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Cancer kanser wtv > pain mgmt > Flashcards

pain mgmt Flashcards

1
Q

Types of pain?

A

Nociceptive, Neuropathic, Referred, Ischemic

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2
Q

Duration to consider pain - “chronic pain”

A

4-6 weeks, to some 3 months

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3
Q

What are the stages to nociceptive pain?

A

Transduction, Transmission, Modulation, Perception

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4
Q

Types of nociceptive pain?

A

Somatic, Visceral

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5
Q

What is somatic pain described as?

A

Throbbing, aching, stabbing. Localized to injury site and constant

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6
Q

What are the stimulus that cause somatic pain?

A

Chemical, mechanical, thermal

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7
Q

What fibres are the nociceptive pain signals carried by?

A

Small myelinated A-Delta fibres (for mechanical and thermal stimulus)
C fibres to the dorsal horn of spinal cord (for all type types of pain stimulus)

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8
Q

What are visceral pain mediated by?

A

Stretch receptors

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9
Q

What is visceral pain described as?

A

Dull, gnawing, cramping. Poorly localised

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10
Q

What causes neuropathic pain?

A

Damage to nerves due to diseases or treatment

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11
Q

What are the types of neuropathic pain?

A

Peripheral, Central

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12
Q

What is the pathophysiology of peripheral neuropathic pain

A

Abnormal nerve generation + Nerve sprouts formation

Ectopic neuronal pacemaker formation

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13
Q

What is the pathophysiology of central neuropathic pain?

A

Reorganisation of central somatosensory processing leading to

1) Deafferentation of pain
2) Sympathetically maintained pain

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14
Q

How is neuropathic pain described?

A

Tingling, numbing, electric shock-like, burning, prolonged

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15
Q

How is referred pain described as?

A

Pain is located away from point of origin

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16
Q

What causes referred pain?

A

Signal from different pain of the body travels along the same pathway going to the spinal cord and the brain

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17
Q

What causes Ischemic pain ?

A

Loss of blood flow to tissue, lack of perfusion, leading to tissue hypoxia and damage

Tissue hypoxia causes the release of inflammatory mediators and chemicals that stimulate the nociceptors.

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18
Q

Autonomic signs associated with pain?

A

Increased RR, HR, BP and diaphoresis

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19
Q

What are the components of SOCRATES framework?

A

Site, Onset, Character, Radiation, Associations, Time course, Exacerbating/Relieving factors, Severity

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20
Q

What are assessment tools use to assess pain?

A

FLACC scale, Wong-Baker Faces rating scale, Numerical rating scale, Visual analog scale, Adjective rating scale, McGill Pain Questionnaire

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21
Q

What are the pharmacological therapies available for pain?

A

Non-opioids analgesics, Opioids analgesics, Nerve blocks, Adjuvant analgesics

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22
Q

What are the electrical stimulation therapies available for pain?

A

Transcutaneous electrical nerve stimulation (TENS)

Percutaneous electrical nerve stimulation (PENS)

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23
Q

What are the alternative therapies available for pain?

A

Acupuncture, physiotherapy, chiropratic, surgery

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24
Q

What are the pharmacologic treatments suggested by WHO ladders?

A

Mild pain - Non-opioids +/- adjuvants
Moderate pain - Weak opioids +/- adjuvants
Severe pain - Strong opioids +/- adjuvants

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25
Q

What are recommendations made by WHO for management of cancer pain?

A

1) Oral administration of analgesic (if possible)
2) Analgesics should be given at regular intervals
3) Dosing of pain medication should be adapted to the individual
4) Analgesic should be prescribed according to pain intensity as evaluated by a scale of intensity of pain
5) Analgesics should be prescribed with a constant concern for detail

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26
Q

Pharmacological options for mild pain?

A

Acetaminophen, NSAIDs (1st line: Ibuprofen)

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27
Q

Benefits of COX-2 selective NSAIDs?

A

Lesser GI side effects, no platelet inhibition

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28
Q

What are the uses of adjuvants?

A

Co-administered to improve analgesia

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29
Q

Adjuvants used for neuropathic pain?

A

Gabapentin, Pregabalin, Antidepressants, Antiepileptics, Topical lidocaine, Corticosteroids

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30
Q

Adjuvants used for bone pain?

A

NSAIDs, Corticosteroids, Bisphosphonates

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31
Q

Adjuvant used for intestinal colic?

A

Hyoscine butylbromide

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32
Q

Adjuvant used for muscle cramps/ spasms?

A

Muscle relaxants, benzodiazepines

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33
Q

Corticosteroid is an adjuvant indicated for?

A

Bone pain, neuropathic pain, raised intracranial pressure pain, liver capsule stretch pain

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34
Q

MOA of opioids?

A

Modifies central perception of pain by binding to Mu-1, Mu-2, Kappa and Delta opioid receptors

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35
Q

Examples of Weak opioids?

A

Codeine, Tramadol

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36
Q

Examples of Moderate opioids?

A

Tapentadol

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37
Q

Examples of Strong Opioids?

A

Morphine, Fentanyl, Oxycodone, Pethidine, Methadone

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38
Q

Conversion of PO codeine to PO morphine?

A

10:1 , 100 mg of PO codeine = 10 mg of PO morphine

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39
Q

Codeine is a substrate of?

A

CYP2D6, CYP3A4

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40
Q

DDIs of Codeine?

A

CYP2D6 inhibitors such as Chlorpromazine, Fluoxetine can decrease the effects of codeine

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41
Q

Indication for Codeine?

A

Moderate pain

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42
Q

Indication of Tramadol

A

Moderate pain

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43
Q

MOA of Tramadol

A

Opioid receptor agonist, inhibitor of noradrenaline and serotonin uptake

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44
Q

Onset of Tramadol?

A

1 hour

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45
Q

Duration of Action of Tramadol

A

9 hours

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46
Q

Absorption of Tramadol?

A

Rapid and complete

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47
Q

Onset of Codeine?

A

Oral: 0.5-1 hours
IM: 10-30 mins

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48
Q

Duration of action of Codeine?

A

4-6 hours

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49
Q

Metabolism of Codeine?

A

Hepatically to morphine

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50
Q

Excretion of codeine?

A

Urinary

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51
Q

What is codeine available as?

A

Injection and tablet

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52
Q

Dosing adjustment for codeine in patient with renal impairment?

A

CLCR 10-50ml/min: 75% dose

CLCR <10 ml/min: 50%

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53
Q

Dosing adjustment for codeine in patient with hepatic impairment?

A

Necessary in hepatic insufficiency

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54
Q

ADR of Codeine?

A

Drowsiness, Constipation

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55
Q

Metabolism of Tramadol?

A 
Extensively hepatically by CYP2D6 via 
1) Demethylation
2) Glucuronidation
3) Sulfation
to active metabolite O-desmethyl tramadol
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56
Q

Excretion of tramadol?

A

Urine

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57
Q

Conversion of PO tramadol to PO morphine?

A

5:1, 50mg PO Tramadol = 10 mg PO morphine

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58
Q

Dosing adjustment for Tramadol in patient with renal impairment?

A

Immediate release:
CLCR < 30ml/min: 50-100 mg q12h (Max: 200mg)

Extended release:
Should not be used in patient with CLCR <30ml/min

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59
Q

Dosing adjustment for Tramadol in patient with hepatic impairment?

A

Immediate release:
Cirrhosis: 50mg q12h
Extended release:
Should not be used in pts with severe hepatic dysfunction

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60
Q

Tramadol is a substrate of?

A

CYP2D6, CYP3A4

61
Q

DDIs of Tramadol?

A

CYP2D6: Chlorpromazine, Fluoxetine

Carbamazepine: Decreases half life of tramadol

Increases risk of tramadol induced seizure:
Naloxone
Neuroleptic agents
SSRIs
Tricyclic antidepressants

Warfarin: Elevation of prothrombin times

62
Q

ADR of Tramadol

A

Dizziness, Constipation, Nausea, at high dose decreases the seizure threshold

63
Q

Indication of Morphine

A

For moderate to severe pain

64
Q

Conversion of PO Morphine to IV morphine

A

3:1, 30 mg of PO = 10mg of IV

65
Q

Tramadol is available as?

A

Injection and tablet

66
Q

Benefits of Tramadol over other opioids?

A

Lesser cardiovascular and respiratory adverse effects, lower potential of abuse.

67
Q

Onset of action for Morphine?

A

Oral (immediate release): 30 minutes

IV: 5-10 minutes

68
Q

Absorption of Morphine

A

Variable

69
Q

Metabolism of morphine

A

Hepatic via conjugation via glucuronic acid to

1) Morphine-3-glucuronide (inactive)
2) Morphine-6-glucuronide (active)
3) Morphine-3,6-diglucuronide
4) Normorphine (active)
5) 3-ethereal sulfate

70
Q

Excretion of morphine

A

Mainly in urine, 10% in bile

71
Q

Morphine is available as?

A

Tablet, capsule, injection, mixture

72
Q

Dosing adjustment for Morphine in patient with renal impairment?

A

CLCR 10-50 ml/min: 75% dose

CLCR < 10 ml/min: 50%

73
Q

Dosing adjustment for Morphine in patient with hepatic impairment?

A

No change in mild liver disease, excessive sedation may occur in cirrhosis

74
Q

DDIs of Morphine

A

Antipsychotic agent: Increase hypotensive effects of morphine

Increase effect/toxicity:
CNS depressant, MAO inhibitors

75
Q

DFIs of Morphine

A

Ethanol: Increase CNS depression

Herb/Nutraceutical: Valerian, St John’s Wort, Kava Kava, Gotu Kola increases CNS depression

76
Q

Side effects of Morphine (more important ones)

A

Hypotension, Pruritus, Drowsiness, Urinary retention, N/V, Constipation

77
Q

Indications of Fentanyl

A

Indicated for severe pain

78
Q

Onset of action of Fentanyl?

A

IM: 7-15 mins
IV: Almost immediately

79
Q

Metabolism of Fentanyl?

A

Hepatically, primarily via CYP3A4

80
Q

Excretion of Fentanyl

A

Urinary, mainly as metabolites

81
Q

Conversion of TD Fentanyl to PO Morphine

A

Refer to manufacturer guide

12 MCG TD= 30 MG PO /24 hours

82
Q

Dosing adjustment for Fentanyl in patient with renal impairment?

A

Nil

83
Q

Dosing adjustment for Fentanyl in patient with hepatic impairment?

A

Monitor

84
Q

SE of Fentanyl (more impt ones)

A

Hypotension, N/V, Constipation, Respiratory depression, Drowsiness

85
Q

Availability of Fentanyl

A

Injection and Dermal patch

86
Q

What kind of patients are TD Fentanyl indicated for?

A

1) Intolerable SE from Morphine
2) Renal failure
3) Dysphagia
4) ‘Tablet phobia’ or poor oral compliance

87
Q

Bioavailability of TD Fentanyl?

A

> 92%

88
Q

Time taken to reach steady state for TD Fentanyl?

A

36-48 hours

89
Q

Elimination half-life of TD Fentanyl?

A

13-22 hours after removing patch

90
Q

Duration of action of TD Fentanyl?

A

72 hours, for some pts 48 hrs

91
Q

MOA of Methadone?

A

Mu-opioids receptor agonist, NDMA receptor channel blocker, Presynaptic blocker of serotonin re-uptake

92
Q

Bioavailabilty of Methadone?

A

80% (range from 40-100%) PO

93
Q

Onset of action of Methadone?

A

30 minutes PO

94
Q

Metabolism of Methadone?

A

Hepatically. N-demethylation primarily via CYP3A4, CYP2B6, CYP2C19

95
Q

Excretion of Methadone?

A

Urine, increased with urine pH <6

96
Q

Methadone is a substrate of?

A

CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4 (major)

97
Q

DDIs of Methadone?

A

CYP3A4 inducers, may decrease levels /effects of methadone

CYP3A4 inhibitors, may increase levels/ effect of methadone

Agonist/antagonist analgesics: May decrease analgesic effect of methadone

98
Q

DFIs of Methadone?

A

Ethanol: Increase CNS effects

Herb/ Nutraceuticals like St John’s Wort (may decrease Methadone levels as well), Valerian, Kava Kava, Gotu kola increases CNS effects

99
Q

Dosing adjustment for Methadone in patient with renal impairment?

A

CLCR < 10 ml/min: 50-75% dose

100
Q

Dosing adjustment for Methadone in patient with hepatic impairment?

A

Avoid in severe liver disease

101
Q

Significant SEs of Methadone?

A

Hypotension, Constipation, Sweating, Drowsiness, N/V, Respiratory depression

102
Q

Conversion of PO Oxycodone to PO Morphine

A

1:2, 10 mg Oxycodone = 20 mg Morphine

103
Q

Bioavailability of Oxycodone?

A

75% PO (60-87% range)

104
Q

Onset of action of Oxycodone

A

20-30 mins PO

105
Q

Duration of action of Oxycodone

A

4-6 hours; 12 hours for m/r

106
Q

Metabolism of Oxycodone

A

Hepatically by CYP2D6 to oxymorphone (active), BY CYP3A4 to noroxycodone

107
Q

Excretion of Oxycodone?

A

Via Urine

108
Q

Dosing adjustment for oxycodone in patient with renal impairment?

A

Use with caution. Renal impairment decrease the clearance of oxycodone, noroxycodone and conjugated oxymorphone

109
Q

Dosing adjustment for oxycodone in patient with hepatic impairment?

A

Reduce dosage in pts with severe liver disease

110
Q

Significant SEs of Oxycodone?

A

Drowsiness, Constipation, N/V

111
Q

Main difference in dosing between Oxycodone and Morphine?

A

Oxycodone is given q6h rather than q4h

112
Q

Oxycodone is the substrate of?

A

CYP2D6, CYP3A4

113
Q

DDIs of oxycodone?

A

CYP2D6 inhibitors: Decrease effect of oxycodone (Chlorpromazine, Fluoxetine)

114
Q

DFIs of oxycodone?

A

Ethanol

Valerian, St John’s wort, Kava Kava, Gotu kola

115
Q

Indication of Tapentadol?

A

Acute moderate to severe pain

116
Q

MOA of tapentadol

A

Mu-opioid receptor, inhibits reuptake of noradrenaline

117
Q

Metabolism of Tapentadol?

A

Metabolized primarily via phase 2 glucuronidation to glucuronides, all metabolites are pharmacologically inactive

118
Q

Excretion of Tapentadol?

A

Urine

119
Q

Absorption of Tapentadol?

A

Rapid

120
Q

Distribution of Tapentadol?

A

Widely distributed, enters human milk

121
Q

Dose of Tapentadol?

A

50-100mg q4h or q6h for acute moderate/acute pain

122
Q

Administration of Tapentadol?

A

Orally with or without food, long acting formula must be swallowed whole

123
Q

Dosing adjustment for Tapentadol in patient with renal impairment?

A

No dose adjustment for mild/moderate impairment

124
Q

Dosing adjustment for TAPENTADOL in patient with hepatic impairment?

A

No dose adjustment for mild impairment

125
Q

Common SEs of Tapentadol?

A

N/V, Dizziness, Drowsiness

126
Q

Indication of Pethidine

A

ACUTE SEVERE PAIN

127
Q

Onset of Pethidine?

A

SC: 10-15 mins
IV: 5 mins

128
Q

Duration of Pethidine effect?

A

SC: 2-4 hours

129
Q

Metabolism of Pethidine?

A

Hepatically to

1) Meperidinic acid (inactive)
2) Norpethidine (active)

130
Q

Excretion of Pethidine?

A

Urine as metabolites

131
Q

Dose of Pethidine?

A

IV 75-100mg q3h

132
Q

Dosing adjustment for Pethidine in patient with renal impairment?

A

Avoid repeated administration in renal dysfunction

CLCR 10-50 ml/min: 75%
CLCR <10 ml/min: 50%

133
Q

Dosing adjustment for Pethidine in patient with hepatic impairment?

A

Increase effect in cirrhosis, may need to reduce dose

134
Q

Why do we avoid Pethidine in Palliative care?

A

1) Quick onset, short duration of action. Not suitable for regular analgesia
2) Toxic metabolite (Norpethidine) accumulate if given regularly
3) More emetogenic than morphine

135
Q

When switching from one opioid to another consider _____ dose reduction?

A

25-50%

136
Q

Exceptions for opioid dose reduction?

A

1) No dose reduction when converting to TD Fentanyl
2) Patient in severe pain
3) Converting to Methadone required larger reduction (75-90%)
4) Elderly patients or those with organ dysfunction, consider reduction

137
Q

Choice and dose of opioid depends on?

A

Severity of pain

138
Q

Dose of breakthrough dose?

A

1/6 of total daily dose

139
Q

Which drug is used for opioid overdose rescue?

A

Naloxone

140
Q

When to use Naloxone?

A

When patient is non responsive, cyanosed, RR < 8/min

141
Q

When to “wait and see”?

A

When patient RR >8/min, easily arousable and not cyanosed

142
Q

Metabolism of Naloxone? Excretion of Naloxone?

A

In the liver, excreted by kidney

143
Q

Onset of action of Naloxone?

A

Around 2 mins (IV)

144
Q

Availability of Naloxone?

A

400 mcg/ml IV injection

145
Q

Dosing of Naloxone

A

Adults: IV 100-200 mcg, can be repeated every 2 mins. Max: 10mg

Child: IV 5-10 mcg/kg, can be repeated every 2 mins

146
Q

Common SEs of Opioid therapy?

A

Somnolence, mental clouding, constipation, N/V

147
Q

Management of Sedation and cognitive dysfunction?

A

Psychostimulants like
Caffeine (100-200mg PO daily)

Dextroamphetamine (2.5-10mg PO BDS)

Methylphenidate (5-10 mg PO BDS)

148
Q

Management of Myoclonus?

A

Clonazepam (0.5-2mg PO TDS) and anticonvulsants

149
Q

Monitoring outcomes of Opioid Tx?

A

Pain relief, SEs, Function (Physical and Psychosocial), Drug related behaviour

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