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PHAR 557 > Pain 1 > Flashcards

Pain 1 Flashcards

1
Q

Prevalence of chronic pain in Canada

A

1 in 5

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2
Q

Chronic pain is more common in which gender?

A

Females

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3
Q

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

A

Indigenous ppls

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4
Q

Classifications of pain:

A
  1. Nociceptive
  2. Neuropathic
  3. Nociplastic
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5
Q

What is nociceptive pain?

A

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

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6
Q

Synonym for nociceptive pain?

A

Adaptive pain

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7
Q

What’s neuropathic pain?

A

pain that arises from direct damage to the nervous sys itself

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8
Q

What’s nociplastic pain?

A

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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9
Q

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

A

nociceptive

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10
Q

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

A

neuropathic OR nociplastic (depending on the initial cause)

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11
Q

From where does somatic adaptive (aka nociceptive) arise?

A

skin, bone, joint, muscle, or connective tissue

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12
Q

From where does visceral adaptive (aka nociceptive) arise?

A

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

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13
Q

What’s the job of nociceptors?

A

distinguish between harmful/noxious and innocuous stimuli, and transmit appropriate signals to the spinal cord via afferent nerve fibers

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14
Q

How do glutamate and substance P affect pain?

A

they intensify it

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15
Q

What endogenous substances attenuate pain?

A

endorphins, enkephalins, GABA, NE, and serotonin

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16
Q

Two synonyms for neuropathic pain

A

maladaptive pain

pathophysiologic pain

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17
Q

How does neuropathic pain develop?

A

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

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18
Q

Two main types of maladaptive pain:

A

neuropathic

centralized

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19
Q

How long does acute pain typically last for?

A

< 3-6 months

usually less than 3 months

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20
Q

Acute pain is usually characterized by what type of pain?

A

nociceptive

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21
Q

How long does chronic pain typically last?

A

≥ 3 months

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22
Q

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

A

“Mixed” pain

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23
Q

Are the two types of chronic pain?

A

Chronic primary pain (no identifiable cause)

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

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24
Q

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

A

chronic pain

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25
Q

How do the goals of tx differ b/w acute and chronic pain?

A

goal of acute pain: cure (pain reduction/elimination)

goal of chronic pain: functionality (return to normal life with manageable amt of pain)

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26
Q

Depression is uncommon in this type of pain.

A

Acute pain

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27
Q

What’s the risk of overtx’ing pain?

A

May cause hyperalgesia and increased AEs

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28
Q

How is pain assessed?

A

OPQRST

onset
provoking/palliative
quality
region/radiation
severity (1-10 scale)
temporal/treatments tried
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29
Q

Realistic pain reduction? (percentage)

A

30-50%

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30
Q

How should we use regimens initially for acute pain, as well as for chronic pain?

A

Around-the-clock

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31
Q

How should we use regimens for acute pain as the pain subsides?

A

PRN

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32
Q

Name some non-pharm stuff a pt can do for pain

A

Distraction + relaxation, TENS, cold, heat, CBT, positioning, exercise, acupuncture, massage, biofeedback, education

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33
Q

When is it appropriate to put heat on an injury?

A

≥ 48h post-injury

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34
Q

What can happen if we don’t tx an acute pain episode?

A

It can progress to chronic pain

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35
Q

What approach is recommended by the WHO for tx’ing acute pain?

A

3-step ladder approach: non-opioids, then weak opioids, the strong opioids

36
Q

3-step ladder approach to nociceptive pain management: what drugs are on the first rung?

A

acetaminophen, ASA, NSAIDs

37
Q

3-step ladder approach to nociceptive pain management: what drugs are on the second rung?

A

codeine

38
Q

3-step ladder approach to nociceptive pain management: what drugs are on the third rung?

A

morphine, hydromorphone, fentanyl

39
Q

3-step ladder approach to nociceptive pain management: When would you move to the next rung on this ladder?

A

if the pain persists or increases

40
Q

There’s a higher risk of bleed with this class of pain med.

A

NSAIDs

41
Q

Which first-line pain meds would you choose during severe liver disease?

A

Acetaminophen (although Tylenol can make it worse, NSAIDs have a higher risk of acute bleeds)

42
Q

Name 3 simple analgesics:

A

aspirin, acetaminophen, NSAIDs

43
Q

How should simple analgesics be taken initially to tx acute pain?

A

Around the clock at appropriate doses

44
Q

T or F: Pts cannot use acetaminophen and an NSAID due to toxicity concerns

A

F

45
Q

MOA of acetaminophen?

A

inhibit prostaglandins in CNS and blocks pain impulse generations peripherally

46
Q

Acute pain dosing of immediate release reg strength acetaminophen

A

325-650 mg q4-6h prn (max = 4g/day)

47
Q

Acute pain dosing of immediate release extra strength acetaminophen

A

500-100mg q4-6h prn (max = 4g/day)

48
Q

Acute pain dosing of extended release acetaminophen (e.g. Tylenol Arthritis)

A

1300mg q8h prn (max = 4g/day)

49
Q

Acute pain dosing of reg strength acetaminophen in children?

A

10-15 mg/kg q4-6h prn (max 75 mg/kg/day or 4g/d - whichever comes first)

50
Q

Biochemically, what happens during cellular injury?

A

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

51
Q

Which COX enzyme is responsible for mucosal protection?

A

COX-1

52
Q

Which COX enzyme is only induced during inflammation?

A

COX-2

53
Q

Which COX enzyme is targeted by COXIBs?

A

COX-2

54
Q

MOA of ASA?

A

irreversibly inhibits COX-1/2 via acetylation which decreases formation of prostaglandin precursors

55
Q

MOA of NSAIDs?

A

non-selectively inhibits COX-1/2 which decreases formation of prostaglandin precursors

56
Q

In which trimester of pregnancy are NSAIDs CI’ed?

A

3rd trimester

57
Q

ASA dosing for acute pain?

A

325-650 mg po q4h prn (max 4g/day)

58
Q

ibuprofen OTC dosing?

A

200-400mg po q4-6h prn (max 1200 mg/day)

59
Q

ibuprofen Rx dosing?

A

600 mg po q6h prn (max 2400mg/day)

60
Q

naproxen sodium (Aleve) dosing (OTC)

A

125-500 mg bid (max 1.5g/d)

61
Q

naproxen base (Naprosyn) dosing (Rx)

A

250-500 mg po bid (prn) (max 1000 mg/day)

62
Q

What kind of drug inhibits COX-2 exclusively?

A

Coxibs

63
Q

What’s the advantage of coxib drugs?

A

Spare COX-1 inhibition > reduces risk of GI complications (ulcer, bleed)

64
Q

T or F: Coxibs inhibit COX-2 at all doses.

A

F (specificity is lost at higher doses)

65
Q

What risks do not decrease, even when using coxibs?

A

Renal and clotting risk (i.e. same renal and clotting risk with COX-1’ and COX-2’s)

66
Q

Celecoxib dosing for acute pain

A

400mg po as a single dose on first day, followed by 200mg po OD ≤ 7 days (max dose = 400mg/d for ≤ 7d)

67
Q

How do NSAIDs increase risk of CV events?

A

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

68
Q

T or F: CV risk of NSAIDs is not dose related.

A

F

it IS dose-related (higher dose = more risk)

69
Q

Which COX enzyme is assoc w/ GI risk?

A

COX-1

70
Q

How does COX-1 protect the GI tract?

A

It increases GI mucosal blood flow, mucous and HCO3 production, and epithelial growth

71
Q

How do NSAIDs increase GI risk?

A

they inhibit COX-1 > reduce prostaglandins > reduce gastroduodenal mucosal protection > GI ulcer

72
Q

How should an NSAID be taken if pt has low GI risk and low CV risk?

A

NSAID alone

73
Q

How should an NSAID be taken if pt has moderate GI risk (1-2 risk factors) and low CV risk?

A

NSAID + PPI or misoprostol

74
Q

How should an NSAID be taken if pt has high GI risk (hx of GI ulcer or >2 risk factors) and low CV risk?

A

don’t use NSAID
or
COX-2 inhibitor + PPI or misoprostol

75
Q

How should an NSAID be taken if pt has low GI risk and high CV risk?

A

naproxen + ppi or misoprostol

76
Q

How should an NSAID be taken if pt has mod GI risk and high CV risk?

A

naproxen + ppi or misoprostol

77
Q

How should an NSAID be taken if pt has high GI risk (hx of GI ulcer or >2 risk factors) and high CV risk?

A

avoid NSAIDs and COX-2 inhibitors

USE ALTERNATE TX

78
Q

How do NSAIDs/coxibs affect kidneys?

A

inhibit prostaglandins > vasoconstriction of afferent renal arteriole > reduced ability for kidneys to regulate blood flow

79
Q

CrCl of ___ = avoid NSAIDs/Coxibs

A

≤ 40 mL/min

80
Q

How do NSAIDs/Coxibs interact w/ ACE-i’s/ARBs/BBs/thiazides (HTN meds)?

A

NSAIDs/Coxibs reduced their anti-HTN effect (since they increase vasoconstriction)

81
Q

What’s the risk of combining NSAIDs/Coxibs w/ warfarin/heparin/CSs/SSRIs?

A

increased risk of GI bleed

82
Q

What might happen if we combine NSAIDs/Coxibs w/ ACEi’s/ARBs/diuretics?

A

Increase risk of nephrotoxicity

83
Q

Muscle relaxant place in tx for acute pain.

A

NOT useful (they’re actually anti-spasmodics)

84
Q

Which analgesic is preferred in renal and hepatic impairment?

A

acetaminophen

85
Q

When should you refer for acute pain?

A

When simple analgesics are used for more than 10d in adults or longer than 5d in children

86
Q

What did the Chang trial show?

A

That NSAID-acetaminophen combos may be just as good as opioid-only tx’s for severe pain (de-emphasizes role of opioids, basically)

PHAR 557 (36 decks)

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