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BDS3 Oral surgery > Analgesics in oral surgery > Flashcards

Analgesics in oral surgery Flashcards

1
Q

What are the analgesia considerations?

A
  1. “think” postoperative analgesia
  2. start systemic analgesics before the local anaesthetic wears off
  3. “Sell” the prescription to obtain optimal response
  4. Use local anesthetics more
  5. Watch for risk groups
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2
Q

What analgesics are included in the dental practitioners formulary

A
  1. Asprin (NSAID)
  2. Ibuprofen (NSAID)
  3. Diclofenac (NSAID)
  4. Paracetamol
  5. Dihydrocodeine (opioid)
  6. Carbamazepine
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3
Q

what do we need to know about the drugs we prescribe for analgesia

A
  • mechanism of action
  • doses
  • side effects
  • interactions
  • groups of patients to avoid
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4
Q

what pain aspirin effective for

A

dental and TMJ

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5
Q

what has superior anti-inflammatory properties: aspirin or paracetamol

A

aspirin

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6
Q

can aspirin be bought over the counter

A

yes

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7
Q

what effects does aspirin have

A
  1. analgesic
  2. antipyretic
  3. anti-inflammatory
  4. anti-platelet
  5. metabolic
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8
Q

how does pain occur from trauma to the mouth

A
  • trauma and infection lead to the breakdown of membrane phospholipids producing arachidonic acid
  • arachidonic acid can be broken down to form prostaglandins
  • prostaglandins sensitise the tissues to other inflammatory products which results in pain
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9
Q

why does reducing prostaglandin production moderate pain

A
  • prostaglandins don’t cause pain directly

- they sensitise the tissues to other inflammatory products such as leukotrienes

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10
Q

what enzymes convert arachidonic acid to result in inflammatory mediators being produced

A

cyclo-oxygenases (COX-1 and COX-2)

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11
Q

what is the mechanism of action of aspirin

A
  • reduces production of prostaglandins
  • inhibits cyclo-oxygenases
  • more effective at inhibiting COX-1 (by 150x) therefore reducing platelet aggregation and predisposes to damage of the gastric mucosa
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12
Q

what are the analgesic properties of aspirin

A
  • mainly a peripherally acting agent

- inhibition of prostaglandin synthesis in inflamed tissues (cyclo-oxygenase inhibition)

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13
Q

what are the antipyretic properties of aspirin

A
  • reduces temperature during a fever (doesn’t alter normal)

- happens by preventing temp raising effects of interleukin-1 and the rise in brain prostaglandin levels

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14
Q

what are the anti-inflammatory properties of aspirin

A
  • reduces redness, swelling and pain at site of injury
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15
Q

what are the metabolic effects of aspirin

A
  1. increased BMR
  2. platelets
  3. prothrombin
  4. decreased blood sugar
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16
Q

what adverse effects does aspirin have

A
  1. GIT problems
  2. hypersensitivity
  3. overdose- tinnitus, metabolic acidosis
  4. aspirin burns-mucosal
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17
Q

How does aspirin cause GIT problems

A
  • mainly mucosal lining of stomach
  • prostaglandins inhibit gastric acid secretion, increase blood flow through the gastric mucosa and help prodution of mucin by cells in stomach lining (cytoprotective action)
  • care must be taken in pt’s with GIT problems e.g. ulcers or gasto-oesophageal reflux
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18
Q

what hypersensitivity reactions does aspirin cause

A
  • acute bronchospasm/asthma type attacks (care when prescribing to asthmatics)
  • minor skin rashes
  • other allergies
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19
Q

what can an overdose in aspirin result in

A
  • hyperventilation
  • tinnitus, deafness
  • vasodilation and sweating
  • metabolic acidosis
  • coma
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20
Q

why can aspirin cause mucosal burns

A
  • direct effect of salicylic acid
  • aspirin applied locally to oral mucosa results in chemical burns
  • aspirin has no topical effect
  • ensure aspirin is taken with water
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21
Q

what groups should be avoided/caution with aspirin

A
  1. peptic ulceration
  2. epigastric pain
  3. bleeding abnormalities
  4. anticoagulants
  5. pregnancy/breast-feeding
  6. patients on steroids
  7. renal/hepatic impairment
  8. children/adolescents under 16 years
  9. asthma
  10. hypersensitivity to other NSAIDs
  11. Taking other NSAISs
  12. Elderly
  13. G6PD-deficiency
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22
Q

why should people with peptic ulcerations not have aspirin

A

gastric or duodenal ulcer could result in perforation

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23
Q

why should people with epigastric pain not have aspirin

A

potential ulcer??

history of epigastric pain/discomfort or gastro-oesophageal reflux but no ulcer diagnosed

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24
Q

why should people on anticoagulants avoid aspirin

A
  • aspirin enhances warfarin and other coumarin anticoagulants (displaces warfarin from binding sites on plasma proteins and increases free warfarin)
  • the majority of warfarin is bound (inactive). If more is released this will become active increasing bleeding tendency
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25
Q

why should pt’s in their 3rd trimester of pregnancy avoid asprin

A
  • nearer delivery and may cause impairment of platelet function
  • increased risk of haemorrhage
  • increased risk of jaundice in baby
  • can prolong/delay labour
  • contraindicated in breastfeeding (Reye’s syndrome)
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26
Q

why should patients on steroids avoid aspirin

A
  • approx 25% of pt’s on long term systemic steroids will develop a peptic ulcer
  • if they have an undiagnosed ulcer, aspirin may result in perforation
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27
Q

why should pts with renal/hepatic impairment avoid aspirin

A
  • aspirin metabolism in liver and excretion 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
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28
Q

how can aspirin cause nephrotoxicity

A
  • prostaglandins (PGE2 and PGI2) are powerful vasodilators synthesized in the renal medulla and glomeruli respectively, and are involved in the control of renal blood flow and excretion of salt and water
  • inhibition of renal prostaglandin synthesis can result in sodium retention, reduced renal blood flow, renal failure
  • NSAIDs may cause interstitial nephritis and hyperkalaemia
  • prolonged analgesic abuse over a period of years is associated with papillary necrosis and chronic renal failure
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29
Q

why should children and adolescents under 16 years avoid aspirin

A

risk of Reye’s syndrome

  • very serious, up to 50% mortality
  • contraindicated if under 16 years
  • avoid during fever or viral infection in adolescents
  • contraindicated in breast-feeding
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30
Q

what is Reye’s syndrome

A
  • fatty degenerative process in liver (and to a lesser extent kidney)
  • profound swelling in brain
  • clinically: initially nausea, vomiting, lethergy and later seizures and coma
  • mortality (50%) related to brain damage due to encephalopathy
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31
Q

should asthma be a contraindication for aspirin

A
  • some have a problem with NSAIDs and others don’t

- ask patient

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32
Q

why should aspirin be avoided in groups allergic to other NSAIDs

A

because asprin is an NSAID

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33
Q

why should groups taking other NSAIDs avoid aspirin

A

combinations of NSAIDs increase risk of side effects, only use if necessary and monitor closely

34
Q

why should elderly pts avoid aspirin

A
  • more susceptible to side effects
  • often smaller/smaller circulating blood volume
  • on other medications
  • have other medical problems
35
Q

why should groups with a G6PD deficiency avoid asprin

A
  • predisposes to red blood cell break down
  • susceptible to developing acute haemolytic anaemia on taking a number of common drugs
  • aspirin carries a possible risk of haemolysis in some G6PD-deficicient individuals
36
Q

what groups is aspirin contraindicated in

A
  1. children and adolescents under 16 years; breast feeding
  2. previous or active peptic ulceration
  3. haemophilia
  4. hypersensitivity to aspirin or any other NSAID
37
Q

what is the aspirin dose if you are suspecting a stroke/mi

A

300mg

38
Q

what is the maintenance treatment dose of aspirin for thrombotic prophylaxis

A

75mg daily

39
Q

what can protect the gastric lining from effects of aspirin

A

proton pump inhibitor e.g. omeprazole

40
Q

What are the effects of ibuprofen

A
  • similar to aspirin
  • less effect on platelets
  • irritant to gastric mucosa but lower risk than aspirin
  • may cause bronchospasm
  • popular as post-operative analgesia following oral surgery
  • paediatric suspension avaliable
41
Q

what is the maximum dose for ibuprofen in adults

A

2.4g in adults (600mg 4x a day but don’t normally prescribe as high as that)

42
Q

what groups should we be cautious when prescribing ibuprofen to

A
  1. previous or active peptic ulceration
  2. elderly
  3. pregnancy and lactation
  4. renal, cardiac or hepatic impairment
  5. history of hypersensitivity to aspirin and other NSAIDs
  6. asthma
  7. patient taking other NSAIDs
  8. patients on long term systemic steroids
43
Q

what are the side effects of ibuprofen

A
  1. GIT discomfort, occasionally bleeding and ulceration
  2. hypersensitivity reactions e.g. rashes, angioedema and bronchospasm
  3. lots of others see BNF
44
Q

what are the potential drug interactions for ibuprofen

A

check BNF (lots)

45
Q

what are the symptoms of overdosing on ibuprofen

A
  • nausea
  • vomiting
  • tinnitus

(activated charcoal followed by symptomatic measures are indicated if more than 400mg/kg has been ingested within the preceding hour

46
Q

what is the prescription we write called in scotland

A

GP14

47
Q

how do NSAIDs reduce pain

A

NSAIDs inhibit cyclo-oxygenases and so reduce prostaglandins (which sensitise the tissues to other inflammatory mediators resulting in pain)

48
Q

what is COX-1 responsible for

A

catalysing the reaction that produces prostaglandins associated with platelet aggregation and protection of the gastric mucosa

49
Q

what is COX-2 responsible for

A

generation of most of the inflammatory prostaglandins (although in some situations COX-1 is also involved)

50
Q

what do the actions of prostaglandins depend on

A
  • the pathological situation
  • whether they are formed by COX-1 or COX-2
  • whether they are formed in excessive amounts
51
Q

why does it make sense to have COX-2 selective inhibitors

A

since the analgesic actions of NSAIDs appear to result form inhibition of COX-2 (mainly, although COX-1 may be involved) it would make sense to have selective cox-2 inhibitors and spare COX-1, therefore less gastric effect

52
Q

what is an example of a selective COX-2 inhibitor

A

celecoxib (celebrex)

- anti-inflammatory actions and fewer GIT damaging actions compared with non-selective NSAIDs

53
Q

what is important to note about selective COX-2 inhibitors

A
  • all NSAIDs (including selective COX-2 inhibitors) are contraindicated in pts with active peptic ulceration
  • non-selective NSAIDs are contraindicated in patients with a history of peptic ulceration
  • BNF recommends not to use more than 1 oral NSAID at a time
54
Q

what is the BNF recommendation regarding selective cox-2 inhibitors for dental and orofacial pain

A

only use in patients at high risk of gastric or duodenal ulceration e.g. those with a history of peptic ulcer

55
Q

why might selective cox-2 inhibitors be better tolerated by tps with clotting disorders

A

they don’t have an effect on platelet aggregation

56
Q

why have selective cox-2 inhibitors been withdrawn from dental list

A

due to cardiovascular risk

57
Q

is paracetamol an NSAID

A

yes, but in reality is a simple analgesic without anti-inflammatory activity

58
Q

what are the characteristics of paracetamol

A
  1. analgesic
  2. antipyretic
  3. little or no anti-inflammatory action
  4. no effects on bleeding time
  5. does not interact significantly with warfarin
  6. less irritant to GIT
  7. suitable for children
59
Q

what is the mode of action for paracetamol

A
  • 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
  • reduction in prostaglandins in the pain pathways of the CNS, such as the thalamus is the main site of action of paracetamol
60
Q

what does the mode of action of paracetamol result in

A
  • analgesia
  • antipyretic action
  • no reduction in peripheral inflammation
61
Q

what effect does paracetamol have on the gastric mucosa

A

very little = “safe analgesic”

  • because it doesn’t have much effect on peripheral prostaglandins
62
Q

what groups do you have to be cautious when prescribing paracetamol

A
  1. hepatic impairment
  2. renal impairment
  3. alcohol dependence
63
Q

what are the side effects of paracetamol

A

side effects are rare but:

  1. rashes
  2. blood disorders
  3. hypotension reported on infusion
  4. liver damaged (and less frequently kidney damage) following overdose
64
Q

what are the interactions for paracetamol

A

see BNF

  • anticoagulants
  • cytotoxics
  • domperidone
  • lipid-regulating drugs
  • metoclopramide
65
Q

what is the dose for paracetamol

A

500mg tablets

adults: 1-2 tablets, 4-6 hourly

66
Q

what is the max dose for paracetamol for adults

A

4g daily (8 tablets)

67
Q

what is the max dose of paracetamol for children

A

depends on weight/age (see BNF)

68
Q

what is a really important warning you must say to patients about paracetamol

A

always warn patient with regard to maximum dose and emphasize that they should not exceed this

69
Q

if someone has taken as little as 20-30 tablets or 150mg/kg of paracetamol within 24 hours what are they at risk of

A

severe hepatocellular necrosis, renal tubular necrosis

70
Q

what are the only features of paracetamol poisoning

A
  • anorexia, nausea and vomiting

- usually settle within 24 hrs

71
Q

what are the signs of overdose on paracetamol

A
  1. anorexia, nausea, vomiting
  2. abdominal pain, right subcostal pain and tenderness (usually indicates development of hepatic necrosis)
  3. liver damage is maximal at 3-4 days after ingesion and may lead to jaundice, renal failure, haemorrhage, hypoglycaemia, encephalopathy, cerebral oedema and death
72
Q

if you think someone has overdosed on paracetamol what should you do

A

transfer them immediately to hospital

73
Q

what medicines also contain paracetamol (easier to overdose)

A

co-codamol

co-proxamol

74
Q

what opoid can dentists prescribe

A

dihydrocodeine

75
Q

how does opioid analgesics work

A
  • act in the spinal cord (especially in the dorsal horn pathways associated with paleo-spinothalamic pathway)
  • central regulation of pain in periaqueductal grey matter, nucleus reticularis paragigantocellularis, raphe magnus nucleus
76
Q

how do opiod analgesics work

A
  • via specific recptors which are closely associated with the neuronal pathways that transmit pain to the CNS
  • opioid is a term for both naturally occuring and synthetic molecules that produce their effects by combining with opiod receptors
77
Q

what does the BNF state about opiod analgesics

A

they are relatively ineffective in dental pain

78
Q

what are the main problems with opioid analgesics

A
  • dependence (psychological and physical)

- tolerance (only to depressant effects)

79
Q

what dependece problems do opioids have

A

phychological and physical

- withdrawel of the drug will lead to cravings and pt feeling physically ill

80
Q

what tolerance problems do opiods have

A

to achieve the same therapeutic effects the dose of the drug needs to be progressiely increased

81
Q

what effects do opioid have on smooth muscle

A
  • constipation

- urinary and bile retention

BDS3 Oral surgery (5 decks)

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