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Therapeutics I > NSAIDs and DMARDs > Flashcards

NSAIDs and DMARDs Flashcards

1
Q

How do prostaglandins potentiate pain?

A

They potentiate the stimulation of nerve endings produced by histamine or bradykinin (these cause pain)

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2
Q

What does pyrogen do?

A

Stimulate prostaglandin production in the hypothalamus, which increases body temperature (fever)

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3
Q

What are the GI side effects of NSAIDs?

A 
Dyspepsia
N/V
 blood loss
 ulcer
 GI hemorrhage
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4
Q

How can you decrease GI side effects of NSAIDs?

A

Administer w/food

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5
Q

What causes GI side effects?

A
  1. NSAIDs are acidic
  2. NSAIDs inhibit PGE2, which is cytoprotective in the gastric mucosa
  3. NSAIDs inhibit platelet aggregation –> bleeding
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6
Q

What can be used to decrease hypersensitivity from NSAIDs?

A

Lipoxygenase inhibitors–hyposensitivity caused by leukotrienes

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7
Q

What disease state is more likely to have hypersensitivity to NSAIDs?

A

Asthma

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8
Q

What is Reye’s syndrome?

A

A rare, acute, life-threatening condition characterized by vomiting, delirium, and coma

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9
Q

Who is at risk for Reye’s syndrome?

A

Children (<12) who have flu or chicken pox

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10
Q

What class of NSAIDs causes Reye’s Syndrome?

A

Salicylates

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11
Q

What are the CNS side effects of NSAIDs?

A

Tinnitus
Dizziness
Headache

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12
Q

Who is at risk for renal failure from use of NSAIDs?

A

Patients with cardiovascular, hepatic, and renal diseases

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13
Q

Order of side effect frequency of aspirin, indomethacin, naproxen, and sulindac?

A

Aspirin = indomethacin > naproxen > sulindac

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14
Q

What two drugs are used to prevent GI side effects with NSAIDs?

A

PPIs and misoprostol

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15
Q

What is misoprostol?

A

PGE1 analog–mucus protectant

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16
Q

Why is naproxen used in combination products?

A

It has fewer side effects than other NSAIDs

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17
Q

What causes the drug interactions associated with NSAIDs?

A

NSAIDs are highly bound to albumin

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18
Q

What class of drugs commonly interacts with NSAIDs?

A

anticoagulants

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19
Q

What should be done to anticoagulant dosing when administered with NSAIDs?

A

Decrease (NSAIDs compete for albumin, which causes more free anticoagulant in the blood PLUS NSAIDs are already antithrombotic)

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20
Q

What functional group do most NSAIDs have?

A

Carboxylic acid

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21
Q

Where is the acidic group located in salicylates?

A

Directly off of the carbon ring

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22
Q

Where is the acidic group located in arylacetic acids and arylpropionic acids?

A

1 carbon between the acid and the ring

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23
Q

What is the structural difference between arylpropionic acids and arylacetic acids?

A

Arylpropionic acids have an alpha methyl group on the carbon next to the COOH

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24
Q

What does a methyl group on the carbon atom separating the acidic group from the aromatic ring due to activity levels?

A

Increases

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25
Q

What does a second area of lipophilicity that is noncoplanar with the aromatic ring due to activity levels?

A

Enhances

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26
Q

What was the first salicylate derived from?

A

Willow and poplar bark

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27
Q

What form are salicylates absorbed in?

A

Ionic in small intestine mainly, also unionized in stomach

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28
Q

What enzyme do salicylates inhibit?

A

COX-1 and COX-2

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29
Q

What are the three salicylates?

A

Aspirin
Salsalate
Diflunisal

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30
Q

How does aspirin irreversibly inhibit COX?

A

Acetylates a serine residue in the active site

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31
Q

What is aspirin hydrolyzed into?

A

Salicylate

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32
Q

How does aspirin reduce the risk of MI?

A

It blocks TXA2–which causes platelet aggregation?

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33
Q

Is aspirin found in solution form?

A

No–not stable

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34
Q

What is the structure of salsalate?

A

Dimer of salicylic acid?

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35
Q

Does salsalate cause GI bleeding?

A

No–not active in the stomach b/c it needs to be cleaved

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36
Q

Where is salsalate get hydroylzed?

A

small intestine

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37
Q

Is diflunisal a more potent alangesic than aspirin?

A

Yes

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38
Q

Is diflunisal a more potent antipyretic than aspirin?

A

No

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39
Q

Does diflunisal have fewer side effects than aspirin?

A

yes

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40
Q

Does diflunisal have a longer half-life than aspirin?

A

Yes (3-4 times)

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41
Q

What are the arylacetic acids?

A

Indomethacin
Sulindac
Etodalc
Diclofenac

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42
Q

Which arylacetic acids are somewhat selective for COX-2?

A

Etodalc and Diclofenac

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43
Q

Which arylacetic acid inhibits both COX and lipoxygenase pathways?

A

Diclofenac

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44
Q

Which arylacetic acid is a prodrug?

A

Sulindac–sulfoxide group reduced

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45
Q

What is the least potent arylacetic acid?

A

Sulindac

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46
Q

Which arylacetic acids can be used for long-term use?

A

Sulindac, etodalc

47
Q

Which arylacetic acids have lesss GI side effects?

A

Sulindac (prodrug)

Etodalc (COX-2 selective)

48
Q

Which aryacetic acid is not stable in solution due to hydrolysis of the amide bond?

A

Indomethacin

49
Q

Which arylacetic acid has high incidents of side effects?

A

Indomethacin

50
Q

What is the most commonly used NSAID?

A

Diclofenac

51
Q

What is etodalc used for?

A

Osteoarthritis

52
Q

What is sulindac used for?

A

Chronic inflammation

53
Q

What are the arylpropionic acids?

A

ibuprofen, naproxen, ketoralc

54
Q

Which of the arylpropionic acids is a racemic mixture?

A

Ibuprofen

55
Q

How does ibuprofens potency compare to aspirin and indomethacin?

A

In between them

56
Q

Is naproxen or ibuprofen more potent?

A

Naproxen

57
Q

What is naproxen used for?

A

Rheumatoid arthritis and osteoarthritis

58
Q

What is the structure of ketorolac?

A

Cyclized heteroarylpropionic acid derivative

59
Q

What is ketorolac used for?

A

Short term management of severe pain (as strong as an opioid)

60
Q

What are the non-carboxylate NSAIDs?

A

Nabumetone

Meloxicam

61
Q

What is the active form of nabumetone?

A

6-MNA

62
Q

What is nabumetone good at?

A

Anti-inflammation (weak analgesic activity)

63
Q

Does nabumetone have many gastric side effects?

A

Nope (prodrug)

64
Q

Which NSAID is longest acting?

A

Meloxicam

65
Q

How does meloxicam’s potency compare to aspirin and indomethacin?

A

About as potent as indomethacin

66
Q

Which of the non-carboxylates is selective for COX-2

A

Meloxicam

67
Q

What are the most potent anti-inflammatory NSAIDs?

A

Meloxicam
Indomethacin
Diclofenac
Sulindac

68
Q

what are the safest and most potent NSAIDs?

A

Meloxicam

Diclofenac

69
Q

What is the least potent NSAID?

A

Aspirin

70
Q

What is the difference between the COX-1 and COX-2 active site?

A

COX-2 has a valine instead of isoleucine–makes it a larger active site

71
Q

How are COX-2 selective inhibitors structurally different from non-selective?

A

They have larger and more rigid functional groups (b/c COX-2 has bigger binding site)

72
Q

What are the 3 FDA classified COX-2 Inhibitors?

A

Celecoxib
Rofecoxib
Valdecoxib

73
Q

What is the only selective COX-2 inhibitor still in market?

A

Celecoxib (Celebrex)

74
Q

How do selective COX-2 inhibitors increase the risk of cardiovascular events?

A

They inhibit PGI2 (inhibiting platelet aggregation) but not TXA2 (which causes platelet aggregation)–> increased risk of clots (strokes, MIs, etc)

75
Q

What drug is celebrex’s potency similar to?

A

Naproxen

76
Q

What is celecoxib used for?

A

Rheumatoid arthritis
Osteoarthritis
Pain/inflammation/fever

77
Q

What does acetaminophen do?

A

Reduce pain and fever (not inflammation)

78
Q

How does acetaminophen work?

A

It scavenges peroxynitrite which is required for PGHS (COX)–only works with low levels of peroxynitrite, not during inflammation when levels are high

79
Q

What is the major caution with acetaminophen?

A

Hepatotoxicity

80
Q

What causes hepatotoxicity from acetaminophen?

A

It is made into N-acetylmidoquinone by CYP450, which is reduced by glutathione, Too much APAP means more is made, which means more glutathione is used. Glutathione is needed for cells, so this causes cell damage in the liver

81
Q

What can make acetaminophen toxicity worse? How?

A

Alcohol–induces CYP450 enzyme so more N-acetylmidoquinone is made form APAP more quickly

82
Q

How long do DMARDs take to act?

A

1 to 6 months

83
Q

What is the common mechanism of action of DMARDs?

A

Immunosuppression

84
Q

What are the 3 uses for DMARDs?

A

Rheumatoid arthritis
Inflammatory bowel disease
Reduce rejection in organ transplant

85
Q

WHat is the first line treatment of RA?

A

Methotrexate

86
Q

What is the MOA of methotrexate?

A

Inhibits ribonucleotide transformylase and thymidylate synthetase to decrease purine and pyrimidine synthesis

87
Q

What are side effects of methotrexate?

A

Gi symptoms, stomatitis, rash, hair loss
Myelosuppression (decreased bone marrow activity)
Hepatotoxicity
Pulmonary toxicity

88
Q

When is methotrexate contraindicated?

A

Pregnancy

89
Q

What is the MOA of leflunomide?

A

Pyrimidine synthesis inhibitor and T cell proliferation inhibitor

90
Q

What are the side effects of leflunomide?

A

Heptotoxicity, diarrhea, hair loss, rash

91
Q

What should you monitor when taking leflunomide?

A

Hepatotoxicity

92
Q

When is leflunomide contraindicated?

A

Any women of childbearing age

93
Q

Is leflunomide a prodrug?

A

Yep

94
Q

What is hydroxychloroquine?

A

Protein secretion inhibitor–in lysosomes

95
Q

What should be monitored when taking hydroxychloroquine?

A

Opthalmologic monitoring for reversible retinal toxicity

96
Q

What does sulfasalazine do?

A

Suppress release of cytokines from macrophages

97
Q

How long does sulfasalazine take to work?

A

Several months

98
Q

What needs to be monitored with sulfasalazine use?

A

myelosuppression

99
Q

What are the active components of sulfasalazine?

A

sulfapyridine and 5-aminosalicylic acid

100
Q

What is infliximab?

A

TNF blocker–chimeric

101
Q

How is infliximab given?

A

IV every 8 weeks

102
Q

What is adalimumab?

A

Human antibody to TNF-alpha

103
Q

How is adalimumab given?

A

Subcutaneously every 2 weeks

104
Q

What is etanercept?

A

TNF-alpha receptor antibody (competitively inhibits TNF-alpha)

105
Q

What is the IL-1 receptor antagonist?

A

Anakinra

106
Q

Can anakinra be used with TNF blockers?

A

No

107
Q

What is rituximab?

A

Monoclonal antibody against CD20–induces apoptosis of B cells
Blocks activation of T cells

108
Q

When is rituximab used?

A

With methotrexate if TNF-alpha blockers don’t work

109
Q

What is the risk with rituximab?

A

Serious infection (antibody production decreases)

110
Q

What is abatacept?

A

Fusion protein of cytotoxic T-lymphosyte associated protein 4 (CTLA4) and FC region of human antibody

111
Q

How does abatacept work?

A

It mimics CTLA4 to bind to CD80 on APCs, thereby preventing activation of T cells

112
Q

Can abatecept be combined with TNF-alpha blockers?

A

no

113
Q

What are the side effects of abatacept?

A

Risk of serious infection

Risk of lymphomas

Therapeutics I (9 decks)

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