Analgesic agents Flashcards

1
Q

What would be the appropriate treatment of dental pain?

A
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2
Q

What is pain? Can pain always be cured? If not, what % of people in the UK suffer from persistent pain?

A

An unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of tissue damage or both (IASP definition).

Inadequate pain relief is a global concern for patients and practitioners. Pain is not always cured and requires continuous medical management, the same as any other disease process.

About 40%, or as many as 28 million people, in the UK suffer from persistent pain.

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3
Q

What is congenital insensitivity to pain? Why is it dangerous?

A

Can’t feel pain - on the pic the fingers are completely burnt as the pt couldnt feel pain so didnt retract the hand fast enough.

Congenital insensitivity to pain is caused by SCN9A gene mutation in humans.

Children with this condition don’t survive very long.

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4
Q

What are the 2 main sources of pain?

A

INJURY - via sport, surgery damage, etc

DISEASE - migraine, osteomalacia, psoriasis

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5
Q

How do we feel pain?

A

Receptors in our nerve endings are activated in response to certain stimuli. They activate a cascade of different signals along sensory fibres.

They send the info to higher regions of the brain like the thalamus / cortex.

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6
Q

What are some factors that can modulate pain?

A

Emotion and attention profoundly modulate nociception.

The amount of pain experienced does not necessarily relate to the severity of tissue damage

Anxiety increases pain transmission

Complex cultural and contextual influences

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7
Q

What can we generally use to relieve pain? When is this not always effective?

A

In normal circumstances we have an injury that produces pain.

Can generally use NSAIDs / opioids.

But in chronic pain patients, we dont have the perfect analgesic treatment. Some NSAIDs/opioids are not always enough to relieve the pain.

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8
Q

What different types of dental pain can we have?

A

infection - acute inflammation

exposed nerve endings = neurogenic pain

swelling in confined space = pressure effects

fear and anxiety

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9
Q

What are the different ways in which we can treat pain involving:

nerve block?

spinal cord?

CNS?

A

Nerve block - local anaesthetics

Spinal cord - opioids

CNS - opioids / psychological factors

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10
Q

How can we reduce tissue damage and therefore pain?

A
  • NSAIDs (non-steroidal anti-inflammatory drugs)
  • Steroids
  • Cooling
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11
Q

What are the WHO 1996 pain relief guidelines for managing a patient presenting with pain?

A
  • Believe the patient
  • History of symptoms
  • Assessment of severity
  • Physical examination
  • Appropriate pain management
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12
Q

What is the WHO analgesic ladder from step 1 (mild pain) to step 3 (severe pain)?

A

step 1 = MILD pain

  • non-opioids (e.g. paracetamol)
  • +/- NSAIDs

step 2 = MODERATE pain

  • weak opioid (e.g. tramadol, dihydrocodeine)
  • +/- non-opioid (e.g. paracetamol and/or NSAID)

step 3 = SEVERE pain

  • strong opioid (e.g. morphine, diamorphine, fentanyl patch)
  • +/- non-opioid (e.g. paracetamol and/or NSAID)
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13
Q

What are the co-analgesics that could be involved in the WHO analgesic ladder?

A

other drugs, nerve blocks, surgery, radiotherapy, complementary therapies, addressing psychosocial issues

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14
Q

What are some analgesic ladder ASSUMPTIONS?

A

Synergism

Overall philosophy assessing severity, starting at lowest level and increasing if necessary

Joint Royal Colleges Report (1988) quality of analgesia in hospital practice is inadequate

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15
Q

What is a placebo and what is the placebo effect?

A

A placebo is anything administered which is pharmacologically and physiologically inert

Placebo is not ineffective therapeutically. Can have a measurable effect

Reassurance and confidence in one’s therapy may also have an effect.

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16
Q

PARACETAMOL. Describe:

It’s mechanism of action?

Is it anti-inflammatory?

Forms it can be taken in?

Maximum adult dosage?

A

Mechanism of action unknown – but it is an inhibitor of the synthesis of prostaglandins.

Analgesic and antipyretic, but doesn’t have much anti-inflammatory effect.

Can be taken orally, as soluble potions, intravenously or rectal

1g (1000mg) 4-6 hourly adult dose (maximum 4g in 24h)

17
Q

What are the adverse effects of paracetamol? What if the patient overdoses?

A

Adverse effects are uncommon.

Hepatotoxicity if overdose. Early treatment with N-acetyl-cysteine.

Paracetamol use isnt entirely contraindicated in liver disease.

18
Q

NSAIDs. Explain…

Different NSAIDs?

How they work?

Why adverse effects may occur?

A

Aspirin, Ibuprofen, Naproxen, Indomethacin…

NSAIDs are an irreversible inhibitor of cyclo-oxygenase (COX1 and/or COX2) enzyme.

  • COX generates inflammatory mediators: prostaglandins and thromboxanes.
  • COX is widely distributed and there are different isotypes of it.
  • COX inhibitors (i.e. NSAIDs) are effective at reducing acute inflammation.

Adverse effects are due to the extension of therapeutic effects.

19
Q

What are the main NSAIDs prescribed? (3)

What are some newer COX2 inhibitors being introduced? (2)

A

ibuprofen, naproxen and diclofenac

Newer COX2 inhibitors - parecoxib and celecoxib

20
Q

What are some of the adverse effects of NSAIDs on:

GI tract?

Renal function?

Platelets?

Cardiovascular?

Respiratory?

A

GI tract: GI blood loss from minor breaches in mucosa (loss of PGE). Peptic ulceration. General GI upset, indigestion.

Renal Function: Reduction in intrarenal blood flow can cause renal failure

Platelets: COX inhibition, bleeding tendency

Cardiovascular: As a result of altered renal function, fluid retention can precipitate heart failure

Respiratory: Some ‘aspirin sensitive’ asthmatics

21
Q

Why are COX2 inhibitors sometimes preferred to COX1 inhibitors?

BUT, when are COX2 inhibitors contraindicated and why?

A

COX2 causes less bleeding as the GI tract and platelets mainly have COX1.

It is not less nephrotoxic though (kidneys)

Contraindicated in heart disease as there is the abscence of anti-platelet effects, it is slightly pro-thrombotic and there is an increased risk of MI and stroke

22
Q

What are the guidelines for taking NSAIDs before elective surgery?

A

Need to STOP taking them at least 5 days before elective surgery.

Bleeding at operation = platelet transfusion

Consider platelets if emergency surgery.

23
Q

What are 2 examples of weak opioids used for moderate-severe pain?

How do they work?

A

Codeine and dihydrocodeine.

Both are metabolised to morphine. Metabolism varies. Some people have minimal enzyme and hence less effective.

They have weak opioid effects.

24
Q

What are the adverse effects of weak opioids? Consider:

Cardiovascular?

Respiratory?

GI tract?

A
  • Cardiovascular - reduced sympathetic outflow, increased vagal tone, bradycardia, hypotension, excitation.
  • Respiratory - inhibit cough reflex, respiratory depression.
  • GI tract - reduced gastric motility, constipation, nausea and vomiting.
25
Q

What are the CNS opioid effects generally?

What are their analgesic effects on the spinal cord and brainstem?

A

They cause sedation, euphoria (dysphoria), excitation.

Spinal cord analgesia = reduced pain fibre transmission. Kappa opioid receptors.

Brainstem analgesia = reduced pain projection to higher centres. Mu opioid receptors.

They also cause respiratory depression and a reduced brainstem response to hypoxia and hypercarbia.

26
Q

How can you reverse opioid effects? When is this less effective?

A

Naloxone 400mcg intravenously = dramatic reversal of Mu receptor opioid effects.

This is far less effective on newer synthetic opioid-like substances as their effects in the CNS are less well defined.

27
Q

What does chronic opioid use / opioid dependency lead to?

A

Chronic opioid use: opioids have a reduced effect as CNS becomes more tolerant. Dose increase.

Acute withdrawal: Hypertension, tachycardia, tachypnoea, diarrhoea, sweating, anxiety, hallucinations.

Any chronic opioid medication will precipitate some withdrawal reaction if stopped suddenly.

28
Q

What are the newer oral opioids (2) and why are they being prescribed more?

What are their effects?

A

Tramadol and nefopam

As effective as codeine, less variability, much less constipation hence very frequently prescribed.

“Oramorph”is lower dose oral morphine.

Usual opioid effects: sedation, dizziness, nausea. Occasionally flushing / sweating with tramadol

29
Q

What are the adverse effects of TRAMADOL? What is the new legislation regarding it?

A

Increasing number of fatalities from tramadol overdose as it causes respiratory depression.

Dependency develops with long term use, which is difficult to withdraw.

New legislation: Controlled drug (class 3). Limit to maximum prescription. Must be signed for.

30
Q

What are some common combinations of weak opioid / paracetamol?

Why are they less popular now?

A

Co-codamol, co-proxamol, etc.

Now less popular than either nefopam or tramadol (the newer oral opioids). Need to include the paracetamol in the total 24 h maximum of 4g

Check BNF if an unfamiliar oral analgesic

31
Q

Before prescribing opioids why should you look at patient’s medical history?

A

Dependent on hepatic metabolism and renal excretion of metabolites. Some active metabolites.

Prolonged effect in liver or renal impairment

Respiratory disease, sleep apnoea, increased sensitivity

32
Q

What are some strong opioids used for severe pain? (3)

For the same efficacy, what must the oral dose be compared to the i.v. dose?

A
  • Morphine; taken either oral, s.c., i.v.
  • Diamorphine: taken either s.c., i.v.
  • Fentanyl patch (transdemal)

The oral dose is approximately 3x the i.v. dose for the same efficacy

33
Q

What are the route options for opioid administration?

A

Oral, i.v., s.c.and i.m., rectal, intrathecal, epidural, buccal, transdermal

34
Q

What is common post-operative analgesia if required?

A

If required: i.v. in recovery 2mg increments every 3 minutes until comfortable (10 to 20mg) in a recovery setting. Must be given by trained staff

Ward care: Morphine 10mg s.c. 3 hourly. This is usually co- prescribed with an anti-emetic; Ondansetron or cycizine

35
Q

How does morphine patient-controlled analgesia work?

A

Syringe driver intermittent i.v. bolus delivery initiated by patient (push button)

1mg minimum frequency every FIVE minutes

Multiple studies show that this gives approximately 1/3 dose compared to nurse administered subcutaneous morphine

36
Q

What can severe, chronic pain be treated with?

A

Oral morphine syrup or tablets.

Morphine s.c. infusion

Diamorphine s.c. infusion.

Patches: fentanyl transdermal patch (lasts 5 days), buprenorphine patch.

37
Q

What are adjuvant therapies?

A

Applied after initial therapy (particularly in cancer - adjuvant therapies would aim to suppress secondary tumour formation).

38
Q

Which 2 drugs are effective for chronic neurogenic pain? What do they do and what are their adverse effects?

A

Gabapentin and pregabalin

They reduce central transmission and pain projection.

Adverse effects: sedation, dizziness, nausea, occasionally hypotension.

39
Q

What some antidepressant drugs (3)? What do they do? What do their adverse effects affect?

A

Amitryptiline, duloxetine and citalopram.

They have useful adjuvant effects in neurogenic pain. Also have some antidepressant effects.

Adverse effects on GI and CVS.