Analgesia Flashcards
what are the 6 main analgesics prescribed
- aspirin (NSAID)
- ibuprofen (NSAID)
- diclofenac (NSAID)
- paracetamol
- dihydrocodeine (opioid)
- carbamazepine
what causes pain
production of prostaglandins which sensitise the tissues to other inflammatory products e.g. leukotrienes which results in pain
how are prostaglandins formed
trauma/infection lead to breakdown of membrane phospholipids producing arachidonic acid which is then broken down to form prostaglandins
how to reduce pain
decrease prostaglandin production
describe the arachidonic acid pathway
tissue injury -> injury to phospholipid cell membrane causing release of arachidonic acid ->
1. cyclooxygenase pathway (COX-1/COX-2) -> prostaglandin (PGG2) -> prostaglandin H2 (PGH2) -> prostacyclin / prostaglandin (cause pain, inflammation), thromboxane (cause platelet aggregation)
OR
2. 5-lipooxygenase pathway -> leukotrienes (cause bronchoconstriction / asthma attacks / smooth muscle contraction)
main properties of aspirin
- analgesic
- antipyretic (prevent / reduce fever)
- anti inflammatory
- metabolic
aspirin mechanism of action
inhibits cyclooxygenases (COX 1&2) so reduced production of prostaglandins
more effect at inhibiting COX-1 which reduces platelet aggregation (predisposes to damage of gastric mucosa)
analgesic properties of aspirin
analgesic action exerted both peripherally & centrally
peripheral actions predominate
analgesic action results from inhibition of prostaglandin synthesis in inflamed tissues (COX inhibition)
antipyretic properties of aspirin
prevents temperature rising effects of interleukin-1 and rise in brain prostaglandin levels so reduces elevated temp in fever
NB - doesn’t reduce normal temp
anti inflammatory properties of aspirin
prostaglandins are vasodilators and as such affect capillary permeability
aspirin = good anti inflammatory and will reduce redness / swelling as well as pain at site of injury
adverse effects of prescribing aspirin (4)
- GIT problems
- hypersensitivity
- overdose - tinnitus, metabolic acidosis
- aspirin burns - mucosal
describe adverse aspirin effect on GIT
mostly on mucosal lining of stomach; prostaglandins PGE2 & PGI2 inhibit gastric acid secretion, increase blood glow through gastric mucosa & help production of mucin by cells in stomach lining (cytoprotective action)
care must be taken for patients with ulcers & GORD
describe adverse effect of hypersensitivity when prescribing aspirin
reactions include:
- acute bronchospasm / asthma type attacks
- skin rashes / urticaria / angioedma
- other allergies
caution when prescribing to asthmatics
adverse effect of overdose when prescribing aspirin
- hyperventilation
- tinnitus, deafness
- vasodilation & sweating
- metabolic acidosis (can be life threatening)
- coma
adverse effect of mucosal burns when prescribing aspirin
direct effect of salicylic acid as aspirin applied locally to oral mucosa results in chemical burns. it has no topical effect. ensure it is taken with water
name 13 groups you should avoid prescribing aspirin to
- peptic ulceration
- epigastric pain
- bleeding abnormalities
- anticoagulants
- pregnancy / breast feeding
- patients on steroids
- renal / hepatic impairment
- u16s
- asthmatics - ask if used before and if any problems
- hypersensitivity to other NSAIDs
- taking other NSAIDs
- elderly
- G6PD deficiency
why avoid prescribing aspirin to those on anticoagulants
it enhances warfarin & other coumarin anticoagulants; displaces warfarin from binding sites on plasma proteins and increases free warfarin.
majority of warfarin in bound i.e. inactive so if more is released this will become active thus increasing bleeding tendency
why avoid prescribing aspirin in pregnancy/lactation
esp in 3rd trimester as nearer delivery and may cause impairment of platelet function:
- increased risk of haemorrhage & jaundice in baby
- can prolong / delay labour
contraindicated in breastfeeding - reye’s syndrome
why avoid prescribing aspirin to those on steroids
approx 25% of patients on long term systemic steroids will develop a peptic ulcer & if they have undiagnosed ulcer, aspirin will result in perforation
why avoid prescribing aspirin in renal / hepatic impaired
aspirin metabolised in liver & excreted mainly in kidney
if renal impairment excretion may be reduced / delayed
not a complete contraindication but administer with care and avoid if severely impaired
relationship between prostaglandins and the kidney
prostaglandins PGE2 & PGI2 are powerful vasodilators synthesised in renal medulla and glomeruli respectively & are involved in control of renal blood flow and excretion of salt & water
inhibition of renal prostaglandin synthesis may result in
sodium retention
reduced renal blood flow
renal failure
NSAIDs may cause interstitial nephritis & hyperkalaemia
why avoid prescribing aspirin in u16s
reye’s syndrome - up to 50% mortality due to encephalopathy so contraindicated in u16s, avoid during fever or viral infection
fatty degenerative process in liver that causes profound swelling in brain
why avoid prescribing aspirin to those with G6PD deficiency
glucose-6-phosphate dehydrogenase deficiency
susceptible to acute haemolytic anaemia and aspirin carries risk of haemolysis in some of these individuals
what groups is aspirin completely contraindicated in
- u16s & breast feeding
- previous or active peptic ulceration
- haemophilia
- hypersensitivity to aspirin or any other NSAID
ibuprofen v aspirin
less effect on platelets
irritant to gastric mucosa but less than aspirin
may cause bronchospasm
paediatric suspension available
max adult dose of ibuprofen
2.4g
8 groups to be cautious of prescribing ibuprofen to
- previous or active peptic ulceration
- elderly
- pregnancy & lactation
- renal, cardiac or hepatic impairment
- history of hypersensitivity to aspirin & other NSAIDs
- asthma
- patient taking other NSAIDs
- patients on long term systemic steroids
side effects of ibuprofen
- GIT discomfort, occasionally bleeding & ulceration
- hypersensitivity reactions e.g. rashes, angioedema & bronchospasm
- headache, dizziness, insomnia, vertigo, fluid retention etc
ibuprofen overdose
symptoms = nausea, vomiting, tinnitus
treat = activated charcoal followed by symptomatic measures are indicated if more than 400mg/kg ingested within preceding hr
how does paracetamol differ from other NSAIDs
it is a simple analgesic without anti-inflammatory activity
7 main characteristics of paracetamol
- analgesic
- antipyretic
- little or no anti-inflammatory action
- no effects on bleeding time
- does not interact significantly with warfarin
- less irritant to GIT
- suitable for children
mode of action of paracetamol
hydroperoxides are generated from the metabolism of arachidonic acid by COX and exert a positive feedback to stimulate COX activity
this feedback is blocked by paracetamol thus indirectly inhibiting COX especially in the brain
main action site of paracetamol
the thalamus
caution when prescribing paracetamol to
- hepatic impairment
- renal impairment
- alcohol dependence
side effects of paracetamol
are rare but include:
- rashes
- blood disorders
- hypotension reported on infusion
- liver damage following overdose
interactions of paracetamol with other drugs
- anticoagulants (prolonged regular use of paracetamol possibly enhances anticoag effects of coumarins)
- cytotoxics
- domperidone
- lipid regulating drugs
- metoclopramide
paracetamol dosage
adults - 1-2 500mg tablets 4-6 hourly
children - depends on weight / age
max dose paracetamol
4g daily i.e. 8 tablets
paracetamol overdose
as little as 150mg/kg or 20-30 tablets taken in 24hrs can cause severe hepatocellular necrosis or less frequently renal tubular necrosis
liver failure maximal at 3-4 days after ingestion
despite lack of early significant symptoms patients who have overdosed on paracetamol should be transferred immediately to hospital
paracetamol, ibuprofen and aspirin are what types of analgesics
non opioid analgesics
how do opioid analgesics act
they act in the spinal cord in dorsal horn pathways - central regulation of pain
they produce their effects via specific receptors which are closely associated with neuronal pathways that transmit pain to CNS
opioids and dentistry
opioid analgesics are relatively ineffective in dental pain
opioid dependence
psychological & physical - withdrawal of drug will lead to psychological cravings + ptx will be physically ill
opioid tolerance
to achieve same therapeutic effects the dose of the drug needs to be progressively increased
opioid effect on smooth muscle
constipation
urinary & bile retention
CNS effects of opioids
depresses
- pain centre; alters awareness / perception of pain
- higher centres
- respiratory centre
- cough centre
side effects of opioids
most common - nausea, vomiting, drowsiness
larger doses - respiratory depression & hypotension
others include - dry mouth, sweating, facial flushing, bradycardia
caution prescribing opioids to
- hypotension
- hypothyroidism
- asthma
- decreased respiratory reserve
- pregnancy / breast feeding
- hepatic impairment
- renal impairment
- elderly & debilitated
- convulsive disorders
- dependence
contraindications of prescribing opioids
acute respiratory depression
acute alcoholism
raised intracranial pressure / head injury - interferes with respiration & affects pupillary responses vital for neurological assessment
why use codeine
1/12th potency of morphine
effective orally
low dependence
usually in combination with NSAIDs / paracetamol
effective cough suppressant
available over counter
what codeine combination is on the dental list
dihydrocodeine (orally)
dosage of dihydrocodeine
30mg every 4-6hrs as necessary
no other mg on dental list
side effects of dihydrocodeine
same as general opioid e.g. nausea/vomiting, constipation, drowsiness
larger doses - respiratory depression, hypotension
serious drug interactions of dihyrocodeine
antidepressants MAOIs
dopaminergics (parkinsonism)
caution prescribing dihydrocodeine to
hypotension
asthma
pregnancy/lactation
renal/hepatic disease
elderly/children
never prescribe in raised intracranial pressure or suspected head injury
opioid overdose
varying degrees of coma, respiratory depression and pinpoint pupils
specific antidote naloxone indicated if coma/bradypnoea
close monitoring & repeated infusion may be required
what neuropathic & functional pain requires analgesics in dentistry
trigeminal neuralgia
post herpetic neuralgia
functional - TMJ / atypical face pain
what is the only drug on the dental list for neuropathic & functional pain
carbamazepine - an anti convulsant
proprietary brand e.g. tegretol
drugs that can be used to treat trigeminal neuralgia
carbamazepine 100 or 200mg tablets start on 100mg 1-2 x daily but increase according to response to 200mg 3-4 x daily
following 2 not on dental list
gabapentin
phenytoin
clinical features of trigeminal neuralgia
- severe spasms of pain ‘electric shock’ lasts seconds
- usually unilateral
- trigger spot identified
- F > M
- older age group
- periods of remission
- recurrences often greater severity
