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Professional Clinical Practice > HX1.2 - Cancer Pain Management > Flashcards

HX1.2 - Cancer Pain Management Flashcards

1
Q

What percentage of cancer patient experience pain?

A

(60-80%)

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2
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual / potential tissue damage

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3
Q

What are the two processes at work when pain is experienced?

A
  1. Cognitive Process

2. Emotional Process

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4
Q

How does emotional process affect sensitivity/perception of pain?

A

These influence pain processing at the level of the spinal cord.

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5
Q

What is the result of the physical and emotional process of experiencing pain?

A

Pain is an individual experience.

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6
Q

What are the goals of assessing pain?

A
  1. Classify the pain
  2. Determine the cause
  3. Estimate severity
  4. Impact on patient
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7
Q

What are the steps in assessing pain?

A
  1. History
  2. Examination
  3. +/- Investigations
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8
Q

How do we classify pain?

A
  1. Type of pain

2. Time course

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9
Q

Who is the primary assessor of pain?

A

Patient

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10
Q

What should be elicited in the pain Hx?

A

SOCRATES

Site
Onset
Character
Radiation
Associations
Time course
Exacerbating / Relieving factors
Severity
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11
Q

What are the two broad types of pain?

A
  1. Nociceptive

2. Neuropathic

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12
Q

What are the subcategories of nociceptive pain?

A

NOCICEPTIVE=

  1. Visceral
  2. Somatic
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13
Q

What brings about Visceral pain? What is its character?

A

Diffuse, achy, cramping

Results from the activation of nociceptors of the thoracic, pelvic, or abdominal viscera (organs). Visceral structures are highly sensitive to distension (stretch), ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain such as cutting or burning

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14
Q

What brings about Somatic pain? What is its character?

A

Well-localised, throbbing, achy.

These specialized nerves, called nociceptors, pick up sensations related to temperature, vibration and swelling in the skin, joints and muscles.

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15
Q

What brings about Neuropathic Pain? What is its character? What may accompany neuropathic pain?

A

Burning / tingling
+/- referred
+/- altered sensation

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16
Q

What are the two types of neuropathic pain?

A

Peripheral (Due to Nerve Damage)

Central (Spinal Cord Damage)

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17
Q

In what patterns might neurogenic pain occur?

A

Spontaneous Discharge (due to degeneration of nerve sprouts)

Evoked

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18
Q

What causes the spontaneous pattern of neurogenic pain?

A

Degeneration of nerve sprouts

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19
Q

What is the name given to neurogenic pain caused by the reduced activation threshold of fibres?

A

Allodynia

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20
Q

What is the name given to neurogenic pain caused by the shift to the left of the stimulus response curve?

A

Hyperalgesia

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21
Q

Can pain be more or less neuropathic?

A

Yes can exist on a spectrum, Can be mixed.

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22
Q

How do we diagnose neurogenic pain?

A

Tools = LANSS Scale (Local Assessment of Neuropathic Symptoms and Signs).

Clinical = Pain in an area of altered sensation is pathogenomic.

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23
Q

How do we classify the time course of pain?

A

Acute
Chronic
Background
Breakthrough (Incident e.g. on walking, Spontaneous)

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24
Q

What are the broad causes of pain (in cancer care?)

A
  1. Cancer
    e. g. Bony involvement, nerve compression
  2. General Debility
    e. g. Constipation, pressure sores
  3. Treatment
    e. g. Mucositis with chemotherapy
  4. Concurrent disorder
    e. g. Osteoarthritis
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25
Q

How do we assess the severity of pain?

A

Children: Wong Baker Scal
Adults: 0-10

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26
Q

How do we assess the impact of pain on a patient?

A

We Ask -_-

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27
Q

What are the consequences of uncontrolled pain?

A

Distress, anxiety, fear, low mood
Loss of mobility, independence
Poor quality of life
Admissions to hospital; need for practical assistance at home

Spiritual, Social, Psychological aspects.

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28
Q

What are the problems regarding the evidence base for cancer pain management?

A
  1. Trials are difficult to perform
  2. Level of evidence available often low
  3. Evidence often drawn from post-operative and chronic non-malignant pain experience
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29
Q

What are the 3 broad strategies for pain control?

A
  1. Modification of Pathology
  2. Non-Pharmacological
  3. Pharmacological
30
Q

Give examples of how we might modify the pathology to help manage pain?

A

Chemotherapy
Radiotherapy
Hormone therapy
Surgery

31
Q

Give examples of some non-pharmacological methods of managing cancer pain?

A

Radiotherapy

Physical methods – TENS, physiotherapy, acupuncture

32
Q

What are the 3 broad categories of pharmacological pain management?

A

Opioid analgesics

Non-opioid analgesics

Adjuvant agents – antidepressants, anticonvulsants, local anaesthetics, ketamine, capsaicin

33
Q

What is the main supporting framework for cancer pain relief? Strength?

A

The WHO Ladder

Not rigorously validated in trials but extensive experience and validation in practice

34
Q

What is the saying for effective cancer pain management?

A

By the mouth, by the clock, by the ladder, individual assessment, and attention to detail

35
Q

What is step 1 on the WHO ladder?

A

Step 1 - non-opioid analgesia

NSAIDs and paracetamol for cancer pain

36
Q

Which NSAID?

A

No clear evidence for superior safety / efficacy of one NSAID over another.

37
Q

What is the efficacy of combining NSAIDs to opioid regimes?

A

Paracetamol

No additional benefit with strong opioids

38
Q

What are the side affects of NSAIDs?

A

Ulcers, bleeding, kidney failure, and, rarely, liver failure.

High dose diclofenac or ibuprofen (>1200mgs) associated withl increased risk of thrombotic / CV events

39
Q

What is Step 2 on the WHO ladder?

A

Weak opioids

40
Q

At what dose is Codeines ceiling effect reached?

A

240mgs / day

41
Q

What race are poor metabolizers of codeine? What are the implications?

A

7% of Caucasians are poor metabolisers leading to poor or absent analgesic effect

42
Q

What is the efficacy of combining weak opioids with Adujvent Analgesics?

A

Combined preparations (60mgs codeine / paracetamol 1g) more effective than paracetamol alone or 8mgs codeine / paracetamol)

43
Q

What is the MOA of Tamadol?

A

Mu-receptor agonism (M1 metabolite)
Serotonin reuptake inhibition (tramadol)
Norepinephrine reuptake inhibition (tramadol)

44
Q

What is the efficacy of Tramadol v Codeine/Paracetamol?

A

Evidence that is safe and well-tolerated but…

No evidence that is superior to codeine / paracetamol combination for management of cancer pain

45
Q

What is step 3 on the WHO ladder?

A

Strong opioids

46
Q

What are the mainstay of strong opioid therapies?

A

Morphine,
Oxycodone,
hydromorphone

47
Q

What are valid alternative opioid therapies?

A

Fentanyl and Buprenorphine

48
Q

Why is methadone not a first line opioid?

A

Methadone not first line due to side effect profile

49
Q

Which type of pain will likely require adjuvant intervention to strong opioid to be managed properly?

A

Neuropathic pain – yes +/- other interventions

50
Q

By what routes can strong opioids be delivered?

A

Oral (First line)

Subcutaneous

Intravenous

Transmucosal (Rapid onset, rapid offset)

Transdermal (Fentanyl / buprenorphine, Stable analgesia only)

51
Q

Outline some of the approaches to determining formulation of analgesic drugs?

A

Multiple possible different approaches (e.g. rapid IV titration, subcutaneous infusion)

Oral titration
No evidence of superiority of starting with either oral immediate-release preparation or modified-release preparation

Dose titrated to pain; reassess at least daily if uncontrolled severe pain

52
Q

What is breakthrough pain?

A

‘abrupt, short lived and intense pain that ‘breaks through’ the around the clock analgesia that controls persistent pain’

53
Q

What are the subcategories of breakthrough pain?

A

Incident (Voluntary/Involuntary)
Spontaneous
End of dose failure

54
Q

What is the Tx for breakthrough pain?

A

Dose of 1/6 of total daily opioid dose

55
Q

When should background pain prompt analgesia to be reviewed?

A

Background analgesia should be reviewed if more than 4 breakthrough episodes / day

56
Q

What are the S/E’s of opioid use?

A
  1. Dry mouth
  2. Transient drowsiness x 24 hours – driving
  3. Nausea and vomiting – 40%, 3 – 5 days after initiation
    (NB co-prescribe anti-emetic PRN – metoclopramide)
  4. Constipation
    (NB NB co-prescribe laxative regularly)
  5. Respiratory depression
    (Exceptionally rare….)
57
Q

What should be discussed with the patient prior to prescribing opioids?

A

What are the patient’s beliefs / fears?

Explain anticipated side effects

  • Prescribe laxative
  • Anti-emetic as needed

Encourage them to persevere despite initial side effects

58
Q

Which is the active component of Morphine? S/E’s?

A

M6G
-Mu receptor agonist – ‘useful’ analgesic metabolite
=Drowsiness, nausea, respiratory depression as crosses blood brain barrier

59
Q

What is the inactive (analegsicless) component of morphine?

A

M3G
-No analgesic effect
=May cause neuropsychological side effects within the CNS

60
Q

What are the neurophysiological S/E’s of morphine?

A 
Sedation
Cognitive impairment
Myoclonus
Hallucinations
Hyperalgesia
61
Q

How common is psychological dependence on opioids?

A

extremely rare

62
Q

How common is physical dependence? How is it mitigated?

A

Does occur but manageable

Gradual withdrawal if pain reduces e.g. post RT

63
Q

How common is respiratory depression? How is the risk mitigated?

A

Respiratory depression – exceptionally rare
-Careful titration

Pain = antagonist to opioid effects on respiration and conscious level

64
Q

How can opioid toxicity be managed/avoided?

A

Avoid stopping abruptly

Infection or renal failure? Reduced need following RT?

Treat cause (Hydrate)

65
Q

What steps can be taken if pain becomes uncontrolled?

A

Switch / rotate opioid +/- reduce dose

Complex – seek senior help

66
Q

How does opioid toxicity differ from overdose?

A 
Toxicity
Confused / drowsy
Myoclonus
Hallucinations
(Pinpoint pupils irrelevant)
Suspected illicit opioid overdose
Injected iv (fast)
No control of dose taken
Arrive unresponsive
Pinpoint pupils = key clue
Not breathing / v low RR
67
Q

What is the Tx in opioid overdose? Indications? Other steps to be taken?

A 
Toxicity = RR and SpO2 OK, Reduce opioid + monitor
OD = Resuscitate, Naloxone iv +/- infusion
68
Q

Which other drugs have analgesic effects but are not strictly analgesics?

A

ANTIDEPRESSANT
Amitriptyline
Neuropathic pain

ANTI-CONVULSANT
Gabapentin, pregabalin
Neuropathic pain

CORTICOSTEROID
Dexamethasone
Pain due to oedema

ANTISPASMODIC
Hysocine butylbromide
Colic

NMDA-RECEPTOR BLOCKER
Ketamine
Neuropathic pain

BISPHOSPHONATES
Zoledronic acid
Pain due to bone mets

69
Q

When should a cancer patient be referee to palliative care for pain management?

A

Difficult to manage symptoms
Psychological / spiritual distress
Ethical difficulties

70
Q

What are the steps to be taken when prescribing opioids?

A

Titrate according to pain severity
Co-prescribe appropriately
Always prescribe a breakthrough option with a regular opioid

Professional Clinical Practice (8 decks)

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