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3e. BDS3 CDS Oral Surgery > L69. Analgesia in Oral Surgery > Flashcards

L69. Analgesia in Oral Surgery Flashcards

1
Q

How does prostaglandin production effect perceived pain?

A
  • Trauma/ infection lead to the breakdown of membrane phospholipids producing arachidonic acid;
  • Arachidonic acid is broken down to form prostaglandins;
  • Prostaglandins sensitise the tissues to other inflammatory products - pain;
  • Reduction in prostaglandin production moderates pain.
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2
Q

What type of analgesic is aspirin?

A

NSAID (non steroidal anti inflammatory drug)

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3
Q

What is the active ingredient in aspirin?

A

Acetylsalicylic Acid

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4
Q

What properties does aspirin offer?

A
  • Analgesic;
  • Antipyretic;
  • Anti-inflammatory;
  • Anti-platelet;
  • Metabolic.
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5
Q

What is the mechanism of action of aspirin?

A
  • Reduces production of prostaglandins;
  • Inhibits both COX-1 and 2 (150x more effective on COX-1);
  • COX-1 inhibition reduces platelet aggregation and predisposes to damage of the gastric mucosa.
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6
Q

How does aspirin work as an antipyretic?

A
  • Prevents temperature raising effects of interleukin-1 and the rise in brain prostaglandin levels;
  • This reduces elevation in temperature leading to a fever;
  • Doesn’t reduce normal temperature.
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7
Q

How does aspirin work as an anti-inflammatory?

A
  • Inhibits prostaglandin production;
  • Prostaglandins are vasodilators and effect capillary permeability;
  • Reduces redness and swelling.
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8
Q

What adverse side effects can be seen from aspirin?

A
  • GIT problems;
  • Hypersensitivity;
  • Overdose: hyperventilation, vasodilation and sweating, tinnitus, metabolic acidosis, coma (uncommon);
  • Aspirin burns - mucosal.
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9
Q

How can aspirin cause GIT problems?

A
  • Effects mucosal lining of the 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).
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10
Q

How can aspirin cause mucosal burns?

A

Direct effect from salicylic acid when applied directly to mucosa (take with water!)

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11
Q

What groups should be avoided when prescribing aspirin?

A
  • GIT patients (previous or active peptic ulcers [risk of perforation!];
  • Pregnant (especially third trimester) [can impair platelet function/ effect timing of labour];
  • Breast feeding [Reye’s syndrome];
  • Children and <16s [Reye’s syndrome];
  • Hypersensitivity to aspirin or any other NSAIDs;
  • Bleeding abnormalities (e.g. haemophilia);
  • Anticoagulated patients [enhances warfarin/ coumarin anticoagulants by displacing warfarin binding sites and creating more free warfarin - increased bleeding tendency].

N.B. Normally, most warfarin is bound (inactive)

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12
Q

Why groups should you be cautious about when prescribing aspirin?

A
  • Asthmatics (ask if they’ve used NSAIDs before);
  • Renal/ hepatic impairment [aspirin metabolised in liver and excreted by kidneys - either can be delayed with impairment - only a contraindication when impairment is severe];
  • Patients on steroids (~25% of pts. on long-term steroids will develop a peptic ulcer, could be undiagnosed - risk of perforation);
  • Patients with epigastric pain;
  • Patients taking other NSAIDs [combination of NSAIDs will increase the risk of side effect, like seen in GIT];
  • Patients with G6PD-deficiency [can develop acute haemolytic anaemia but up to 1g daily is usually acceptable in these patients];
  • Elderly (more susceptible to drug-induced side effects in general due to smaller blood volume/ being on other medications/ medical problems).
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13
Q

Why can aspirin effect asthmatics?

A
  • Can cause hypersensitivity (acute bronchospasm/ asthma type attacks);
  • Hypersensitivity can also lead to minor skin rashes/ other allergies.
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14
Q

What is Reye’s syndrome?

A
  • Fatty degenerative process in liver (and to a lesser extent in kidneys);
  • Profound swelling in the brain;
  • Clinically: initially nausea, vomiting, lethargy then seizures and coma later;
  • Can lead to mortality (50%) due to brain damage by encephalopathy.
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15
Q

What dose of aspirin should be prescribed for odontogenic pain?

A
  • 300mg;

- 2 tablets, up to 4 times a day.

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16
Q

What dose of aspirin should be given for thrombotic prophylaxis (cerebrovascular/ cardiovascular event)?

A
  • Single dose of 150-300mg given ASAP;

- 75mg maintenance treatment.

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17
Q

What drug is commonly prescribed with aspirin?

A
  • Proton-pump inhibitor;
  • e.g. Omeprazole 20mg, once a day;
  • e.g. Lansoprazole 15mg, once a day.
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18
Q

What property does ibuprofen not offer, that aspirin does?

A

Anti-platelet (less effect so not used therapeutically for this)

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19
Q

What dose of ibuprofen should be prescribed for odontogenic pain/ post-operative pain?

A
  • 400mg;
  • 1 tablet, up to 4 times a day;
  • After food.
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20
Q

What is the maximum daily dose of ibuprofen for an adult?

A

2.4g

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21
Q

Why groups should you be cautious about when prescribing ibuprofen?

A
  • Previous or active peptic ulceration;
  • The elderly;
  • Pregnancy and lactation;
  • Renal, cardiac or hepatic impairment;
  • History of hypersensitivity to aspirin and other NSAIDs;
  • Asthma;
  • Patients taking other NSAIDs;
  • Patients on long-term systemic steroids.
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22
Q

What side effects can be seen from ibuprofen?

A
  • GIT discomfort (occasionally bleeding and ulceration);
  • Hypersensitivity reactions e.g. rashes, angioedema, bronchospasm;
  • Others: headache, dizziness, nervousness, depression, drowsiness, insomnia, vertigo, haematuria, blood disorders, fluid retention, renal impairment, hepatic damage, pancreatitis, eye changes, Stevens-Johnson syndrome and others (see BNF).
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23
Q

What drugs can ibuprofen potentially interact with?

A
  • ACE inhibitors;
  • Other analgesics;
  • Antibiotics;
  • Anticoagulants;
  • Antidepressants;
  • Antidiabetics;
  • Corticosteroids;
  • Cytotoxics;
  • Diuretics;
  • Beta-blockers;
  • Calcium-channel blockers;
  • Cardiac glycosides;
  • Ciclosporin;
  • Clonidine;
  • Clopidogrel (anti-platelet drug);
  • Lithium;
  • Tacrolimus;
  • Vasodilator antihypertensives;
  • CHECK BNF.
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24
Q

What are the symptoms of an ibuprofen overdose?

A
  • Nausea;
  • Vomiting;
  • Tinnitus (more serious toxicity - very uncommon).
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25
Q

How is an ibuprofen overdose treated?

A

Activated charcoal followed by symptomatic measures are indicated if >400mg/kg has been ingested within the preceding hour

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26
Q

What does COX-1 do?

A
  • Cyclo-oxygenase;
  • Catalyses the reaction that produces prostaglandins associated with platelet aggregation and protection of the gastric mucosa.
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27
Q

What does COX-2 do?

A
  • Cyclo-oxygenase;

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

28
Q

What do the actions of prostaglandins depend on?

A
  • The pathological situation;
  • Whether they are formed from COX-1 or COX-2;
  • Whether they are formed in excessive amounts.
29
Q

Provide an example of a selective COX-2 inhibitor:

A

Celecoxib (Celebrex)

[used to treat the pain and inflammation in osteoarthritis, acute pain in adults, rheumatoid arthritis, ankylosing spondylitis, painful menstruation, and juvenile rheumatoid arthritis]

30
Q

Why might a selective COX-2 inhibitor be chosen?

A
  • COX-1 in gastric tissues release PGE2 (a prostaglandin) as a protective effect;
  • COX-1 inhibition can have gastric effects (like aspirin);
  • Are therefore contraindicated in patients with current or hx of peptic ulceration;
  • Selective COX-2 inhibitors should be chosen to manage dental pain of patients at high risk of gastric or duodenal ulceration;
  • These also have no effect on platelets so may be better tolerated by patients with clotting disorders.
31
Q

What is the active ingredient in paracetamol?

A

Acetaminophen

32
Q

Why is paracetamol not considered an NSAID?

A

No anti-inflammatory activity

33
Q

What properties does paracetamol offer?

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.
34
Q

What is the mechanism of action of paracetamol?

A
  • Not fully known;
  • 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;
  • All NSAIDs reduce prostaglandin production of the CNS, such as the thalamus, but this is the main site for paracetamol;
  • Results in analgesia and antipyretic action.
35
Q

Why does paracetamol have little to no effect on gastric mucosal irritation?

A

Does not appear to have much effect on peripheral prostaglandin pathways

36
Q

What groups should you be cautious about when prescribing paracetamol?

A
  • Hepatic impairment;
  • Renal impairment;
  • Alcohol dependence.
37
Q

What adverse side effects can be seen from paracetamol?

[rare!]

A
  • Rashes;
  • Blood disorders;
  • Hyptension reported on infusion;
  • Liver damage (and less frequently kidney damage), following overdose.
38
Q

What drugs can paracetamol potentially interact with?

A
  • Anticoagulants (prolonged regular use of paracetamol possibly enhances the anticoagulant effects of the coumarins);
  • Cytotoxics;
  • Domperidone;
  • Lipid-regulating drugs;
  • Metoclopramide.
39
Q

What dose of paracetamol should be prescribed for odontogenic pain/ post-operative pain?

A
  • 500mg;

- 2 tablets, up to 4 times a day (every 4-6 hours).

40
Q

What is the maximum daily dose of paracetamol for an adult?

A

4g (8 tablets)

41
Q

What is classed as a paracetamol overdose?

A
  • 10-15g (20-30 tablets);
  • OR 150mg/kg, taken within 24 hours;
  • May cause severe hepatocellular necrosis (and less frequently renal tubular necrosis).
42
Q

What are the signs and symptoms of a paracetamol overdose?

A
  1. Anorexia, nausea and vomiting (early features, usually settle within 24 hours);
  2. Persistence of these beyond 24 hours is often associated with abdominal pain (usually indicates development of hepatic necrosis);
  3. Liver damage is maximal at 3-4 days after ingestion and may lead to jaundice, renal failure, haemorrhage, hypoglycaemia, encephalopathy, cerebral oedema and death.
43
Q

What should you do if you suspect a paracetamol overdose?

A

Immediate hospital referral

44
Q

What opioid analgesia can dentists prescribe?

A

Dihydrocodeine

[- aka dihydrocodeine tartrate and DF118 Forte (trade name);

  • Potency similar to codeine;
  • Routes: SC or IM (controlled) or oral (not controlled)]
45
Q

Where do opioid analgesics target?

A
  • Spinal cord [dorsal horn pathways associated with paleo-spinothalamic pathway];
  • Central regulation of pain in periaqueductal grey matter, nucleus reticular paragigantocellularis, raphe magnus nucleus;
  • They produce their effects via specific receptors which are closely associated with the neuronal pathways that transmit pain to the CNS.
46
Q

What are the problems with opioid analgesics?

A
  • Relatively ineffective for dental pain;
  • Dependence: psychological and physical;
  • Tolerance: only to depressant effects;
  • Dose of drug needs to be progressively increased, for same pain relief, as tolerance increases.
47
Q

What common side effects are there of opioid analgesics?

A
  • Effects on smooth muscle: constipation;

- Urinary and bile retention.

48
Q

What effects do opioid analgesics have on the CNS?

A

Depresses:

  • Pain centre (alters awareness/ perception of pain);
  • Higher centres;
  • Respiratory centre;
  • Cough centre;
  • Vasomotor (hypotension).

Stimulates:

  • Vomiting centre (dihydrocodeine often causes nausea and vomiting which limits its value in dental pain);
  • Salivary centre;
  • Pupillary constriction.
49
Q

What side effects can be seen from opioid analgesics?

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 potency;
  • Rashes/ urticaria/ pruritus.
50
Q

What can the effects of opioids be enhanced by?

A

Alcohol

51
Q

What groups should you be cautious about when prescribing opioid analgesics?

A
  • Hypotension;
  • Hypothyroidism;
  • Asthma;
  • Decreased respiratory reserve;
  • Prostatic hyperplasia;
  • Pregnancy/ breast-feeding;
  • Hepatic impairment (may precipitate coma - reduce dose or avoid);
  • Renal impairment (reduce dose or avoid);
  • Elderly and debilitated (reduce dose);
  • Children;
  • Convulsive disorders;
  • Dependence;
  • Suspected head injury.
52
Q

When are opioid analgesics contraindicated?

A
  • Acute respiratory depression;
  • Acute alcoholism;
  • Raised inter cranial pressure/ head injury (interferes with respiration, affects pupillary responses vital for neurological assessment).
53
Q

What is codeine derived from?

A

Opium poppies

54
Q

How potent is codeine, compared to morphine?

A

1/12th

55
Q

What properties can codeine offer?

A
  • Effective orally;
  • Low dependence;
  • Usually in combination with NSAIDs or paracetamol e.g. co-codamol (8mg codeine, 500mg paracetamol);
  • Effective cough suppressant;
  • Available OTC.
56
Q

What is a typical dose for oral dihydrocodeine?

A
  • 30mg;

- Every 4-6 hours, as necessary.

57
Q

What drugs can dihydrocodeine potentially interact with (serious)?

A
  • Antidepressants MAOIs;

- Dopaminergics (Parkinsonism).

58
Q

What signs and symptoms are there of an opioid overdose?

A
  • Varying degrees of coma;
  • Respiratory depression;
  • Pinpoint pupils.
59
Q

What antidote drug is indicated if there is a coma or bradypnoea (as a result of opioid overdose)?

A

Naloxone

[shorter duration of action than many opioids so close monitoring required and repeated injections/ infusions may be necessary according to respiratory rate and depth of coma]

60
Q

What neuropathic or functional pain might be seen in dentistry?

A

Neuropathic:

  • Trigeminal neuralgia;
  • Post-herpetic neuralgia.

Functional:

  • TMJ pain;
  • Atypical facial pain.
61
Q

What drug can dentists prescribe for neuropathic or functional pain?

A

Carbamazepine (Tegretol)

[anti-convulsant]

62
Q

What other drugs are used to treat trigeminal neuralgia? (not on dental list)

A
  • Gabapentin;

- Phenytoin.

63
Q

What are the clinical features of trigeminal neuralgia?

A
  • Severe spasms of pain, ‘electric shock’ - lasts seconds;
  • Usually unilateral;
  • Older age-group;
  • Trigger spot identified;
  • Females more than males;
  • Periods of remission;
  • Recurrences often greater sensitivity.
64
Q

What dose of carbamazepine should be prescribed for trigeminal neuralgia?

A

Initially:

  • 100 or 200mg tablets (starting dose 100mg but some patients require higher);
  • 1 or 2 times daily;
  • Gradually increase according to response.

Usual dose:

  • 200mg;
  • 3-4 times daily;
  • Up to 1.6g daily in some patients.
65
Q

What side effects can be seen with carbamazepine?

A
  • Dizziness;
  • Ataxia;
  • Drowsiness;
  • Leucopenia and other blood disorders;
  • SEE BNF.

[Patient blood monitoring: blood count and liver fn]

66
Q

When is carbamazepine contraindicated?

A
  • AV conduction abnormalities (unless paced);
  • History of bone marrow depression;
  • Porphyria.
67
Q

What groups should you be cautious about when prescribing carbamazepine?

A
  • Hepatic/ renal/ cardiac disease;
  • Skin reactions;
  • History of haematological reactions to other drugs;
  • Glaucoma;
  • Pregnancy/ breast-feeding;
  • Avoid abrupt withdrawal.

3e. BDS3 CDS Oral Surgery (5 decks)

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