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.Pharmacology > Chapter 18: NSAIDs and Acetaminophen > Flashcards

Chapter 18: NSAIDs and Acetaminophen Flashcards

1
Q

What is pain?

A

basic bodily sensation introduced by noxious stimulus

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2
Q

t/f pain is a protective response to keep us from hurting ourselves

A

t

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3
Q

thermal stimuli are sensed by ___ receptors

A

TRP heat sensitive cation channels

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4
Q

mechanical stimuli are sensed by ___ receptors

A

mechanosensitive ion channel

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5
Q

after the initial pain stimulus, how is pain taken to be processed?

A

AP travels back through the spinal cord and brain stem to the cortex to be processed

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6
Q

the greater the pain stimuli, the AP is ____

A

more frequent

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7
Q

what is adaptive pain?

A

painful stimulus that has a physiological purpose

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8
Q

in adaptive pain, as soon as the noxious stimulus is removed, what happens to the pain stimulus?

A

goes away

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9
Q

nociceptive/mechanical pain experienced when you’ve touched something hot and move your hand is an example of ____ pain

A

adaptive

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10
Q

inflammatory pain when you’ve injured yourself and the immune system is helping to repair the damage and prevent infection is an example of ____ pain

A

adaptive

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11
Q

what is maladaptive pain?

A

painful stimulus that has no physiological purpose

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12
Q

maladaptive pain occurs when theres been ___ or ___ normal pain transduction

A

damage or disruption

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13
Q

persistant pain that remains after an injury is healed is called ___ and is an example of ___type pain

A

chronic pain; maladaptive

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14
Q

nerve pain may cause ___ pain where pain signals are initiated w/o a noxious cause

A

neuropathic

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15
Q

neuropathic pain is a form of ___ type pain

A

neuropathic

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16
Q

when can inflammatory pain be maladaptive?

A

if in an autoimmune disease that cause over production of cytokines and pro inflammatory mediators

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17
Q

cytokines and pro inflammatory mediators stimulate ___ causing pain

A

nociceptive nerve fibers

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18
Q

autoimmune diseases can cause ___ damage

A

tissue

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19
Q

t/f pain is very subjective

A

true

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20
Q

what are the 3 categories of pain perception?

A

mild, moderate, severe

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21
Q

t/f pain intensity scales are useful for knowing if an analgesic is needed and what type

A

t

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22
Q

for acute mild pain (1-3 on scale) what is the appropriate Rx treatment?

A

NSAIDs and acetaminophen

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23
Q

for acute moderate pain (4-6 on scale) such as after minor surgery, the appropriate treatment is __

A

weak opioid such as codeine w/ or w/o a NSAID or acetaminophen

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24
Q

for acute severe pain (7-10 on scale) such as after major trauma or surgery, the appropriate treatment is ___

A

opioids

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25
Q

t/f to best treat pain, you need to go to the root of the pain

A

t

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26
Q

arthritis pain is managed with what type of analgesic?

A

anti-inflammatory (steroids and NSAIDs)

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27
Q

disease modifying anti rheumatic drugs (DMARDs) and immunomodulators are a mainstay of therapy to reduce ___ caused by chronic inflammation

A

tissue damage

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28
Q

neuropathic pain can be modulated with drugs that affect ___

A

neurotransmission

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29
Q

decreasing the ___ of damaged nerves will reduce pain transmission

A

excitability

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30
Q

t/f antidepressants and anti seizure drugs have analgesic effects bc they decrease excitability of damaged nerves

A

t

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31
Q

if the underlying cause of pain is unknown, or treatment with other analgesics is not sufficient, what treatment option may be needed>

A

opioids

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32
Q

t/f once you get to the top of the analgesic ladder, you’re stuck there and cant get anymore help

A

false

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33
Q

t/f non-pharm is important to chronic pain management

A

true

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34
Q

what are some non-pharm options that may be used for chronic pain?

A

physiotherapy, acupuncture, lifestyle modification

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35
Q

what are the steps of the analgesic ladder?

A
  1. non-opioids +/- adjuvants
  2. mild opioids + non-opioids +/- adjuvants
  3. severe opioids +/- non-opioids +/- adjuvants
  4. invasive treatment
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36
Q

ASA, ibuprofen, naproxen, indomethacin, diclofenac, and celecoxib are all ___ analgesics

A

NSAIDs

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37
Q

NSAIDs reduce inflammation by decreasing the production of ___ which reduces the stimulation of ___ receptors on nerve fibers and also reduces ___ that often accompanies inflammation

A

pro inflammatory mediators; chemical; swelling

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38
Q

does acetaminophen have significant anti-inflammatory effects

A

no

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39
Q

what is the normal protective function of inflammation?

A

avoid infection and repair tissue damage

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40
Q

in some cases, pain of inflammation persists due to sensitization of ___fibers

A

nociceptive

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41
Q

peripheral sensitization occurs when the nociceptive nerve fibre is stimulated by inflammatory mediators like __, and other signalling molecules like ___, __ and __

A

prostaglandins; bradykinins, adenosine, and neuropeptides

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42
Q

peripheral sensitization causes nociceptive nerve fibers to become more sensitive to pain so when pain is felt, it is perceived as being more __

A

intense

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43
Q

t/f sensitization of nociceptive fibers can become so intense that even stimulus that shouldn’t cause pain will be perceived as painful

A

t

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44
Q

when a non-painful stimulus causes pain, it is called ___

A

allodynia

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45
Q

prostaglandins, leukotrienes, prostacyclin and thromboxane are all mediators of the ___ pathway

A

arachidonic acid

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46
Q

in the arachidonic acid pathway, ___ are used to make inflammatory mediators

A

phospholipids

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47
Q

what are the 2 cyclooxyrgenase isoforms?

A
  1. COX1

2. COX2

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48
Q

COX___ is expressed in many tissues and helps maintain cellular functions such as mucous secretion, regulation platelet aggregation, and smooth muscle contraction

A

1

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49
Q

COX__ is expressed in many tissues, including kidneys and endothelium.

A

2

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50
Q

COX___ is responsible for increased inflammation

A

2

51
Q

prostaglandins are pro-___ and have ___ activity

A

inflammatory; cytoprotective

52
Q

thromboxane and prostacyclin regulate platelet ___

A

aggregation

53
Q

COX 2 promotes the production of pro-inflammatory prostaglandins, particularly ___

A

PGE2

54
Q

PGE2 drives the ___ response

A

immune

55
Q

increased prostaglandins causes ___ in the periphery and ___ in the CNS

A

inflammation pain/swelling; fever

56
Q

COX__ is the target of anti-inflammatory drugs

A

2

57
Q

until the late __(year) it was not possible to selectively inhibit COX2

A

1990s

58
Q

___ is currently the only clinically available, selective COX-2 inhibitor for human use in Canada

A

celecoxib

59
Q

t/f Celebrex (celecoxib) requires a RX in Canada

A

t

60
Q

all COX inhibitors are ____antagonists

A

competitive

61
Q

indomethacin is typically only used in the clinical treatment of ___

A

gout

62
Q

what is gout?

A

acute inflammation of the joints due to uric acid bulid0up and crystallization

63
Q

in reversible inhibition of COX by something like ibuprofen, during periods when drug is not bound to the COX, it can function, but overall there is a decrease in ___ production

A

prostaglandin

64
Q

when ibuprofen is used, higher concentration of ___ are needed to out-compete the drug to produce prostaglandins

A

arachidonic acid

65
Q

what is the deference in stimulating an enzyme vs stimulating a receptor?

A

enzyme stimulation results in direct influence on cellular product production

receptor stimulation results in altered signalling pathway

66
Q

in the presence of a competitive antagonist, the concentration needed to produce a product causes that curve to shift to the ___

A

right

67
Q

as a reversible inhibitor of an enzyme is cleared from the body, the functionality of the enzyme is ___

A

restored to normal

68
Q

even with repeated and continued dosing of COX inhibitors, if the cell received ____, a greater amount of arachidonic acid would be produced and could block out the drug

A

large inflammatory signal

69
Q

what is an example of an irreversible COX inhibitor?

A

ASA

70
Q

ASA binds to COX in what way?

A

covalently

71
Q

when ASA binds to COX, it adds a ___ group to the enzyme active site

A

acetyl

72
Q

___ is the byproduct of ASA interacting with COX

A

salicylate

73
Q

what is the effect of ASA adding acetyl to COX?

A

prevents it from making prostaglandins

74
Q

ASA acts as a ___antagonsit at the COX enzymes

A

non-competitive

75
Q

when ASA is used, can enough arachidonic acid be made to reach peak prostaglandin production?

A

no, not until more COX are made

76
Q

why are the irreversible effects of ASA not notable in most cell types?

A

most cells make new COX continually

77
Q

t/f ASA is a poor anti-inflammatory compared to other NSAIDs

A

t

78
Q

ASA is commonly used as a ___ agent

A

anti platelet

79
Q

platelets express COX1 to produce ___ which is involved in platelet activation and aggregation

A

thromboxane A2

80
Q

platelet aggregation is one of the first steps in ___

A

blood clotting

81
Q

reducing the production of thromboxane A2 in platelets reduces the risk of ___ and __

A

heart attack and stroke

82
Q

why is taking low-dose ASA as effective as taking an antiplatelet therapy?

A

bc ASA binds irreversibly to COX-1 and bc platelets are anuclear, they cannot make more platelets so the effect is maintained for the lifetime of the platelet

83
Q

platelets express COX__

A

1

84
Q

what is the lifetime of platelet?

A

8-9 days

85
Q

if we inhibit every COX1 in every platelet at once, what would happen to the patient?

A

bleed out

86
Q

why is ASA a better anti-platelet than anti-inflammatory / analgesic?

A

higher affinity for COX1 than COX 2

87
Q

naproxen has a slight preference for COX___

A

2

88
Q

why are diclofenac and indomethacin not used systemically or in particular cases only?

A

high affinity for COX and bc that includes COX1, there will be the ADR of blocking COX1

89
Q

Celecoxib and Naproxen have much ___ half-lives compared to the other NSAIDs

A

longer

90
Q

what is the dose of ASA required for anti-platelet function?

A

81 mg / day

91
Q

what is the dose of ASA required for analgesic or anti inflammatory function?

A

650 mg Q4hr

92
Q

the primary ADR related to NSAID use are related to the inhibition of ___, ___ and ___ synthesis that are used in normal processes

A

prostaglandin, thromboxane, prostacyclin

93
Q

reduction in prostaglandin synthesis ny NSAIDs in the GI tract reduces ___, which makes the stomach and intestine more susceptible to peptic ulcers

A

secretions

94
Q

t/f there is conflicting evidence if celecoxib has risk of peptic ulcers

A

t

95
Q

if long-term NSAID use is needed, a ___ such as misoprostol or a ___ like omeprazole may be added to reduce risk of developing a peptic ulcer

A

cytoprotective agent; proton pump inhibitor

96
Q

bc celecoxib does not block COX1, it has a lower risk of __ compared to other NSAIDs

A

GI bleeding

97
Q

are NSAIDs contraindicated in patients with renal impairment? why/ why not?

A

yes; risk of nephrotoxicity

98
Q

nephrotoxicity of NSAIDs is caused by ___ in the kidneys, which reduces renal function

A

inhibition of COX1/2

99
Q

are NSAIDS contraindicated in patients with CVD / risk factors? Why/why not?

A

yes; reduction of COX2 production of prostacyclin in the endothelium which is important to blood clotting

100
Q

t/f there are conflicting studies as to if celecoxib increases risk for MI and stroke

A

t

101
Q

NSAIDs are contraindicated in the ___ trimester of pregnancy. why?

A

third; importance of COX in normal physiological processes

102
Q

t/f short term use in trimesters 1-2 has no significant risk to the fetus

A

t

103
Q

small amounts of NSAIDs can be excreted in the breast milk, so what type of NSAID should be chosen?

A

short-half life like ibuprofen

104
Q

wherever possible ___ application of analgesic for local pain is preferred over systemic

A

topical

105
Q

t/f topical application can still accumulate to have some systemic effects

A

t

106
Q

post-surgery use of NSAIDs can have negative impact on ___ and ___

A

wound healing and bone remodelling after orthopaedic surgery

107
Q

t/f even though NSAIDs are available OTC, they can still have serious ADR and interactions/contraindications

A

true

108
Q

t/f the MOA of acetaminophen is not completely clear

A

true

109
Q

the best evidence suggests that acetaminophen works by

A

being metabolized in the CNS into a compound that affects the endocannabinoid system that increases 5-HT in the spinal cord, giving analgesia

110
Q

what are 3 benefits of using acetaminophen for analgesia?

A
  1. low risk of GI ulcers
  2. no anti-platelet effects
  3. safe in pregnancy
111
Q

acetaminophen has risk of toxicity in what organ?

A

liver

112
Q

what is the max dose of acetaminophen daily?

A

4 g

113
Q

acetaminophen use is contraindicated in patients with ___ and/or ___ impairment

A

renal; hepatic

114
Q

hepatotoxicity of acetaminophen is worsened in the presence of ___

A

alcohol

115
Q

the major metabolic pathways of acetaminophen are phase __ metabolism to ___ or ___ metabolites which are excreted by the kidneys

A

2; glucuronide; sulfate

116
Q

a minor pathway exists where acetaminophen is oxidized by CYP enzyme into a toxic metabolite called___

A

NAPQI

117
Q

what normally happens to the toxic NAPQI metabolite of acetaminophen?

A

further metabolized (phase 2) to make a glutathione conjugate which is excreted

118
Q

what happens if there is not enough glutathione to convert the toxic NAPQI?

A

will accumulate and cause hepatotoxicity

119
Q

why does alcohol worsen hepatotoxicity of acetaminophen?

A

induces the CYP enzymes that create the NAPQI metabolite

120
Q

in acute acetaminophen overdose ___ can be administered to promote the glutathione rxn that eliminates the toxic metabolite

A

N-acetylcysteine

121
Q

t/f treatment for hepatoxicity must be prompt

A

t

122
Q

t/f in chronic alcohol users, even a normal dose of acetaminophen can cause liver toxicity

A

t

123
Q

t/f the liver is resilient, but severe damage can be fatal

A

t

.Pharmacology (55 decks)

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