Chronic Nonmalignant Pain

Question 1

Types of Chronic Nonmalignant Pain

Answer 1

nociceptive (trauma/mechanical damage)

neuropathic (nerve damage)

Question 2

Examples of diseases associated with chronic nonmalignant pain

Answer 2

Arthritis, spinal stenosis, neuropathies, neuralgias, mylagias

Question 3

Pathophysiology of chronic pain

Answer 3

perception of pain
normal pain pathway
endogenous pain relief
chronic pain cycle

Question 4

Perception of pain

Answer 4

transduction
transmission
perception
modulation

Question 5

normal pain pathway

Answer 5

tissue injury leads to chemical release, leads to inflammation, leads to pain signal (electrical impulse), goes to spinal cord, goes to brain (where it is perceived, localized, and interpreted)

Question 6

endogenous pain relief (modulation)

Answer 6

anti-nociceptive system

endorphins and enkephalins are natural pain relievers

Question 7

chronic pain cycle

Answer 7

chemical changes (hypersensitive to pain signals, resistant to endogenous pain relief)
physiological changes (reflex is formed in spinal cord- body learns to transmit signals towards and away from the brain)

result: pain signals generated without continued injury

Question 8

neuropathic pain

Answer 8

“nerve pain” from damage to sensory nerves

more responsive to adjuvant analgesics, and are typically not responsive to other medications such as opioids

Question 9

effective management of chronic nonmalignant pain includes

Answer 9

medication and rehabilitation

multi-disciplinary approach (education, rehab, counseling, meds)

Question 10

systematic 3-step ladder plan for medication management of chronic nonmalignant pain; recommendations

Answer 10

Step 1: non-opioid +/- adjuvant
Step 2: if persists, opioid for mild-moderate pain +/- non-opioid +/- adjuvant
Step 3: if persists, opioid for moderate-severe pain +/- non-opioid +/- adjuvant

• for severe or acute pain or end of life, go from steps 3 to 1
• long acting for “controlling” and short acting for “breakthrough” plus or minus adjuvants

Question 11

NSAIDS

Answer 11

ex: ASA, ibuprofen, naproxen (Naprosyn), diclofenac (Voltaren), indomethacin (Indocin), nabumetone (Relafen)
MOA: block COX enzymes and block prostaglandin production
SE: GI, ulcers, RF, sodium and fluid retention, CV

• consider GI protective medications
• available OTC

Question 12

COX-2 Inhibitors

Answer 12

ex: celecoxib, (rofecoxib and valdecoxib taken off the market due to CV side effects)
MOA: selectively block COX-2 enzyme and block prostaglandin production
SE: GI, ulceration (possibly less than NSAIDS), RF, fluid retention, CV complications (prothrombotic effect)

• usually cost more- poorly covered by insurance due to no real increased benefit over NSAIDS
• lowest effective dose for shortest duration possible

Question 13

Acetaminophen

Answer 13

MOA: “central mechanism” not well understood
SE: liver toxicity

*available OTC, contained in many OTC products- good patient teaching to prevent OD

Question 14

Tramadol

Answer 14

MOA: short-acting, non-narcotic for moderate to severe pain
SE: decrease dose in liver and kidney dysfunction, decrease dose in elderly, may cause seizure (avoid in pts with pre-existing seizure disorder)

Question 15

Opioids

Answer 15

ex: oxycodone, morphine, fentanyl, hydrocodone, codeine, methadone, prophxyphene, etc (can by ER or IR)
MOA: interact with CNS opioid receptors and mimic endorphins and enkephalins
SE: sedation/dizziness (decrease with use), n/v (decrease with use), constipation

• no ceiling effect; tolerance developed
• abuse potential

Question 16

List of types of adjuvant pain medications

Answer 16

anticonvulsants
antidepressants
local anesthetics/antiarrhythmics
muscle relaxants
alpha-2 adrenergic antagonists

others: capsaicin cream, oral steroids, antihistamines, calcitonin, benzodiazepines; stimulants may reverse sedation from opioids; implanted pumps may be considered when unable to relieve pain with oral pain meds
etc.

Question 17

Adjuvant analgesics: anticonvulsants

Answer 17

ex: carbamazepine, oxycarbazepine, phenytoin, divalproex, gabapentin, tiagabine, lamotrigine, topiramate (Topamax), zonisamide (Zonegran), etc.
MOA: activate sodium channels to interrupt transmission of pain signals
SE: dizziness, drowsiness, unsteadiness, clumsiness, Stevens Johnson syndrome

*no need to draw blood levels when taking for pain- dose to effects

Question 18

Adjuvant analgesics: antidepressants

Answer 18

ex: amitriptyline, imipramine, desipramine, doxepin, nortriptyline, trazodone, mirtazapine, venlafaxine, fluoxetine, sertraline, paroxetine, citalopram, etc
MOA: increase seratonin and norepinephrine
SE: agent-specific

*typically given in lower doses than when given for depression

Question 19

Adjuvant analgesics: local anesthetics/antiarrhythmics

Answer 19

ex: lidocaine patch, bupivocaine, mexilitine
MOA: membrane stabilizers; disrupt pain signal transmission
SE: cardiac effects at higher doses

Question 20

Adjuvant analgesics: muscle relaxants

Answer 20

ex: cyclobenzaprine, carisoprodol (Soma), metaxalone, tizanidine, baclofen
MOA: muscle relaxant for musculoskeletal pain/spasms
SE: drowsiness/dizziness, feeling “out of it”

*abuse potential with carisoprodol (Soma) due to some opioid effect

Question 21

Adjuvant analgesics: alpha-2 adrenergic agonists

Answer 21

ex: clonidine
MOA: nociceptive and neuropathic pain; potentiates opioid analgesia; analgesia via central mechanism
SE: effects on blood pressure limit the dosing