Analgesia in Oral Surgery Flashcards
(115 cards)
1
Q
What are the analgesia in the dental practitioners formulary
A
aspirin ibuprofen diclofenac paracetamol dihydrocodein (opioid) carbamazepine
2
Q
What kind of pain is aspirin effective for
A
dental and TMJ
3
Q
How does aspirin compared to paracetamol
A
it has superior anti-inflammatory properties
4
Q
What is the properties of aspirin
A
analgesic antipyretic anti-inflammatory anti-platelet metabolic
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
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
7
Q
If prostaglandin production decreases what will this result in
A
it will moderate the pain
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
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)
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
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
12
Q
What are the metabolic effects of aspirin
A
increased basal metabolic rates
effects platelets, prothrombin and blood sugar
13
Q
What are the adverse effects of aspirin
A
GIT problems
hypersensitivity
overdose - tinnitus, metabolic acidosis
aspirin burns - mucosal
14
Q
What are the adverse effects of aspirin on the GIT
A
it is mostly on the mucosal lining of the stomach
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
16
Q
Which GIT patients require care in prescription of aspirin
A
those with GIT problems such as ulcers or GORD
17
Q
What do the hypersensitivity reactions to aspirin result in
A
acute bronchospasm / asthma type attacks
minor skin rashes
other allergies
18
Q
What should be done to reduce the risk of hypersensitivity to aspirin
A
take care when prescribing to asthmatics
19
Q
What are the adverse effects of overdose of aspirin
A
hyperventilation tinnitus, deafness vasodilation and sweating metabolic acidosis coma
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
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
22
Q
Why should aspirin be avoided in those with metic ulceration
A
is it could result in perforation
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
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
25
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
26
Why is aspirin contraindicated in those breastfeeding
due to reye's syndrome
27
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
28
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
29
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
30
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
31
Why is aspirin avoided in children and U16s
reyes syndrome
32
What is Reye's syndrome
fatty degenerative process in the liver (and to a lesser extend in the kidney)
profound swelling in the brain
33
What is the clinical presentation of Reye's syndrome
initially nausea, vomiting, lethargy
later seizures and coma
34
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
35
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
36
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
37
Why should NSAIDs not be combined
increases risk of side effects
only done if necessary
38
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
39
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
40
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)
41
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
```
42
What is the dose for aspirin
300mg
40 tablets
2 tablets, 4 times daily, after food
43
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
44
If someone has active peptic ulcer disease and requires NSAID, what else should be prescribed
lansoprazole or omeprazole
| 5 capsules - 5 days
45
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
46
What is the dose for ibuprofen
400mg
20 tablets
1 tablet, 4 times daily, preferably w food
47
What is the maximum dose of ibuprofen in adults
2.4g
48
Who should be prescribed ibuprofen with caution
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
What are the most important side effects of ibuprofen
1. GIT discomfort, occasionally bleeding and ulceration
| 2. hypersensitivity reactions e.g rashes angiodema, bronchospasm
50
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
51
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
```
52
What are the symptoms of ibuprofen overdose
nausea
vomiting
tinnitus
53
What is done if more than 400mg/kg has been ingested within the preceding hour
activated charcoal followed by symptomatic measures
54
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
55
What is COX2 responsible for
generation of most of the inflammatory prostaglandins (although in some situations (COX-1) is also involved
56
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
57
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
58
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
59
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
60
What is an example of a COX-2 inhibitor
celecoxib
61
What is celexocib useful for
has useful anti-inflammatory actions and fewer GIT damaging actions compared with non-selective NSAIDs
62
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
63
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
```
64
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
65
Where is the main action of paracetamol
pain pathways of the CNS such as the thalamus
66
Does paracetamol cause gastric irritation
no as it doesn't have much effect on peripheral prostaglandins
67
Who should you be cautious about prescribing paracetamol to
those with
hepatic impairment, renal impairment, alcohol dependence
68
What are the side effects of paracetamol
rare
rashes
blood disorders
hypotension reproved on infusion
liver damage (and less frequently kidney damage) following overdose
69
What are the interactions of paracetamol
```
anti-coagulants
cytotoxic
domperidone
lipid regulating drugs
metoclopramide
```
70
How can paracetamol interact with anti-coagulants
prolonged regular use of paracemtol possibly enhances the anticoagulant effects of the coumarins
71
What is the dose of paracetamol
500mg
40 tablets
1-2 tablets 4-6 hourly
72
What is the max dose of paracetamol
4g daily
| 8 tablets
73
How much paracetamol can result in severe hepatocellular necrosis or renal tubular necrosis
10-15g (20-30 tablets) or 150mg/kg
74
What are the early features of paracemtol poisoning
anorexia
nausea
vomitting
usually settle within 24h
75
What is the indication of hepatic necrosis from paracetol
persistence of the early features and abdominal pain, right subcostal pain and tenderness
76
What other drugs also contain paracetamol
cocodomal and coproxamol
77
Which opioid can be prescribed by dentists
dihydrocodeine
78
Where do opioid analgesics act
on the spinal cord
| especially in the dorsal horn pathways associated with palateo-spinothalamic pathway
79
Where is the central regulation of pain for opioids
periaqueductal grey matter
nucleus retictularis paragigantocellulais
raphe magnus nucleus
80
How do opioids produce their effects
via specific receptors which are closely associated with the neuronal pathways that transmit pain to the CNS
81
What are the problems with opioids
dependence - physiological and physical
tolerance - only to depressant effects
82
Describe how the dependance on opioids presents
withdrawal of the drug will lead to psychological cravings and the patient will be physically ill
83
Describe how tolerance to opioids presents
to achieve the same therapeutic effects the dose of the drug needs to be progressively increased
84
What are the effect of opioids on smooth muscle
constipation - can occur after a few doses of dihydrocodeine
urinary and bile retention
85
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
```
86
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
87
What are the most common side effects
nausea, vomiting, drowsiness
larger doses produce respiratory depression and hypotension
88
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
```
89
What are the effects of opiods enhanced by
alcohol
90
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
```
91
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
92
What are the effects of codeine
effective orally
low dependence
usually in combination with paracetamol
cough suppressant
93
What is a common side effect of cocodomol
consitpation
94
What codeine combination is on the dental list
dihydrocodeine
95
What are the routes for dihydrocodeine
subcutaneous or intramuscular (controlled)
oral (not controlled)
96
What is the oral dose for dihydrocodeine
30mg even 4-6 hrs as necessary
| higher doses not available to dentists
97
What are the common dihydrocodeine side effects
general opioids side effects
nausea/vomiting
constipation
drowsiness
98
What are the larger dose effects of dihydrocodiene
respiratory depression
hypotension
ureteric spasm
biliary spasm
99
What are the serious drug interactions of dihydrocodiene
antidepressants MAOIs
| dopaminergics
100
What are the cautions for dihydrocodeine
```
hypotension
asthma
pregnancy/lactaiton
renal/hepatic disease
elderly/children
```
101
When should dihydrocodeine never be prescribed
in raised intracranial pressure/suspected head injury
102
What are the uses of dihydrocodeine
moderate to severe pain
103
Why is dihydrocodeine not used for dental pain much
side effects of nausea and vomiting
104
What happens if there is opioid overdose
can cause varying degrees of coma, rest depression and pinpoint pupils
105
What is the specific antidote for opioid overdose
naloxone if there is coma or bradypnoea
106
What is the other category of analgesics in the BNF
those that are related to neuropathic and functional pain
107
What is a neuropathic functional pain
trigeminal neuralgia
post-herpetic neuralgia
functional (TMJ or atypical facial pain)
108
What is the only drug used in dentistry for neuropathic and functional pain
carbamazepine
109
What is carbamazepine
its a proprietary brand
| anti convulsant
110
What is prescribed for trigeminal neuralgia
carbamazepine - only one on dental list
gabapentin
phenytoin
111
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
```
112
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
113
What is the main side effects of carbamazepine
dizziness
ataxia
drwosiness
leucopenia and there blood disorders
114
What are contraindications of carbamazepine
AV conduction abnormaliteit (unless paced)
history of bone marrow depression
porphyria
115
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
