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92 Cards in this Set
- Front
- Back
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What is pain
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signalling system
cant see pain sensory & emotional experience |
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acute pain
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temporary
usually from injury response to healing |
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chronic pain
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continues after healing
no clear pathology CNS changes physical and psycological often leads to sleep disturbances, depression, social withdrawal |
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pallative care
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e.g. cancer
aim is to provide best quality of life and reduce pain |
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4 types of cancer pain
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malignant (increasing tumor size)
treatment pain (chemotherapy) debilitating (bed sore) unrelated (low BP) |
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3 types of pain
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mechanical (OA)
neuropathic (nerve damage) inflammatory (arthritis) |
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nociceptive pain
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pain due to stimulation of superficial or deep tissue pain receptors resulting from inflammation
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neuropathic pain
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pain due to dysfunction or primary legion in CNS or PNS
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analgesia
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absense of pain in presence of stimulation
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allodynia
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pain from stimulation which would not normally be painful (e.g. run tissue across wrist)
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hyperalgesia
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increased pain in normally painful stimuli
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central pain
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initiated/caused by pain lesion or dysfunction of CNS (neuropathic pain)
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damage to cells releases which 4 chemicals (e.g.)
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histamine, arachadonic acid (leukotrienes, prostaglandins), bradykins, 5-HT
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What do chemical mediators do
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lower threshold for pain to prevent further injury
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A-delta fibers
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sports carsssss
myelinated, large diameter, quick initial sharp pain reflex withdrawal |
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C fibers
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family carrr :(
dull local aching pain unmyelinated, slow after stimuli and withdrawal |
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inhibitory neurons
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when activated reduce pain
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facilatory neurons
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lower pain threshold
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Gate system
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blocks pain via descending inhibitory pathways on spinal cord
open - due to emotion, stress, anxiety transmits pain closed - due to drugs/body chemicals, relaxation, distractions or massage. blocks pain. |
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LINDOCARRF
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location
intensity nature duration onset concomitants aggrivating relieving radiation frequency |
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numerical pain scale
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10 = worst pain ever
0 = no pain |
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quality pain scale
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1 (dull) -> 9 (stabbing)
person to put where pain is |
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biopsychological aspect of chronic pain
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affects sleep, appetite, energy, depression
pain is influenced by psychological factors, emotional factors and the situation |
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treatment for acute pain
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passive, hands on, rest, resume normal life, prn treatment, short term
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treatment for chronic pain
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active, hands off, readjusting, constant tx, active, long term
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non pharmacological treatments for pain
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hot/cold packs, exercise, TENS machines, physiotherapy, hydrotherapy, massage
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psychological
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cognitive behaviour, stress & anxiety management, music therapy, distraction techniques
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drug classes to treat pain: 5
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analgesics, anticonvulsants, antidepressants, membrane stabilisers, opioids
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analgesic ladder
step 1-3 |
step 1 - NSAID, non-opioid analgesic (paracetamol), adjuvant medication.
step 2 - NSAID, non-opioid analgesic, adjuvant medication AND weak opioid (codine) Step 3 - NSAID, non-opioid analgesic, adjuvant medication AND strong opioid (morphine/oxycodone) |
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by the ladder
by the mouth by the clock |
... start low, go slow
... oral first, avoid injections ... take at regular intervals |
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wind up
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sensitization of nervous system with inadequate analgesia
more pain AHH |
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paracetamol
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analgesic, antipyretic, acts centerally on PG, no anti-inflammatory, few se, 1-2tabs QID max 4g.
1st line therapy for pain (equally goodness to aspirin and ibuprofen) best choice for children MAX 8 DAILY |
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side effects
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poisoning due to overdose
liver damage worse if dehydrated, malnourished, alcohol (chronic) common: N/V, diziness, sedation less common: headache, skin rash |
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paracetamol and NSAID
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can be used together because work on different mechanisms
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why was vioxx withdrawn from the market
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only knocks out COX2 which produces prostacyclin (anti-clotting)
this causes increased clotting effect (from thromboxane in cox 1) which increases risk of MI or stroke. |
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NSAID
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analgesic, antipyretic, anti-inflammatory
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how long does antiinflammatory effect from NSAIDs take to work
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7 days of regular dosing for anti-inflammatory process to work.
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Adverse effects of NSAIDs
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gi bleeding, ulceration, upset stomach
stops COX-1 which produces PG which lines GI tract |
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most at risk from side effects from NSAIDs
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elderly women in first six weeks of therapy
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risk factors for GI bleeding with nsaid use
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prior bleed, anticoagulant use (warfarin), elderly, high dose
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nsaid with unstable hypertension
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increases bp/oedema
indomethacin |
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nsaids with asthmatics
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can cause bronchospasm (10-15%)
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nsaids use with pregnancy
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dont use
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nsaids with breast feeding
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dont use
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drug interactions with nsaids
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LOTS e.g. warfarin, lithium.... the list goes on
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opioids
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growing acceptance, thorough assesment with one doctor, trial before long term, long acting are best
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opioids and pallative care
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not only used anymore for that...
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opioid dependence
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pyschological response, will occur in all patients taking chronic opioids, much titrate downwards to prevent withdrawal symptoms.
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opioid addiction
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psychological response, behaviour patterns (craving) using for other than pain control, continues despite high interference to social life/job and high adverse effects, 1-2%, lots of time thinking about next 'fix', crushing SR or injection of tabs
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where do opioids act
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brain, spinal cord, peripherally in nociceptors
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how do opioids act
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mu, delta, kappa.
coupled to GPCR also in other tissues (GIT, immune cells, other cells) |
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desired effect
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analgesia
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unwanted effects
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analgesia tolerance, physical dependence, respiratory depression, nausea, vomitting, sedation
also constipation, endocrine (may need testosterone supplements), neuro-excitatory (muscle jerks, allodynia, seizures) |
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laxatives
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ALWAYS USE WITH PAIN MANAGEMENT
bisacodyl and coloxyl 2bd constipation can increase pain must treat early start high and titrate down |
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why does caution need to be taken if opioid has active metabolite
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can cause problems in renal impairment
e.g. codine must be metabolised to morphine to have effect, if not metabolised only will get side effects |
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how to treat with opioids
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start low, go slow
start with short acting and titrate up till reach analgesic dose then switch to controlled release |
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breakthrough pain treatment
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give 1/6 to 1/12 of TDD
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convert to morphine dose
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dose of drug x conversion factor = dose of morphine
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multiple medications e.g. panadine forte and oxycodone to single product of morphine what must you do
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calculate morphine equivalent
reduce dose by 20% then give morphine. |
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norspan patches
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buprenorphine
semi synthetic opioid mixed agonist (mu)/antagonist (Kappa) mu = primary site of reward effects of opiates (euphoria, analgesia) - buprenorphine binds more strongly than morphine at these receptors yet in doses in the patches only occupy about 10% of receptors antagonists at kappa (negative effects occur at kappa e.g. depression) buprenorphine inhibits these effects but not at doses in patches |
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why is buprenorphine used in patches
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it has low molecular weight, water solubility, lipophilic.
cant be taken oral (extensive 1st pass metabolism) |
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matrix patch
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new
polymer matrix system with active drug |
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reservoir patch
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old patches with drug in reservoir
could inject needle and get drug out so bad |
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advantages of norspan patches
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avoid first pass metabolism, effective if experiencing side effects, less constipation, high analgesic potency, long lasting analgesia, high safety margin.
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pharmacokinetics of bupronorphine
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7 days delievey
peak analgesia after 3 days conc decreases by 50% within 12 hrs of removing patch |
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place of buprenorphine in therapy
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not used in cancer pain
often low doses and clean drug so used in elderly |
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fentanyl
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patch
2 days analgesia another option but kinda gay |
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pethidine
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'pro emetic with mild analgesic properties'
do not use for longer than 2 days can accumulate and cause severe side effects potential seizures interacts with other drugs |
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morphine/hydromorphone
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have active metabolites *shrugs shoulders*
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which opioid drugs do not have active metabolites
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fentanyl, methadone, oxycodone, buprenorphine
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metabolism of morphine
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20% metabolised to M6G which gives 20X potent analgesia
80% metabolised M3G which is anti-analgesic and causes seizures, myoclonus and sedation |
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what to do if patient has moderate of severe impairment (toxicity)
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reduce dose or possibly change drug
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problem with codeine e.g. panadeine forte
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10% of people cant metabolise codeine to morphine therefore SE with no analgesic benefit
CYP 2D6 deficent |
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why is panadeine forte pointless (10mg codeine)
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no good evidence that 8-10mg of codeine has analgesic effect (SE but no analgesia) but used to be S2 so thats why companies did that
25-30 mg = good evidence of effect |
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mersyndol
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codeine, paracetamol, doxylamine
feel stoneeeedddd haha codeine (no analgesic effect) doxylamine (highly sedating) useful if migraine headache, dental pain. |
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doxylamine
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sedation
NOT anti-anxiety or muscle relaxing effects not used in elderly cause contributes to fall in elderly. strongly anticholinergic |
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tramadol - 2 mechanisms
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1. acts on mu receptors (similar to morphine) metabolised
2. inhibits reuptake of NA and 5-HT similar to codeine a group cannot metabolise problems in renal impairment max 400mg!!!!!!!! can cause hyperthermia (seratonin syndrome) interactions |
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NNT
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no of patients needed to treat to get 50% reduction in pain
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NNH
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numbers needed to harm
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neuropathic pain
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pain due to dysfunction of, or damage to a nerve or group of nerves
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central pain
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dull, aching
due to compression by nerves |
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peripheral pain
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shooting, stabbing pain
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causes of neuropathic pain
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shingles (post herpetic neuralgia), phantom limb pain, postoperative pain, diabetes neuropathy
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damage to nerve
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causes remodelling -> movement of Na+ channels to area of damage
multiple action potentials firing to try and get past damaged area may branch off and hit other nerves whcih can cause dull aching pain to become sharp and stabbing (if c fibre hits adelta fibre) |
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treatment of neuropathic pain
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antidepressants, anticonvulsants, opioids, topical agents
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anticonvulsant
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good for shooting stabbing pain
old - cbz, valproate, phenytoin, clonazepam new - gabapentin, pregabalin, lamotrigine |
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anticonvulsant for neuropathic pain vs epilesy
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lower doses for neuopathic pain
low NNT = good gabapentin and pregablin (slighly higher doses can be used because better tolerated) |
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how does gabapentin and progablin work
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block Ca+ channels presynaptically and post synaptically
block excitation of nerve |
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Antidepressants in neuropathic pain MOA
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increases DA, 5-HT and NA
blocks Na+ channels anticholinergic effect increases endorphines TCA hits multiple paths in pain pathways |
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Antidepressants e.g.
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amitriptyline, doxepin, dothiepin
much lower doses than in depression cant use with cardiac conditions (can cause arythmias) |
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draw summary of pain
opioids nsaids paracetamol tca anticonvulsants local anaesthetics |
look it up pain slide 130
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interactions with tramadol
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TCA, MAO, SSRI, warfarin
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