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BDS3 CLINICAL Oral Surgery > Analgesia in Oral Surgery > Flashcards

Analgesia in Oral Surgery Flashcards

1
Q

What are the analgesia in the dental practitioners formulary

A 
aspirin 
ibuprofen
diclofenac 
paracetamol
dihydrocodein (opioid) 
carbamazepine
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2
Q

What kind of pain is aspirin effective for

A

dental and TMJ

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3
Q

How does aspirin compared to paracetamol

A

it has superior anti-inflammatory properties

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4
Q

What is the properties of aspirin

A 
analgesic
antipyretic
anti-inflammatory
anti-platelet
metabolic
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5
Q

How is pain produced

A

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

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6
Q

What is the role of prostaglandins

A

they don’t cause pain directly but they do sensitive the tissues to other inflammatory products e.g leukotrienes

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7
Q

If prostaglandin production decreases what will this result in

A

it will moderate the pain

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8
Q

What is the mechanism of action of aspirin

A

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

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9
Q

What are the analgesic properties of aspirin

A

it is mainly a peripherally acting agent

the analgesic action results from inhibition of prostaglandin synthesis in inflamed tissues (COX inhibition)

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10
Q

What are the antipyretic properties of aspirin

A

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

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11
Q

What are the anti-inflammatory properties of aspirin

A

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

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12
Q

What are the metabolic effects of aspirin

A

increased basal metabolic rates

effects platelets, prothrombin and blood sugar

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13
Q

What are the adverse effects of aspirin

A

GIT problems

hypersensitivity

overdose - tinnitus, metabolic acidosis

aspirin burns - mucosal

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14
Q

What are the adverse effects of aspirin on the GIT

A

it is mostly on the mucosal lining of the stomach

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15
Q

What is the action of prostaglandins on the stomach lining

A

inhibit gastric acid secretion

increase blood flow through the gastric mucosa

help production of mucin by cells in stomach lining

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16
Q

Which GIT patients require care in prescription of aspirin

A

those with GIT problems such as ulcers or GORD

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17
Q

What do the hypersensitivity reactions to aspirin result in

A

acute bronchospasm / asthma type attacks

minor skin rashes

other allergies

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18
Q

What should be done to reduce the risk of hypersensitivity to aspirin

A

take care when prescribing to asthmatics

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19
Q

What are the adverse effects of overdose of aspirin

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

How can mucosal burns occur from aspirin

A

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

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21
Q

What are the groups to avoid/take caution with when it comes to aspirin

A 
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
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22
Q

Why should aspirin be avoided in those with metic ulceration

A

is it could result in perforation

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23
Q

When do we not prescribe aspirin to those with epigastric pain

A

if they have a history of epigastric pain/discomfort or GORD but no ulcer diagnosed

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24
Q

Why should aspirin be avoided by px on anticoagulants

A

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

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25
Q

Why should aspirin be avoided for those who are pregnant

A

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

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26
Q

Why is aspirin contraindicated in those breastfeeding

A

due to reye’s syndrome

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27
Q

Why should aspirin be avoided/used with caution in those on steroids

A

as 1/4 on long term systemic steroids develop a peptic ulcer

higher chance of having an undiagnosed ulcer, aspirin may result in perforation

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28
Q

Why should aspirin be avoided/given with caution for those with renal or hepatic impairment

A

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

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29
Q

What role do prostaglandins play in the kidney

A

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

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30
Q

How can aspirin result in nephrotoxicity

A

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

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31
Q

Why is aspirin avoided in children and U16s

A

reyes syndrome

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32
Q

What is Reye’s syndrome

A

fatty degenerative process in the liver (and to a lesser extend in the kidney)
profound swelling in the brain

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33
Q

What is the clinical presentation of Reye’s syndrome

A

initially nausea, vomiting, lethargy

later seizures and coma

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34
Q

How does Reyes syndrome present clinically

A

initially nausea, vomiting, lethargy

later seizures and coma

mortality is 50% and is related to brain damage due to encephalopathy

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35
Q

Why is aspirin avoided or given in caution to asthmatics

A

not completely contraindicated

as px if used NSAIDs before and if there were any issues

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36
Q

Why is aspirin avoided due to hypersensitivity

A

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

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37
Q

Why should NSAIDs not be combined

A

increases risk of side effects

only done if necessary

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38
Q

Why should aspirin be avoided/ given in caution to elderly px

A

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

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39
Q

Where is glucose 6-phosphate dehydrogenase deficiency most common in

A

individuals originating from

most parts of africa, asia
oceana
southern europe
can occur rarely in other individuals

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40
Q

What are individuals with G6PD-deficiency more susceptible to

A

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)

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41
Q

What groups is aspirin fully contraindicated in

A 
children and adults under 16 years 
breast feeding
previous or active peptic ulceration 
haemophilia
hypersensitivity to aspirin or any other NSAID
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42
Q

What is the dose for aspirin

A

300mg
40 tablets
2 tablets, 4 times daily, after food

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43
Q

What is the dosage for aspirin as thrombotic prophylaxis

A

a single dose of aspirin (150-300mg) is given ASAP after ischemic event and maintenance tx is 75mg daily

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44
Q

If someone has active peptic ulcer disease and requires NSAID, what else should be prescribed

A

lansoprazole or omeprazole

5 capsules - 5 days

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45
Q

What is the effect of ibuprofen

A

it has less effect on platelets than aspirin

it is an irritant to gastric mucosa but lower risk than aspirin

may cause bronchospasm

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46
Q

What is the dose for ibuprofen

A

400mg
20 tablets
1 tablet, 4 times daily, preferably w food

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47
Q

What is the maximum dose of ibuprofen in adults

A

2.4g

48
Q

Who should be prescribed ibuprofen with caution

A
  1. previous or active peptic ulceration
  2. the 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
49
Q

What are the most important side effects of ibuprofen

A
  1. GIT discomfort, occasionally bleeding and ulceration

2. hypersensitivity reactions e.g rashes angiodema, bronchospasm

50
Q

What are the other effects of ibuprofen

A

headache, dizziness, nervousness, depression, drowsiness insomnia, vertigo, hearing disturbances/tinnitus, photosensitivity, hematuria, blood disorders, fluid retention, renal impairment, hepatic damage, pancreatitis, eye changes

51
Q

What are the drugs that ibuprofen can interact with

A 
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
52
Q

What are the symptoms of ibuprofen overdose

A

nausea
vomiting
tinnitus

53
Q

What is done if more than 400mg/kg has been ingested within the preceding hour

A

activated charcoal followed by symptomatic measures

54
Q

What is COX1 responsible for

A

it is the cyclo-oxygenase predominantly responsible for catalyzing the reaction that produces prostaglandins associated with platelet aggregation and protection of the gastric mucosa

55
Q

What is COX2 responsible for

A

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

56
Q

What does the action of the formed prostaglandin’s depend on

A

the pathological situation

whether they are formed by COX-1 or COX-2

whether they are formed in excessive amounts

57
Q

How are prostaglandins produced in the physiological state

A

PGE2 is generated in low physiological amounts by COX-1 in gastric tissues and has a protective effect

58
Q

How are prostaglandins produced in inflammation

A

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

59
Q

Why are COX-2 selectives a good idea

A

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

60
Q

What is an example of a COX-2 inhibitor

A

celecoxib

61
Q

What is celexocib useful for

A

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

62
Q

What are selective COX-2 inhibitors still not used for

A

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

63
Q

What is the action of paracetamol

A 
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
64
Q

What is the mode of action of paracetamol

A

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

65
Q

Where is the main action of paracetamol

A

pain pathways of the CNS such as the thalamus

66
Q

Does paracetamol cause gastric irritation

A

no as it doesn’t have much effect on peripheral prostaglandins

67
Q

Who should you be cautious about prescribing paracetamol to

A

those with

hepatic impairment, renal impairment, alcohol dependence

68
Q

What are the side effects of paracetamol

A

rare

rashes
blood disorders
hypotension reproved on infusion
liver damage (and less frequently kidney damage) following overdose

69
Q

What are the interactions of paracetamol

A 
anti-coagulants 
cytotoxic
domperidone
lipid regulating drugs
metoclopramide
70
Q

How can paracetamol interact with anti-coagulants

A

prolonged regular use of paracemtol possibly enhances the anticoagulant effects of the coumarins

71
Q

What is the dose of paracetamol

A

500mg
40 tablets
1-2 tablets 4-6 hourly

72
Q

What is the max dose of paracetamol

A

4g daily

8 tablets

73
Q

How much paracetamol can result in severe hepatocellular necrosis or renal tubular necrosis

A

10-15g (20-30 tablets) or 150mg/kg

74
Q

What are the early features of paracemtol poisoning

A

anorexia
nausea
vomitting

usually settle within 24h

75
Q

What is the indication of hepatic necrosis from paracetol

A

persistence of the early features and abdominal pain, right subcostal pain and tenderness

76
Q

What other drugs also contain paracetamol

A

cocodomal and coproxamol

77
Q

Which opioid can be prescribed by dentists

A

dihydrocodeine

78
Q

Where do opioid analgesics act

A

on the spinal cord

especially in the dorsal horn pathways associated with palateo-spinothalamic pathway

79
Q

Where is the central regulation of pain for opioids

A

periaqueductal grey matter
nucleus retictularis paragigantocellulais
raphe magnus nucleus

80
Q

How do opioids produce their effects

A

via specific receptors which are closely associated with the neuronal pathways that transmit pain to the CNS

81
Q

What are the problems with opioids

A

dependence - physiological and physical

tolerance - only to depressant effects

82
Q

Describe how the dependance on opioids presents

A

withdrawal of the drug will lead to psychological cravings and the patient will be physically ill

83
Q

Describe how tolerance to opioids presents

A

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

84
Q

What are the effect of opioids on smooth muscle

A

constipation - can occur after a few doses of dihydrocodeine

urinary and bile retention

85
Q

What are the depressor CNS effect of opioids

A

it depresses:

pain centre (alters awareness of perception of pain)
higher centres
resp centres
cough centre
vasomotor
86
Q

What are the stimulatory CNS effects of opiods

A

vomiting centre (dihydrocodeine often causes nausea and vomitnig which limits its value in dental pain)

salivary centre

pupillary constriction

87
Q

What are the most common side effects

A

nausea, vomiting, drowsiness

larger doses produce respiratory depression and hypotension

88
Q

What are the opioids side effects

A 
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
89
Q

What are the effects of opiods enhanced by

A

alcohol

90
Q

What are cautions for opioids

A 
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
91
Q

What are contraindications of opioids

A

acute respiratory depression

acute alcoholism

raised intracranial pressure/head injury

  • interferes with respiration
  • affects pupillary responses vital for neurological assessment
92
Q

What are the effects of codeine

A

effective orally
low dependence
usually in combination with paracetamol
cough suppressant

93
Q

What is a common side effect of cocodomol

A

consitpation

94
Q

What codeine combination is on the dental list

A

dihydrocodeine

95
Q

What are the routes for dihydrocodeine

A

subcutaneous or intramuscular (controlled)

oral (not controlled)

96
Q

What is the oral dose for dihydrocodeine

A

30mg even 4-6 hrs as necessary

higher doses not available to dentists

97
Q

What are the common dihydrocodeine side effects

A

general opioids side effects

nausea/vomiting
constipation
drowsiness

98
Q

What are the larger dose effects of dihydrocodiene

A

respiratory depression
hypotension
ureteric spasm
biliary spasm

99
Q

What are the serious drug interactions of dihydrocodiene

A

antidepressants MAOIs

dopaminergics

100
Q

What are the cautions for dihydrocodeine

A 
hypotension
asthma
pregnancy/lactaiton
renal/hepatic disease
elderly/children
101
Q

When should dihydrocodeine never be prescribed

A

in raised intracranial pressure/suspected head injury

102
Q

What are the uses of dihydrocodeine

A

moderate to severe pain

103
Q

Why is dihydrocodeine not used for dental pain much

A

side effects of nausea and vomiting

104
Q

What happens if there is opioid overdose

A

can cause varying degrees of coma, rest depression and pinpoint pupils

105
Q

What is the specific antidote for opioid overdose

A

naloxone if there is coma or bradypnoea

106
Q

What is the other category of analgesics in the BNF

A

those that are related to neuropathic and functional pain

107
Q

What is a neuropathic functional pain

A

trigeminal neuralgia
post-herpetic neuralgia
functional (TMJ or atypical facial pain)

108
Q

What is the only drug used in dentistry for neuropathic and functional pain

A

carbamazepine

109
Q

What is carbamazepine

A

its a proprietary brand

anti convulsant

110
Q

What is prescribed for trigeminal neuralgia

A

carbamazepine - only one on dental list
gabapentin
phenytoin

111
Q

What are the clinical features of trigeminal neuralgia

A 
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
112
Q

What dose is given for trigeminal neuralgia of carbamazepine

A

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

113
Q

What is the main side effects of carbamazepine

A

dizziness
ataxia
drwosiness
leucopenia and there blood disorders

114
Q

What are contraindications of carbamazepine

A

AV conduction abnormaliteit (unless paced)

history of bone marrow depression

porphyria

115
Q

What are the cautions for carbamazepine

A

hepatic/renal/cardiac disease

skins reactions

history of hematological reactions to other drugs

gluacoma

pregnancy/breast feeding

avoid abrupt withdrawal

BDS3 CLINICAL Oral Surgery (6 decks)

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