Analgesia in Oral Surgery Flashcards
What are the analgesia in the dental practitioners formulary
aspirin ibuprofen diclofenac paracetamol dihydrocodein (opioid) carbamazepine
What kind of pain is aspirin effective for
dental and TMJ
How does aspirin compared to paracetamol
it has superior anti-inflammatory properties
What is the properties of aspirin
analgesic antipyretic anti-inflammatory anti-platelet metabolic
How is pain produced
trauma and infection –> breakdown of membrane of phospholipids –> arachidonic acid produced
arachidonic acid broken down to form prostaglandins
prostaglandins sensitize the tissue to other inflammatory products –> pain
What is the role of prostaglandins
they don’t cause pain directly but they do sensitive the tissues to other inflammatory products e.g leukotrienes
If prostaglandin production decreases what will this result in
it will moderate the pain
What is the mechanism of action of aspirin
reduces production of prostaglandins
it inhibits COX1 and 2 but more effective at inhibiting COX1
COX1 inhibiting reduces platelet aggregation and predisposes to damage of the gastric mucosa
What are the analgesic properties of aspirin
it is mainly a peripherally acting agent
the analgesic action results from inhibition of prostaglandin synthesis in inflamed tissues (COX inhibition)
What are the antipyretic properties of aspirin
it prevents the temperature raising effects of interleukin-1 and the rise in brain prostaglandin levels
it reduces elevated temperature in fever
it doesn’t reduce normal temperature
What are the anti-inflammatory properties of aspirin
prostaglandins are vasodilators and as such also effect capillary permeability
aspirin is a good anti-inflammatory and will reduce redness and swelling as pain at the site of the injury
What are the metabolic effects of aspirin
increased basal metabolic rates
effects platelets, prothrombin and blood sugar
What are the adverse effects of aspirin
GIT problems
hypersensitivity
overdose - tinnitus, metabolic acidosis
aspirin burns - mucosal
What are the adverse effects of aspirin on the GIT
it is mostly on the mucosal lining of the stomach
What is the action of prostaglandins on the stomach lining
inhibit gastric acid secretion
increase blood flow through the gastric mucosa
help production of mucin by cells in stomach lining
Which GIT patients require care in prescription of aspirin
those with GIT problems such as ulcers or GORD
What do the hypersensitivity reactions to aspirin result in
acute bronchospasm / asthma type attacks
minor skin rashes
other allergies
What should be done to reduce the risk of hypersensitivity to aspirin
take care when prescribing to asthmatics
What are the adverse effects of overdose of aspirin
hyperventilation tinnitus, deafness vasodilation and sweating metabolic acidosis coma
How can mucosal burns occur from aspirin
it is the direct effect of salicylic acid
aspirin has no topical effect and if applied locally to oral mucosa it results in a chemical burn
What are the groups to avoid/take caution with when it comes to aspirin
peptic ulceration epigastric pain bleeding abnormalities anticoagulants pregnancy/breast feeding patients on steroids renal/hepatic impairment children & adolescents under 16 years asthma hypersensitivity to other NSAIDs taking other NSAIDs elderly G6PD-defieincy
Why should aspirin be avoided in those with metic ulceration
is it could result in perforation
When do we not prescribe aspirin to those with epigastric pain
if they have a history of epigastric pain/discomfort or GORD but no ulcer diagnosed
Why should aspirin be avoided by px on anticoagulants
it enhances warfarin and other coumarin anticoagulants
it displaces warfarin from binding sties on plasma proteins
it increases free warfarin
the majority of warfarin is bound (inactive) and if more of this is released then there will be an increase in bleeding tendency
Why should aspirin be avoided for those who are pregnant
especially in the third trimester which is near delivery, it can cause impairment of platelet function
this results in an increased risk fo hemorrhage, increased risk of jaundice in baby, can prolong/delay labour
Why is aspirin contraindicated in those breastfeeding
due to reye’s syndrome
Why should aspirin be avoided/used with caution in those on steroids
as 1/4 on long term systemic steroids develop a peptic ulcer
higher chance of having an undiagnosed ulcer, aspirin may result in perforation
Why should aspirin be avoided/given with caution for those with renal or hepatic impairment
aspirin
metabolism in liver and excretion mainly in the kidney
if renal impairment excretion may be reduced/delayed
not a complete contraindication but administer with care/reduce dose and avoid if renal or hepatic impairment is severe
What role do prostaglandins play in the kidney
prostaglandins are powerful vasodilators synthesized in the renal medulla and glomeruli and are involved in control of renal blood flow and excretion of salt and water
How can aspirin result in nephrotoxicity
inhibition of renal prostaglandin synthesis may result in sodium retention, reduced renal blood flow, renal
NSAIDs may cause interstitial nephritis and hyperkalaemia
prolonged analgesic abuse over a period of years is associated with papillary necrosis and chronic renal failure
Why is aspirin avoided in children and U16s
reyes syndrome
What is Reye’s syndrome
fatty degenerative process in the liver (and to a lesser extend in the kidney)
profound swelling in the brain
What is the clinical presentation of Reye’s syndrome
initially nausea, vomiting, lethargy
later seizures and coma
How does Reyes syndrome present clinically
initially nausea, vomiting, lethargy
later seizures and coma
mortality is 50% and is related to brain damage due to encephalopathy
Why is aspirin avoided or given in caution to asthmatics
not completely contraindicated
as px if used NSAIDs before and if there were any issues
Why is aspirin avoided due to hypersensitivity
contraindicated in patients with a history of hypersensitivity to aspirin or any other NSAIDS
this includes those in whom attacks of asthma, angioedema,urticaria or rhinitis have been precipitated by aspirin or any other NSAIDS
Why should NSAIDs not be combined
increases risk of side effects
only done if necessary
Why should aspirin be avoided/ given in caution to elderly px
they are more susceptible to drug induced side effects in general
they are often smaller and have a smaller circulating blood volume
they are on other medications and often have other medical issues
Where is glucose 6-phosphate dehydrogenase deficiency most common in
individuals originating from
most parts of africa, asia
oceana
southern europe
can occur rarely in other individuals
What are individuals with G6PD-deficiency more susceptible to
developing acute hemolytic anaemia on taking a number of common drugs
aspirin carries a possible risk of hemolysis in some G6PD-deficient individuals (acceptable up to a dose of at least 1g daily in most G6PD-deficient individuals)
What groups is aspirin fully contraindicated in
children and adults under 16 years breast feeding previous or active peptic ulceration haemophilia hypersensitivity to aspirin or any other NSAID
What is the dose for aspirin
300mg
40 tablets
2 tablets, 4 times daily, after food
What is the dosage for aspirin as thrombotic prophylaxis
a single dose of aspirin (150-300mg) is given ASAP after ischemic event and maintenance tx is 75mg daily
If someone has active peptic ulcer disease and requires NSAID, what else should be prescribed
lansoprazole or omeprazole
5 capsules - 5 days
What is the effect of ibuprofen
it has less effect on platelets than aspirin
it is an irritant to gastric mucosa but lower risk than aspirin
may cause bronchospasm
What is the dose for ibuprofen
400mg
20 tablets
1 tablet, 4 times daily, preferably w food
What is the maximum dose of ibuprofen in adults
2.4g
Who should be prescribed ibuprofen with caution
- previous or active peptic ulceration
- the elderly
- pregnancy and lactation
- renal, cardiac or hepatic impairment
- history of hypersensitivity to aspirin and other NSAIDs
- asthma
- patient taking other NSAIDs
- patients on long term systemic steroids
What are the most important side effects of ibuprofen
- GIT discomfort, occasionally bleeding and ulceration
2. hypersensitivity reactions e.g rashes angiodema, bronchospasm
What are the other effects of ibuprofen
headache, dizziness, nervousness, depression, drowsiness insomnia, vertigo, hearing disturbances/tinnitus, photosensitivity, hematuria, blood disorders, fluid retention, renal impairment, hepatic damage, pancreatitis, eye changes
What are the drugs that ibuprofen can interact with
ACE inhibitors other analgesics antibiotics anticoagulants antidepressants antidiabetics corticosteroids cytotoxics diuretics beta blockers calcium- channel blockers cardiac glycosides ciclosporin clonidine clopidogrel (an antiplatelet drug) lithium tacrolimus vasodilator antihypertensives
What are the symptoms of ibuprofen overdose
nausea
vomiting
tinnitus
What is done if more than 400mg/kg has been ingested within the preceding hour
activated charcoal followed by symptomatic measures
What is COX1 responsible for
it is the cyclo-oxygenase predominantly responsible for catalyzing the reaction that produces prostaglandins associated with platelet aggregation and protection of the gastric mucosa
What is COX2 responsible for
generation of most of the inflammatory prostaglandins (although in some situations (COX-1) is also involved
What does the action of the formed prostaglandin’s depend on
the pathological situation
whether they are formed by COX-1 or COX-2
whether they are formed in excessive amounts
How are prostaglandins produced in the physiological state
PGE2 is generated in low physiological amounts by COX-1 in gastric tissues and has a protective effect
How are prostaglandins produced in inflammation
prostaglandins (esp PGE2) are generated in excessive amounts during inflammation via elevated COX-2 levels
PGE2 in large amounts produces increased vasodilation, increased vascular permeability and densities nerve fibre endings to other inflammatory mediators
Why are COX-2 selectives a good idea
inflammatory effects come mainly from COX-2 but NSAIDs target mainly COX-1
these selectives would spare COX-1 and so have less of a gastric effect
do not effect platelet aggregation
What is an example of a COX-2 inhibitor
celecoxib
What is celexocib useful for
has useful anti-inflammatory actions and fewer GIT damaging actions compared with non-selective NSAIDs
What are selective COX-2 inhibitors still not used for
ALL NSAIDS (including selective COX-2 inhibitors) are contraindicated in patients with active peptic ulceration AND non selective NSAIDs are contraindicated in patients with a history of peptic ulceration
also not on dental list
What is the action 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
What is the mode of action of paracetamol
hydroperxoides are generated from the metabolism of arachidonic acid by COX and exert a positive feedback to stimulate COX activity
this feedbacks blocked by paracetamol thus indirectly inhibiting COS especially in the brain
this results in analgesia, antipyretic action but no reduction in peripheral inflammation
Where is the main action of paracetamol
pain pathways of the CNS such as the thalamus
Does paracetamol cause gastric irritation
no as it doesn’t have much effect on peripheral prostaglandins
Who should you be cautious about prescribing paracetamol to
those with
hepatic impairment, renal impairment, alcohol dependence
What are the side effects of paracetamol
rare
rashes
blood disorders
hypotension reproved on infusion
liver damage (and less frequently kidney damage) following overdose
What are the interactions of paracetamol
anti-coagulants cytotoxic domperidone lipid regulating drugs metoclopramide
How can paracetamol interact with anti-coagulants
prolonged regular use of paracemtol possibly enhances the anticoagulant effects of the coumarins
What is the dose of paracetamol
500mg
40 tablets
1-2 tablets 4-6 hourly
What is the max dose of paracetamol
4g daily
8 tablets
How much paracetamol can result in severe hepatocellular necrosis or renal tubular necrosis
10-15g (20-30 tablets) or 150mg/kg
What are the early features of paracemtol poisoning
anorexia
nausea
vomitting
usually settle within 24h
What is the indication of hepatic necrosis from paracetol
persistence of the early features and abdominal pain, right subcostal pain and tenderness
What other drugs also contain paracetamol
cocodomal and coproxamol
Which opioid can be prescribed by dentists
dihydrocodeine
Where do opioid analgesics act
on the spinal cord
especially in the dorsal horn pathways associated with palateo-spinothalamic pathway
Where is the central regulation of pain for opioids
periaqueductal grey matter
nucleus retictularis paragigantocellulais
raphe magnus nucleus
How do opioids produce their effects
via specific receptors which are closely associated with the neuronal pathways that transmit pain to the CNS
What are the problems with opioids
dependence - physiological and physical
tolerance - only to depressant effects
Describe how the dependance on opioids presents
withdrawal of the drug will lead to psychological cravings and the patient will be physically ill
Describe how tolerance to opioids presents
to achieve the same therapeutic effects the dose of the drug needs to be progressively increased
What are the effect of opioids on smooth muscle
constipation - can occur after a few doses of dihydrocodeine
urinary and bile retention
What are the depressor CNS effect of opioids
it depresses:
pain centre (alters awareness of perception of pain) higher centres resp centres cough centre vasomotor
What are the stimulatory CNS effects of opiods
vomiting centre (dihydrocodeine often causes nausea and vomitnig which limits its value in dental pain)
salivary centre
pupillary constriction
What are the most common side effects
nausea, vomiting, drowsiness
larger doses produce respiratory depression and hypotension
What are the opioids side effects
difficulty with micturition ureteric or biliary spasm dry mouth sweating facial flushing headache vertigo bradycardia tachycardia palpitations postural hypotension hypothermia hallucinations dysphoria mood changes dependence miosis decreased libido or ptoency rashes
What are the effects of opiods enhanced by
alcohol
What are cautions for opioids
hypotension hypothyroidism asthma decreased respiratory reserve prostatic hyperplasia pregnancy/breast feeding may precipitate coma in hepatic impairment (reduce dose or avoid) renal impairment (reduce dose or avoid) elderly and debilitated (reduce dose) convulsive disorders dependence
What are contraindications of opioids
acute respiratory depression
acute alcoholism
raised intracranial pressure/head injury
- interferes with respiration
- affects pupillary responses vital for neurological assessment
What are the effects of codeine
effective orally
low dependence
usually in combination with paracetamol
cough suppressant
What is a common side effect of cocodomol
consitpation
What codeine combination is on the dental list
dihydrocodeine
What are the routes for dihydrocodeine
subcutaneous or intramuscular (controlled)
oral (not controlled)
What is the oral dose for dihydrocodeine
30mg even 4-6 hrs as necessary
higher doses not available to dentists
What are the common dihydrocodeine side effects
general opioids side effects
nausea/vomiting
constipation
drowsiness
What are the larger dose effects of dihydrocodiene
respiratory depression
hypotension
ureteric spasm
biliary spasm
What are the serious drug interactions of dihydrocodiene
antidepressants MAOIs
dopaminergics
What are the cautions for dihydrocodeine
hypotension asthma pregnancy/lactaiton renal/hepatic disease elderly/children
When should dihydrocodeine never be prescribed
in raised intracranial pressure/suspected head injury
What are the uses of dihydrocodeine
moderate to severe pain
Why is dihydrocodeine not used for dental pain much
side effects of nausea and vomiting
What happens if there is opioid overdose
can cause varying degrees of coma, rest depression and pinpoint pupils
What is the specific antidote for opioid overdose
naloxone if there is coma or bradypnoea
What is the other category of analgesics in the BNF
those that are related to neuropathic and functional pain
What is a neuropathic functional pain
trigeminal neuralgia
post-herpetic neuralgia
functional (TMJ or atypical facial pain)
What is the only drug used in dentistry for neuropathic and functional pain
carbamazepine
What is carbamazepine
its a proprietary brand
anti convulsant
What is prescribed for trigeminal neuralgia
carbamazepine - only one on dental list
gabapentin
phenytoin
What are the clinical features of trigeminal neuralgia
severe spasms of pain: 'electric shock' usually unilateral older age group trigger spot identified females more than males periods of remission recurrences often greater severity
What dose is given for trigeminal neuralgia of carbamazepine
100 or 200 mg tablets
starting dose is 100mg once or twice daily but some patients may require higher initial dose
increase gradually according to response
usual dose is 200mg 3-4 times daily up to 1.6g daily in some px
What is the main side effects of carbamazepine
dizziness
ataxia
drwosiness
leucopenia and there blood disorders
What are contraindications of carbamazepine
AV conduction abnormaliteit (unless paced)
history of bone marrow depression
porphyria
What are the cautions for carbamazepine
hepatic/renal/cardiac disease
skins reactions
history of hematological reactions to other drugs
gluacoma
pregnancy/breast feeding
avoid abrupt withdrawal
