Pain 1 Flashcards by J G

Prevalence of chronic pain in Canada

1 in 5

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Chronic pain is more common in which gender?

Females

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This pop in Canada experiences the highest prevalence of chronic pain in Canada

Indigenous ppls

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Classifications of pain:

Nociceptive
Neuropathic
Nociplastic

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What is nociceptive pain?

pain experienced as a result of injury, dz, or inflammation

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Synonym for nociceptive pain?

Adaptive pain

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What’s neuropathic pain?

pain that arises from direct damage to the nervous sys itself

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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

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A pt complains of aching and throbbing pain. What kind of pain is this?

nociceptive

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A pt complains of radiating and burning pain. What kind of pain is this?

neuropathic OR nociplastic (depending on the initial cause)

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From where does somatic adaptive (aka nociceptive) arise?

skin, bone, joint, muscle, or connective tissue

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From where does visceral adaptive (aka nociceptive) arise?

internal organs (e.g. lg intestine, pancreas)

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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

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How do glutamate and substance P affect pain?

they intensify it

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What endogenous substances attenuate pain?

endorphins, enkephalins, GABA, NE, and serotonin

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Two synonyms for neuropathic pain

maladaptive pain

pathophysiologic pain

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How does neuropathic pain develop?

either damage or abnormal fn’ing of the PNS +/- CNS

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Two main types of maladaptive pain:

neuropathic

centralized

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How long does acute pain typically last for?

< 3-6 months

usually less than 3 months

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Acute pain is usually characterized by what type of pain?

nociceptive

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How long does chronic pain typically last?

≥ 3 months

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What kind of pain is usually present in those suffering from chronic pain?

“Mixed” pain

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Are the two types of chronic pain?

Chronic primary pain (no identifiable cause)

Chronic secondary pain (s.th else is causing it)

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Substance use disorders are more common in inds who tx what kind of pain?

chronic pain

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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

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)