analgesia Flashcards
dental practitioners formulary analgesia
aspirin ibuprofen diclofenac paracetamol dihydrocodeine carbamazepine
what does pain result from?
trauma and infection - breakdown of membrane phospholipids into arachidonic acid
breaks down into prostaglandins
sensitise the tissues to other inflammatory products which results in pain
writing a prescription
GP14 (scotland)
write name and address - not label as could be removed
line underneath if you only partially fill box so no-one can add to it
use child’s weight to calculate dose
aspirin advantage over paracetamol
superior anti-inflammatory properties
aspirin full name
acetylsalicylic acid
aspirin properties
analgesic
antipyretic
anti-inflammatory
metabolic
aspirin - mechanism of action
decrease prostaglandin production
inhibits COX1 (and COX2)
- reduces platelet aggregation and predisposes to damage of gastric mucosa
aspirin - analgesic
mainly peripherally acting
inhibition of prostaglandin synthesis in inflamed tissues (COX inhibition)
aspirin - antipyretic
prevents temp raising effects of IL-1 and the rise in brain prostaglandin levels
therefore reduces elevated temperature in fever
doesn’t reduce normal temp
aspirin - anti-inflammatory
prostaglandins are vasodilators therefore also affect capillary permeability
good anti-inflammatory
aspirin - metabolic effects
BMR increase
platelets - reduces aggregation
prothrombin - increases PT time
decreases blood sugar
aspirin adverse effects
GIT problems
hypersensitivity
overdose
mucosal burns
aspirin adverse effects - GIT problems
stomach mucosa
prostaglandins (PGE2 and PGI2)
- inhibit gastric acid secretion
- increase blood flow through gastric mucosa
- help production of mucin by cells in stomach lining (cytoprotective action)
aspirin adverse effects - hypersensitivity
acute bronchospasm/asthma type attacks
minor skin rashes
other allergies
ask asthmatics if they have taken it before
aspirin adverse effects - overdose
hyperventilation tinnitus, deafness vasodilation and sweating metabolic acidosis - can be life threatening coma (uncommon)
aspirin adverse effects - mucosal burns
direct effect of salicylic acid
aspirin applied locally to oral mucosa results in chemical burns
aspirin has no topical effects
ensure taken with water
aspirin complete contraindications
U16s, breastfeeding
- Reye’s syndrome (50% mortality)
previous/active peptic ulceration
haemophilia
hypersensitivity to aspirin or any other NSAIDs
- inc pts who attacks of asthma, angioedema, urticaria or rhinitis have been ppt by aspirin or any other NSAID
Reye’s syndrome
fatty degenerative process in liver (and to a lesser extent kidney)
profound swelling in brain
clinically
- nausea, vomiting, lethargy
- later seizures and coma
mortality related to brain damage due to encephalopathy
aspirin cautions
epigastric pain anticoagulants pregnancy pts on steroids hepatic/renal impairment asthma - ask taking other NSAIDs elderly G6PD-deficiency
aspirin cautions - epigastric pain
history or GORD but no ulcer diagnosed
aspirin cautions - anticoagulants
enhances warfarin and other coumarin anticoagulants
- displaces warfarin from binding sites on plasma proteins so increases free warfarin
- majority of warfarin is bound (inactive) so if more released therefore active - increases bleeding tendency
aspirin cautions - pregnancy
esp 3rd trimester - may impair platelet fct
- increased risk of haemorrhage
- increased risk of jaundice in baby
- can prolong/delay labour (don’t know why)
aspirin cautions - pts on steroids
around 25% on systemic long-term steroids will develop a peptic ulcer
if they have an undiagnosed ulcer aspirin may = perforation
aspirin cautions - hepatic/renal impairment
metabolism liver, excretion mainly kidney
care/reduce dose/avoid if severe
aspirin cautions - taking other NSAIDs
combinations increase risk of SEs
aspirin cautions - elderly
more susceptible to SEs - smaller circulating blood vol, on other meds, have co-morbidities
aspirin cautions - G6PD deficiency
possible risk of acute haemolytic anaemia/haemolysis
acceptable up to a dose of at least 1g daily in most
prescribing aspirin
300mg tablets
send 40 tablets
2 tablets x4 daily, preferably after food
not licensed for U16s
aspirin thrombotic prophylaxis
thrombotic cerebrovascular/CV disease
- a single dose 150-300mg given as soon as possible after the ischaemic event
- maintenance tx 75mg daily
aspirin nehrotoxicity
PGE1 and PGI2 are powerful vasodilators synthesised renal medulla and glomeruli involved in control of renal blood flow and excretion of salt and water inhibition of synthesis may = - sodium retention - reduced renal blood flow - renal failure
NSAIDs may cause interstitial nephritis and hyperkalaemia
prolonged abuse over years associated with papillary necrosis and chronic renal failure
aspirin in pts with history or active PUD needing NSAIDs
prescribe a PPI in conjunction
- lansoprazole 15mg x1 daily, 5 days
- omeprazole 20mg x1 daily, 5 days
paracetamol full name
acetaminophen
is paracetamol an NSAID?
not really
paracetamol properties
analgesic
antipyretic
little/no anti-inflammatory action
does paracetamol interact with warfarin?
not significantly
can paracetamol be given to children?
yes
why is paracetamol called a “safe” analgesic?
doesn’t appear to have much effect on peripheral prostaglandins - little/no gastric mucosal irritation
no effects on bleeding time
but causes severe problems in overdose
paracetamol mode of action
COX metabolises arachidonic acid into hydroperoxidases, which exert a positive feedback to stimulate COX activity
paracetamol blocks this therefore indirectly inhibiting COX - esp in brain
works centrally
reduction of prostaglandins in the pain pathways of the CNS e.g. thalamus - main site of action
exact mode of action still unclear
paracetamol alternative central mechanisms
decrease 5HT production
interference with excitatory a.a. NMDA in spinal cord pathways
exact mode of action still unclear
paracetamol cautions
hepatic impairment
renal impairment
alcohol dependence (CNS depressant)
paracetamol side effects
rare rashes blood disorders hypotension reported on infusion liver damage (and less freq kidney damage) following overdose
paracetamol interactions
anticoagulants - prolonged regular use possibly enhances the anticoagulant effect of the coumarins cytotoxics domperidone (anti-emetic) lipid-regulating drugs metoclopramide (for nausea and vomiting)
paracetamol dosage
500mg tablets
1-2 tablets every 4-6hours
max dose 4g daily (8 tablets)
always warn pt with regard to max dose and emphasise that they should not exceed this
what amount of paracetamol can cause overdose?
10-15g (20-30 tablets) or 150mg/kg of paracetamol taken within 24hrs may cause severe hepatocellular necrosis and less freq renal tubular necrosis
features of paracetamol overdose
anorexia, nausea, vomiting
- only early features of poisoning
- usually settle within 24hrs
persistence of these features beyond 24hrs is often associated with abdominal pain: right subcostal pain and tenderness, usually indicates development of hepatic necrosis
liver damage maximal at 3-4 days - jaundice, renal failure, haemorrhage, hypoglycaemia, encephalopathy, cerebral oedema and death
anyone who has taken an overdose - urgently hospital
what has the long-term use of ibuprofen recently been associated with an increased risk of?
cardiac events
compare ibuprofen to aspirin
similar effect to aspirin
- less effect on platelets
- slightly less irritant to gastric mucosa
NSAIDs that can be prescribed
aspirin
ibuprofen
diclofenac
ibuprofen dosage
400mg tablets x4 daily
preferably after food
max dose 2.4g
ibuprofen cautions
prev or active peptic ulceration elderly pregnancy and lactation renal, cardiac and hepatic impairment history of hypersensitivity to aspirin and other NSAIDs asthma pt taking other NSAIDs pt on long-term systemic steroids
ibuprofen overdose
nausea, vomiting, tinnitus
more serious toxicity v uncommon
activated charcoal followed by symptomatic measures indicated if >400mg/kg ingested in last hour
ibuprofen SEs
GIT discomfort
- occ bleeding and ulceration
hypersensitivity reactions e.g. rashes, angioedema and bronchospasm
others e.g. headache, dizziness, fluid retention etc
COX
predominantly responsible for catalysing the reaction that produces prostaglandins associated with:
- platelet aggregation
- protection of gastric mucosa
COX-2
enzyme responsible for generation of most of inflammatory prostaglandins (sometimes COX-1 also involved)
what does PGE2 by COX2 in large amounts result in?
increased vasodilation
increased vascular permeability
sensitises pain fibre nerve endings to bradykinin, 5HT and other mediators
what do the actions of prostaglandins depend on?
the pathological situation
whether they are formed by COX1 or COX2
whether they are formed in excessive amounts
when can PGE2 have a protective effect?
when generated in low physiological amounts by COX-1 in gastric tissues
COX2 selectives
analgesic actions of NSAIDs appear to result from inhibition of COX-2
so have selective COX2 inhibitors and spare COX1 - less gastric effect
e.g. celecoxib/celebrex
advantage of COX2 selectives
fewer GIT damaging actions
COX2 generated P may also contribute to gastric mucosal integrity and damage repair
- but can say selective COX-2 inhibitors associated with lower risk of serious upper GIT SEs
what are all NSAIDs (inc selective) contraindicated in?
pts with active peptic ulceration
what are non-selective NSAIDs contraindicated in?
pts with history of peptic ulceration
BNF NSAID recommendations dental
don’t use >1 oral NSAID at a time (inc selective)
for dental and orofacial pain only use selective in those with history of peptic ulcer
highly selective COX2 inhibitors don’t have effect on platelet aggregation - may be better tolerated by pts with clotting disorders
several selectives withdrawn due to CV risk
celecoxib not on dental list
where does opioid analgesia act?
spinal cord - esp the dorsal horn pathways associated with paleo-spinothalamic pathway
central regulation of pain
produce their effects via specific receptors which are closely associated with the neuronal pathways that transmit pain to the CNS
opioid
naturally occurring and synthetic molecules that produce their effects by combining with opioid receptors
BNF opioid analgesia
relatively ineffective in dental pain
SEs
opioid analgesia problems
dependence - physical, psychological tolerance - only to depressant effects - to achieve the same therapeutic effects the dose of the drug needs to progressively increase effects on smooth muscle - constipation - urinary and bile retention
opioid analgesia CNS effect
depresses - pain centre (alters awareness/perception of pain) - higher centres - respiratory centre - cough centre - vasomotor stimulate - vomiting centre (why dihydrocodeine limited value in dental pain) - salivary centre - pupillary constriction
opioid analgesia common SEs
nausea, vomiting, drowsiness
larger doses - respiratory depression and hypotension
opioid analgesia cautions
hypotension hypothyroidism asthma decreased respiratory reserve prostatic hyperplasia pregnancy/breastfeeding may ppt coma in hepatic impairment (reduce dose or avoid) renal impairment (reduce dose/avoid) elderly and debilitated (reduce dose) convulsive disorders dependence
opioid analgesia contraindications
acute respiratory depression
acute alcoholism (effects enhanced by alcohol)
raised ICP/head injury
- interferes with respiration
- affects pupillary responses vital for neurological assessment
codeine potency
1/12 morphine
advantages of codeine
OTC
low dependence
effective orally
effective cough suppressant
codeine SE
constipation
codeine common OTC dose
usually in combination with NSAIDs or paracetamol
e.g. cocodamol 8mg codeine 500mg paracetamol
dihydrocodeine potency
similar to codeine
dihydrocodeine methods of administration
SC/IM (controlled drug)
oral (not controlled)
dihydrocodeine dose
30mg every 4-6hrs
dihydrocodeine SEs
nausea/vomiting
constipation
drowsiness
larger doses - respiratory depression, hypotension, ureteric spasm, biliary spasm etc
dihydrocodeine key interactions
MAOI antidepressants
dopaminergics (Parkinsons)
dihydrocodeine cautions
hypotension asthma pregnancy/lactation renal hepatic disease elderly/children
dihydrocodeine contraindications
never in raised ICP/suspected head injury
dihydrocodeine dental use
mod/severe pain
but BNF states due to vomiting SE little value for dental pain
opioid overdose
varying degrees of coma, respiratory depression and pinpoint pupils
specific antidote Naloxone indicated if coma/bradypnoea
Naloxone shorter duration of action than many opioids so need close monitoring +/- repeated injections/infusion according to respiratory rate and depth of coma
carbamazepine
on dental list
Tegretol
anticonvulsant
trigeminal neuralgia
other drugs used for trigeminal neuralgia
gabapentin
phenytoin
clinical features of trigeminal neuralgia
severe spasms of pain 'electric shock' lasts seconds usually unilateral older trigger spot identified F>M periods of remission recurrences often greater severity
carbamazepine dose for trigeminal neuralgia
start 100mg x1-2 daily (but some pts may require higher initial dose) increase gradually according to response usual dose 200mg x3-4 daily put to 1.6g daily in some pts follow up - need bloods checked
carbamazepine side effects
dizziness
ataxia
drowsiness
blood disorders
carbamazepine contraindications
AV conduction abnormalities - unless paced
history of bone marrow depression
porphyria
carbamazepine cautions
hepatic/renal/cardiac disease skin reactions history of haematological reactions to other drugs glaucoma pregnancy/breastfeeding avoid abrupt withdrawal
