Pain 1 Flashcards
Prevalence of chronic pain in Canada
1 in 5
Chronic pain is more common in which gender?
Females
This pop in Canada experiences the highest prevalence of chronic pain in Canada
Indigenous ppls
Classifications of pain:
- Nociceptive
- Neuropathic
- Nociplastic
What is nociceptive pain?
pain experienced as a result of injury, dz, or inflammation
Synonym for nociceptive pain?
Adaptive pain
What’s neuropathic pain?
pain that arises from direct damage to the nervous sys itself
What’s nociplastic pain?
Pain that arises due to changes in the way sensory neurons fn (no nerve damage) –> sensory neurons are more sensitized, essentially
A pt complains of aching and throbbing pain. What kind of pain is this?
nociceptive
A pt complains of radiating and burning pain. What kind of pain is this?
neuropathic OR nociplastic (depending on the initial cause)
From where does somatic adaptive (aka nociceptive) arise?
skin, bone, joint, muscle, or connective tissue
From where does visceral adaptive (aka nociceptive) arise?
internal organs (e.g. lg intestine, pancreas)
What’s the job of nociceptors?
distinguish between harmful/noxious and innocuous stimuli, and transmit appropriate signals to the spinal cord via afferent nerve fibers
How do glutamate and substance P affect pain?
they intensify it
What endogenous substances attenuate pain?
endorphins, enkephalins, GABA, NE, and serotonin
Two synonyms for neuropathic pain
maladaptive pain
pathophysiologic pain
How does neuropathic pain develop?
either damage or abnormal fn’ing of the PNS +/- CNS
Two main types of maladaptive pain:
neuropathic
centralized
How long does acute pain typically last for?
< 3-6 months
usually less than 3 months
Acute pain is usually characterized by what type of pain?
nociceptive
How long does chronic pain typically last?
≥ 3 months
What kind of pain is usually present in those suffering from chronic pain?
“Mixed” pain
Are the two types of chronic pain?
Chronic primary pain (no identifiable cause)
Chronic secondary pain (s.th else is causing it)
Substance use disorders are more common in inds who tx what kind of pain?
chronic pain
How do the goals of tx differ b/w acute and chronic pain?
goal of acute pain: cure (pain reduction/elimination)
goal of chronic pain: functionality (return to normal life with manageable amt of pain)
Depression is uncommon in this type of pain.
Acute pain
What’s the risk of overtx’ing pain?
May cause hyperalgesia and increased AEs
How is pain assessed?
OPQRST
onset provoking/palliative quality region/radiation severity (1-10 scale) temporal/treatments tried
Realistic pain reduction? (percentage)
30-50%
How should we use regimens initially for acute pain, as well as for chronic pain?
Around-the-clock
How should we use regimens for acute pain as the pain subsides?
PRN
Name some non-pharm stuff a pt can do for pain
Distraction + relaxation, TENS, cold, heat, CBT, positioning, exercise, acupuncture, massage, biofeedback, education
When is it appropriate to put heat on an injury?
≥ 48h post-injury
What can happen if we don’t tx an acute pain episode?
It can progress to chronic pain
What approach is recommended by the WHO for tx’ing acute pain?
3-step ladder approach: non-opioids, then weak opioids, the strong opioids
3-step ladder approach to nociceptive pain management: what drugs are on the first rung?
acetaminophen, ASA, NSAIDs
3-step ladder approach to nociceptive pain management: what drugs are on the second rung?
codeine
3-step ladder approach to nociceptive pain management: what drugs are on the third rung?
morphine, hydromorphone, fentanyl
3-step ladder approach to nociceptive pain management: When would you move to the next rung on this ladder?
if the pain persists or increases
There’s a higher risk of bleed with this class of pain med.
NSAIDs
Which first-line pain meds would you choose during severe liver disease?
Acetaminophen (although Tylenol can make it worse, NSAIDs have a higher risk of acute bleeds)
Name 3 simple analgesics:
aspirin, acetaminophen, NSAIDs
How should simple analgesics be taken initially to tx acute pain?
Around the clock at appropriate doses
T or F: Pts cannot use acetaminophen and an NSAID due to toxicity concerns
F
MOA of acetaminophen?
inhibit prostaglandins in CNS and blocks pain impulse generations peripherally
Acute pain dosing of immediate release reg strength acetaminophen
325-650 mg q4-6h prn (max = 4g/day)
Acute pain dosing of immediate release extra strength acetaminophen
500-100mg q4-6h prn (max = 4g/day)
Acute pain dosing of extended release acetaminophen (e.g. Tylenol Arthritis)
1300mg q8h prn (max = 4g/day)
Acute pain dosing of reg strength acetaminophen in children?
10-15 mg/kg q4-6h prn (max 75 mg/kg/day or 4g/d - whichever comes first)
Biochemically, what happens during cellular injury?
Cell damage releases phospholipids, which get converted into arachidonic acid
Cyclooxygenase pathway:
Arachidonic acid is then converted into…
1. prostaglandins and thromboxanes via COX-1 (physiologic enzyme) > GI mucosal protection, renal blood flow, and hemostasis
2. prostaglandins via COX-2 (inflammatory sites) > inflammation, pain, and fever
Which COX enzyme is responsible for mucosal protection?
COX-1
Which COX enzyme is only induced during inflammation?
COX-2
Which COX enzyme is targeted by COXIBs?
COX-2
MOA of ASA?
irreversibly inhibits COX-1/2 via acetylation which decreases formation of prostaglandin precursors
MOA of NSAIDs?
non-selectively inhibits COX-1/2 which decreases formation of prostaglandin precursors
In which trimester of pregnancy are NSAIDs CI’ed?
3rd trimester
ASA dosing for acute pain?
325-650 mg po q4h prn (max 4g/day)
ibuprofen OTC dosing?
200-400mg po q4-6h prn (max 1200 mg/day)
ibuprofen Rx dosing?
600 mg po q6h prn (max 2400mg/day)
naproxen sodium (Aleve) dosing (OTC)
125-500 mg bid (max 1.5g/d)
naproxen base (Naprosyn) dosing (Rx)
250-500 mg po bid (prn) (max 1000 mg/day)
What kind of drug inhibits COX-2 exclusively?
Coxibs
What’s the advantage of coxib drugs?
Spare COX-1 inhibition > reduces risk of GI complications (ulcer, bleed)
T or F: Coxibs inhibit COX-2 at all doses.
F (specificity is lost at higher doses)
What risks do not decrease, even when using coxibs?
Renal and clotting risk (i.e. same renal and clotting risk with COX-1’ and COX-2’s)
Celecoxib dosing for acute pain
400mg po as a single dose on first day, followed by 200mg po OD ≤ 7 days (max dose = 400mg/d for ≤ 7d)
How do NSAIDs increase risk of CV events?
They upset the balance b/w vasoconstricting and platelet aggregating activities of thromboxane A2 (produced by COX-1) and vasodilating prostacyclin (produced by COX-2) –> More thromboxane A2 activity and less prostacyclin activity = higher clotting risk
T or F: CV risk of NSAIDs is not dose related.
F
it IS dose-related (higher dose = more risk)
Which COX enzyme is assoc w/ GI risk?
COX-1
How does COX-1 protect the GI tract?
It increases GI mucosal blood flow, mucous and HCO3 production, and epithelial growth
How do NSAIDs increase GI risk?
they inhibit COX-1 > reduce prostaglandins > reduce gastroduodenal mucosal protection > GI ulcer
How should an NSAID be taken if pt has low GI risk and low CV risk?
NSAID alone
How should an NSAID be taken if pt has moderate GI risk (1-2 risk factors) and low CV risk?
NSAID + PPI or misoprostol
How should an NSAID be taken if pt has high GI risk (hx of GI ulcer or >2 risk factors) and low CV risk?
don’t use NSAID
or
COX-2 inhibitor + PPI or misoprostol
How should an NSAID be taken if pt has low GI risk and high CV risk?
naproxen + ppi or misoprostol
How should an NSAID be taken if pt has mod GI risk and high CV risk?
naproxen + ppi or misoprostol
How should an NSAID be taken if pt has high GI risk (hx of GI ulcer or >2 risk factors) and high CV risk?
avoid NSAIDs and COX-2 inhibitors
USE ALTERNATE TX
How do NSAIDs/coxibs affect kidneys?
inhibit prostaglandins > vasoconstriction of afferent renal arteriole > reduced ability for kidneys to regulate blood flow
CrCl of ___ = avoid NSAIDs/Coxibs
≤ 40 mL/min
How do NSAIDs/Coxibs interact w/ ACE-i’s/ARBs/BBs/thiazides (HTN meds)?
NSAIDs/Coxibs reduced their anti-HTN effect (since they increase vasoconstriction)
What’s the risk of combining NSAIDs/Coxibs w/ warfarin/heparin/CSs/SSRIs?
increased risk of GI bleed
What might happen if we combine NSAIDs/Coxibs w/ ACEi’s/ARBs/diuretics?
Increase risk of nephrotoxicity
Muscle relaxant place in tx for acute pain.
NOT useful (they’re actually anti-spasmodics)
Which analgesic is preferred in renal and hepatic impairment?
acetaminophen
When should you refer for acute pain?
When simple analgesics are used for more than 10d in adults or longer than 5d in children
What did the Chang trial show?
That NSAID-acetaminophen combos may be just as good as opioid-only tx’s for severe pain (de-emphasizes role of opioids, basically)
