neuronal AP firing: 
  • increases K+ conductance out of the cell via KATP and Kir channels, hyperpolarising the cell 
  • decreases Ca2+ release from IC stores --> prevents release of neurotransmitter from IC vesicles and their fusion with the PM 

17

LO: Revise drug classes commonly used in management of pain, MOA and side effects: 

What are the two reversal agents for opiod overdose? 

Opiod antagonists: 

Naloxone (T half of 1-2 hrs) 

Naltrexone (T half of 12 hrs) 

18

LO: Revise drug classes commonly used in management of pain, MOA and side effects: 

What are the sites of action of opiods in the CNS? 

Opioid receptors widely expressed in both brain and spinal cord 

Found in a number of brain regions: insular cortex, amygdala, hypothalamus 

Found in a number of brainstem nuclei: PAG, NRM, LC (periaqueductal gray, nucleus raphe magnus, locus coerulus) 

Activates descending inhibition via dorsolateral funiculus

Inhibit nociceptive neurones presynaptically (prevent NT release) and postsynaptically (reduce excitability) in dorsal horn of the spinal cord. 

19

What are the side effects and signs of opiod intoxication? 

CARDINAL SIGNS of OD: 

  • Respiratory depression 
  • COMA (GCS < 7) 
  • Mioisis ("Pinpoint Pupils" - key diagnostic sign) 

GI: 

  • reduced GI motility 
  • Nausea/ Vomiting 

Hypersensitivity: 

  • Histamine release from mast cells
  • Smooth muscle spasm 
  • Bronchoconstriction 
  • Anaphylaxis 

Pyschiatric: 

  • Euphoria 
  • Sedation 
  • Mood changes 

Tolerance and dependency: 

  • desensitisation of the opioid R's 
  • physiological withdrawal 

20

What are the management steps for Opioid OD? 

Oh God Take No drugs CHildren

To resolve coma: 

Oxygen 

Glucose

Thiamine 

IV Naloxone (shorter acting 2-4 hrs)/ naltrexone (longer acting 10hrs)

Activated CHarcoal (if concious and within 1 hr of OD,  give charcoal and 0.8-2mg i.v naloxone every 2-3 mins) 

21

LO: Outline the principles of management of neuropathic pain: 

Drugs for neuropathic pain? 

PAIN GAP:

Gabapentin 

Amitryptiline 

Pregabalin

22

What is the management for neuropathic pain? 

Medicines are first line with goal of reducing sx --> membrane stabilising anticonvulsants (gabapentin, pregabalin) and tricyclic antidepressants (amitryptiline) 

Serotonin- noradrenaline reuptake inhibitor duloxetine may be useful in patients that cant tolderate tricyclics 

Second line therapy = topical capsaicin and dermal lidocaine patch 

Opiods = third line treatment 

Pts with significant impairment in daily activities, work dutie or social activity/ mood from neuropathic pain should be evaluated by physical, occupational and psychological therapists. 

Physical therapy includes posture correction, stretching exercises and active ROM (range of motion) 

TENS may be useful in diabetic neuropathy or chronic back pain 

For post herpetic neuralgia use antiviral agents 

Complex regional pain syndrome should be managed by physical and drug therapy, may use sympathetic blocks, spinal cord stimulation or IV immunoglobulin treatment for patients with immunoglobuln responsive CRPS