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Pharm U2 > 5) Rheumatoid Arthritis and Gout > Flashcards

5) Rheumatoid Arthritis and Gout Flashcards

1
Q

What is the class for Indomethacin (Indocin)

A

Non-selective NSAID

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2
Q

What is the mechanism for Indomethacin (Indocin)

A

Eliminate pain; reduce inflammation (but does not slow disease progression)

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3
Q

What are the therapeutics for Indomethacin (Indocin)

A

Rheumatoid arthritis; acute gouty arthritis

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4
Q

What are the important side effects for Indomethacin (Indocin)

A

Gastric and duodenal ulcers

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5
Q

What is the class for Naproxen (Aleve)

A

Non-selective NSAID

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6
Q

What is the mechanism for Naproxen (Aleve)

A

Eliminate pain; reduce inflammation (but does not slow disease progression)

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7
Q

What are the therapeutics for Naproxen (Aleve)

A

Rheumatoid arthritis; acute gouty arthritis

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8
Q

What are the important side effects for Naproxen (Aleve)

A

Gastric and duodenal ulcers

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9
Q

What is the class for COX-2 inhibitors

A

Selective NSAID

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10
Q

What is the mechanism for COX-2 inhibitors

A

Eliminate pain; reduce inflammation (but does not slow disease progression)

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11
Q

What are the therapeutics for COX-2 inhibitors

A

Superseding conventional NSAIDs for rheumatoid arthritis

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12
Q

What are the important side effects for COX-2 inhibitors

A

50% fewer gastric and duodenal ulcers than traditional NSAIDs

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13
Q

What is the class for Quinolones

A

DMARD (antimalarial)

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14
Q

What is the mechanism for Quinolones

A

Reduces T-cell activation & chemotaxis

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15
Q

What are the therapeutics for Quinolones

A

Rheumatoid arthritis, SLE

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16
Q

What are the important side effects for Quinolones

A

Retinal damage (chloroquine)

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17
Q

What are the miscellaneous for Quinolones

A

Used for patients who no longer respond to NSAIDS or can’t tolerate other DMARDs

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18
Q 
What is the class for Glucocorticoids
(Corticosteroids)
A

DMARD

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19
Q

What is the mechanism for Glucocorticoids

Corticosteroids

A
  1. Inhibits phospholipase A2 (inhibiting release of arachidonic acid and, thus, formation of prostaglandins)
  2. Inhibits cytokine production (which prevents induction of COX-2)
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20
Q

What are the therapeutics for Glucocorticoids

Corticosteroids

A

Rheumatoid arthritis; acute gouty arthritis (intraarticular injection for relief of acute monoarticular gout)

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21
Q

What are the important side effects for Glucocorticoids

Corticosteroids

A

Cushingoid symptoms

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22
Q

What are the miscellaneous for Glucocorticoids

Corticosteroids

A 
Started initially (fast acting) before other drugs become effective
Can give orally or intra-articularly
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23
Q

What is the class for Sulfasalazine (Azulfidine)

A

DMARD

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24
Q

What is the mechanism for Sulfasalazine (Azulfidine)

A

Likely inhibition of IL-1 & TNF-alpha release

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25
Q

What are the therapeutics for Sulfasalazine (Azulfidine)

A

Rheumatoid arthritis

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26
Q

What are the important side effects for Sulfasalazine (Azulfidine)

A

N/V, skin rashes, neutropenia (30% of patient discontinue drug)

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27
Q

What are the other side effects for Sulfasalazine (Azulfidine)

A

Headaches

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28
Q

What are the miscellaneous for Sulfasalazine (Azulfidine)

A

Acts more quickly than other drugs

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29
Q

What is the class for Methotrexate (Trexall)

A

DMARD

Immunosuppressive

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30
Q

What is the mechanism for Methotrexate (Trexall)

A
  1. Inhibition of aminoimidazolecarboxamide (AICAR) transformylase and
    thymidylate synthetase, with secondary effects on PMN chemotaxis
  2. Causes adenosine accumulation, which inhibits inflammation
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31
Q

What are the therapeutics for Methotrexate (Trexall)

A

Rheumatoid arthritis

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32
Q

What are the important side effects for Methotrexate (Trexall)

A

Nausea, stomatitis, hepatotoxicity (rare)

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33
Q

What are the miscellaneous for Methotrexate (Trexall)

A

Takes several weeks to start working; “gold standard” of therapy

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34
Q

What is the class for Leflunomide (Arava)

A

DMARD

Immunosuppressive

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35
Q

What is the mechanism for Leflunomide (Arava)

A

Inhibits dihydroorotate dehydrogenase (DHODH), which inhibits T-lymphocyte response to stimuli

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36
Q

What are the therapeutics for Leflunomide (Arava)

A

Rheumatoid arthritis

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37
Q

What are the important side effects for Leflunomide (Arava)

A

Diarrhea, hepatotoxity

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38
Q

What are the miscellaneous for Leflunomide (Arava)

A

Takes several weeks to start working; oral prodrug

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39
Q

What is the class for Etanercept (Enbrel)

A

Biologic Response Modifiers

40
Q

What is the mechanism for Etanercept (Enbrel)

A

Blocks binding of TNF to TNF receptors

41
Q

What are the therapeutics for Etanercept (Enbrel)

A

Rheumatoid arthritis

42
Q

What are the miscellaneous for Etanercept (Enbrel)

A

Twice weekly subcutaneous injections

43
Q

What is the class for Infliximab (Remicade)

A

Biologic Response Modifiers

44
Q

What is the mechanism for Infliximab (Remicade)

A

Blocks binding of TNF to TNF receptors

45
Q

What are the therapeutics for Infliximab (Remicade)

A

Rheumatoid arthritis

46
Q

What are the important side effects for Infliximab (Remicade)

A

Antigenic response to murine monoclonal Ab

47
Q

What is the class for Adalimumab (Humira)

A

Biologic Response Modifiers

48
Q

What is the mechanism for Adalimumab (Humira)

A

Blocks binding of TNF to TNF receptors

49
Q

What are the therapeutics for Adalimumab (Humira)

A

Rheumatoid arthritis

50
Q

What are the miscellaneous for Adalimumab (Humira)

A

Fully human, so no antigenic response; twice monthly injections

51
Q

What is the class for Golimumab

A

Biologic Response Modifiers

52
Q

What is the mechanism for Golimumab

A

Blocks binding of TNF to TNF receptors

53
Q

What are the therapeutics for Golimumab

A

Rheumatoid arthritis

54
Q

What are the important side effects for Golimumab

A

Risk of serious infections

55
Q

What is the class for Certolizumab

A

Biologic Response Modifiers

56
Q

What is the mechanism for Certolizumab

A

Blocks binding of TNF to TNF receptors

57
Q

What are the therapeutics for Certolizumab

A

Rheumatoid arthritis

58
Q

What are the important side effects for Certolizumab

A

Risk of serious infections

59
Q

What are the miscellaneous for Certolizumab

A

Conjugated to PEG for stabilization

60
Q

What is the class for Anakinra (Kineret)

A

Biologic Response Modifiers

61
Q

What is the mechanism for Anakinra (Kineret)

A

IL-1 Receptor Antagonist

62
Q

What are the therapeutics for Anakinra (Kineret)

A

Rheumatoid arthritis

63
Q

What are the miscellaneous for Anakinra (Kineret)

A

Short (6 hr) plasma half-life; daily treatment with high doses

64
Q

What is the class for Tocilizumab (Actemra)

A

Biologic Response Modifiers

65
Q

What is the mechanism for Tocilizumab (Actemra)

A

IL-6 Receptor Antagonist

66
Q

What are the therapeutics for Tocilizumab (Actemra)

A

Rheumatoid arthritis

67
Q

What is the class for Rituximab (Rituxan)

A

Biologic Response Modifiers

68
Q

What is the mechanism for Rituximab (Rituxan)

A

Anti-CD20 mAb, reduces circulating B cells

69
Q

What are the therapeutics for Rituximab (Rituxan)

A

Rheumatoid arthritis

70
Q

What are the important side effects for Rituximab (Rituxan)

A

Infections; hypersensitivity reactions

71
Q

What are the miscellaneous for Rituximab (Rituxan)

A

Used for RA refractory to TNF-alpha inhibitors

72
Q

What is the class for Abatacept (Orencia)

A

Biologic Response Modifiers

73
Q

What is the mechanism for Abatacept (Orencia)

A

Inhibits T-cell activation and induces T-cell apoptosis

74
Q

What are the therapeutics for Abatacept (Orencia)

A

Rheumatoid arthritis

75
Q

What are the important side effects for Abatacept (Orencia)

A

Headaches; infections

76
Q

What are the miscellaneous for Abatacept (Orencia)

A

Used in patients for RA refractory to MTX or TNF-alpha inhibitors

77
Q

What is the mechanism for Colchicine (Colcrys)

A

Prevents tubulin polymerization & leads to inibition of leukocyte migration, phagocytosis, and release of cytokines

78
Q

What are the therapeutics for Colchicine (Colcrys)

A

Acute gouty arthritis

79
Q

What are the important side effects for Colchicine (Colcrys)

A

Long-term use causes peripheral neuropathy & neutropenia

80
Q

What are the other side effects for Colchicine (Colcrys)

A

Nausea, vomiting, abdominal pain, troublesome diarrhea

81
Q

What are the miscellaneous for Colchicine (Colcrys)

A

Works in 12-24 hours!

82
Q

What is the class for Probenecid (Benemid)

A

Uricosuric Agent

83
Q

What is the mechanism for Probenecid (Benemid)

A

Compete with urate at the anionic transport site of the renal tubule and inhibit urate reabsorption

84
Q

What are the therapeutics for Probenecid (Benemid)

A

Chronic tophaceous gout

85
Q

What are the important side effects for Probenecid (Benemid)

A

Urate crystal mobilization and acute gouty arthritis

86
Q

What are the other side effects for Probenecid (Benemid)

A

Gastrointestinal irritation

87
Q

What are the miscellaneous for Probenecid (Benemid)

A

Secretion of some weak acids (e.g., penicillin) is reduced

88
Q

What is the mechanism for Allopurinol (Zyloprim)

A
  1. Reduces uric acid synthesis by inhibiting xanthine oxidase (competitive inhibition) –> alloxanthine
  2. Alloxanthine is a non-competitive inhibitor of xanthine oxidase
89
Q

What are the therapeutics for Allopurinol (Zyloprim)

A

Chronic tophaceous gout

90
Q

What are the important side effects for Allopurinol (Zyloprim)

A

Acute attacks of gouty arthritis early in treatment due to mobilization of urate crystals

91
Q

What is the mechanism for Febuxostat (Uloric)

A

Non-purine, non-competitive antagonist of xanthine oxidase

92
Q

What are the therapeutics for Febuxostat (Uloric)

A

Chronic tophaceous gout

93
Q

What are the important side effects for Febuxostat (Uloric)

A

Nausea, rash, arthralgias

94
Q

What are the miscellaneous for Febuxostat (Uloric)

95
Q

What is the class for Pegloticase (Krystexxa)

A

Recombinant, stabilized uricase

96
Q

What is the mechanism for Pegloticase (Krystexxa)

A

Converts uric acid to allantoin

97
Q

What are the therapeutics for Pegloticase (Krystexxa)

A

Chronic tophaceous gout

Pharm U2 (11 decks)

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