Pain Flashcards
Causes & Pathophysiology
Pain = unpleasant sensory and emotional experience coming from actual/potential tissue damage as warning signals to react to stimulus or withdraw from harm.
Pain is subjective and intensity based on person perception.
Pain classes:
- Neuropathic pain: abnormal processing of stimuli from the PNS/CNS and thought to serve no useful purpose. (From damage to a nerve)
- Nociceptive pain: normal neural processing of pain happens when free nerve endings are activated by tissue damage or inflammation. (can be acute, chronic, primary chronic).
Acute pain is self limiting - resolves after stimuli removal.
Inflammatory leads to persistence of pain for weeks, months, or years.
Poorly controlled acute pain can lead to chronic pain, needing to be hospitalised or stay longer.
Chronic pain > 12weeks
Chronic primary pain - No clear underlying cause
Chronic secondary pain - Underlying condition (OA)
Assessment
SOCRATES - Site, Onset, Character, Radiation,
Associated features, Time course, Exacerbating or Alleviating Factors, Severity
number or graph rating scale
visual scale
verbal scale
Treating Acute Pain
WHO PAIN LADDER:
Non opioid (+-adjuvant) –> opioid mild to moderate (+-non opioid, or adjuvant) –> opioid moderate to severe (+-non opioid, or adjuvant)
1. Opioid:
bind to certain receptor sites in PNS & CNS, once activated pain signal transmission is blocked i.e., by opening K+ channel causing hyperpolarisation so no action potential= analgesia.
Examples: Morphine, fentanyl, diamorphine, codeine
hydromorphone, and oxycodone, are µ (mu) agonist.
- Bind mainly to the µ opioid receptors = wanted (analgesia) and unwanted (AEs).
- AEs: N+V, severe itching, constipation, sedation, respiratory depression, euphoria, pupil constriction.
stool softener + laxative for constipation. OR to remove AE reduce dose. Should start with lowest dose too.
BEWARE of respiratory depression - asses respiratory status within 24 hour of opioid treatment.
if this occurs give NALOXONE (µ receptor antagonist) = sedating reversed and respiratory depression effect gone.
2. Adjuvant analgesics:
- Local anaesthesia (lignocaine, bupivacaine)- block Na ion channels to prevent the conduction of nerve impulses. forms: gels, creams, or infusion via intrathecal, epidural or through surgical sites.
- Muscle relaxant (benzos) used only for pain associated with muscle spasm.
AE- sedation and risk of respiratory depression (FLUMAZENIL reversal agent)
3. Non Opioid:
(NSAID, Paracetamol, tramadol [binds to µ receptors and it also weakly inhibits NA and serotonin reuptake, which is thought to cause pain signal transmission inhibition])
- Methadone: µ agonist opioid and NMDA antagonist with two-compartment kinetics (long acting)
- Ketamine: NMDA antagonist that provide analgesia
- Anti seizure medication: by stabilizing nerve membranes, reducing excitability, and reducing spontaneous neuronal firing
4. Non pharmacological: physical modalities (acupuncture, massage, positioning, deep breathing, application of heat or cold),
psychosocial modalities (CBT and psychotherapy).
Treating Chronic pain
Lasts >3 months.
Primary = no known origin
Secondary = from previous injury.
- Secondary can be a behavioural issue that just needs attention i.e. by meds, people, time off usage) or internally (relief from emotions guilt, fear, sex, responsibilities). Can happen without stimulus.
Non pharmacological:
- Application of heat and cold compressions,
- transcutaneous electrical nerve stimulation (TENS)(RA & OA), massage,
-Acupuncture,
- Hypnosis,
- Psychophysiological therapy (counselling, relaxation therapy, stress management programs, and CBT),
- Physiotherapy,
- Occupational therapy and social prescribing.
Pharmacological:
WHO pain ladder + (any of)
Combinations example:
- Paracetamol + codeine (Co-Codamol), ibuprofen + paracetamol (NUROMOL), Ibuprofen + codeine ( NUROFEN)
- Benzos/NSAID for secondary CPS
- Antidepressants improve mood and pain
- Anti seizure (Gabpentinoids)
Calcitonin/Bisphosphonates in phantom limb pains post amputation.
Neuropathic pain
- Peripheral (Diabetic neuropathy, trigeminal neuralgia, post surgery neuropathic pain, cancer neuropathic pain) OR
- Central (stroke, spine injury, multiple sclerosis)
Causes:
- Postherpetic neuralgia from shingles
- Nerve damage from surgery
- Multiple sclerosis
- Diabetic neuralgia typically affects the feet
- Trigeminal neuralgia
- Complex Regional Pain Syndrome (CRPS) - can be intermittent or constant, and spontaneous or provoked
Descriptions of pain: shooting, stabbing, electric shock, burning, tingling, numb, itching)
Treatment
1st line - neuropathic pain:
- Nortriptyline (better tolerated) OR Amitriptyline -TCA
- Duloxetine - SNRI
- Gabapentin AED
- Pregabalin AED
Amitriptyline + pregab can be effective combo if other max tolerated doses FAIL
ALT
- OPIOD - Tramadol ONLY as a rescue for short term control of flares, Morphine or oxycodone - specialist
- Topical Lidocaine
- Capsaicin cream (burning sensation when used) - localised pain
- Corticosteroid possible to relieve pressure in neuropathy = reduce pain.
- Physiotherapy to maintain strength
- Psychological input to help with understanding and coping
Trigeminal neuralgia - Carbamazepine 1st line
- high doses monitor FBC and Electrolytes.
Chromic facial pain - TCA useful
Nociception process: (DONT NEED TO KNOW)
- Transduction- tissue damage releases chemical mediators like PG, bradykinin, 5HT, substance P, histamine. Substances activate nociceptors = transduction or make action potential.
- Transmission- action potential moves from injury site along nerves to nociceptors at spine. release substance P and other neurotransmitter carries the action potential across the spine ascending to spinothalamic tract to thalamus then midbrain. The message spreads across the brain lobes and to limbic system where perception happens.
- Perception- pain exp. involves sensory and affective components of pain. limbic system produces emotional response to pain activating midbrain leading to modulation.
- Modulation- multiple neurotransmitters (endorphins, enkephalins, 5-HT and dynorphin) descend to lower areas in the CNS. causing release of more neurotransmitters = release of endogenous opioids and inhibit pain impulse at dorsal horn.
PRSC extra notes
Sickle cell disease
Paracetamol, NSAIDs, Opioids
Severe crisis - Morphine, Diamorphine
AVOID pethidine cam cause seizures
EXAM Q - Paracetamol/Ibuprofen doses - ALWAYS COME UP
- Check PICS
Dental pain
NSAIDs, Paracetamol temporarily
Benzydamine mouthwash/spray
- can prescribe diazepam short term
Dysmenorrhoea
- Antiemetic can be used for vomiting
- Paracetamol/NSAID for pain relief
- Oral contraceptive for pain with cycles
Other notes
Nefopam can be used for normal pain but has more AEs
EXAM Q - Respiratory depression a key AE of opioids - treat with naloxone.
Over dose signs: Coma, Respiratory depression, pin point pupils, sedation, NV, constipation, dry mouth,
- Larges doses: Hypotension, Muscle rigidity, respiratory depression
- Long term use: Hypogonadism and adrenal insufficiency
(MORPHINE mnemonic)
Codeine linctus now POM
Hyoscine hydrobromide patches - antimuscarinic AEs
Pholcodine WTHDRAWN
