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Palliative > Pain > Flashcards

Pain Flashcards

1
Q

Pharmacokinetics

A

“What the body does to the drug”

ADME of drugs

Absorption
Distribution
Metabolism
Excretion

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2
Q

Pharmacodynamics

A

“What the drug does to the body”

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3
Q

Factors affecting pharmacokinetics of opioids

A

Age

  • Change at the extreme of age
  • Increased free drug concentrations due to decreased metabolism and volume of distribution
  • Reduced clearance of opioids due to reduced hepatic blood flow
  • Increased CNS sensitivity also found in the elderly

Hepatic disease

  • Unpredictable affects
  • Severe hepatic failure with coexisting encephalopathy can result in marked increase in sensitivity to drug effects
  • Reduced plasma protein concentration (as in liver failure) can also increase plasma concentrations of free, unbound drug

Renal failure

  • Alters concentrations of parent drug and metabolites
  • Drug effects may compound int he uremic state
  • Metabolites may accumulate (e.g. as with morphine)

Obesity

  • Larger volume of distribution
  • Prolonged half life

Hypothermia
Hyperthermia
Hypotension
Hypovolemia

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4
Q

Impact of age on pharmacokinetics of opioids

A
  • Increased free drug concentrations due to decreased metabolism and volume of distribution
  • Reduced clearance of opioids due to reduced hepatic blood flow
  • Increased CNS sensitivity also found in the elderly
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5
Q

Pharmacokinetics: Absorption

A
  • Occurs across a lipid cell membrane, passive across a concentration gradient (greater lipid solubility = greater absorption)
  • Typically occurs in the small bowel
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6
Q

Reasons for altered absorption

A

Delayed or decreased:
- Delayed gastric emptying or motility (either pathological or pharmacologic)

Reduced absorption:

  • Modified/sustained release formulations which need to remain in the small bowel to achieve expected absorption potential
  • Absorption may be reduced if there is increased GI transit time
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7
Q

Pharmacokinetics: Bioavailability

A
  • Percentage of the administered drug that gains access unchanged to the systemic circulation
  • Most relevant with oral administration due to extensive ‘first pass’ effect (drug absorbed through portal vein then metabolised in the liver, resulting in relatively low bioavailability or interindividual variation for some drugs)
  • Difference in bioavailability complicates the challenge of safe dose selection between oral/parenteral and the reason why careful dose titration is safest
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8
Q

Reasons for altered bioavailability

A
  • Disease processes affecting hepatic function (first pass) - e.g. in liver disease, shunting from portal to systemic vessels may bypass the liver and decrease the first pass effect, increasing bioavailability
  • Exposure to drugs that either induce or inhibit enzymes of the cytochrome p450 system
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9
Q

Pharmacokinetics: Distribution

A
  • Volume of distribution is a theoretical volume in which the total amount of drug would need to be uniformly distributed to achieve the targeted blood concentration
  • Note that for very lipophilic drugs that are taken up into fat stores or muscles, the volume may be many times body size
  • Volume of distribution is a determinant of half life and important to the calculation of the loading dose of a drug

High Vd:

  • Propensity to leave the plasma and enter extravascular compartments of the body, meaning a higher dose is required to achieve a given plasma concentration (e.g. lipophilic drugs)
  • Longer elimination half life as only drug in the vasculature can be eliminated by the liver and kidneys

Low Vd:

  • Propensity to remain in the plasma, meaning a lower dose is required to achieve a given plasma concentration
  • Shorter half life
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10
Q

Factors affecting volume of distribution

A
  1. Acid-base disturbances
    - More basic drugs tend to be more lipophilic and leave the systemic circulation, leading to higher VD
    - More acidic drugs haver a higher affinity for albumin and are more likely to remain in the plasma (lower VD)
  2. Lipophicility of the drug
    - Lipophilic drugs more likely to pass through lipid bilayers and go to adipose tissue or brain (Higher VD)
    - Hydrophilic molecules more likely to remain in the bloodstream (lower VD)
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11
Q

Diffusible fraction of opioids

A
  • Proportion of opioid that are unbound to plasma proteins and capable of diffusing to the site of action (note - pH dependent)

Speed of onset is determined by the concentration of the diffusible fraction (depends on pH) and lipid solubility, as this facilitates diffusion across the blood brain barrier

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12
Q

Pharmacokinetics: Metabolism

A
  • Drug transformation mainly takes place in the liver
  • Rate of metabolism usually determines clearance, though if removal/clearance is particularly rapid, the rate of delivery of the drug to the liver rather than metabolism in the liver may determine clearance

Phase I reactions:
- Includes oxidation catalysed by the CYP450 family

Phase II reactions::
- Includes conjugation

In general, reactions involve the production of products that are more water soluble and readily excreted by the kidney

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13
Q

Pharmacokinetics: Elimination

A
  • Two major organs of elimination are liver and kidney

- Determinant of halflife and steady state drug concentration

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14
Q

Pharmacokinetics: Half life

A
  • Elimination half life is a measure of the time taken for half the drug in the body to be removed and generally correlates closely with duration of action
  • After starting regular dosing (or existing dose of a regimen is changed), takes 5-6 half lives to approach steady state concentration (regardless of route)
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15
Q

Significance of a long elimination half life

A
  • Accumulation of the drug for a prolonged period of time
  • Concentration may surpass the effective therapeutic range and build up to toxic levels
  • Methadone is a good example, as long half life but with a variable elimination phase and rapid distribution phas
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16
Q

Pharmacokinetics: Steady state plasma concentration

A
  • Aim of any dosing regimen is to achieve a concentration high enough to give intended effect, without side effects
  • Concentration is never steady - peaks occur at the point of maximum drug absorption after administration, valleys occur immediately before each dose
  • The degree of swing between peaks and valleys is determined by the eliminiation half life and frequency of administration
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17
Q

Pharmacokinetics: Time to ready steady state

A
  • Dependent on half life
  • 5 -6 half lives required to approach steady state drug concentration if the same dose of drug is given at a constant time interval. 95% achieved in 4 half lives.

Note: applies only to drug where elimination is governed by first-order kinetics (most drugs, including opioids)

  • Phenytoin is an notable exception, which has both first and zero order processes
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18
Q

Pharmacodynamics: Overview

A

Drugs exert effects by:

  • Binding with receptors
  • Modifying enzyme processes
  • Direct chemical or physical actions
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19
Q

Opioid receptors

A
  • mu (MOR)
  • kappa (KOR)
  • delta (DOR)
  • nociceptin peptide receptor (NOR)

Widely, yet differentially, distributed in the CNS and PNS

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20
Q

Endogenous opioids

A
  • Encephalins
  • Endorphins
  • Dynorphins
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21
Q

Mu-opioid receptor (Gene, expression, endogenous ligand, function)

A

Gene
- OPRM1

Expression

  • CNS: Brain (cerebral cortex, thalamus, hypothalamus, striatum, amygdala, periaqueductal grey)
  • Spinal cord, pre and post synaptic neurons
  • PNS
  • Immune cells

Endogenous ligand

  • Beta endorphin
  • Encephalins
  • Endomorphins

Function

  • Inhibition of nociceptive pathways, exploited by all exogenous opioids
  • Analgesia
  • Respirator depression
  • Reduced GI motility
  • Miosis (pin point pupils)
  • Euphoria
  • Sedation
  • Physical dependence
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22
Q

Kappa opioid receptor (Gene, expression, endogenous ligand, function)

A

Gene
-OPRK1

Expression

  • CNS (brain - cerebral cortex, thalamus, hypothalamus, striatum, periaqueductal grey) - same as Mu, but no amygdala involvement)
  • Spinal cord
  • PNS

Endogenous ligand
- Dynorphins

Function

  • modulation of pain - may influence chemical visceral pain and thermal nociception
  • analgesia
  • miosis
  • dysphoria
  • hallucinations
  • sedation
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23
Q

Delta opioid receptor (Gene, expression, endogenous ligand, function)

A

Gene
- OPRD1

Expression

  • CNS (cerebral cortext, striatum, olfactory bulb)
  • PNS

Endogenous ligand

  • Encephalins
  • Beta-endorphins

Function

  • modulates mechanical and inflammatory pain
  • Analgesia
  • Respiratory depression
  • Reduced GI motility
  • Tolerance
  • Mood regulation
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24
Q

Opioid receptor effect: Agonists (description, examples)

A
  • Affinity for and binds to cell receptors
  • No clinically relevant ceiling effect to analgesia
  • Most opioids fall into this class

Examples:

  • Morphine
  • Diamorphine
  • Oxycodone
  • Pethidine
  • Hydromorph
  • Methadone
  • Fentanyl
  • Tramadol
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25
Q

Opioid receptor effect: Partial agonist (description, examples)

A
  • Low intrinsic activity/efficacy (degree of analgesia produced following dose escalation)
  • Ceiling effect at less than the maximum effect produced by a full agonist

Example:
- Buprenorphine

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26
Q

Potency as it relates to opioids

A
  • Influenced by pharmacokinetic factors (e.g. how much drug enters systemic circulation, then reaches receptors) and affinity to drug receptors
  • Clinically operationalised as a ratio of doses required to produce the same analgesic effect
  • Commonly based upon a 10mg morphine dose
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27
Q

Opioid receptor effect: Antagonist (description, examples)

A
  • No intrinsic pharmacologic action, but interfere with action of the agonist
  • Competitive antagonists bind to the same receptor and compete with agonists for receptor sites
  • Non-competitive antagonists block the effects of the agonist in another way

Examples:

  • Naloxone
  • Naltrexone
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28
Q

Opioid receptor effect: Mixed agonist/antagonist

A
  • Product agonist effects at one receptor, antagonist effects at another

Examples:

  • Pentazocine
  • Butorphanol
  • Nalbuphine
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29
Q

Opioid therapy: Principles underlying combination therapy

A
  • Aims to improve analgesia while reducing side effects and limiting tolerance
  • Uses inherent differences in pharmacodynamic and pharmacokinetic properties

May be synergism between methadone and other mu-agonist opioids

Requires further research

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30
Q

Opioid side effects: GI system

A
  • Nausea
  • Constipation
  • Dry mouth
  • Vomiting
  • Ileus
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31
Q

Opioid side effects: Nervous system

A
  • Somnolence
  • Confusion
  • Myoclonus
  • Abnormal dreams
  • Hallucinations
  • Hyperalgesia
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32
Q

Opioid side effects: GU system

A
  • Urinary retention
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33
Q

Opioid side effects: Respiratory system

A
  • Decreased cough

- Respiratory depression

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34
Q

Opioid side effects: Skin

A
  • Hyperhidrosis

- Pruritis

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35
Q

Opioid side effects: Endocrine

A
  • Hypogonadism

- Immunosuppression

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36
Q

Adverse drug reaction

A

Unwanted or harmful reaction experienced:

  • following administration of a drug or combination of drugs
  • under normal conditions of use
  • suspected to be related to the drug

Note: Opioids are one of the drugs most frequently associated with ADEs

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37
Q

Pharmacokinetic drug interactions

A

Arise through:

  • alterations in the rate and extent or absorption
  • rate and extent of absorption
  • Changes in metabolism (both pre-systemic and elimination)
  • Distribution
  • Renal excretion

The clinical impact can sometimes be difficult to assess when a theoretical interaction is detected.

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38
Q

Drug interactions related to GI activity:

A

Prokinetics (domperidone, metoclopramide)
- May affect speed of absorption

Antacids, iron salts, cholestyramine
- May bind other drugs in the GI tract and affect bioavailability

Cytochrome p450 induction (phenobarb, carbamazepine, phenytoin, rifampin)
- Increased pre-systemic metabolism, lower drug levels of substrates (methadone, warfarin, steroids, anticonvulsants)

Cytochrome p450 inhibition

Urinary acidifiers (acetazolamide)
- increased renal excretion of methadone
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39
Q

Drug formulations and route of administration: IR and MR

A
  • PO (generally preferred), either IR or MR
  • IR formulations absorbed in the stomach or proximal small bowel, absorption complete within a few hours of ingestion
  • MR/SR formulations allow a drug to be released over 12-24 hours, allowing for smoother concentration profile of the drug in the blood, extended duration of action, and reduction in pill burden
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40
Q

Drug formulations: Transmucosal preparations

A
  • Drugs absorbed through buccal, nasal, or rectal mucosa

- Avoid first pass metabolism, and as such higher bioavailability and faster onset of action

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41
Q

Drug formulations: Transdermal preparations

A
  • Lipid soluble drugs are well absorbed through the skin
  • Transdermal delivery via patches for CR over many hours or days (e.g. fentanyl or buprenorphine)
  • Caution in cachexic (decreased absorption) or pyrexial patients (increased absorption)
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42
Q

Drug formulations: Parenteral route

A
  • Subcut, IV, or intrathecal delivery
  • In PC, preferred parenteral route is subcut (continuous or episodic)
  • If multiple drugs are combined in a subcut infusion, watch that drugs will not precipitate another (e.g. dexamethasone + midazolam)
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43
Q

Opioid pharmacogenomics

A

CYP2D6 enzyme - involved in the metabolism of many opioids (codeine, tramadol, oxycodone).

Four main phenotypes associated with genetic variation: poor metabolisers, intermediate, extensive, ultra metabolizers

For example, 10% of Caucasions are poor metabolisers of codeine and will experience little analgesia, while 3% are ultra metabolizers and will be more likely to experience adverse reactions

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44
Q

Chronic pain (definition)

A

Pain which persists beyond the usual course of healting or is associated with chronic pathological illness
- Continuous pain, or pain that recurs at intervals for months of years

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45
Q

Total pain (definition)

A

Physical, psychological, social, spiritual influence on the experience of pain and the multidimensional effects it has an on individual’s life

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46
Q

Nociceptive pain (definition)

A

Pain arising from actual or threatened damage to non-neural tissue and activation of nociceptors

May be visceral or somatic

47
Q

Neuropathic pain

A

Pain caused by a lesion or disease of the somatosensory nervous system

  • May be classified as peripheral or central, by anatomic site and disease

Quality

  • Numb, burning, sharp or shooting
  • Allodynia (painful response to a non painful stimulis
  • Hyperalgesia (Increased painful response to a painful stimulus
  • Hyperpathia (delayed and prolonged response to painful stimulus)
  • Dysesthesias (altered pain perception)
48
Q

Breakthrough pain

A

Variations in quality, intensity, and timing of pain on a background of stable pain control

  • May be predictable or unpredictable
  • May be same or different quality to baseline pain

Pts with uncontrolled breakthrough pain more likely to have poorer quality of life and depression

49
Q

Prevalence of pain in patients with advanced disease

A

> 50%

50
Q

Somatic pain

A

Type of nociceptive pain

  • Pain experienced in the skin, muscles, bones, and joints
  • Easily localised
  • Type of nociceptive pain
  • Sharp, throbbing, aching
  • Aggravated by movement
51
Q

Visceral pain

A

Type of nociceptive pain

  • Pain due to injury of the internal organs (viscera, peritoneum, or pleural cavity)
  • Poorly localised
  • Type of nociceptive pain from the walls of visceral hollow and solid organs, with receptors responding to stretching
  • Aching, gnawing or cramping, pressure or ‘deep pain’
  • May be referred (e.g. shoulder tip pain secondary to diaphgramatic irritation)
  • May be associated with autonomic symptoms (e.g. nausea, diaphoresis)
52
Q

Assessment of pain

A 
Onset
Provoking/Palliation
Quality
Radiation
Severity
Timing
53
Q

Definition of allodynia

A

Painful response to a non painful stimulus

Associated with neuropathic pain

54
Q

Definition of Hyperalgesia

A

Increased painful response to a painful stimulus

Associated with neuropathic pain

55
Q

Definition of hyperpathia

A

Delayed and prolonged response to painful stimulus

Associated with neuropathic pain

56
Q

Pain Scales

A

Intensity 0-10 (0 = no pin, 10 = pain as bad as you can imagine)

Brief pain inventory (useful to assess pain severity, localization, impact on various domains of life (e.g. activity, mood, sleep, etc.)

McGill pain questionnaire (validated in the cancer population)

57
Q

Chronic pain following cancer

A
  • Increasingly prevalent as cancer care (including surveillance, diagnosis, and treatment) results in longer survival and follow up
  • Goal of the American Cancer Society is to make cancer into a chronic disease state in which long term control is possible
  • Pain may arise due to the cancer, surgery, chemo, steroids, hormones, or radiation
58
Q

Examples of somatic pain in cancer survivors (chronic pain)

A
  • Osteoporotic fractures
  • MSK imbalance with degenerative arthritis
  • Avascular necrosis of the femoral head
59
Q

Examples of visceral pain in cancer survivors (chronic pain)

A
  • Partial SBO from adhesions

- Odynophagia from esophageal narrowing

60
Q

Examples of neuropathic pain in cancer survivors (chronic pain)

A
  • Localised to specific dermatomes, nerve root distribution, or peripheral/distal extremities
  • Chemotherapy induced peripheral neuropathy
  • Scar pain (especialy post mastectomy and post thoracotomy)
61
Q

Chronic pain due to chemotherapy/corticosteroids (type, characteristics, effects)

A

May cause acute paraesthesias or chronic dysasthetic pain (stocking/glove)

Steroids may lead to steroid myopathy

Characteristics of acute paresthesias
- Typically resolves once chemo is discontinued, but can persist in 15-50% of cases

Characteristics of chronic paraesthesias

  • Risk of chronic pain due to cumulative toxicity
  • Often due to cisplatin, oxaliplatin, vincristine, vinblastine, paclitaxel, docetaxel

Effects

  • Chronic peripheral neuropathy may lead to risk of deconditioning and MSK pain
  • Steroid myopathy may lead to somatic pains and weakness
62
Q

Chronic pain due to surgery (type, characteristics)

A

Types:

  • Chronic post op pain, characterised by type of surgery (e.g. thoracotomy, breast surgery, neck dissection, amputations, nephrectomy)
  • Felt due to central sensitization

Characteristics

  • Variable. May have phantom breast pain or phantom limb pain
  • Typically presents 2-12 months post op
  • Intensity of acute post op pain predicts chronic pain
63
Q

Chronic pain due to radiation (type, characteristics)

A

Types:

  • Varies.
  • Plexopathies
  • Peripheral nerve entrapment
  • Myelopathy
  • Enteritis
  • Proctitis
  • Cystitis
  • Visceral strictures
  • Osteoradionecrosis
  • Accelerated osteoporosis
  • Secondary malignancies

Characteristics
- Likely to manifest months or years after treatment is completed

64
Q

Chronic pain due to hormonal therapy - types, effects

A
  • Osteoporosis due to hormonal treatments of breast and prostate CA
  • Cancer-therapy related bone loss is severe and happens at a higher rate than typical osteoporosis

Effects

  • Increased risk of vertebral and non-vertebral fractures resulting in pain and disability
  • Aseptic necrosis of the femoral heads and hip
65
Q

Chronic pain due to bisphosphonages - types, characteristics

A
  • Usually well tolerated, but may increas risk of osteonecrosis of the jaw (particularly when taken >4 years, incidence >11%)

Characteristics

  • Localised pain
  • Swelling
  • Loosening of teeth
  • Exposed bone
  • Non-healing oral ulcers
  • Purulent gingival discharge
  • Numbness or heaviness of the jaw

Chronic and diffuse bone pain may occur as well

66
Q

Chronic pain related to Head and Neck Cancer

A
  • Cervical lymph node mets often treated with radical neck dissection - involve removal of ipsilateral CN XI, IJ, and SCM as well as ipsilateral LNs

‘Shoulder syndrome’

  • Continuous pain
  • Shoulder tilt and drop
  • Limitations in shoulder retraction, anterior flexion movements and active shoulder abduction
  • Winged scapula
  • Abnormal EMG
  • Sensory paresthesias and numbness due to CN XI damage

Osteonecrosis of the jaw

  • May occur due to head and neck rads, then exacerbated by steroids, chemotherapy, infection, poor dental hygiene and periodontal disease
  • Also associated with bisphosphonates (especially in the mandible)
67
Q

Chronic pain associated with rectal cancer

A

‘Pelvic pain syndrome”

  • Associated with radiation to the pelvis for rectal CA
  • Etiology may be chronic radiation enteritis, chronic cystitis, pelvic insufficiency fractures or neuropathies manifesting as burning perineum syndrome

Chronic radiation enteritis

  • Occurs in up to 15% of patients with abdo/pelvic rads
  • Can occur up to 18 months post rads
  • Crampy, colicky abdo pain, tenesmus, blood diarrhea, emesis, anorexia or weight loss

Chronic cystitis

  • Chronic bladder irradiation
  • Diminished bladder capacity, urgency, dysuria

Pelvic insufficiency fractures

  • Uncommon, but significant morbidity
  • Pain intense, acute onset
  • Affects abdomen, low back, pelvis, hip, buttock, thigh

Burning perineum syndrome

  • Pain in the perianal region
  • May encompass scrotum or vagina
  • Rare, onset usually 6-18 months post rads
68
Q

Chronic pain associated with sarcoma

A

Phantom limb pain

  • Perception of painful sensations in an amputated extremity
  • Due to spinal plasticity and cerebral reorganization following an insult
  • Onset in days to weeks following amputation, can be delayed for months or years
  • Occurs acutely in over half of amputees, with risk increasing at higher level of amputation

Presentation:

  • Neuropathic (shooting, stabbing, cramping, burning, itchy)
  • Often localised to distal aspect of the amputated extremity and feel as though the affected limb is in a contorted or awkward position
  • May be exacerbated by cold temps, stress, fatigue, urination, and defecation

Not caused by psychological factors, though this may exacerbate pain

69
Q

Chronic pain associated with prostate cancer

A

Osteoporosis

  • Due to androgen deprivation therapy (surgical via orchidectomy or GnRH agonist treatment)
  • Decreases bone mineral density and increases risk for severe osteoporosis

Chronic testicular pain

  • Well known complication
  • Chronic pelvic pain syndrome (continuous or recurrent pelvic pain for 6 months)
  • Phantom testes syndrome (pain in the removed testis)
70
Q

Chronic pain associated with breast cancer: Phantom breast syndrome

A
  • Condition where patients have the sensation of residual breast tissue, which can often (not always) be painful
  • May manifest as persistent pain and discomfort, numbness or tingling, pressure, burning, and throbbing
  • Onset may occur up to 1 year post surgery
  • Also may occur in those who have undergone either reconstructive or breast-conserving surgery
  • May persist for several years
71
Q

Risk factors for chronic post operative pain

A
  • Severe acute postoperative pain

- Greater postoperative use of analgesics

72
Q

Chronic pain associated with breast cancer: Neuroma pain

A

Pain in the area of a surgical scar on the breast, chest or arm

  • Aggravated or intensified by touch or percussion
  • Benign growth of nerve tissue at the severe ends of a sensory nerve, which may become entrapped by scar tissue
  • Can result in dysesthesia to the overlying skin secondary to atypical connections of the regenerating nerves
73
Q

Chronic pain associated with breast cancer: Intercostobrachial neuralgia

A
  • Post surgical pain in the distribution of the intercostobrachial nerve either with or without axillary LN dissection
  • Generally results in pain, allodynia, or hyperalgesia in the axilla, anterior chest well, or medial upper arm
  • Risk of damage to nerve during the surgery is relatively high due to variability in distribution of the intercostobrachial nerve
74
Q

Chronic pain associated with breast cancer: Radiation induced pain dyndrome

A
  • Adjunctive radiation in breast cancer increases their risk of developing a chronic pain syndrome
  • Most common cause of pain in this setting is radiation-induced plexopathy (especially brachial plexopathy)

Brachial plexopathy

  • Numbness and parasthesias of the hands and fingers, followed by weakness and increasing pain
  • Thought to result from direct cell damage and progressive ischemic changes leading to fibrosis around the nerve
  • Onset may be delayed by months to years
75
Q

Chronic pain associated with breast cancer: Peripheral neuropathy

A
  • Typically due to chemotherapeutic agents
  • Vinca alkaloids (vincristine), taxanes (paclitaxel/docetaxel), and platinums (carboplatin)
  • PN is often the dose limiting side effect of these meds
  • Numbness, paresthesias, tingling, pain in stocking glvoe distribution
  • Majority see improvement over time, others it is irreversible
76
Q

Chronic pain associated with breast cancer: Pain related to breast implants and reconstruction

A
  • Evidence suggests women who undergo breast reconstruction may be at higher risk post surgery for chronic pain than those who have not
77
Q

Chronic pain associated with lung cancer

A

Chronic post thoracotomy pain syndrome

  • Persistent or recurrent pain in the area of a thorocatomy incision for at least two months following surgery
  • Believed to be secondary to intercostal nerve damage as well as suboptimal acute pain control post operatively
  • Significant burning pain with very slow resolution over months and years, often does not decrease
  • High incidence of ipsilateral arm and shoulder dysfunction
78
Q

Chronic pain associated with heme malignancy/stem cell transplantation

A

Bone pain
- Prolonged steroid therapy for GVHD leading to osteonecrosis and osteoporosis

Hemorrhagic cystitis
- Due to cyclophosphamide or total body irradiation

Neurotoxic side effects from calcineurin inhibitors (e.g. tacrolimus, cyclosporin)
- tremor (most common finding), insomnia, headache, vertigo, dysaesthesia, photophobia and mood disturbance

Opportunistic infection
- Due to immune suppression (e.g. herpes zoster)

79
Q

Non-pharm treatments for chronic pain in the cancer survivor

A
  • Multidisciplinary and interdiscplinary treatment teams have been shown to empower patients and provide significant benefit in the non-cancer chronic pain population
  • Physicians, RNs, PT, OT, SW, dietiticians, psychologists
  • Consider the concept of ‘total pain’ and the impact on activity, deconditioning, reduced socialization, etc.
  • Exercise training and behavioural activation my be helpful
80
Q

Damocles syndrome

A
  • state of long term uncertainty, stress, anxiety of having disease recurrence
81
Q

Visceral pain: Innervation

A

Innervation:

  • Predominantly unmyelinated C fibres, some thinly myelinated A fibres
  • Afferent nerves that run parallel with the efferent autonomic nerves comprising the sympathetic and parasympathetic systems
  • Unlikely peripheral afferent fibres, visceral input has a wide spread through the spinal cord and may project to other segments and contralateral tracts
  • Functionally, the vast majority of visceral sensations do not reach consciousness
82
Q

Visceral pain: receptor types

A

Visceral nociceptors are thought to be polymodal

  • Mechanosensory (responding to a range of distention pressures, including tonic/normal, high distention, and inflammation). Located in the walls and muscles of internal organs
  • Chemoreceptors (located in the mucosa and muscular layers)
  • Thermoreceptors (located in the mucosa and muscular layers)
83
Q

Clinical features of visceral pain

A

Obstruction or injury to hollow viscus

  • Poorly localized
  • Vague, gnawing, crampy
  • Intermittently severe in association with visceral contractions

Injury to solid organ capsules or fascia

  • Better localized
  • Sharp, stabbing

All types may be associated with nausea and vomiting, highly aversive emotional reactions

84
Q

Referral sites in visceral pain - underlying principles

A
  • Visceral and somatic afferent fibres can converge on the same lamina on the spinal cord
  • Nociceptive input from a visceral site may be processed by the higher brain centres as emanating from a corresponding somatic site - “Viscerosomatic referred pain”
  • May result in hyperalgesia and allodynia on stimulation of the skin or gentle palpation in the area of the referred pain
  • May also be referred to other visceral organs (e.g. coronary artery disease and disease of the biliary tree have common afferent inputs at T5)
85
Q

Referred pain from esophageal distention

A
  • Pain in the chest and back
86
Q

Referred pain from cervical distention

A
  • Pain in the lower abdomen and lower back
87
Q

Referred pain from bladder distention

A
  • Suprapubic pain
88
Q

Referred pain from thoracic injuries (cardiac, esophageal, lung, etc.)

A
  • Thoracic region pain
  • Persistent pain usually ipsilateral to the affected hemithorax, but mediastinal pain may be distributed bilaterally or more focally
89
Q

Referred pain from upper abdominal organs (stomach, pancreas, liver)

A
  • Upper abdominal wall pain
90
Q

Referred pain from lower abdominopelvic organs (colon, bladder, uterus, kidney)

A
  • Lower abdominal wall
91
Q

Referred pain from the porta hepatis

A
  • Pain in the ipsilateral scapula
92
Q

Injury to the diaphragm

A
  • Pain to the ipsilateral shoulder
93
Q

Pain from perineral invasion from pancreatic cancer

A
  • Inflammatory perineural invasion by pancreatic cancer cells, in up to 75% of those with advanced pancreatic CA
  • Risk factors include tumour size, invasion of the anterior capsule, invasion of the intrapancreatic nerves
  • Typically boring, well-localized upper abdominal pain that may radiate to the back
  • May also shoot toward mid-thoracic spinal level
94
Q

Pain from bowel obstruction

A
  • Fluctuation abdominal pain, distention, regurgitation or N/V, absence of bowel movements
  • Seen most commonly in patients ovarian, cervical, or gastric primary sites
  • Pain is crampy, may rise and fall during the day
95
Q

Pain from hepatic distention syndrome

A
  • Steady pressure sensation in the RUQ
96
Q

Pain from large adrenal masses

A
  • Flank discomfort, may radiate to the ipsilateral inguinal region
97
Q

Pain from enlarged retroperitoneal lymphadenopathy

A
  • May cause severe back pain, either focal or diffuse

- Most prevalent in lymphoma or germ cell tumours

98
Q

Pain from splenic infarction

A
  • May develop in longstanding myeloproliferative diseases with splenomegaly
  • LUQ pain, continuous with exacerbations of stabbing
99
Q

Treatment of visceral pain

A
  • Opioid therapy remains the mainstay
  • Thought that perhaps kappa agonist opioids may be preferable in visceral pain, but no clinical evidence to support (e.g. oxycodone, which works on both kappa and mu, was not superior to morphine)
  • Consider adjuvants to reduce spasm of smooth muscle (e.g. NSAIDs for biliary colic, anticholinergics for bowel obstruction, oxybutynin (anticholinergic) for bladder spasm)
  • Consider stents for obstructions (esophageal) or nerve blocks (e.g. celiac plexus block)
100
Q

Definition of tolerance

A

A need for increasing doses of a medication to facilitate an effect/same level of pain relief

  • Observed in a variety of opioid effects, including analgesia, respiratory depression, and cognitive impairment
  • In the PC population, the need for escalating doses is more commonly related to progression of the underlying illness rather than tolerance
  • Clinical practice does not reliably support that tolerance is a warning signal for substance dependence
  • Significant tolerance is uncommon, but if it arises, can be managed with opioid rotation or adjuvants
101
Q

Definition of dependence

A

Substance dependence
- Syndrome that requires maladaptive substance use with drug-seeking behaviour and physical indicators of use, including withdrawal and dependence

Physical dependence
- Presence of withdrawal alone with cessation of use/administration of an antagonist

Some overlap, but separate entities - physiologic (physical dependence) vs problematic substance use behaviours

102
Q

Definition of substance abuse and dependence

A

Substance abuse and substance dependence

  • Defining normative behaviours can be difficult amongst patients with pain as they may endorse many of the behaviours associated with substance abuse in the context of being ill
  • Use of term in the medically ill population is difficult
  • In general, ‘addiction’ is associated with psychological dependence where the risks or harm of ongoing use of the drug outweigh the benefits
  • When drugs are used appropriate to manage pain in palliative circumstances, risks of addiction is highly unlikely
  • Physical dependence commonly develops with sustained use of opioids, but is only clinicaly significant if the opioid is abruptly withdrawn or dose reduced, or an opioid antagonist is used

DSM-V: Substance abuse

  • Taking substance in larger amounts or for longer than intended
  • wanting to cut down or stop using but being unable
  • Spending significant time getting, using, or recovering from the use of the substance
  • Cravings and urges to use the substance
  • Impact on function (work, home, school)
  • Continuing to use despite causing relationship problems
  • Giving up activities because of substance use
  • Using repeatedly despite risks
  • Continuing to use despite knowing it could worsen health
  • Tolerance
  • Withdrawal symptoms
103
Q

Aberrant drug-related behaviour definition

A

Attempt to develop a concept more useful in clinical decision making

  • Represents an indication to assess patients for problematic substance use including underlying psychiatric illness, poor coping techniques, or inadequate analgesia (full differential)
  • Patients may engage in aberrant behaviours if pain is inadequately controlled

Examples of mildly aberrant behaviour (more likely representative of patient distress):

  • Requests for specific pain meds
  • Aggressive complaints about the need for medication
  • Using drugs prescribed for someone else
  • Frequent prescription losses
  • Hoarding drugs

More highly aberrant (more consistent with problematic substance use):

  • Forging scripts
  • Obtaining drugs from non-medical sources
  • Sale of prescription drugs
  • Crushing SR tablets for snorting or injecting
104
Q

Risk of substance abuse and dependence in the medically ill

A
  • Development of significant substance abuse issue in patients treated for cancer pain with opioids, with no prev abuse history, is a rare occurrence
  • Poor evidence to support a certain risk assessment strategy, but Screener and Opioid Assessment for Patients with Pain (SOAPP) is a self administered questionnaire validated in patients with chronic non-malignant pain
  • Based upon available information, the risk of exacerbating remote or active substance abuse/dependence or dependence issues in medically ill patients is low
  • Small reports seem to support safety
  • In general, ‘addiction’ is associated with psychological dependence where the risks or harm of ongoing use of the drug outweigh the benefits
  • When drugs are used appropriate to manage pain in palliative circumstances, risks of addiction is highly unlikely
  • Physical dependence commonly develops with sustained use of opioids, but is only clinicaly significant if the opioid is abruptly withdrawn or dose reduced, or an opioid antagonist is used
105
Q

Risk factors for problematic-drug related behaviours

A
  • A personal history of alcohol dependence or drug abuse.
  • A family history of alcohol or drug abuse.
  • A major psychiatric disorder
  • Patients with a history of sexual abuse victimization may be at increased risk for opioid abuse/misuse.
  • Patients with a history of legal problems or incarceration.
  • Medication-assisted treatment for substance use disorder. Patients receiving treatment for addiction should be encouraged to continue with therapy and pain management should be carried out in coordination with an addiction specialist.
106
Q

Clinical management of aberrant drug use in patients with advanced illness

A
  • Represents major impediment to appropriate care

Multidisciplinary approach:

  • Teams ideally include a psychologist, adequate nursing and SW support to support potentially complex needs
  • Communication amongst team members

Assessment

  • Involve physician early given physical safety risks
  • Begin a graduated interview that proceeds from open ended questioning to more specific details about substance abuse - allows for development of report and minimises denial
  • Assess for co-occurring psychiatric disorders
  • Consider diagnostic instruments (e.g. Screener and Opioid Assessment for Patients with Pain - SOAPP)
107
Q

Appropriate monitoring of patients who are prescribed opioids for analgesia

A

Four As - analgesia, ADLs, AEs, and Aberrant drug-taking behaviours

Analgesia
- Pain scale

ADLs

  • monitor ADLs to observe increases over time
  • Refers to QOL and functionality

AEs

  • Strive for highest analgesia with most benign side effect profile
  • Make patients aware of side effects inherent in the treatment of their pain condition with opioids and other meds
  • Aggressively manage AEs so that sedation, etc. do not overshadow potential benefits of tx

Aberrant behaviours

  • Monitor carefully, make use of PMP
  • Education patients through agreements or other means about the parameters of acceptable drug taking
  • May require dispensation of pain medicine in a highly structured fashion
108
Q

Management of aberrant drug-related behaviours

A

General:

  • Use empathic listening and attempt to understand
  • Listen and accept pt’s report of distress
  • Use behavioural and non-opioid interventions as part of management, but not as a substitute
  • Consider drugs with slower onset and longer duration (e.g. TD fentanyl, SR opioids) and understand that higher doses may be needed for pain control in patients with a history of abuse or dependence
  • Frequently reassess pain and symptom control

Outpatients

  • Limit amount of drug dispensed per prescription
  • Make refills contingent on clinic attendance
  • Consider urine tox screenings to assess usage, but consider that assessment tools should be used to more reliably identify patients who are at risk. Further, testing should be performed on a randomised basis to minimise the risk of patients predicting testing and deceiving screening
  • Involve family members and key supports in the treatment plan
  • Be cognizant of the risk of diversion to others
  • Consider a written treatment contract governing frequency of urine checks, expectations of refills, etc.

Inpatients

  • Consider placing the patient in a private room near the nurses’ station
  • Consider daily urine collection
  • Be cognizant of the risk of withdrawal, if patients no longer have access to illicit drugs they were using at home, and the risk of patients leaving the floor to make purchases
109
Q

WHO Analgesic ladder

A

Step 1: Non-opioid +/- adjuvant

  • Efficacy limited by ceiling effect (dose beyond which additional analgesia is unlikely or risks of side effects are too great)
  • Generally, acetaminophen or NSAIDs
  • Watch for hepatotoxicity with acetaminophen and renal impairment, PUD, and age-related renal risk with NSAIDs

Step 2: Weak Opioids
Codeine
- prodrug, efficacy is dependent on liver metabolism
Tramadol
- Works on opioid receptors, but also inhibits serotonin and norepi reuptake
- Caution if the patient is already on an SSRI or SNRI

Step 3: Strong Opioids

110
Q

Ddx of increased breakthrough use

A
  1. Disease progression (development or exacerbation of acute pain event)
  2. Development of delirium (possibly neurotoxicity) - may lead to patients struggling to self-assess and express pain
  3. Psychosocial or spiritual distress. May result in a spiral of increasing opioid use, delirium or neurotoxicity, and further opioid use
111
Q

Indications to consider interventional analgesia or neurosurg procedures

A

Indications

  • Pain localised to certain areas or certain dermatomes
  • Pain is poorly controlled
  • Patients who have reached limit of tolerability for high opioid doses

In general
- Patients may need to understand for some interventions (e.g. continuous epidurals or intrathecals) that there will be more contact with the medical system/time spent in hospital

Nerve blocks may be temporary (local anesthetic) or ablative (phenol)

112
Q

Pain crisis - definition and causes

A

Definition:
- Sudden and catastrophic escalation of pain

Causes:

  • Ruptured viscus
  • Internal hemorrhage or tumour erosion
  • Pathological fracture
113
Q

Pain crisis - management

A

Ensure ongoing communication with patient and family. Note that death may be imminent, depending on the underlying case.

Opioids

  • Administer subcut or IV (PO onset time is too slow, and absorption may be unpredictable)
  • Give equivalent to usual oral breakthrough opioid dose by subcut or IV, then repeat q20-30mins until the patient first reports a break in pain. If <50% improved, continue with same dose
  • If opioid naive, start at Morphine 5-10mg or HM 1-2 mg
  • Ensure close observation after ‘stacking’ of doses to ensure respiratory depression does not ensue

If severe pain persists despite several stacked doses:

  • Double dose of parenteral opioid q20-30mins until there is relief of pain and suffering
  • Dangerous technique typically used for end of life situations

Adjuvants

  • Consider benzos for agitation
  • Ketamine has rapid onset
  • Methotrimeprazine for sedation

Goal of treatment is relief of suffering, and death may occur secondary to the catastrophic disease complication

Consider hospital admission for inadequate pain control or persistent side effects

114
Q

Cognitive impairment and pain assessment

A
  • Cognitive impairment can be a barrier to assessment and management
  • As dementia increases, tendency is to underreport pain, though no evidence that there is LESS pain

Approach:

  1. Attempt to elicit patient’s self-report
  2. If self-report is not possible or unreliable, investigate for pathology that could cause pain
  3. Observe the patient for pain behaviours (grimacing, restlessness, moaning, confusion)
  4. Obtain surrogate reports of pain behaviours
  5. Trial analgesics to determine whether treatment reduces pain behaviours
  • Note that patients with cognitive impairment and advanced cancer appear to be very sensitive to opioids
  • Start low and go slow (e.g. morphine 2.5-5mg PO q4H)
  • Caution with PRN doses if the patient will not ask for them

Palliative (71 decks)

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