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4TH YEAR - CPTP > Week 9 - Pain & Palliative Care > Flashcards

Week 9 - Pain & Palliative Care Flashcards

1
Q

What is step 1 of the WHO pain ladder?

A

Non-opioid analgesia

NSAIDS

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2
Q

What is step 2 of the WHO pain ladder?

A

Weak Opiods

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3
Q

What is step 3 of the WHO pain ladder?

A

strong opioids
Methadone
Oral administration
Transdermal patch

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4
Q

What is step 4 of the WHO pain ladder?

A 
Nerve block
Epidural
PCA pump
Neurolytic block therapy
Spinal stimulators
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5
Q

Name a non-opioid analgesic?

A

Paracetamol

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6
Q

What is the indication of paracetamol?

A

Indication: First line analgesic. Efficacy often under-estimated. Reduces opiate requirement and enhances quality of opiate-based analgesia.

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7
Q

What is the MoA of paracetamol?

A

Mechanism of action: Not fully understood.

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8
Q

What is the recommended dose of paracetamol?

A

Dose - 1g QDS, max 4g daily; toxicity from >75mg/kg in 24hr period. Beware use of over-the-counter preparations.

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9
Q

How can paracetamol be administered?

A

Can be given oral / PR / IV / NG

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10
Q

What is the indication of NSAIDS?

A

Indication: Inflammatory pain (arthritis etc.). Reduces opiate requirement and enhances quality of opiate based analgesia.

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11
Q

What is the MoA of NSAIDS?

A

Mechanism of Action: Act by blocking cyclo-oxygenase (COX) and hence prostaglandin synthesis. 2 types of COX:
• COX-1 routine physiological functions
• COX-2 induced by pain and inflammation

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12
Q

what are the adverse effects of NSAIDS?

A

Adverse Effects
• If you use more COX-1, you get increased GI s/e – peptic ulcer disease and GI bleeding.
• If you use more COX-2, you get increased CV s/e – MI, stroke, ischaemic cardiacdisease.
• Ipruprofen and naproxen are your safest options

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13
Q

What are the contraindications of NSAIDS?

A 
Contraindications
•	GI symptoms / peptic ulcer disease
•	Liver or renal impairment 
•	Asthmatic with aspirin sensitivity
•	Coagulation disorders/treatment
•	Caution: 
•	Cardiac failure, elderly patients, dehydration
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14
Q

Name a commonly used weak opioid?

A

Codeine, Tramadol, Dihydrocodeine
Combination therapies:
Co-codamol – Codeine and paracetamol, therefore don’t prescribe with paracetamol
Co-dydramol – Codeine and dihydrocodeine

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15
Q

What are the indications of codeine?

A

Indication: First line step 2 analgesic. Used for mild to moderate pain.

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16
Q

What is the MoA of codeine?

A

Mechanism of Action: Codeine is metabolised to morphine by CYP2D6. Metabolising capacity varies from poor to extensive

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17
Q

What are the adverse effects of codeine?

A

All patients will require laxatives.
Nausea.
Opiate toxicity.

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18
Q

What are the Pharmacodynamics of codeine?

A

Pharmacodynamics: Converted to morphine in the liver and acts on mew-opioid receptors.

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19
Q

What are the Pharmacokinetics of codeine?

A

Pharmacokinetics:
Codeine converted to morphine in the liver.
Variable expression of enzymes in the population producing poor metabolisers in whom codeine is ineffective and excess metabolisers in whom doses may easily become toxic.
• Risk of interaction with medications that affect to CP450 pathway. Codeine, norcodeine and morphine almost entirely excreted by the liver, mainly as conjugates of glucoronic acid.

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20
Q

What is the usual dose of coedine?

A

Dose: 30-60mg QDS (PO / PR / IM)

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21
Q

What conditions are important to consider when prescribing codeine?

A

Hepatic impairment: Liver is the major site of metabolic transformation may not be transformed in cirrhosis therefore may be ineffective. Contributes to manifestations of encephalopathy. Avoid in portal hypertension and encephalopathy.

Renal impairment: Effects are increased and prolonged for any given dose. Avoid if eGFR <30 and/or reduced dose, start low and go slow.

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22
Q

What should you prescribe with codeine?

A

Extremely constipating therefore should be automatically prescribing a regular and prn laxative with codeine.

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23
Q

What are the indications of tramadol?

A

Indication: Most commonly used following bowel surgery. Also frequently used for patients with chronic pain.

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24
Q

What is the MoA of tramadol?

A

Synthetic opioid with multiple active metabolites. Effects not totally reversed by Naloxone.

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25
Q

What is the usual dose of tramadol?

A

Dose: 50-100mg QDS (PO / IV)

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26
Q

When is tramadol most commonly prescribed?

A

Used following bowel surgery as less constipating. Used in chronic pain as less sedating/respiratory depression. Mood boost as well as pain control.

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27
Q

What are the Pharmacodynamics of tramadol?

A

Pharmacodynamics: Inhibits serotonin and nor-epinephrine re-uptake (sympathetic effects, cholinergic inhibitor). NMDA receptor antagonist, 5-HT2c receptor antagonist, Nicotine Ach receptor antagonist, TRPV1 receptor antagonist, M1/M3 receptor antagonist.

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28
Q

What are the Pharmacokinetics of tramadol?

A

Pharmacokinetics: Undergoes hepatic metabolism via the CP450 iso-enzyme. As with codeine 6% of the population have reduced CYP2D6 activity and will therefore have reduced analgesic effect. Phase II hepatic metabolism renders the metabolite soluble and excreted by the kidney.

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29
Q

When are opioids contraindicated?

A
  • Severe renal / hepatic failure
  • Raised intra-cranial pressure
  • Severe respiratory depression
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30
Q

What are the common side effects of opioids?

A
  • Nausea and vomiting
  • Drowsiness/Respiratory depression
  • Pruritus
  • Hallucinations
  • Urinary retention
  • Pinpoint pupils
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31
Q

What makes up co-codamol?

A

Codeine and paracetamol, therefore don’t prescribe with paracetamol

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32
Q

What makes up co-dydramol?

A

Codeine and dihydrocodeine

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33
Q

Whats a severe risk in tramadol use?

A

Serotonin syndrome

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34
Q

When is tramadol not used?

A

Cirrhosis –> not as effective due to competitive antagonism, therefore doesn’t produce active metabolites. Avoid in portal HTN.
Renal impairment –> effects prolonged. Avoid if eGFR is below 30.

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35
Q

What is the most common strong opioid?

A

Morphine

36
Q

What are the indications of morphine?

A

Indication: severe acute pain and chronic pain that has not responded to step 1 and 2 of the analgesic ladder.

37
Q

What is the MoA of morphine?

A

Acts on µ-opioid receptors in the CNS

38
Q

What are the Pharmacokinetics of morphine?

A

Pharmacokinetics: Extensive first pass metabolism so only 40-50% taken PO reaches the CNS. Phase II glucoronidation (UDP glucoronyltransferase) in the liver producing morphine-3-glucoronide (no analgesic effect, 60%) and morphine-6-glucoronide (active metabolite). Glucoronidation also takes place in CNS and kidney. Also small amounts of normorphine, codiene and hydromorphone are produced. Poor lipid solubility so difficult to pass blood brain barrier (diacetlymorphine is lipid soluble). Metabolites are eliminated by renal excretion.

39
Q

What are the Pharmacodynamics of morphine?

A

Pharmacodynamics: Opioid receptor agonist. Strongest affinity to µ-opioid receptors (analgesia, sedation, euphoria, physical dependence and respiratory depression). Also ĸ-opioid (spinal analgesia, miosis) and đ-opioid (analgesia).

40
Q

What are the side effects of morphine?

A 
Respiratory depression
•	Sedation
•	Euphoria
•	Pupil constriction
•	Nausea and vomiting
•	Reduced gut motility / constipation
•	Pruritus
•	Hypotension
•	Bronchospasm
•	Urinary retention
41
Q

What is the recommended break through dose for morphine?

A

1/6th-1/10th of total regular dose in 24hours

42
Q

Apart from morphine, name some other opiates and how they can be administered…

A

Diamorphine (IV / SC) (try and use less of this now, its heroin)
Oxycodone (PO/SC/IV)
Hydromorphone (PO/SC/IV)
Fentanyl (IV / Lozenge / Patch – used commonly as a patch)

43
Q

How can morphine be administered?

A

Morphine (PO / NG / NJ / IV / PR / SC)

44
Q

What receptors does morphine work on?

A

Acts on µ-opioid receptors in the CNS

45
Q

How often should you prescribe immediate release morphine and modified release morphine?

A

Immediate release morphine - 4 hrly

Modified release morphine - 12 hrly

46
Q

What are the features of opiate toxicity?

A

Features: myoclonic jerks, pin-point pupils, hallucinations, confusion, reduced RR.

47
Q

What is the antidote for opiate toxicity?

A

Naloxone

48
Q

Name some adjuvant analgesia to be used along the WHO pain ladder?

A

corticosteroids - Dexamethasone

Antidepressant/Anticonvulsant - Amitriptyline, Gabapentin, Pregabalin

muscle relaxants - Baclofen, Diazepam

bisphosphonates - Ibandronic Acid, Pamidronate, Zolendronic Acid

antispasmodics - Hyoscine Butylbromide (Buscopan)

49
Q

When would you add Corticosteroids to other analgesia on the WHO pain ladder?

A

Raised ICP, nerve compression, liver capsule pain, soft tissue infiltration.

50
Q

When would you add Antidepressant/Anticonvulsant to other analgesia on the WHO pain ladder?

A

Neuropathic pain

51
Q

When would you add muscle relaxants to other analgesia on the WHO pain ladder?

A

Muscle spasm/cramp

52
Q

When would you add bisphosphonates to other analgesia on the WHO pain ladder?

A

Bone pain

53
Q

When would you add antispasmodics to other analgesia on the WHO pain ladder?

A

Bowel colic, Bladder spasm

54
Q

Name a corticosteroid…

A

Dexamethasone

55
Q

Name a Antidepressant/Anticonvulsant…

A

Amitriptyline, Gabapentin, Pregabalin

56
Q

Name a muscle relaxants…

A

Baclofen, Diazepam

57
Q

Name a bisphosphonates…

A

Ibandronic Acid, Pamidronate, Zolendronic Acid

58
Q

Name a antispasmodics…

A

Hyoscine Butylbromide (Buscopan)

59
Q

What drug would you add to normal analgesia if the patient was experiencing - Raised ICP, nerve compression, liver capsule pain, soft tissue infiltration?

A

Corticosteroids - Dexamethasone

60
Q

What drug would you add to normal analgesia if the patient was experiencing - Neuropathic pain?

A

Antidepressant/Anticonvulsant - Amitriptyline, Gabapentin, Pregabalin

61
Q

What drug would you add to normal analgesia if the patient was experiencing - Muscle spasm/cramp?

A

muscle relaxants - Baclofen, Diazepam

62
Q

What drug would you add to normal analgesia if the patient was experiencing - Bone pain?

A

bisphosphonates - Ibandronic Acid, Pamidronate, Zolendronic Acid

63
Q

What drug would you add to normal analgesia if the patient was experiencing - Bowel colic, Bladder spasm?

A

antispasmodics - Hyoscine Butylbromide (Buscopan)

64
Q

What are the 5 symptoms you need to worry about at end of life?

A 
o	Pain
o	Breathlessness
o	Nausea/vomiting
o	Agitation
o	Excess secretions
65
Q

What is the recommended pharmacological treatment at the end of life - for Pain and breathlessness?

A

Prescribing at the end of life: Pain and breathlessness
• eGFR >30
o 2.5mg Morphine SC, every hour, prn pain/breathlessness (if 3 consecutive doses are ineffective then seek advice)
• eGFR ≤30
o 100 micrograms Alfentanil SC, every hour, prn pain/breathlessness (if 3 consecutive doses are ineffective then seek advice)

66
Q

What is the recommended pharmacological treatment at the end of life - for Nausea and vomiting?

A

Prescribing at the end of life: Nausea and vomiting
• eGFR >30
o 50mg Cyclizine SC, 8 hourly, prn nausea/vomiting (MAX 150mg in 24 hours).
• eGFR ≤30
o 1mg Haloperidol SC, 4 hourly, prn nausea/vomiting (if 2 consecutive doses are ineffective then seek advice). Review after 24 hours, if effective consider regular dose of 2.5mg SC nocte.

67
Q

What is the recommended pharmacological treatment at the end of life - for Agitation?

A

Prescribing at the end of life: Agitation
• Any renal function
o 2.5 mg Midazolam SC, every hour, prn agitation (if 3 consecutive doses are ineffective then seek advice)

68
Q

What is the recommended pharmacological treatment at the end of life - for Excess secretions?

A

Prescribing at the end of life: Excess secretions
• eGFR>30
o 400 micrograms Hyoscine Hydrobromide SC, every hour, prn excess respiratory secretions (MAX 2.4mg in 24 hours)
• eGFR≤ 30
o 20mg Hyoscine Butylbromide SC, every hour, prn excess respiratory secretions (MAX 120mg in 24 hours)

69
Q

What is the Effect of renal disease on Drug ABSORPTION?

A
  • Alter drug absorption because of increased gastric pH and oedema in intestinal mucosa (e.g. Nephrotic syndrome)
  • Reduce bioavailability of drugs
70
Q

What is the Effect of renal disease on Drug DISTRIBUTION?

A

Reduced protein binding occurs when renal function is impaired for the following reasons:
1. Reduction in serum albumin concentration.
2. Structural changes in binding sites.
3. Displacement of drug from albumin binding sites by organic molecules that accumulate in uremia.
• Often results in larger apparent Vd (volume distribution) of a drug
o Less binding → more free drug for the same dose → this is more available to go into other tissues → cause a pharmacodynamics effect (drug to the body).

71
Q

What is the Effect of renal disease on Drug METABOLISM?

A
  • The impact of impaired renal function on drug metabolism is dependent on the metabolic pathway
  • Most drugs are not excreted by the kidneys unchanged but are biotransformed to metabolites that are then excreted.
  • Renal failure slow the excretion of metabolites.
  • Elimination half-life is increased → drug has more effect in the body
72
Q

What is the Effect of renal disease on Drug ELIMINATION?

A

• The effect of renal disease on the elimination of a drug depends on the renal status of the patient and the elimination characteristics of the drug.
• For many drugs CLE consists of renal(CLR ) and non renal(CLNR ) components.
o CL E = CL R + CL NR
• Non renal excretion includes Biliary excretion, Pulmonary excretion, salivary excretion etc.
• In renal disease, the renal clearance and elimination rate are reduced

73
Q

What drugs cause pre-renal damage?

A

o Any drug that cause hypotension can increase pre-renal damage, because they reduce renal perfusion.
o ACE Inhibitor

74
Q

Which drugs cause intrarenal damage?

A 
o	Aminoglycoside (Gentamicin)
o	Amphotericin
o	NSAIDs
o	Penicillins/ Cephalosporins
o	Phenytoin
o	Rifampicin
o	Sulphonamides
75
Q

Which drugs cause post-renal damage?

A

o Acetazolamide
o Anticholinergics
o Methotrexate

76
Q

How do you calculate renal clearance?

A

CLR = Rate of urinary excretion / Plasma drug concentration

CLR = (Rate of filtration + Rate of secretion – Rate of reabsorption) / Plasma drug concentration

77
Q

How do you calculate creatine clearance?

A

CLR = Rate of urinary excretion of creatinine / Average serum creatinine concentration
• Normal value = 100-125 ml /min
• Moderate renal failure = 20-50ml/min
• Severe renal failure = < 10 ml/min

78
Q

What is the impact of renal disease on pharmacodynamics?

A

o Reduced renal excretion of a drug or its metabolites may cause toxicity
o Increased sensitivity to some drugs
o Many side-effects are tolerated poorly by patients with renal impairment
o Some drugs are not effective when renal function is reduced

79
Q

Why does ‘normal’ creatinine value change in different people?

A

Creatinine is the function of your muscle mass. If a normally muscular person has a normal creatinine = normal renal function. If someone who is cachectic (starved, 0 muscle) has a normal creatinine, then it means there renal function is poor (i.e its hiding a raised creatinine purely because they have no muscle). So be aware of frail patients with normal creatinine, it doesn’t necessarily mean normal renal function.

80
Q

What are the principles of prescribing in renal disease?

A

Reducte dose depending on the level of renal function

Avoid taking nephrotoxic drugs if possible

Total daily maintenance dose may be reduced by reducing individual doses or the dosing interval may be increased between doses

Loading dose is usually the same

81
Q

What is the calculation for adjusting doses in renal impairment?

A

Corrected dose
= (Normal dose x patient’s creatinine clearance)/
Normal Creatinine clearance

82
Q

Why does tramadol cause serotonin syndrome and when is it more likely?

A

Has 5-HT agonist activity and may cause serotonin syndrome in combination with SSRI/SSNRI

83
Q

What are the best options for neuropathic pain management?

A

Tricyclic antidepressants e.g. amitriptyline

SSRIs and SNRIs
• Less effective than TCADs

Gabapentin

Pregabalin
• First line with amitriptyline in NICE recommendations

Ketamine

Lidocaine patches

84
Q

What are the side effects of SNRI/SSRIs?

A

GI upset, weight gain

85
Q

Whats the MoA of TCAs?

A

Central and peripheral action on histamine, muscarinic and serotonergic receptors

86
Q

Whats the MoA of SNRIs/SSRIs?

A

Reduce reuptake of serotonin/noradrenaline

87
Q

Whats the MoA of Gabapentin/pregabalin?

A

Acts on Ca channels

4TH YEAR - CPTP (19 decks)

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