Module 2.1.2 (Management of Pain) Flashcards

1
Q

What is the acute pain pharmacotherapy guidelines in eTG?

A
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2
Q

What is used for post-operative pain management?

A

Where pain is predictable

  • Use regular paracetamol and NSAIDS

Moderate to severe post-op pain

  • Add pregabalin
  • Add prn opioids

> PCA (patient controlled analgesia)

> If opioids are used for >7 days a slower taper may be required

Major surgery

  • Epidural or intrathecal analgesia, peripheral nerve blocks, field blocks, wound infiltration
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3
Q

What is used for chronic (non-cancer) pain management?

A

Multidisciplinary care is the gold standard 

  • Pain education
  • Psychology strategies
  • Physiotherapy strategies
  • Lifestyle measures

> Sleep hygiene, nutrition, stress mx, smoking cessation

  • Medications as “scaffolding”

> Improve day-to-day function and quality of life

> Provide support while non-pharmacological treatment strategies are built up

> Targeted treatments if available (eg DMARDS in RA)

  • Surgery

> E.g. joint replacement in OA

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4
Q

For chronic pain management;

A) What is used in nociceptive pain?

B) What is used in neuropathic pain?

C) What is used in nociplastic pain?

A

A)

  • Simple analgesia 
  • TCA 
  • SNRI 
  • Opioids – limited evidence of benefit, many harms

B)

  • TCA 
  • SNRI 
  • Gabapentinoids 
  • Lidocaine patch 
  • Capsaicin 
  • Clonidine 
  • Ketamine etc

C)

  • TCA
  • SNRI
  • Gabapentinoids

> fibromyalgia

> caution effects on cogntion and fatigue may worsen some pain states over time

> use low doses

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5
Q

Chronic noncancer pain is often contributed to by more than one pain type (i.e. mixed pain) or multiple mechanisms within a single pain type. What is used if patients unable to use first line strategies (self-mangement strategies) for:

A) nociceptive pain

B) neuropathic pain

C) chronic noncancer pain

A

A)

  • Paracetamol and NSAIDS for nociceptive pain

B)

  • Adjuvants for neuropathic pain.

C)

  • Opioids have a limited role in the management of chronic noncancer pain (see later slides)
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6
Q

Wahat NSAIDs to use in chronic non-cancer pain?

A

Celecoxib, naproxen, ibuprofen

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7
Q

Which adjuvants to use for neuropathic pain? How to use?

A

For neuropathic pain

  • Gabapentinoids, TCA’s, SNRI’s
  • Start at low dose and titrate slowly to improve tolerability
  • May need to use 2 adjuvants if only a partial response
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8
Q

Do BZD, zolpidem and zopiclone have a role in chronic non-cancer pain?

A

No role in chronic non-cancer pain

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9
Q

Opioids in chronic non-cancer pain?

A

Opioids provide little, if any, benefit for chronic noncancer pain and cause significant harm

  • Long-term use of opioids interferes with a patient’s ability to psychologically resolve negative emotions and reduces their problem-solving skills
  • Opioids can reduce a patient’s motivation to participate in self-management strategies (e.g. exercise)

can consider, short term trial

> Buprenorphine patches, morphine, oxycodone, tapentadol or tramadol

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10
Q

Non pharmacological techniques for pain

A) physical

B) social techniques

C) pyschological

A

A)

  • Physiotherapy  Muscle relaxation  Biofeedback  Invasive techniques  Injections and nerve blocks  Electrical stimulation  Neurosurgical procedures  Acupuncture  Ice/heat packs

B)

  • Community support  OT  Self-help group  Work retraining

C)

  •  Assertiveness training  Behaviour modification  Education  Hypnosis  Meditation  Family therapy  Distraction techniques
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11
Q

Early mobilization in acute pain should be done except when?

A

Except in cases of unstable fractures, spinal cord injuries and catastrophic injuries

> Gentle restoration of active range of motion

> Gradual introduction of functional activities

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12
Q

Example of passive treatments?

A

laser, ultrasound, acupuncture, massage, ice and heat

  • Are not a substitute for active participation and offer little to rehabilitation on their own
  • Discourage reliance on passive modalities – need to be used in combination with active treatments
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13
Q

Physical therapy encourages the body to make its own endogenous opioids like endorphins, enkephalins, dopamine, noradrenaline and serotonin

true or false

A

True

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14
Q

What is the most commonly prescribed psychological treatment for chronic pain?

A

Most commonly prescribed psychological treatment for chronic pain is CBT

  1. Assists people living with chronic pain

to reconceptualise their pain –>

how their thoughts (cognitions)

reciprocally interact with their actions

(behaviours)

  1. assists in identifying realistic and

practical goals, reinforces progress

and acknowledges effort and

achievement

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15
Q

What are the four Rs in analgesic prescribing

A

Right drug

  • Type of pain - nociceptive/neuropathic
  • Severity and expected duration of pain

Right dose

  • Age, weight, renal and hepatic function

Right route

  • Speed of onset –> aim of therapy
  • Ability to swallow/absorb

Right interval

  • Type of formulation
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16
Q

For paracetamol:

A) When is it used?

B) What happens in overdose?

C) What factors may increase risk of hepatotoxicity with paracetamol

D) When to reduce dose to 2-3 g per 24 hours?

A

A)

  • Mild to moderate pain
  • Less effective than NSAIDs, good safety profile when used at recommended doses

B)

Potentially life-threatening

C)

  • Depleted glutathione stores (eg prolonged fasting or malnutrition)
  • Treatment with hepatic enzyme inducers
  • Severe renal, hepatic or cardiac impairment
  • Dehydration
  • Chronic alcohol intake

D)

  • Weight < 50 kg
  • ALT >50
  • Prolonged fasting/malnourished 
  • Concurrent hepatic enzyme inducing medication 
  • Chronic etOH 
  • Dehydrated 
  • >65 years old
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17
Q

FOr NSAIDs;

A) when is it used

B) which has highest risk of CV events and lowest?

C) whats best for GI factors

D) risk factors

A

A)

Mild to moderate pain due to inflammation and tissue injury

  • Synergistic with opioids and paracetamol

B)

  • Diclofenac highest risk, naproxen lowest risk

C)

  • Cox-2 selective best, then ibuprofen then diclofenac

D)

>65yo, high dose NSAID, concurrent use of aspirin, SSRIs, corticosteroids or anticoagulants, alcohol overuse, smoking, gord, h.pylori, CVD disease, HTN, waist cirumference, diabetes

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18
Q

When to use opioids in chronic non-cancer pain?

A

Opioids should only be considered for patients with chronic non- cancer pain once non-pharmacological therapies and non-opioid medicines have been optimised.

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19
Q

Which of the opioids are used for:

A) mild to moderate pain

B) moderate to servere pain

C) severe pain/severe chronic pain

A

A)

  • Codeine – mild to moderate pain
  • Tramadol – moderate pain

B)

  • Tapentadol – moderate to severe pain
  • Buprenorphine – moderate to severe pain

C)

  • Morphine – severe pain
  • Oxycodone – severe pain
  • Hydromorphone – severe pain
  • Methadone – severe chronic pain
  • Pethidine – severe pain
  • Fentanyl – severe pain
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20
Q

What are the indications of opioids?

A

Acute or cancer pain.

  • May also be used for dyspnoea in palliative care 
  • Cough suppressant (codeine and derivatives)
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21
Q

What are the precuations for opioids?

A

Other medications that cause CNS/respiratory depression –additive effects

Hx seizures – increased risk of seizures (avoid pethidine and tramadol) 

GI – caution in patients with ileus (avoid codeine and oral medication)

Renal impairment

  • Avoid codeine, pethidine (accumulation of toxic metabolites)
  • Oxycodone, tapentadol, fentanyl preferred (with dose adjustment)

Hepatic impairment

  • Dose adjustment may be required –risk of coma
  • Caution with Targin (oxycodone/naloxone)

Elderly

  • Start low, go slow (increased risk of adverse effects)

Children and breastfeeding

  • Avoid codeine

Patients at risk of Opioid induced ventilatory impairment

  • Hx of obstructive airways disease (eg COPD or OSA)
  • Utilise CPAP or supplemental O2 where appropriate
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22
Q

Who is codeine contraindicated in?

A
  • Children <12 years of age
  • <18 years undergoing tonsillectomy and/or adenoidectomy for obstructive sleep apnoea as deaths have occurred
  • Breastfeeding (infant death has occurred)
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23
Q

What is codeine metabolised to?

A

Codeine metabolised to morphine by CYP2D6

  • Normal metabolism 30mg codeine to 3mg morphine
  • Poor metabolisers – no effect from codeine

> 6–10% of Caucasians and 1–2% of Asians

  • Ultra-rapid metabolisers – increased risk of adverse effects

> Up to 10% of Caucasians, 1–2% of Asians, 21% of people from the Middle East and 29% of Ethiopians

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24
Q

Pharmacology of Tramadol

A

Also inhibits reuptake of serotonin and noradrenaline

  • useful in neuropathic pain

May be used in combination with more potent opioids

Contributes to serotonin syndrome

Lowers seizure threshold (can cause CNS stimulation)

Also metabolised by CYP2D6 

Intra-individual variation in response and drug interactions

Reduce dose in renal impairment

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25
Q

Pharmacology of Tepantadol

A

Also inhibits noradrenaline reuptake

  • Useful in neuropathic pain

Strong analgesic activity

Less CNS and GI AE’s

Reduce dose in moderate to severe hepatic impairment

Does not require metabolic activation

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26
Q

Why may Buprenorphine be used?

A

Partial agonist

  • Ceiling effect on respiratory depression 
  • Less CNS, GI and dependence AE’s 
  • May precipitate withdrawal symptoms in opioid dependent people 
  • Effect is not reversed by naloxone in usual doses
  • Caution in severe renal impairment and mod-severe hepatic impairment
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27
Q

What is the 1st line opioid? What is the AE?

A

Morphine 1st line opioid

  • Oral, IV, IM, SC, epidural, intrathecal
  • Other opioids may be used where adverse effects of morphine are unacceptable or there is concern about the effect of active metabolites

> Accumulates in renal impairment (esp. M6G) prolonging CNS fx

> Commonly causes itch (histamine release), N &V

> Delayed sedation due to delayed crossing of BBB

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28
Q

Compare oxycodone with morphine. What are the forms in comes in?

A

Better tolerated, quicker onset, more potent than morphine

  • Reduce dose in moderate to severe renal impairment

IR and SR

  • Oxycontin: Caution in swallowing disorders and abuse potential
  • Targin: Contains naloxone (reduced constipation and abuse potential)
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29
Q

Pharmacology of fentanyl. What forms does it come in?

A

Potent synthetic opioid

  • Good in renal impairment (no active or toxic metabolites)
  • Caution – may contribute to serotonin toxicity
  • Well tolerated

> IV = quick onset, short duration and patient controlled analgesia (IV)

> Transdermal patch = chronic pain only, not in opioid native patients, 24-72 hours to maximal effect.

> Lozenges, sublingual and buccal tablets – not interchangeable

> Intranasal

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30
Q

Pharmacology of hydromorphone

A

Potent opioid – 5x stronger than morphine

Reduce dose in moderate renal/hepatic impairment

 Injection, mixture, tablets, SR tablets

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31
Q

Pharmacology of pethidine? Why not recommended?

A

Contributes to serotonin toxicity 

Lowers seizure threshold 

Toxic metabolite (norpethidine) 

  • May occur within 24 hours of starting pethidine.
  • Early signs include anxiety and agitation; tremor, muscle twitching and seizures may occur later
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32
Q

Pharmacology of methadone

A

Also has NMDA antagonist effects

  • Benefits in hyperalgesia, chronic pain

Watch for QT prolongation and CYP3A4 interactions

Complicated kinetics

  • Long and variable t ½ (15-60h) –> autoinduction of hepatic enzymes with chronic use
  • Complicated dose equivalence = pain specialist
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33
Q

What to do if adverse effects of opioids is limiting ability to control pain?

A

Control symptoms of adverse effect 

Reduce dose of opioid 

Add adjuvant/non-opioid 

Switch to an alternate opioid (opioid rotation)

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34
Q

What are the adverse effects of opioids?

A

 Nausea, vomiting (give antiemetic initially – improves with time) 

Constipation/gastroparesis (give laxative ongoing, watch diet, mobility and fluids) 

Itch (change opioid - avoid morphine, fentanyl ok) 

Confusion/hallucinations (reduce dose, change opioid – caution tramadol, consider if pain causing symptoms or opioid) 

Dry mouth (good oral hygiene) 

Urinary retention

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35
Q

What is the most serious AE of Opioids

A

Respiratory depression

  • Most serious adverse effect
  • Decreased sensitivity to CO2
  • Best judged by degree of sedation (use sedation score)
  • RR reduction a late and unreliable indicator
  • Worsen OSA
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36
Q

What are the long term adverse effects of opioids?

A

Immune compromise

Neuroendocrine symptoms

  • Oedema, gynecomastia, amenorrhoea, osteoporosis, low testosterone
  • Long term use of opioids suppresses the HPA axis resulting in suppression of all hormones – monitor hormone levels

Opioid induced hyperalgesia

Affects mood and sleep quality

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37
Q

What is opioid tolerance? what happens?

A

Decrease in drug effect over time, such that an increase in dosing is required to have the same effect

> Differential diagnosis: opioid induced hyperalgesia

  • Increased dose doesn’t help the pain 
  • Pain can be widespread 
  • Opioid use increases the levels of pain
38
Q

What to do for opioid dependence?

A

Withdrawal symptoms occur if chronic treatment is stopped suddenly or an antagonist is given

  • This is NOT addiction
  • Gradually reduce doses before cessation
39
Q

What guides opioid use in elderly patients?

A

Generally require lower doses

>80years ~half the dose of a younger person

Constipation – prophylactic laxatives required

More sensitive to CNS effects

> falls risk

40
Q

What guides opioid use in chronic pain patients?

A

Consider their usual background analgesia plus new pain requirements (eg post-op)

  • Multimodal analgesia

> Eg ketamine infusions

> May need higher doses of breakthrough opioids

41
Q

What to use in patients who still require pain management?

A

Regional or epidural anaesthesia

  • Ideally managed with input from addiction specialist liaising with regular prescriber and pain specialists
42
Q

What to do before/during using opioids?

A

Assess pain intensity, cardiorespiratory status, level of sedation and adverse effects regularly

Use small increments for dose increases 

For SR products initially increase the dose (not the frequency) if required

  • Occasionally an increase in frequency maybe appropriate

High dose or rapid IV admin may rapidly cause respiratory depression, circulatory collapse and even cardiac arrest

  • Have naloxone and resus facilities available

consider take home naloxone for high risk patients

43
Q

What is naloxone nasal spray used for? How long does it take to work? Who is it recommended for?

A

Naloxone is part of emergency rescue treatment for known or suspected opioid overdose. It can be administered via nasal spray or intramuscular injection and takes effect 2 to 5 minutes later.

  • Naloxone nasal spray is recommended for patients at increased risk of opioid overdose or people who are likely to witness opioid overdose

When prescribing opioids for patients with increased overdose risk, incorporate strategies to minimise risk including coprescribing naloxone: high dose potent opioid use, hx substance use disorder, comorbidities that increase the risk of respiratory depression (eg OSA, renal or hepatic impairment)

44
Q

What opioids to use in acute short term pain?

A

Consider if an IR (immediate release) opioid is needed in combination with paracetamol +/- NSAID +/- other analgesia

Both pain and the need for opioids should reduce over time

  • Typically quite rapidly
  • Short-stay and emergency department patients do NOT need SR opioids
  • Patients shouldn’t need opioids for the entirety of their recovery
  • Opioid supply should reflect anticipated need or follow-up – NOT pack size!

Sustained release opioids are NOT licenced or recommended for the management of acute pain

45
Q

What opioids to use in chronic pain (cancer pain)?

A

Use a SR opioid regularly and calculate a prn IR dose for breakthrough or incident pain

Never use SR opioids prn!

Always use opioids in combination with other analgesics

Always have a plan for the use of opioids

Duration, expected outcome, review date

46
Q

What are SR examples of opioids

A

Targin® SR (oxycodone/naloxone) usually bd 

Oxycontin® SR (oxycodone) usually bd 

MS Contin® or Kapanol® SR (morphine) usually bd 

Norspan® patches (buprenorphine) change patch weekly 

Fentanyl patches (potent opioid – not in opioid naïve) change every 3 days 

Jurnista® SR (hydromorphone – potent opioid) usually once daily 

Palexia® SR (tapentadol) usually bd 

Tramadol SR usually bd (Durotram® is once a day)

47
Q

What are IR examples of opioids?

A

Oxycodone IR tablets, capsules, liquid 

Morphine IR tablets, liquid 

Buprenorphine sublingual tablets 

Fentanyl lozenges, sublingual and orally disintegrating tablets 

Hydromorphone liquid and IR tablets 

Tapentadol IR tablets 

Tramadol IR capsules and liquid

48
Q

What not to do for SR tablets

A

do not crush them

49
Q

What are the harms of opioids?

A
  • Constipation
  • Death
  • Depression
  • Falls and fractures
  • Hormonal effects
  • Hyperalgesia
  • Motor vehicle collisions
  • Opioid use disorder
  • Respiratory depression and sleep disordered breathing
  • Tolerance, physical dependence and withdrawal
50
Q

What are the ways to optimise non-pharmacological management before and during opioid trial

A

Active physiical therapies

  • hydrotherapy
  • exercise based physiotherapy
  • occupational therapy
  • activity pacing

Psychological therapies

  • CBT
  • relaxation training

Other treatment options

  • acupuncture
51
Q

What are the options for non-opioid treatrment in chronic-non cancer pain?

A

simple analgesia

  • paracetamol and NSAIDs

TCA (amitryptilline and nortripytilline)

  • for neuropathic pain
  • nortriptyliine = less sedating

Gabapentinoids

  • Adjuvant for neuropathic pain
  • AE include drowsiness and peripheral oedema

SNRI (duloxetine and venlafaxine)

  • Recommended for neuropathic pain
52
Q

When is the risk of harm from opioids increased?

A

For patients with complex co-morbidities, and when co-prescribed with BZDs and other sedatives

> avoid prescribing opioids for these patients

53
Q

What is BRAN

A

decision making process

  • Benefits
  • Risks
  • Alternatives
  • Nothing (what if we do nothing…)
54
Q

How to set expectations when starting an opioid in chronic non-cancer pain?

A

Duration: acceptable trial period is up to 8 weeks, syccess or faulure should be determined within 2-4 weeks

Formulation and dose: start at a low dose, any response should be evident at oral morphine equivalent dose at less than 60mg

Treatment outcomes: agree on goals of opioids treatment and how these will be monitored, goals for physical and cognitive functioning

exit strategy: important to agree in which opioid treatment will be stopped

follow up: review patient every 1-2 weeks to monitor progress

55
Q

How to start an opioid in chronic non-cancver pain? Tips and advice.

A
  • Opioids have a time-limited benefit, generally no longer than 3 months
  • Conside use of paracetamol for opioid sparing benefits
  • Trial regular opioid free periods
56
Q

What are the 5As in opioid therapy as a monitoring tool?

A

Activity

  • What progress has been made in the patients functional goals

Analgesia

  • How does the patient rate the pain over the last 24 hours

Adverse effects

  • Constipation, nausea, dizziness, drowsiness etc

Aberrant behaviours

  • Any problematic behaviour or signs of misuse/abuse

Affect

  • Any changes to how the patient has been feeling
57
Q

What are the four principles of motivational interviewing?

A
  1. Empathy
  2. Developing discrepancy
  3. Rolling with resistance
  4. Supporting self-efficacy
58
Q

What are the five key skills for motivational interviewing?

A
  1. Open-ended questioning
  2. Affirmations
  3. Reflections
  4. Summarisations
  5. Elicit – provide – Elicit
59
Q

Why is tapering of opioids good?

A
  • Tapering has been shown to improve function without worsening pain
  • Benefits of opioids reduce over time while risk of harms increase
  • Pain management alternatives have fewer side effects
60
Q

Who are the patients at risk of overdose?

A

Using >60 mg OMEDD (oral morphine equivalent daily dose) or >30mg OMEDD for certain populations (older patients)

  • concomitant use with other CNS depressants (alcohol, benzodiazepines)
61
Q

How to rapid taper for short term exposure in reponse to misuse or intolerable adverse effects?

A

reduce the daily dose by 10– 25% each week

62
Q

How to slowly taper (eg after years of exposure)?

A

Reduce the daily dose by 10–25% each month

63
Q

What to do for moderate to severe OUD (overuse of opioid)?

A

Rotation to opioid agonist treatment (OAT) may be more appropriate

  • Taper may increase risk due to loss of tolerance
64
Q

What is used for opioid agonist treatment?

A

May be a better long term option

  • Methadone and buprenophrine are both effective in prescription opioid dependence
  • Buprenorphine less restrictive and has a good safety profile
65
Q

How to reduce opioid harms in community pharmacy?

A
  • recommend and supply OTC nasal naloxone
  • recommend staged supply where appropriate
  • perform a chronic pain medscheck
  • consider a HMR for the aptient
66
Q

How to reduce opioid harms in hospital pharmacsists?

A
  • Limit supply of opioids at discharge to clinical need by using new half pack sizes
  • Adopt an opioid stewardship program in hospital
  • Add information about the opioid to the discharge summary (including indication, intended duration and recommendation for GP to assess at next consultation)
67
Q

All patients with moderate to severe cancer pain should try?

A

Opioid analgesia

  • Once adequate control is achieved with immediate release products, consider conversion to slow release formulations
68
Q

What to use for metastaic bone pain (cancer)

A

Radiotherapy, NSAIDS, bisphosphonates, corticosteroids, radioactive strontium-89

69
Q

What to use for pain due to inflammation and oedema in confined spaces?

A

raised ICP, hepatic capsular pain, nerve compression/infiltration

  • Dexamethasone
70
Q

What needs to be kept in mind for opioid conversion?

A

GUIDE ONLY – need close monitoring

  • Effectiveness
  • Adverse effects
  • Toxicity

Use 50-75% of calculated dose

> Monitor closely and titrate dose as necessary

> Have breakthrough opioid analgesia available

71
Q

What is the equianalgesic dose of morphine for 200 micorgram buprenorphine tablet?

A

8-16 mg

72
Q

When is a breakthrough (rescue) opioid used? How much sould be used?

A

In patients receiving long-acting opioid formulations for chronic pain (SR, transdermal), a “rescue” dose for breakthrough pain is recommended.

> an immediate-release form of the same opioid is used (e.g. morphine IR with morphine SR)>

  • The size of the breakthrough dose should be 1/6th – 1/12th (5%-15%) of the patient’s 24-hour baseline opioid dose

> Inpatient setting, rescue doses can be provided IV every 15-30 minutes.

> Oral rescue doses can be offered as needed over the normal dosing interval of the drug (typically every 4 hours and not <1hr)

> If pain not controlled after 3 doses, overall management reviewed

73
Q

What is an adjuvant?

A

An adjuvant is a substance that is not primarily used for the treatment of pain but can increase analgesia

74
Q

Outline some information and what type of drugs are used in the folloowing adjuvant categories:

A) Antiepileptics

B) TCA

C) SNRI

D) Skeletal muscle relaxant

E) NMDA-receptor antagonists

F) Hormones, hormonal analogues

G) Biphosphonates

H) BZD

I) LA

J) Capsaicin

K) Botulinium toxin A (botox)

L) Alpha 2 agonists

M) Steroids

N) Inhaled agents

O) PEA (Palmitoylethanolamide)

sucrose, vitamin C and cannabinoids also used.

A

A)

Neuropathic pain 

Carbamazepine (trigeminal neuralgia), gabapentin, pregabalin, valproate, topiramate, clonazepam

gabapentinoids: black box warning, caution in combo with other CNS depressants.

B)

Neuropathic pain, musculoskeletal pain (eg chronic nociceptive pain)

Amitriptyline, nortriptyline (least anticholinergic fx), doxepin

C)

Neuropathic pain, musculoskeletal pain (eg chronic nociceptive pain)

Duloxetine (most evidence – can use up to 120mg), venlafaxine, milnacipran

D)

Muscle spasms

Baclofen, diazepam

E)

Ketamine wafers and infusion

Neuropathic pain

F)

Calcitonin: Malignant bone pain, burn pain, phantom limb pain
Octreotide: Bowel obstruction (reduce secretions)

G)

IV bisphosphonates, denosumab

Bone pain in malignancy (also use NSAID, glucocorticoids, radium 223)

H)

Diazepam, midazolam, lorazepam

Skeletal muscle relaxant, antianxiety

I)

Lignocaine = Topical, 5% patch and infusion  Patch for focal/regional pain

Flecainide = Refractory neuropathic pain

J)

Topical in refractory post-herpetic neuralgia and painful polyneuropathy

Cream and patches

K)

Local injection

L)

Clonidine

M)

Nerve compression, raised intracranial pressure, bone pain, bowel obstruction, lymphoedema

Prednisolone, dexamethasone

N)

Methoxyflurane

Nitrous Oxide (watch B12 and folate with regular use)

O) Endogenous anti-inflammatory (low levels in ppl with chronic pain)

75
Q

For cannabis, what is THC and CBD?

Nabiximols (Sativex) is the only medicinal cannabis registered in Australia for spasticity in MS

A

THC (delta-9-tetrahydrocannabinol) – S8  Responsible for intoxicating and some therapeutic effects

CBD (Cannabidiol) – S4 if CBD only  Wide range of pharmacological but no intoxicating effects

76
Q

What is AE of THC?

A

At higher doses –> dizzy, “spaced out”, sedated 

Increased appetite

Paranoia, severe anxiety and psychotic reactions

> Driving risk with THC

> Withdrawal (THC)

77
Q

What is the AE of CBD?

A

Can reduce these AE’s – possible anxiolytic and antipsychotic effects

Well tolerated at high doses (up to 5000mg) – diarrhoea can be reported

Potent inhibitor of various CYP450 enzymes

> Interactions do not appear to be clinically significant in adults (risk in children with epilepsy) – more research required

78
Q

What neuropathic pain? How to treat? What are the types?

A

Chronic and difficult to treat

Often refractory to simple analgesics, including NSAIDs

  • Poor relief with opioids alone
  • Antidepressants and antiepileptics (adjuvants) drugs of choice

Types: Peripheral neuropathy (e.g. postherpetic neuralgia (PHN), painful peripheral diabetic neuropathy) and central sensitisation pain syndromes (CRPS, CVPS, CWP)

79
Q

What is used as 1st,2nd,3rd,4th,5th line treatment in neuropathic pain?

A

1st line

TCA’s  SNRI’s  Localised – lignocaine 5% patch

2nd line

Pregabalin, gabapentin

3rd line

Tramadol, tapentadol

4th line

Opioids

5th line

Valoprate, sublingual ketamine

80
Q

What to use for trigeminal neuralgia (neuropathic pain)

A

Carbamazepine

81
Q

What are interventional therapies for neuropathic pain?

A

Spinal stimulators 

Percutaneous radiofrequency neurotomy 

Epidural block  Local anaesthetic and corticosteroid

82
Q

summary for acute pain management

A

A tolerable level of pain that allows optimal physical and emotional function 

  • Early mobilisation 

Multimodal pharmacotherapy 

  • Early control of pain 
  • Simple analgesia, adjuvants, inhaled analgesics, local anaesthetics, opioids where necessary 
  • Opioids – use for minimum time, have plan 

Whole person approach 

Manage acute pain well to avoid acute –> chronic

83
Q

Summary for chronic non-cancer pain

A

Goals of care

To provide strategies to live a meaningful/functional life with pain

Biopsychosocial model or “whole person” approach

Multidisciplinary care is the gold standard

  • Pain education
  • Psychology strategies
  • Physiotherapy strategies
  • Lifestyle measures –> sleep hygiene, nutrition, stress mx, smoking cessation

> medications as scaffolding

  • Medications only if demonstrated benefit – as part of overall plan
  • Improve day-to-day function and quality of life
  • Provide support while non-pharmacological treatment strategies are built up

> Limited evidence paracetamol + NSAIDS– only if nociceptic pain

> adjuvants for neuropathic pain

  • Regular review and consideration of deprescribing
  • Opioids – little benefit, significant harms

> Targeted treatments if available (eg DMARDS in RA)

Language guidelines for chronic pain

  • Using language that is empowering, accurate, respectful and inclusive
  • A cause of iatrogenic pain?
84
Q

Summary of non-pharmacological techniques in acute and chronic pain

A

Non-pharmacological techniques

Physical, social and psychological –> imp in both acute and chronic pain

acute pain

> RICE = Relative rest, ice, compression, elevation AND Early mobilisation is important in most cases AND Discourage reliance on passive modalities

chronic pain

Physical therapies

> Encourage body to make it’s own endogenous opioids, reduce falls risk, reduces muscle atrophy and improves gait

> Meditative movement tx can help sleep, depression, fatigue and QOL

> Pacing vs boom and bust

> Discourage reliance on passive modalities

CBT

85
Q

Summary of paharmacological management?

A

Multi-modal analgesia

  • Synergistic or additive effects, ↓doses and ↓AE’s, opioid sparing

Simple analgesia

  • Paracetamol - risk in overdose, caution hepatic impairment -
  • NSAIDS - contraindications and co-morbidities

Opioids

Adjuvants

86
Q

Summary of opioids?

A

Tramadol

  • Serotonin toxicity, lowers seizure threshold

Tapentadol

  • NRI (neuropathic pain)

Buprenorphine

  • Partial agonist. Available patch and sublingual

Morphine and oxycodone

  • Standard opioids. Watch Targin® in hepatic impairment

Fentanyl and hydromorphone

  • Potent

Pethidine

  • Serotonin toxicity, lowers seizure threshold, toxic metabolite

Methadone

  • NMDA antagonist, QT prolongation, pain specialist only
87
Q

Summary of core competencies for pharmacists in the safe supply of opioids.

A
  1. Understand mandatory legislative requirements
  2. Recognise clinical side effects of opioids
  3. Recognise risks associated with interactions
  4. Provide appropriate patient education
  5. Identify when collaboration with a prescriber is necessary
  6. Determine when pain management is inadequate
  7. Evaluate and address overdose risk
88
Q

Opioid epidemic, summary of chronic non cancer pain

A

Opioid analgesia attenuates with time, while the harm persists or increases with time and increasing doses

  •  AE’s in 80% patients on long-term opioids
  • ↑ risk of harm if complex comorbidities or other sedative use

> Tapering opioids improves pain, function and QOL

> Regulatory changes –> Pack sizes, authority indications, 12 month review

Optimise non opioid management

  • Active physical tx - pacing 
  • Psychological tx- CBT and mindfulness 
  • If appropriate other pharmacotherapy –> para/NSAID/TCA/gabapentinoids/SNRIs
89
Q

Summary of opioid trial in chronic non-cancer pain

A

Trial of up to ~8 weeks, start with low dose, agree on goals of treatment (physical/functional goals), exit plan

  • Review every 1-2 weeks, written opioid agreement
  • 5 A’s – activity, analgesia, adverse effects, aberrant behaviours, affect
90
Q

summary of tapering opioid in chronic non-cancer pain

A

To reduce risk of harm and improve pain, function and quality of life

  • Especially if function has not improved, risk of opioid use disorder, risk of overdose

Engage with patient – patient must agree to taper – provide support –> motivational interviewing

  • Open-ended questions, affirmations, reflective listening, summarise discussion

Taper

  • Rapid taper for short-term exposure or in response to misuse or intolerable adverse effects: reduce the daily dose by 10–25% each week
  • Slow taper (eg after years of exposure): reduce the daily dose by 10–25% each month.
  • Aim to reduce to lowest effective dose (including cessation)

Opioid use disorder

  • May need to consider buprenorphine/methadone
  • Taper may increase risk due to loss of tolerance
91
Q

Summary of cancer pain and palliative care

A

Paracetamol, NSAIDS, adjuvants, opioids

  • Bone pain and inflammation

Opioid conversion

  • Practice converting opioids – not exact– need to monitor
  • Incomplete cross-tolerance -use 50-75% of calculated dose

Breakthrough opioids

  •  1/6th – 1/12th (5%-15%) of 24-hour baseline opioid dose