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MSRA Content > BASIC - PAIN & PALLIATIVE CARE > Flashcards

BASIC - PAIN & PALLIATIVE CARE Flashcards

1
Q

Name of strong opioids?

A

Morphine, diamorphine, Oxycodone

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2
Q

4 indications for strong opioids?

A
  • Acute pain relief – ACS, post-operative
  • Chronic pain relief – Step 3 of ladder
  • Relieve breathlessness in palliative care
  • Acute pulmonary oedema (along with oxygen, furosemide, nitrates)
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3
Q

Mechanism of action for strong opioids?

How is oxycodone different?

A
  • Activation of opioid u (mu) receptors in CNS
  • Reduces neuronal excitability and pain transmission
  • In medulla – blunt response to hypoxia and hypercapnoea – reducing respiratory drive
  • Reduce SNS activity
  • Oxycodone is synthetic analogues of morphine
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4
Q

Adverse effects of strong opioids?

A 
o	Nausea and vomiting
o	Constipation
o	Pupillary constriction
o	Skin – itching, vasodilation, sweating
o	Respiratory depression
o	Neurological depression
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5
Q

Can you develop tolerance and dependence in strong opioids?

A 
o	Tolerance does develop and may need to higher the dose over time
o	Dependence apparent with cessation
	Anxiety, pain, breathlessness
	Dilated pupils, skin cool and dry
o	Not a problem in therapeutic doses
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6
Q

Symptoms of toxicity in strong opioids?

A 
o	Persistent nausea and vomiting
o	Drowsiness
o	Confusion
o	Visual Hallucinations
o	Myoclonic jerks
o	Respiratory Depression 
o	Pinpoint pupils (not always useful if on long term)
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7
Q

When should dose reduction be done in strong opioids? What caution must you have?

A
  • Dose reduction in hepatic failure and renal impairment and in elderly
  • Do not give in respiratory failure except in palliative care
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8
Q

Avoid strong opioids when? Why?

A
  • Avoid in biliary colic – may cause spasm in sphincter of Oddi (use pethidine)
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9
Q

What other drugs should you avoid ideally with strong opioids?

A
  • Ideally avoid with other sedating drugs (antipsychotics, benzodiazepines, TCAs)
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10
Q

Route of administration of strong opioids in acute and chronic setting?

A

o In acute setting – given IV

o Chronic pain – oral, IM, SC available

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11
Q

What is oral morphine available as?

A
  • Normal/Immediate release tablets and liquid – lasts 4 hours e.g. Oramorph
  • Modified/Slow release tablets, granules, capsules – lasts 12 hours e.g. morphine sulphate tablets (MSTs), Zomorph capsules
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12
Q

When would modified release morphine be used?

A

o Modified release morphine prescribed in regular treatment

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13
Q

What is an appropriate dose of MR morphine? When would the dose be reduced?
How much % increase needed if not adequate?

A

 Dose usually MST 20mg bd appropriate as Step 3
• Elderly, frail or renal impairment patients (fentanyl used in renal excretion) may need lower doses
• Titrate dose up by 30-50% increments to relieve pain

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14
Q

For breakthrough pain, how much IR morphine given?

A

1/10-1/6 of the total daily regular dose in the PRN

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15
Q

What names would you use in prescription?

A

Brand name prescribing for strong oral opioids

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16
Q

What needs communicating to patient? (4)

A

o Explain that it is a highly effective painkiller and that ‘addiction’ is not an issue when it is used for pain control
o Warn patients that the dose may need to be increased over time as they become tolerant to its effects; this is normal and should not cause alarm
o Offer antiemetic (metoclopramide) and laxative (co-danthrusate or movicol)
o Do not operate heavy machinery or drive if feel drowsy or confused

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17
Q

When would you review strong opioid prescription?

A

o Review in 1-2 weeks to assess effectiveness

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18
Q

When given parenternally, what is the potency of MS and diamorphine?
What dose should be given of diamorphine then?

A

 Parenteral diamorphine 3 times more potent than oral morphine
 Parenteral MS is 2 times more potent
 Total 24-hour SC continuous infusion diamorphine dose should be 1/3 of total 24-hour oral morphine dose

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19
Q

Which strong opioids are given transdermally?

What do they look like?

A

o Fentanyl transdermal patches last 72 hours (can have buprenorphine patches)
 Suitable for severe chronic pain already stabilised on other opioids
 Buprenorphine looks like plaster and fentanyl is clear patch

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20
Q

When oxycodone used, what are the MR and IR names?

A

• Immediate release (oxynorm) and slow release (oxycontin)

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21
Q

Name of weak opioids?

A

Codeine, co-codamol, dihydrocodeine

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22
Q

Indications of weak opioids?

A
  • Step 2 on WHO analgesic ladder when simple analgesia (paracetamol) is insufficient
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23
Q

Metabolism of weak opioids? Mechanism of weak opioids? Why is codeine sometimes not effective?
Tramadol is what?

A
  • Metabolised in liver to produce small amounts of morphine (from codeine) or dihydromorphine (dihydrocodeine)
  • Agonists of opioid u (mu) receptors
  • 10% of Caucasians has less active form of key metabolising enzyme (CYP450 2D6) so may be ineffective
  • Tramadol is synthetic analogue of codeine, also a 5-HT and NA reuptake inhibitor – not a great drug
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24
Q

Side effects of weak opioids?

A
  • Nausea
  • Constipation
  • Dizziness
  • Drowsiness
  • Neurological and respiratory depression
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25
Q

Interactions of weak opioids? When should tramadol not be used?

A
  • Ideally do not combine opioids and other sedating drugs (antipsychotics, benzodiazepines, TCAs)
  • Tramadol should not be used with drugs that lower seizure threshold (SSRIs, TCAs)
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26
Q

Contraindications of weak opioids?

A
  • NEVER GIVE CODEINE OR DIHYDROCODEINE IV – histamine anaphylaxis
  • Acute respiratory depression, comatose patients
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27
Q

When are weak opioids used in caution and dose reduction necessary?

A
  • Both renal and hepatic impairment – dose reduction

- Tramadol lowers seizure threshold – caution in epilepsy

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28
Q

Prescription of weak opioids? Typical codeine starting dose?

Any other considerations?

A
  • Can be prescribed orally, IM
  • Starting dose – codeine 30mg orally 4-hourly
  • Consider prescribing laxative (Senna) for regular administration
  • Should be withdrawn gradually to avoid symptoms
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29
Q

Communication to patient about weak opioids?

A
  • Advise patients to avoid driving or operating heavy machinery if they become drowsy or confused while taking the new painkiller
  • Mention that painkillers should always be stored out of reach of children
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30
Q

Review of weak opioids?

A
  • Review after 1-2 weeks and assess need to move up and down ladder
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31
Q

What strengths does co-codamol come in? Typical starting dose of Step 2 on WHO ladder?

A
  • Co-codamol comes in 3 strengths:
    o 8mg codeine and 500mg paracetamol
    o 15mg codeine and 500mg paracetamol
    o 30mg codeine and 500mg paracetamol
  • Prescribe codeine 30mg when progressing from ‘Step 1’
  • Paracetamol can be given with opioids too
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32
Q

Indications of paracetamol?

A
  • 1st line analgesic for acute and chronic pain

- Antipyretic

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33
Q

Mechanism of paracetamol?

A
  • Weak cyclooxygenase (COX) inhibitor, involved in prostaglandin metabolism
  • Increase pain threshold and reduce (PGE2) concentrations in thermoregulatory region, controlling fever
  • Specifically, COX-2 isoform (inflammation) rather than COX-1 isoform (protecting gastric mucosa, regulating renal blood flow and clotting)
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34
Q

Adverse effects of paracetamol?

A

Few

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35
Q

Normal metabolism of paracetamol? What happens in overdose of paracetamol? Treated with?

A
  • Overdose – liver failure
    o Metabolised by CYP450 enzymes to toxic N-acetyl-p-benzoquinone imine (NAPQI) which is conjugated with glutathione before elimination
    o NAPQI accumulation causes hepatocellular necrosis
    o Treated with acetylcysteine (depending on plasma paracetamol level, <12 hours and not vomiting) and activated charcoal (if <4 hours)
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36
Q

Dose reduction in paracetamol?

A
  • Dose reduced in liver toxicity
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37
Q

Cautions about use of paracetamol?

A

o Chronic excessive alcohol use
o Malnutrition
o Low body weight
o Hepatic impairment

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38
Q

Which drugs increase rate of NAPQI production in overdose?

A
  • CYP450 inducers
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39
Q

Prescription of paracetamol?

A
  • Oral paracetamol can be purchased in retail outlets
  • Regular administration or PRN
  • Available as tablets, caplets, capsules, soluble tablets or oral suspensions
  • IV is possible
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40
Q

Communication to patient about paracetamol?

When should effects be felt?

A
  • Effects should be felt around half an hour after taking it
  • Warn them not to exceed the recommended maximum daily dose because of the potential risk of liver poisoning
  • Advise them that many medicines purchased from the chemist (e.g. cold and flu preparations) contain paracetamol
  • Warn them to check the label
41
Q

Typical paracetamol dose?

A

0.5-1g every 4-6 hours, maximum 4g per day

42
Q

Name of NSAIDs

A

Ibuprofen, diclofenac, etoricoxib

43
Q

Indications of NSAIDs?

A
  • PRN for mild-to-moderate pain

- Regular treatment of pain related inflammation

44
Q

Mechanism of NSAIDs?

How is etoricoxib different?

A
  • Inhibit synthesis of prostaglandins from arachidonic acid by inhibiting cyclooxygenase (COX
  • COX-1 stimulates prostaglandin synthesis essential to preserve gastric mucosa, maintain renal perfusion (by dilating afferent glomerular arterioles) and inhibit thrombus formation at the vascular endothelium
  • COX-2 expressed in response to inflammatory stimuli stimulates production of prostaglandins that cause inflammation and pain
  • Therapeutic benefits of NSAIDs are principally COX-2 inhibition and adverse effects by COX-1 inhibition
  • Selective COX-2 inhibitors (e.g. etoricoxib) developed to reduce the adverse effects
45
Q

SE of NSAIDs?

A
  • GI toxicity
  • Renal impairment
  • Increased risk of MI/CVA
  • Fluid retention
46
Q

Interactions of NSAIDs in:
GI ulceration
GI bleed
Renal impairment

A 
-	GI Ulceration
o	Aspirin, corticosteroid
-	GI bleeding
o	Anticoagulants, SSRIs, venlafaxine
-	Renal Impairments
o	ACEi, diuretics
47
Q

Contraindications of NSAIDs

A

o Severe renal impairment
o Heart Failure
o Liver failure

48
Q

Cautions of NSAIDs in prior history of?

A

o Peptic ulcer disease
o GI bleeds
o CVD

49
Q

Prescription of NSAIDs?

A
  • Available as tablets, suspensions, gels, suppositories, injectable
  • Acute pain treatment should be stopped when resolved
  • Taken with food to minimise GI upset
50
Q

Communication to patients about NSAIDs?
Any time you should stop NSAIDs?
What other meds could be prescribed?

A
  • Warn patients that the most common side effect is indigestion and advise them to stop treatment and seek medical advice if this occurs
  • For patients with acute pain, explain that long-term use, e.g. beyond 10 days, is not recommended due to the risk of side effects
  • Advise patients requiring long-term treatment (particularly if they have renal impairment) to stop NSAIDs if they become acutely unwell or dehydrated to reduce the risk of damage to the kidneys
  • Can use gastroprotection for patients at increased risk
51
Q

Names of antimuscarinics? (antispasmodics)

A

Hyoscine butylbromide (Buscopan)

52
Q

Indications of antimuscarinics?

A
  • IBS
  • Colicky pain in cancer
  • Palliative care - Reduce copious respiratory secretions (death rattle)
53
Q

Mechanism of antimuscarinics?

What are the effects?

A
  • Competitive inhibitor of Ach
  • Blocks the parasympathetic ‘rest and digest’ effects so:
    o Increase HR and conduction
    o Reduces smooth muscle tone
    o Reduces peristaltic contraction
    o Relax pupillary constrictor and ciliary muscles preventing accommodation
54
Q

SE of antimuscarinics?

A
  • Tachycardia
  • Dry mouth
  • Constipation
  • Urinary retention
  • Blurred vision
55
Q

Contraindications of antimuscarinics?

A

Avoid

  • GI obstruction
  • Urinary retention
  • Arrhythmias
56
Q

Cautions in antimuscarinics?

A

Caution

- Angle-closure glaucoma

57
Q

Interactions of antimuscarinics?

A
  • Adverse effects enhanced with other antimuscarinics e.g. TCAs
58
Q

How are antimuscarinics given?

A
  • Usually given SC, either by injection or syringe driver
59
Q

Typical hyoscine dose in palliative care?

A

SC 20mg every 4 hours PRN, can be adjusted up to 20mg every hour
Syringe driver - 20-120mg/24 hours

60
Q

Name of 5-HT antagonist antiemetics?

A

Ondansetron, granisetron

61
Q

Indications of 5-HT antagonists?

A
  • Nausea and vomiting – prophylaxis and treatment

- Particularly chemotherapy

62
Q

Mechanism of 5-HT antagonists?

A
  • 5-HT3 antagonists in the CTZ and gut

- Particularly good at stopping emetogenic substances in blood causing nausea

63
Q

SE of 5-HT antagonists?

A
  • Constipation, diarrhoea, headaches
64
Q

Contraindications of 5-HT antagonists?

A
  • Prolonged QT interval
65
Q

Which drugs should be avoided and why?

A

Avoid in drugs that prolong QT interval:

- Antipsychotics, amiodarone, ciprofloxacin, macrolides, quinine, SSRIs

66
Q

Prescription of 5-HT antagonists?

A
  • Oral, rectal or IV administration - 8mg BDS for 5 days starting before chemotherapy
  • Dose to be taken an hour before symptoms anticipated if oral (IV immediately)
  • Expensive so only used for chemotherapy N&V
67
Q

Names of phenothiazine antiemetics?

A

Levomepromazine, prochlorperazine

68
Q

Indications of phenothiazine antiemetics?

A
  • Nausea and vomiting treatment and prophylaxis

- First generation antipsychotic

69
Q

Mechanisms of phenothiazine antiemetics?

A
  • Blockage of D2 receptors in CTZ and gut, H1 and Ach in vomiting centre and vestibular system
70
Q

SE of phenothiazine antiemetics?

A
  • Drowsiness
  • Postural hypotension
  • Extrapyramidal syndromes – acute dystonic reaction and tardive dyskinesia
  • Prolong QT interval
71
Q

Contraindications of phenothiazine antiemetics?

A

o Severe liver disease

o Prostatic hypertrophy

72
Q

Which drugs should be avoided and why?

A
  • Drugs that prolong QT interval

o Antipsychotics, amiodarone, ciprofloxacin, macrolides, quinine, SSRIs

73
Q

When is this prescribed? What monitoring is needed?

A 
Prescribing
-	Specialist advice usually needed
Monitoring
-	Prolactin baseline and 6 months, then yearly
-	EPSE
74
Q

Typical dose of levomepromzine?

A

Oral - 6mg OD at bed

Syringe Driver - 5-25mg/24 hours

75
Q

Names of H receptor antagonists antiemetics?

A

Cyclizine, promethazine

76
Q

Indications of H antagonists?

A
  • Prophylaxis and treatment of nausea and vomiting
    o Palliative care – cerebral and cerebellar problems
    o Motion sickness and vertigo
77
Q

Mechanism of H antagonists?

A
  • Blockage of the Histamine-1 and acetylcholine receptors predominate in vomiting centre and communication with vestibular system
78
Q

SE of H antagonists?

A
  • Drowsiness (cyclizine least drowsy)
  • Anticholinergic – dry mouth, throat, blurred vision, constipation
  • IV - tachycardia
79
Q

Contraindications of H antagonists?

A
  • Hepatic encephalopathy

- Prostatic hypertrophy (develop urinary retention)

80
Q

Interactions with H antagonists?

A
  • Sedation – benzodiazepines, opioids

- Anticholinergics increased with ipratropium or tiotropium

81
Q

Prescription of H antagonists? Typical dose?

What communication is needed?

A
  • Given orally, IV, IM
  • Typical prescription 50mg 8-hourly PRN (syringe driver 150mg/24 hours)
  • Communication
    o May affect driving and skills tasks
82
Q

Name of dopamine antagonists antiemetics?

A

Metoclopramide, domperidone

83
Q

Indications of dopamine antagonist antiemetics?

A
  • Prophylaxis and treatment of nausea and vomiting in reduced gut motility
  • Palliative care – Nausea and vomiting due to gastric stasis and irritation, hiccups
84
Q

Mechanism of dopamine antagonist antiemetics?

A
  • D2 receptor is main receptor in chemoreceptor trigger zone (CTZ)
  • Dopamine promotes relaxation of stomach and LOS and inhibits gastroduodenal coordination
  • Blocking D2 has prokinetic effect
85
Q

SE of dopamine antagonist antiemetics?

Why does domperidone not have some of these effects?

A
  • Diarrhoea
  • Metoclopramide
    o Extrapyramidal syndromes – acute dystonic reaction (facial and skeletal muscle spasms)
    o Galactorrhoea, gynaecomastic
  • Domperidone does not cross BBB
86
Q

Contraindications of dopamine antagonist antiemetics?

A
  • Children and young adults
  • Parkinson’s (Metoclopramide)
  • Gastrointestinal obstruction/perforation, 3-4 days after GI surgery
87
Q

Caution in dopamine antagonist antiemetics?

A
  • Reduce dose in renal and hepatic impairment
88
Q

Interactions of dopamine antagonists antiemetics?

A
  • Risk of EPSE increased with antipsychotics

- Do not combine with dopaminergic agents for Parkinson’s - antagonise

89
Q

Prescription of dopamine antagonist antiemetics?

A

o Short term use – 5 days
o Dose 10mg up to TDS
o Metoclopramide available IV/IM and orally

90
Q

What monitoring should be done in dopamine antagonists antiemetics?

A

o Monitor extrapyramidal symptoms if prolonged use

91
Q

Name of neuropathic agents?

A

Gabapentin, pregabalin

92
Q

Indications of gabapentin/pregabalin?

A
  • Focal epilepsies (if carbamazepine and other antiepileptics not adequate)
  • Neuropathic pain (diabetic nephropathy, palliative/cancer neuropathic pain)
  • Migraine prophylaxis (Gabapentin)
  • GAD (pregabalin)
93
Q

Mechanism of gabapentin/pregabalin?

A
  • Gabapentin is closely related to GABA neurotransmitter
  • Binds to voltage-sensitive calcium (Ca2+) channels, preventing inflow of Ca and neurotransmitter release
  • Reduces neuronal excitability
  • Pregabalin is structural analogue of gabapentin
94
Q

SE of gabapentin/pregabalin?

A
  • Drowsiness
  • Dizziness
  • Ataxia
  • Usually improve over first few weeks
95
Q

When is dose reduction needed in gabapentin/pregabalin?

A
  • Dose reduced in renal impairment
96
Q

Interactions of gabapentin/pregabalin?

A
  • Sedative effects enhanced when combined with sedating drugs (benzos)
97
Q

Prescription of gabapentin/pregabalin?

A
  • Oral, start at low dose and increase over weeks

- Appropriate escalating-dose regimens are listed in the BNF

98
Q

What to avoid when on gabapentin/pregabalin?

A
  • Avoid driving or operating machinery until confident side effects have settled

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