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Pharm > Drugs to treat RA and gout > Flashcards

Drugs to treat RA and gout Flashcards

1
Q

Which cytokines are involved in RA?

A

TNFa, IL-6, IL-1, PG

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2
Q

Drugs to decrease acute joint pain

A

NSAIDS (indomethacin, naproxen)
Analgesics (acetaminophen, capsacin, opioids)
Glucocorticoids (dexamethasone)

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3
Q

What do you typically use NSAIDS/analgesics/glucocorticoids for in the rx of RA?

A

minimize symptomatic effects of disease while waiting for clinical effects of slow acting DMARDS/BRMs

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4
Q

DMARDS

A

Disease Modifying Anti-Rheumatic Drugs (DMARDs)

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5
Q

DMARDS indication

A

reduce/prevent joint damage

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6
Q

How long till DMARDS show efficacy?

A

Weeks to months

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7
Q

Commonly used DMARDS

A

Hydroxychloroquine, Sulfasalazine, Methotrexate, Leflunomide

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8
Q

Less frequently used DMARDS

A

Azathioprine, D-Penicillamine, Gold Salts, Cyclosporin, Cyclophosphamide

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9
Q

Hydroxychloroquine Indication

A

Mild RA

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10
Q

Which RA drug is a anti-malarial drug?

A

Hydroxychloroquine

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11
Q

Hydroxychloroquine MOA

A

inhibition of TLR signaling/ antigen presentation to T cells

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12
Q

Hydroxychloroquine time to effect

A

3-6 months

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13
Q

Which drugs are often given in combination with Hydroxychloroquine

A

sulfasalazine

Methotrexate

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14
Q

Is hydroxychloroquine safe in pregnancy/lactation?

A

YEs

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15
Q

Rare side effect of hydroxychloroquine

A

Ocular toxicity

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16
Q

Sulfasalazine

A

Decreases signs and symptoms of disease
Slow joint destruction
*More toxic than hydroxychloroquine
*Similar efficacy to methotrexate

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17
Q

What is the active component of sulfasalazine?

A

sulfapyridine

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18
Q

Sulfasalazine MOA

A

? interfer with T/B cell immune response

Inhibits NF-KB

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19
Q

Sulfasalazine time to effect

A

1-3 months

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20
Q

Is sulfasalazine safe during pregnancy?

A

Yes

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21
Q

Which other DMARDS is sulfasalazine often combined with

A

Hydroxychloroquine

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22
Q

Adverse effects of sulfasalazine

A

Agranulocytosis

Hepatotoxicity *reversible

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23
Q

Methotrexate

A

DRUG OF CHOICE for active moderate/severe disease

Decreases appearance of new bone erosions
Improves long term clinical outcome

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24
Q

Methotrexate time to effect

A

4-6 weeks

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25
Q

Methotrexate MOA

A

increases production of adenosine > immunosuppressive

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26
Q

Common side effect of Methotrexate

A

hepatoxicity

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27
Q

What should patients on methotrexate obtain from?

A

Alcohol

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28
Q

Rare side effects of methotrexate?

A

Pulmonary toxicity
Bone marrow suppression
Increased risk of lymphoma

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29
Q

Methotrexate is contraindicated in?

A

pregnancy/breast feeding
pre-existing liver disease
renal impairment

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30
Q

How is methotrexate excreted?

A

80-90% renally

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31
Q

is methotrexate safe in pregnant?

A

NO!

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32
Q

Leflunomide

A

= effective to sulfasalazine and methotrexate

Low cost alternative to TNF inhibtors

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33
Q

Leflunomide time to effect

A

1-2 months

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34
Q

Leflunomide MOA

A

inhibits dihydroorotate dehydrogenase, decreases synthesis of uridine

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35
Q

Adverse effects of Leflunomide

A

HTN (w/ NSAIDS)
Diarrhea, nausea, rash
Hepatotoxicity (w/ methotrexate)

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36
Q

What is Leflunomide contraindicated in?

A

Pregnancy/breast feeding

Pre-existing liver disease

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37
Q

Biologic response modifiers

A

specifically designed to inhibit either cytokines (TNFa, IL-6, IL-1) or cell types (T-cells, B-cells)

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38
Q

Which cells synthesize TNF-a?

A

CD 4+T cells, macs, mast cells

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39
Q

What does TNF-a cause?

A 
Joint inflammation (endothelials)
Cartilage breakdown (chondrocyte/synoviocyte)
Bone erosion (osteoclast)
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40
Q

How are anti-TNFa drugs given?

A

SQ or IV

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41
Q

How often are TNF-a drugs given?

A

Weekly/biweekly

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42
Q

Anti TNFa drugs time to effect

A

1-4 weeks

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43
Q

Effects of anti-TNFa

A

Decrease join pain and swelling
Decreased formation of new bone erosions
Decreased progression of structural joint damage

44
Q

What can the anti-TNFa drugs be used in combo with?

A

Methotrexate

45
Q

Adverse effects of anti-TNFa

A

increased risk of infections
Potential reactivation of latent TB, HBV
Exacerbation of pre-existing CHF
Developing of demyelinating disease (MS)

46
Q

What are the 3 anti-TNFa drugs?

A

Etanercept
Infliximab
Adalimumab

47
Q

Abatacept MOA

A

Recombinant CTLA4+ IgG

Inhibits T cell activation

48
Q

Abatacept Indication

A

slows damage to bone and cartilage

effective in pts non-responsive to TNF-a inhibitors

49
Q

Abatacept adverse effects

A

Increase risk of infection

50
Q

Abatacept contraindication

A

DO not give with TNF-a blocker

51
Q

Rituximab MOA

A

binds CD20

Depletes B cells

52
Q

Rituximab time to effect

A

3 months

53
Q

How long do the effects of rituximab last?

A

6 months- 2 years with one infusion

54
Q

Rituximab adverse effects

A

Increased infections
Reactivation of latent viruses (CMV, HSV, HBV, HCV)
PML

55
Q

Anakinra

A

Anti- IL-1R
Competitively inhibits the pro-inflammatory effects of IL-1
* less effective than anti-TNFa

56
Q

What is the half life of anakinra?

A

short (4-6 hours)

57
Q

How often must you give anakinra and how administered?

A

Sub Q once a day

58
Q

Anakinra adverse effects

A

Neutropenia
Serious infections
* complications more frequent when given with Anti-TNF-a

59
Q

Tocilizumab

A

anti- IL-6 R

60
Q

Indications of Toxilizumab

A

Patients non-responsive to TNF inhibitors

or in combo with methotrexate

61
Q

Tocilizumab Adverse effects

A 
BM suppression
serious infection 
Hepatotoxicity
Increased cholesterol
Increased malignancy
62
Q

Tocilizumab Contraindications

A

pre-existing liver disease

Low blood counts/immunosuppresives

63
Q

Tofacitinib

A

Small molecule inhibitor of cytokine signaling (anti-JAK)

64
Q

Tofacitinib adverse effects

A

BM suppression
serious infections
Increased cholesterol
Hepatotoxicity

65
Q

What co-morbidities is gout associated with?

A 
obesity
HTN
hyperlipidemia
DM II
Hyperuricemia
66
Q

What is a high serum uric acid

A

> 7 mg/dL

67
Q

What is the most common cause of high serum uric acid?

A

Decreased excretion

68
Q

Which joint is often first affected in gout?

A

first metatarophalangeal joint

69
Q

What are tophi?

A

Urate crystal deposits around the joint that promote inflammation and joint destruction

70
Q

Treatment of acute gout (relieve symptoms)

A

Clochicine

NSAIDS

71
Q

Treatment of Chronic Gout

A

Drugs that lower uric acid levels by promoting excretion
Drugs that lower uric acid levels by inhibiting synthesis
Drugs that directly degrade uric acid

72
Q

Drugs that lower uric acid levels by promoting excretion

A

Probenecid

Lesinurad

73
Q

Drugs that lower uric acid levels by inhibiting synthesis

A

Allopurinol

Febuxostat

74
Q

Drugs that directly degrade uric acid

A

Pegloticase

75
Q

Which NSAIDS are used to treat gouty attack

A

Indomethacin

Naproxen

76
Q

How do NSAIDS help in gout?

A

Reduce production of prostaglandins

77
Q

Indication of NSAIDS in gout?

A 
prophylactic Rx (w/ other anti-gout drugs)
relieve symptoms of acute gouty attack
78
Q

Which drugs are NOT used in treated acute gouty attack?

A

Aspirin

Salicylates

79
Q

Colchicine MOA

A

Prevents tubulin polymerization into microtubules

Decreases leukocyte migration and phagocytosis

80
Q

Colchicine effects

A

Anti-inflammatory

NOT analgesic

81
Q

When should you give colchicine

A

within 24-48 hours of attack

82
Q

Colchicine side effects

A

Narrow therapeutic window

Nausea, vomiting, diarrhea

83
Q

Probenecid

A

inhibits anion transporters (URAT1) in proximal renal tubules that reabsorb uric acid > increased uric acid excretion

84
Q

Probenecid indications

A

Patient that under excrete uric acid

85
Q

When should you give probenecid

A

2-3 weeks after initial attack

86
Q

What is the risk of giving probenecid too early?

A

Can initiate/ prolong acute gouty attach

87
Q

What should you give with probenecid prophylactically?

A

NSAIDs

88
Q

Probenecid contraindications

A

pts who overproduce uric acid
pts w/ kidney stones
pts with renal insufficiency

89
Q

Drug interactions with Probenecid

A

Probenecid increases excretion of drugs that are normally reabsorbed by URAT1 (indomethacin, naproxen, lorazepam, cephalosporins, methotrexate, captopril, AZTM ganciclovir)

90
Q

Allopurinol

Febuxostat

A

Inhibits xanthine oxidase

91
Q

Allopurinol

Febuxostat Indications

A

high level of uric acid synthesis
recurrent kidney stones
renal impairment
TOPHI

92
Q

Adverse effects of allopurinol and febuxostat

A

induce acute gout attack if NSAID not provided

Rash, leukopenia, thrombocytopenia

93
Q

Rare side effect of allopurinol

A

allopurinol hypersensitivity syndrome

94
Q

allopurinol hypersensitivity syndrome

A

life threatening

-excessive doses, renal failure, diuretics, HLA-B*5801 allele

95
Q

Which gene is associated with allopurinol hypersensitivity syndrome

A

HLA-B*5801

96
Q

What drugs interact with allopurinol and febuxostat

A

6-mercaptopurine

Azathioprine

97
Q

If a patient has hyperuricemia, but no symptoms, do you treat?

A

NO

unless VERY high >12

98
Q

What is our goal for serum uric acid levels?

A
99
Q

Effective therapy of gout will require treatment for how long

A

life time

100
Q

Treatment of drug-resistant chronic gout

A

Pegloticase

101
Q

Pegloticase MOA

A

Enzymatic conversion of URIC acid to soluble metabolite

102
Q

Pegloticase Indication

A

Advanced, active gout

Uncontrolled with other drug

103
Q

How often do you give pegloticase, how is it administered?

A

IV infusion, every 2 weeks

104
Q

How quickly is pegloticase effective

A

months

105
Q

Adverse effects of pegloticase

A

Anti-drug antibodies

Pharm (20 decks)

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