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Pharm > Pain Management: NSAIDs/APAP > Flashcards

Pain Management: NSAIDs/APAP Flashcards

1
Q

4 types of pain

A

nociceptive
inflammatory
neuropathic
functional

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2
Q

nociceptive pain

A

occurs in response to noxious stimuli, in order to prevent further damage

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3
Q

inflammatory pain

A

occurs in response to tissue damage or infection in order to promote healing

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4
Q

neuropathic pain

A

occurs as the result of damage or pathological changes in either the PNS or the CNS

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5
Q

functional pain

A

occurs due to an abnormality in processing by, or functioning of, the CNS in response to normal stimuli

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6
Q

acute pain is typically from what types of pain?

A

nociceptive or inflammatory

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7
Q

chronic pain is typically from which types of pain?

A

neuropathic, inflammatory, functional.

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8
Q

mild/moderate acute pain

two tiers of treatment

A

1st tier: NSAIDs or APAP

2nd tier: opioids

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9
Q

severe acute pain

two tiers of treatment

A

1st tier: opioids

2nd tier: opioids plus NSAIDS or APAP

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10
Q

acute pain treatment modailities

A

NSAIDS, APAP, opioids

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11
Q

chronic pain treatment modalities (8)

A 
TCAs
AEDs
lidocaine
SSRI/SNRI
long acting opioids
clonidine or bactrim
pregabalin
APAP/NSAIDs (inflammatory)
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12
Q

nociceptor stimulation pathology:

what 6 substances does injured tissue cause the release of?

A 
bradykinin
serotonin
potassium
histamine
prostaglandins
substance P
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13
Q

nociceptor stimulation pathology

A

injured tissue causes the release of bradykinin, serotonin, potassium, histamine, prostaglandin, and substance P. they further sensitize or activate nociceptors. This results in a lowering of the pain threshold.

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14
Q

nociceptor activation

A

action potentials are produced and transmitted to the spinal cord along myelinated a-delta-fibers and unmyelinated c-fibers

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15
Q

pain signals are transmitted via the spinal cord to

A

the thalamus

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16
Q

after pain signals reach the thalamus,

A

they are transmitted to cortical regions where pain is actually perceived.

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17
Q

a-delta-fibers transmit

A

sharp and fast pain

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18
Q

c-fibers transmit

A

slower, dull, diffuse pain

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19
Q

modulation of pain occurs through what 3 processes?

A

endogenous opioids
descending pathway
cognitive behavioral treatments

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20
Q

pain modulation: endogenous opioids

A

endorphins act on opioid receptors in the CNS to inhibit pain impulses

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21
Q

pain modulation: descending pathway

A

inhibition of pain transmission in the dorsal horn of the spinal cord

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22
Q

pain modulation: cognitive behavioral treatments

A

reduce pain perception by altering pain processing in the cortex

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23
Q

inflammatory pathway produces

A

prostaglandins

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24
Q

arachidonic acid

A

liberated from CMs when cells are damaged. from there, it can convert to prostaglandins by cox enzymes

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25
Q

3 prostaglandins

A

thromboxane (TXA2)
prostaglandin e2 (PGE2)
prostacyclin (PGI2)

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26
Q

in response to tissue injury, nociceptors release which prostaglandins?

A

PGE2 & PGI2

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27
Q

PGE2 & PGI2 actions

A

Prostaglandins which facilitate inflammation and sensitize nociceptors to painful stimuli

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28
Q

COX inhibitor drug uses

A

anti inflammatory
analgesic
antipyretic

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29
Q

adverse effects of cox inhibitors

A

gastric ulceration
bleeding
renal impairment

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30
Q

cox inhibitor MoA

A

inhibit cox which is the enzyme that converts arachidonic acid into prostaglandins and related compounds.

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31
Q

inhibition of COX-1 also leads to

A

gastric ulceration
bleeding
renal impairment

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32
Q

which COX is good cox and which is bad cox?

A

COX-1 : goood

COX-2: bad

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33
Q

what is the one benefit of inhibiting cox 1

A

decreased risk for MI on low dose daily ASA

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34
Q

When cells are damaged and release cox2, what will be produced?

A

PGE2 and PGI2, sensitizing nociceptors and facilitating inflammation

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35
Q

cox 2 inhibition Thera effects

A

anti inflammatory
analgesic
anti pyretic
potential for reducing tumorigenic growth

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36
Q

Cox inhibiting drugs with anti inflammatory properties

A

NSAIDS

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37
Q

cox inhibiting drug that does not have an anti inflammatory property

A

APAP (acetaminophen)

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38
Q

why isn’t acetaminophen anti inflammatory?

A

Distributes almost exclusively in the CNS.
Binds to and inhibits cox in the CNS, leading to analgesia and antipyretic
Does not effect COX in peripheral tissues

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39
Q

NSAIDS are nonselective, meaning

A

they bind to and inhibit COX 1 and 2

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40
Q

only FDA approved sole cox-2 inhibitor

A

celecoxib

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41
Q

benefit of acetaminophen over nsaid

A

no renal impairment, gastric ulcers, or risk of bleeding.

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42
Q

aceta MoA

A

inhibits cox in the CNS

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43
Q

PO bioavailability of aceta

A

85-100%

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44
Q

peak plasma time of po aceta

A

within 1 hour

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45
Q

protein binding of aceta vs NSAIDs

A

aceta: low protein binding
NSAIDs: high protein binding

46
Q

metabolism of aceta

excretion

A

mainly in the liver
undergoes phase I via CYP2E1 and II, but vastly done in phase II.
in phase II, aceta is conjugated to glucoronic acid, sulfuric acid, and cysteine. then excreted.

small proportion of aceta goes through phase I. If not able to complete and this metabolite builds up, hepatotoxicity can occur.

47
Q

elimination of aceta in adults time

A

2-3 hours

48
Q

acetaminophen in the setting of inflammatory pain

A

may be used as an analgesic adjunct but is inadequate for this type of pain as a single agent.

49
Q

acetaminophen in neuropathic or functional pain

A

lacks efficacy

50
Q

current FDA recommended daily dose of aceta

A

4g

can effect liver function

51
Q

what dose of acetaminophen can be fatal and why?

A

15g

severe hepatotoxicity and potentially renal failure via acute tubular necrosis

52
Q

treatment for acetaminophen overdose

A

acetylcysteine

53
Q

NAPQI

A

toxic metabolite of acetaminophen

54
Q

NAPQI and glutathione

A

glutathione binds to NAPQI, renders it harmless, and it is excreted in the urine

55
Q

NAPQI with insufficient glutathione

A

hepatotoxicity

56
Q

N-acetylcysteine will

A

act as glutathione, bind to NAPQI for excretion.

57
Q

single and daily doses of aceta are not to exceed…

A

single: 1g
daily: 4g

58
Q

at what adult weight must daily and single aceta doses be adjusted?

A

<50kg

59
Q

which CYP enzyme metabolizes aceta in phase I? (3)

A

CYP2e1
CYP1a2
CYP3a4

60
Q

Alcohol does what to CYP450?

A

induces it

61
Q

CYP450 does what in aceta metabolism?

A

converts aceta to NAPQI

62
Q

glutathione is effected how by alcohol?

A

depleted

63
Q

alcohol + aceta

metabolism

A

CYP450 is induced by alcohol. More of the toxic metabolite, NAPQI, is produced. Alcohol reduces glutathione, which neutralizes NAPQI. this leads to too much NAPQI -> hepatotoxicity.

64
Q

why are renal impaired patients susceptible to aceta toxicity?

A

kidney produces some degree of NAPQI because small amounts of phase I metabolism occur in the kidney. If you have impaired renal function, the NAPQI isn’t able to clear out of the nephron. the kidney is then damaged by the NAPQI.

65
Q

first generation NSAIDs inhibit

A

cox-1 and cox-2

66
Q

first generation NSAID therapeutic indications: (5)

A
  • inflammatory disorders ie: RA
  • mild/moderate pain
  • antipyretic
  • dysmenorrhea/heavy menstrual bleeding
  • promote closure of patent ductus arteriosus
67
Q

first generation of NSAIDS suppress inflammation but

A

pose risk of serious harm

68
Q

first generation NSAIDs in dysmenorrhea

A

uterus SM produces prostaglandins associated with cramping. blocking cox can alleviate.
cox 2 is associated with heavy bleeding. blocking can alleviate.

69
Q

prototype of 1st gen NSAID

A

ASA

70
Q

low dose ASA indication

A

antithrombotic

71
Q

higher dose ASA indication

A

antipyretic
analgesic
anti inflammatory

72
Q

absorption of ASA

A

within 1hr

73
Q

protein binding of ASA

A

high

74
Q

traditional NSAIDS (tNSAIDs) were developed to

A

be safer alternatives to asa

75
Q

what is the primary difference between ASA and tNSAIDs?

A

the way they bind to cox.

asa: irreversible inhibition
tNSAIDs: reversible inhibition

76
Q

ASA inhibition of COX1&2

A

irreversible, meaning that the ASA binds for life. as ASA concentrations fall, ASA is still bound to the cox.

77
Q

ASA prior to surgery & rationale

A

ASA must be stopped a week prior to surgery. the life of a platelet is 8-10 days. ASA will bind to a PLT for its entire life. you need a week to give the body a chance to make PLTs that have not been bound to ASA

78
Q

tNSAID inhibition type of COX

A

reversible.
as the concentration of tNSAIDs decrease below therapeutic, cox are able to produce prostaglandins again. Dosing needs to be repeated to keep this effect.

79
Q

two most common OTC tNSAIDs

A

ibuprofen

naproxen

80
Q

ibuprofen vs naproxen

A

ibuprofen: better for dysmenorrhea
naproxen: better for joint pain but more GI effects

81
Q

FDA warning for tNSAIDs

A

can cause MI or stroke in those treated chronically with tNSAIDs.

82
Q

thromboxane prostacyclin imbalance hypothesis

A

We have a balance between prostaglandin signaling and plts/endothelial cells. Endothelial cells express COX 2, producing prostacyclin (required for normal vasodilation/inhibition of plt agg). that balances out thromboxane production by cox1 and plts. in plts, cox1 produces thromboxane a2, promoting vasoconstriction and plt agg. normally there is this balance between the two, promoting homeostasis.
-balance between prostaglandin signaling and plts/endo cells. endothelial cells express cox2. cox 2 produces prostacyclin which does vasodilation and prevents aggregation. so endo cells = open vessels and free flowing plts.

-thromboxane production by cox1 and plts = thromboxane 2 which = vast con and agg. so cox1-> thromboxane-> constricted vessels and sticky platelets.

when you inhibit cox2, you’re tipping the scales more towards constricted vessels and platelet aggregation.

selective cox2 inhibitors are well known for propensity to cause mi/stroke because they inhibit cox2 in endothelial cells. decrease prostacyclin signaling = thromboxane production in platelets, vasoconstriction and plt agg. this leads to mi and stroke. tNSAIDs and ASA (non selective), promote inhibition of cox2 and prostacyclin. then youre tilted toward thromboxane - vasoconstriction, htn, plt agg, clot formation.

83
Q

Cox 2 selective inhibitor suffix

A

coxibs

84
Q

cox 2 selective inhibitors were created

A

to be safer alternatives to tNSAIDs in terms of GI bleed/ulcerations

85
Q

some tNSAIDs are now known to be cox-2-selective. they are:

A

meloxicam
diclofenac
etodolac

86
Q

cox-2-selective inhibitors are ____ inhibitors of cox-2

A

reversible

87
Q

T or F: cox-2-inhibitors are just as effective as tNSAIDs in suppressing inflammation and pain

A

true.

88
Q

adverse effects of cox-2-selective inhibitors

A

impaired renal function
htn
edema
inc risk for MI/stroke

89
Q

Vioxx

A

former cox-2-selective inhibitor drug which was very effective/had low GI effects but was pulled from the market because of MI/strokes after studies showed a link. The results were suppressed initially until more organizations did their own studies and the link was stronger established.

90
Q

celecoxib new research is showing

A

higher risk for cardiac calcification and aortic stenosis

91
Q

acute, mild to moderate, nociceptive and inflammatory pain treatment modality

A

aspirin, tNSAIDs, coxibs

92
Q

chronic mild to moderate pain

A

ASA*
tNSAIDs

*ASA is not really used anymore in a chronic way.

93
Q

NSAIDs in neuropathic and functional pain

A

are not effective

94
Q

precision trial: celecoxib

A

evaluating CV safety of celecoxib compared to naproxen or ibuprofen in pts with arthritis.

suggesting that the risk, in moderate doses, is equal among these meds.

95
Q

why is GI mucosa damaged in NSAID use?

A

Arachidonic acid is converted to prostaglandins in the GI tract.
COX 1 is expressed in GI tract, which converts arachidonic acid to PGE2 and PGI. These things have gastric protective effects like mucous secretion, bicarb, and increased mucosal blood flow. When inhibited, peptic ulcers and GI bleeding may occur.

96
Q

why are kidneys damaged in NSAID use?

A

cox 1 and 2 are expressed in the kidney. They produce PGE2&PGI which facilitate GFR and Na/water excretion.
when these enzymes are blocked, we get edema, HTN, and kidney injury.

97
Q

why are there CV effects in NSAID use?

A

we have a natural balance between cox 1 and 2 in the CV system’s endothelial cells and platelets. when the balance is disturbed, constriction effects become dominant, leading to MI/stroke.

98
Q

GI effects of NSAIDs

A 
pain
nausea
diarrhea (rare)
gastic ulcers
bleeding
99
Q

platelet effects in NSAID use

A

inhibited activation, therefore a risk of hemorrhage.

100
Q

renal effects in NSAID use

A

salt/water retention
edema
decrease FX of anti-HTN/diuretics
hyperkalemia

101
Q

CV effects in NSAID use

A

MI

stroke

102
Q

hypersensitivity effects in NSAID use

A

rhinitis
edema
asthma

103
Q

hypersensitivity in NSAID use: rationale

A

arachidonic acid can be converted into lipoxygenase as well. these are known to produce inflammation. if you inhibit cox, there will be more arachidonic acid available to be converted by things like lipoxygenase, which can convert arachidonic acid into leukotrienes which promote bronchospasm, mucous plugging, and further inflammation. aka leukotriene shunt.

104
Q

combining asa with any other nsaid

A

contraindicated.

synergistic effects on GI mucosa

105
Q

risk of ulcer complications by ASA or tNSAIDs is increased by what other drugs? (3)

A

warfarin
glucocorticoids
SSRIs

106
Q

NSAIDs and ACE inhibitors

A
  1. ACEs will be less effective

2. additive effects against renal function

107
Q

Which meds that bind to albumin may be displaced due to NSAIDs binding to albumin as well?

A

warfarin
mtx
sulfonylureas

108
Q

ibuprofen blocks the interaction of ASA with _____

A

cox 1

109
Q

what should you do if a patient on daily ASA needs inbuprofen or another NSAID? and why?

A

take ASA 1-2 hours before ibuprofen.

ASA binds irreversibly to cox1 and platelets. When you introduce ibuprofen, it will have no effect because the plts will be bound to asa.

110
Q

Options for preventing GI bleeding on NSAIDs/ASA

A
  • lowest effective dose possible
  • substitute acetaminophen instead
  • use a cox-2 selective instead
  • administer NSAID/ASA with a PPI
  • reduce NSAID/ASA dose and add opioid.
111
Q

Advil dual action

A

new drug

250mg aceta/125mg ibuprofen

Pharm (31 decks)

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