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BDS3 Oral Surgery > analgesia in oral surgery > Flashcards

analgesia in oral surgery Flashcards

1
Q

pain control

post op pain Vs during operative procedure

A

In dental practice pain control is an important aspect of pt management

  • During
  • After/post-op

Local anaesthetics are used everyday to control pain, BUT we also need to consider the use of systemic analgesic drugs to control post-operative pain

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2
Q

5 analgesia considerations

A
  1. ‘think’ postoperative analgesia
  2. Start systemic analgesics before the LA wears off – tell the pt to start 4 hours after if LA wears of 6 hours after
  3. ‘sell’ the prescription to obtain optimal response
  4. Use LA more
  5. Watch for risk groups
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3
Q

6 analgesia in dental practitioners formularly

A
  • Aspirin (NSAID)
  • Ibuprofen (NSAID)
  • Diclofenac (NSAID)
  • Paracetamol
  • Dihydrocodeine (opioid)
  • Carbamazepine
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4
Q

key facts of analgesia to know (5 topics)

A
  • Mechanism of action
  • Doses
  • Side effects
  • Interaction
  • Groups pt to avoid
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5
Q

aspirin

use

A
  • In the past aspirin was one of the more commonly used NSAIDs
  • Effective for dental and TMJ pain
  • Superior anti-inflammatory properties to paracetamol
  • Less commonly used in dentistry now (iburprofen more)
  • Can be bought over the counter as well as prescribed

Blood thinning uses

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6
Q

aspirin a.k.a

A

Acetylsalicylic Acid

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7
Q

5 properties of aspirin

A
  1. Analgesic
  2. Antipyretic
  3. Anti-inflammatory
  4. Anti-platelet
  5. metabolic
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8
Q

what is the common reason why pts are on aspirin

A

antiplatelet

  • low dose 75mg (prevent strokes, heart attacks in past) on long term
  • common in elderly pt
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9
Q

pain

A

Unpleasant sensation conveyed to the brain by sensory neurons, the discomfort signals actual or potential injury to the body

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10
Q

pain causes

A

production of prostaglandins

  • 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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11
Q

how do drugs moderate pain

A

Prostaglandins do not cause pain directly BUT they sensitise the tissues to other inflammatory products such as leukotrienes

  • so if prostaglandin production decreases this will moderate the pain
  • How drugs work – minimise prostaglandin*
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12
Q

sequence of trauma to prostaglandin production (pain)

A
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13
Q

aspirin mechanism of action

A
  • aspirin reduces production of prostaglandins
  • it inhibits cyclo-oxygenases (COX-1 & 2)
    • more effective at inhibiting COX-1
  • COX-1 inhibition reduces platelet aggregation and predisposes to damage of the gastric mucosa
    • Gastric mucosa – watch pt groups to avoid
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14
Q

can you develop a tolerance or dependence to aspirin

A

no

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15
Q

analgesic properties of aspirin

A
  • Good for mild to moderate pain
  • Mainly a peripherally acting agent
    • Analgesic action of NSAIDs is exerted both peripherally and centrally
      • Peripheral action predominate
    • The analgesic action results from inhibition of prostaglandin synthesis in inflamed tissues (Cylclo-oxygenase inhibition)
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16
Q

antipyretic properties of aspirin

A
  • Aspirin prevents the temperatures raising effects of interleukin-1 and the rise in brain prostaglandin levels
    • So reduces elevated temperature in fever

Doesn’t reduce normal temperature

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17
Q

anti-inflammatory properties of aspirin

A
  • Prostaglandins are vasodilators and as such also affect capillary permeability
  • Aspirin is a good anti-inflammatory and will reduce redness and swelling as well as pain at site of the injury
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18
Q

metabolic effects of aspirin (4)

A
  • Increase
    • BMR
    • Platelets
    • Prothrombin
  • Decrease
    • Blood sugar
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19
Q

problems with aspirin use

A
  • Adverse/side effects
  • Groups to avoid
  • Caution when prescribing

Not tend to prescribe for analgesia now

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20
Q

4 main adverse affects of aspirin

A
  • GIT problems
  • Hypersensitivity
  • Overdose
  • Aspirin burns
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21
Q

GIT problems associated with aspirin

A
  • Mostly on mucosal lining of stomach
  • Prostaglandins (PGE2 and PGI2)
    • Inhibit gastric acid secretion
    • Increase blood flow through the gastric mucosa
    • Help production of mucin by cells in stomach lining (cytoprotective action)
  • Care must be taken in patients with GIT problems
    • Ulcers
    • Gastro-oesophageal reflux
  • Most pts taking aspirin will suffer some blood loss from GIT
    • Not detectable macroscopically and asymptomatic
      • Not effect day to day life – blood loss
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22
Q

hypersensitivity problems with aspirin use

A
  • Reactions include
    • Acute bronchospasm/asthma type attacks
    • Minor skin rashes
    • Other allergies
  • NSAID allergy inc aspirin
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23
Q

overdose of aspirin affects

A
  • Hyperventilation
  • Tinnitus, deafness
  • Vasodilation and sweating
  • Metabolic acidosis (can be life threatening)
  • Coma (uncommon)
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24
Q

mucosal burns due to aspirin use

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
  • Can be large and significant
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25
Q

groups of people to have caution/avoid giving 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 and adolescents under 16 years
  9. Asthma
  10. Hypersensitivity to other NSAIDs
    • Aspirin is an NSAID
  11. Taking other NSAIDs
  12. Elderly
    • Generally careful in elderly with all medications
  13. G6PD-deficiency
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26
Q

why avoid aspirin if

peptic ulceration

A

gastric or duodenal bleeding could result in perforations

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27
Q

why avoid aspirin if

epigastric pain

A

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

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28
Q

why avoid aspirin if

bleeding abnormalities

A

have known bleeding problems e.g. haemophilia

  • high risk of bleeding - don’t want to exacerbate
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29
Q

why avoid aspirin if

anticoagulant medication

A
  • Aspirin enhances warfarin and other coumarin anticoagulants
    • Displaces warfarin from binding sites on plasma proteins
    • 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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30
Q

why avoid aspirin if

pregnant/lactation

A
  • Especially 3rd trimester
    • This is nearer delivery and may cause impairment of platelet function (Aspirin has antiplatelet property)
      • Increased risk of haemorrhage
      • Increased risk of jaundice in baby
      • Can prolong/delay labour (unsure why)
  • Contraindicated in breastfeeding -> Reye’s syndrome
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31
Q

why avoid aspirin if

renal/hepatic impairment

A
  • Aspirin metabolism is in liver and excretion mainly in 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 severe

Always caution renal and hepatic – most Mx metabolised in liver and excreted by kidney – like aspirin

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32
Q

nephrotoxicity and NSAID use

A

Prostaglandins PGE2 and PGI2 are powerful vasodilators synthesised in the renal medulla and glomeruli respectively,

  • are involved in the control of renal blood flow and excretion of salt and water

inhibition of renal prostaglandin synthesis may result in:

  • sodium retention
  • reduced renal blood flow
  • renal failure

NSAID may cause interstitial nephritis and hyperkalaemia

  • Prolonged analgesic abuse over a period of years is associated with papillary necrosis and chronic renal failure
    • Severe derangement of pt urea and electrolytes
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33
Q

inhibition of renal prostaglandin synthesis may result in (3)

A
  • sodium retention
  • reduced renal blood flow
  • renal failure
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34
Q

why avoid aspirin in

children and adolescents under 16 years (inc breastfeeding)

A

Reye’s syndrome

  • Rare
    • Under 20s affected mainly
  • Very serious, up to 50% mortality
    • Related to brain damage due to encephalopathy
  • Fatty degenerative process in liver (and lesser extent kidney)
    • Profound swelling in brain
  • Clinically
    • Initially nausea, vomiting, lethargy
    • Later seizures and coma

Contraindicated if under 16 years or breastfeeding

Avoid during fever or viral infection in adolescents

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35
Q

why avoid aspirin in

asthma pts

A
  • NSAID not completely contraindicated as some asthmatics have no problems with them
    • ask if used before and if any problems
      • any shadow of doubt avoid NSAIDs
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36
Q

why avoid aspirin in

hypersensitivity to NSAIDs

A
  • contraindicated in pts 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 NSAID
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37
Q

why avoid aspirin

if taking other NSAIDs

A
  • combination of NSAIDs will increase risk of side effects
    • e.g. the combination of an NSAID and low dose aspirin may increase the risk of GIT side effects; and should be used if absolutely necessary and the pt monitored closely
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38
Q

why avoid aspirin in

elderly

A
  • more susceptible to drug induced side effects in general
    • they are often smaller/smaller circulating blood volume
    • on other medications
      • Higher risk interactions when polypharmacy
    • Have other medical problems
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39
Q

G6PD - deficiency

A

glucose 6-phosphate dehydrogenase deficiency

Rare

Prevalent In individuals from:

  • Most parts Africa,
  • Most parts Asia
  • Oceania
  • Southern Europe

Inborn error of metabolism, predisposes RBC breaking down

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40
Q

why avoid aspirin in

G6PD-deficiency

A

Inborn error of metabolism, predisposes RBC breaking down

Susceptible to develop acute haemolytic anaemia on taking a number of common drugs

  • Aspirin – possible risk of haemolysis 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

absolute contraindication groups for aspirin use (4)

A
  1. Children and adolescents under 16 years; breast feeding (Reye’s syndrome)
  2. Previous or active peptic ulceration
  3. Haemophilia
  4. Hypersensitivity to aspirin or any other NSAID
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42
Q

thrombotic prophylaxis

A
  • Thrombotic cerebrovascular/cardiovascular disease (HA, stroke)
  • A single dose of aspirin (150-)300mg given as soon as possible after ischaemic event, provided no contraindications
  • Maintenance treatment: 75mg daily
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43
Q

how to prevent aspirin damage to gastric lining

A

prescribe with PPI to protect (lansoprazole capsules, 15mg; gastro-resistant omeprazole capsules, 20mg)

  • 5 day regime usually
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44
Q

iburpofen

use

A

Used more commonly than aspirin in dentistry

  • Long term use recently associated with increased risk of cardiac events

NSAID

Available over the counter

Popular as post-operative analgesia following oral suragery

Paediatric suspension available

  • Safely given to children
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45
Q

ibuprofen Vs aspirin

A

Similar but not identical effect as aspirin

Less effect on platelets

Not used therapeutically for this - Not used for MI or stroke

Irritant to gastric mucous – but lower risk than aspirin

May cause bronchospasm (care in asthmatics but not completely contraindicated)

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46
Q

max dose ibuprofen in adults

A

2.4g

47
Q

usual dosage of ibuprofen for adults

A

iburpofen tablets, 400mg

  • 1 tablet, 4 times a day, preferably after food ‘

send 20 tablets (last 5 days)

48
Q

ibuprofen

caution when prescribing (8)

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. Patient on long term systemic steroids
49
Q

side effects of iburpofen

A

GIT discomfort, occasionally bleeding and ulceration

Hypersensitivity reactions e.g. rashes, angioedema and bronchospasm

  • Others – headache, dizziness, nervousness, depression, drowsiness, insomnia, vertigo, hearing disturbance/tinnitus, photosensitivity, haematuria, blood disorders, fluid retention, renal impairment, hepatic damage, pancreatitis, eye changes, Steven- Johnson (rare and severe) and more, see BNF
50
Q

drug interactions with ibuprofen

A
  • ACE inhibitors Beta blockers Other analgesics*
  • Cytotoxics Antibiotics Cardiac glycosides*
  • Anticoagulants Cyclosporin Antidepressants*
  • Clonidine Antidiabetics Clopidogrel (antiplatelet)*
  • Corticosteroids Lithium Calcium channel Blockers*
  • Diuretics Tacrolimus Vasodilator Antihypertensives*

Many interactions - check BMF

51
Q

ibuprofen overdose

A
  • Rare but be aware of esp for emergency pts (more serious toxicity very uncommon)

Symptoms

  • Nausea
  • Vomiting
  • Tinnitus

A&E

  • Activated charcoal followed by symptomatic measures are indicated id more than 400mg/kg been ingested within the preceding hour
    • Absorb excess
52
Q

writing prescription

A
  • GP14 (Scotland)
  • FP10D (England)
  • WP10D (Wales)

https://bnf.nice.org.uk/guid ance/prescription-writing.html

No hospital labels on prescription

  • write out – confirm with pt to ensure correct

Most dental tx 5 days

  • e.g. 400mg ibuprofen tables*
  • 3 times a day for 5 days*
  • Send 15 tablets*
53
Q

NSAID general method of action

A

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

inhibit COX-1 as well as COX-2

  • Predominantly COX-1 inhibition
    • Aspirin 150 times more effective at inhibiting COX-1 than COX-2
54
Q

COX-1

A

cyclo-oxygenase predominantly responsible for catalysing the reaction that produces prostaglandins associated with:

  • Platelet aggregation
  • protection of gastric mucosa
55
Q

COX-2

A
56
Q

aspirin potency on COX-1 Vs COX-2

A

Aspirin 150 times more effective at inhibiting COX-1 than COX-2

  • Amount of Aspirin needed to have sufficient anti-inflammatory effects by inhibition of COX-2 will cause gastric damage due to the amount of COX-1 inhibition
57
Q

action of formed prostaglandins depend on (3)

A
  • Pathological situation
  • Whether they are formed by COX-1 or COX-2
  • Whether they are formed in excessive amounts

e. g. PGE2 generated in low physiological amounts by COX-1 in gastric tissues and has a protective effect
* 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 sensitises pain fibre nerve endings to bradykinin, 5HT and other mediators

58
Q

PGE2

A

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

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 sensitises pain fibre nerve endings to bradykinin, 5HT and other mediators
59
Q

why selective COX-2 inhibitors

A

less gastric effect

Since the analgesic actions of NSAIDs appear to result from inhibition of COX-2 (mainly, although COX-1 can be involved (but aspirin and ibuprofen more COX-1)) it would make sense to have Selective COX-2 Inhibitors and spare COX-1

60
Q

selective COX-2 inhibitors

e.g.

A

Celecoxib (celebrax)

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

Useful for rheumatoid arthritis

61
Q

pts with active peptic ulceration are contraindicated to

A

all NSAIDs

inc selective COX-2 inhibitors

62
Q

pts with history of peptic ulceration are contraindicated to

A

non-selective NSAIDs

63
Q

BNF NSAID use recommendation

A

do not use more than one oral NSAID at a time (inc selective COX-2 inhibitors)

(dental and orofacial pain) – COX-2 selective should be chosen to manage dental pain only in pts at high risk of gastric or duodenal ulceration (e.g. those with a history of peptic ulcer)

64
Q

side effects of selective COX-2 inhibitors

A
  • Highly selective COX-2 inhibitors do not have an effect on platelet aggregation and so may be better tolerated by patients with clotting disorders
  • Several COX-2 selectives have been withdrawn due to cardiovascular risk
    • Other COX-2 selective NSAIDs not withdrawn e.g. celecoxib – but no longer of the Dental List
      • So cannot prescribe as dentists – but if patient cannot have NSAIDs (ibuprofen or aspirin) may beconsidered if liaise with GMP
65
Q

paracetamol a.k.a

A

acetaminophen

66
Q

paracetamol is

A

simple analgesic without anti-inflammatory activtiy

NOT NSAID

  • common
  • relatively safe
67
Q

7 properties of paracetamol

A
  1. Analgesic
  2. Antipyretic
  3. Little or no anti-inflammatory action
  4. No effect on bleeding time
  5. Does not interact significantly with warfarin
  6. Less irritant to GIT
  7. Suitable for children
68
Q

anti-pyretic

A

reduction in temperature

69
Q

mode of action of 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 – especially in the brain

Results in:

  • Analgesia
  • Antipyretic action
  • No reduction in peripheral inflammation

A small component of the analgesic action of all NSAIDs is the reduction of prostaglandins in the pain pathways of the CNS, such as in the thalamus

  • MAIN site of action of paracetamol - CENTRALLY – thalamus

Alternative central mechanisms have also been proposed, inc reduced 5HT production or interference with the excitatory amino acid NMDA (N-Methyl-D-Aspartate) in spinal cord pathways

  • Exact mode of action still unclear

Since paracetamol does not appear to have much effect on peripheral prostaglandins there is little/no gastric mucosal irritation

  • Described as ‘safe analgesic’ although causes severe problems in overdose
70
Q

paracetamol

Central or peripheral action?

A

A small component of the analgesic action of all NSAIDs is the reduction of prostaglandins in the pain pathways of the CNS, such as in the thalamus

  • MAIN site of action of paracetamol
    • CENTRALLY – thalamus

Since paracetamol does not appear to have much effect on peripheral prostaglandins there is little/no gastric mucosal irritation

  • Described as ‘safe analgesic’ although causes severe problems in overdose
71
Q

3 groups to be cautious when prescribing paracetamol

A
  1. Hepatic impairment
  2. Renal impairment
  3. Alcohol dependence
72
Q

paracetamol side effects

A
  1. Rashes
  2. Blood disorders
  3. Hypotension reported on infusion (IV)
  4. Liver damage (and less frequently kidney damage) following overdose – hepatotoxic in high doses
73
Q

paracetamol interactions (4 main)

A
  • Anticoagulants (prolonged regular use of paracetamol possibly enhances the anticoagulant effect of the coumarins)
  • Cytotoxics
  • Domperidone
  • Lipid-regulating drugs
  • Metoclopramide

See BNF

74
Q

paracetamol dose

A

500mg tablets; 1-2 tablets; 4 times a day (4-6 hourly)

8 x 500mg a day – max for adults (4g)

Children depends on age/weight

75
Q

paracetamol warning

A

Always warn pt with regard to maximum dose and emphasize that they should not exceed this

  • Overdose in emergency pts (extreme dental pain)

As little as 10-15g (20-30 tablets) or 150mg/kg paracetamol taken within 24 hours may cause severe hepatocellular necrosis and less frequently renal tubular necrosis (liver and kidneys)

76
Q

paracetamol overdose symptms

A

Anorexia, nausea, vomiting

  • The only early features of poisoning
  • Usually settle within 24 hours

Persistence of these features beyond is often associated with abdominal pain (right subcostal pain and tenderness, usually indicates development of hepatic necrosis)

  • Liver damage is maximal at 3-4 days after ingestion and may lead to jaundice, renal failure, haemorrhage, hypoglycaemia, encephalopathy, cerebral oedema and death
  • Pain ->develop into hepatic necrosis*
  • Therefore, despite a lack of significant early symptoms – pts who have taken an overdose of paracetamol should be transferred immediately to hospital – liver risk
77
Q

warning of many OTC preparation

A

contain paracetamol

e.g. Lemsip, Co-codamol and co-proxamol

78
Q

opioid analgesia in dental practitioners formularly

A

dihyrdrocodeine

79
Q

opioid analgesia

method of action

A
  • Act in spinal cord
    • Especially in the dorsal horn pathways associated with paleo-spinothalamic pathway
  • Central regulation of pain in:
    • Periaqueductal gey matter
    • Nucleus reticularis paragigantocellularis
    • Raphe magnus nucleus
  • They produce their effects via specific receptors which are closely associated with neuronal pathways that transmit pain to the CNS
  • Opioid is a term used for both naturally occurring and synthetic molecules that produce their effects by combining with opioid receptors

BNF state – opioid analgesics are relatively ineffective in dental pain

80
Q

2 main opioid problems

A

dependece - psychological and physical

tolerance - only to depressant effects

81
Q

dependence on opioids

A

Psychological and physical

  • Withdrawal of the drug will lead to psychological cravings and the pt will also be physically ill
82
Q

tolerance to opioids

A

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

83
Q

effects on opioids on body

A

effects smooth muscles

CNS effects

84
Q

opioid effects on smooth muscles

A
  • Constipation (can occur after few doses of dihydrocodeine)
  • Urinary and bile retention

Long term opioid – uncomfortable

85
Q

CNS effects of opioids

A
  • Depresses
    • Pain centre (alters awareness/perception of pain)
    • Higher centres
    • Respiratory centre
    • Cough centre cough suppression
    • Vasomotor
  • Stimulates
    • Vomiting centre
      • Dihydrocodeine often causes nausea and vomiting which limits its value in dental pain – not able to ingest drug fully
    • Salivary centre
    • Pupillary constriction
86
Q

opioids depress 5 aspects of CNS

A
  • Pain centre (alters awareness/perception of pain)
  • Higher centres
  • Respiratory centre
  • Cough centre cough suppression
  • Vasomotor
87
Q

opioids stimulate 3 aspects of CNS

A
  • Vomiting centre
    • Dihydrocodeine often causes nausea and vomiting which limits its value in dental pain – not able to ingest drug fully
  • Salivary centre
  • Pupillary constriction
88
Q

opioid side effects

A

The most common are nausea, vomiting and drowsiness

Larger doses produce respiratory depression and hypotension (LBP)

Many more

  • Difficulty with micturition
  • Postural Hypotension
  • Uretic or biliary spasm
  • Hypothermia
  • Dry mouth
  • Hallucinations
  • Sweating
  • Dysphoria
  • Facial Flushing
  • Mood Changes
  • Headache
  • Dependence
  • Vertigo
  • Miosis
  • Bradycardia
  • Decreased libido or potency
  • Tachycardia
  • Rashes/urticaria/Pruritis
  • Palpitations
89
Q

effect of opioids enhanced by

A

alcohol

90
Q

groups to have caution with in opioids prescription (11)

A
  • Hypertension
  • Hypothyroidism
  • Asthma
  • Decreased respiratory reserve
  • Prostatic hyperplasia
  • Pregnancy/breast feeding
  • Many precipitate come in hepatic impairment
    • reduce dose/avoid
  • Renal impairment
    • Reduce dose/avoid
  • Elderly and debilitated
    • Reduce dose
  • Convulsive disorders (epilepsy)
  • Dependence
91
Q

hepatic impairment impact on drug metabolism

A

unable to metabolism if liver not functioning

92
Q

renal impairment impact on drug metabolism

A

unable to excrete if kidneys not functioning

93
Q

absolute contraindications to opioid use (3)

A
  • Acute respiratory depression
  • Acute metabolism
  • Raised intracranial pressure/head injury
    • Interferes with respiration
    • Affects pupillary responses vital for neurological assessment
94
Q

codeine

A

opioid analgesic

A natural alkaloid found in opium poppy

  • 1/12th the potency of morphine
    • Still relatively strong

Effective orally

Lower dependence than morphine

Usually in combination with NSAIDs or paracetamol

  • E.g. OTC 8mg codeine in 500mg paracetamol

Prescription 30mg codeine in 500mg paracetamol – not Dental list

Effective cough suppressant

Common side effect – constipation

Available over the counter

95
Q

dihydrocodeine

A

Only codeine combination on dental list is Dihydrocodeine

Codeine phosphate – not on dental list

96
Q

dihyrdocodeine a.k.a

A

dihydrocodeine tartrate;

DF118 Forte (trade name)

97
Q

dihydrocodeine potency

A

similar to codeine

98
Q

dihydrocodeine

routes (2)

A
  • Sub cutaneous or intra-muscular (controlled drug)
  • Oral (not controlled)
99
Q

controlled Vs non-controlled routes

A
  • Controlled – need prescribed*
  • Not controlled - OTC*
100
Q

dihydrocodeine dose

A

Oral (only route on dental list)

  • 30mg every 4-6 hours as necessary

40, 60, 120mg not on dental list

101
Q

side effects of dihydrocodeine

A

General Opioid side effects (see side effects of codeine)

  • Nausea/vomiting
  • Constipation
  • Drowsiness

Larger doses

  • Respiratory depression
  • Hypotension
  • Uretic spasm
  • Biliary spasm

Etc

102
Q

serious drug interactions of dihydrocodeine

A
  • Antidepressants MAOIs
  • Dopaminergic (Parkinsonism)

many - see BNF

103
Q

groups to have caution when prescribing dihydrocodeine

A
  • Hypotension
  • Asthma
  • Pregnancy/lactation
  • Renal/hepatic disease
  • Elderly/children

Remember – never prescribe in raised intracranial pressure/suspected head injury

see general opioid cautions

104
Q

dihyrdocodeine

uses

A
  • moderate to severe pain
    • However, BNF states that due to the side effects of nauseas and vomiting it is of little value for dental pain (pts look very pale and ill due to vomitting)
      • And not very effective for post-operative dental pain

Not commonly prescribed by dentist

105
Q

opioid overdose

A

cause varying degrees of coma, respiratory depression and pinpoint pupils

Specific antidote Naloxone indicated if there is coma or bradypnea

  • Naloxone has a shorter duration of action than many opioids
    • So, close monitoring and repeated injections/infusion may be necessary according to respiratory rate and depth of coma
106
Q

neuropathic and functional pain e.g. (3)

A
  • Trigeminal neuralgia
  • Post-herpetic neuralgia
  • Functional – TMJ or atypical facial pain
107
Q

drug on dental list for neurological and functional pain

A

Carbamazepine

  • Proprietary brand e.g. Tegretol
  • Anti-convulsant - Emergency – epilepticus

also used for trigeminal neuralgia

108
Q

trigeminal neuralgia

drugs

A
  • Carbamazepine on Dental Practitioner’s Formulary

Other drugs used for trigeminal neuralgia include: (not on dental list)

  • Gabapentin
  • Phenytoin
109
Q

7 clinical features of trigeminal neuralgia

A
  1. Severe spasms of pain – ‘electric shock’, lasts seconds
  2. Usually unilateral (One branch usually – but can be more)
  3. Older age group
  4. Trigger spot identified e.g. wash face, wind hit
  5. Females more than male
  6. Periods of remission
  7. recurrence of greater severity
110
Q

carbamazepeine use for trigeminal neuralgia

A

100 or 200mg tablets

Starting dose 100mg once or twice daily (some pts require higher initial dose)

  • Increase gradually according to response
    • Usual dose 200mg 3-4 times daily
      • Up to 1.6g daily in some patients (8 x 200mg)

Low dose and increase dose slowly

111
Q

carbamazepeine side effects

A

Extensive list – see BNF e.g.

  • Dizziness
  • Ataxia
  • Drowsiness – issue in elderly as more susceptible to falls and brittle bones
  • Leukopenia and other blood disorders

Patient blood monitoring – full blood count and liver function tests

  • Get pre-emptively so know in advance and monitor through Tx
112
Q

3 absolute contraindication groups for carbamazepine use

A
  1. AV conduction abnormalities (unless paced)
  2. History of bone marrow depression
  3. Porphyria
113
Q

6 caution groups for carbamazepeine use

A
  • Hepatic/renal/ cardiac disease (metabolised by liver; excreted by kidney)
  • Skin reactions
  • History of haematological reactions to other drugs
  • Glaucoma
  • Pregnancy/breast feeding
  • Avoid abrupt withdrawal

BDS3 Oral Surgery (8 decks)

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