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MSK Exam 2 Spring 2015 > Drugs for Rheumatic Diseases - Linger > Flashcards

Drugs for Rheumatic Diseases - Linger Flashcards

1
Q

agents that slow or stop progression of rheumatic disease, reduce pain and inflammation
-longer remission free phases and better quality of life

A

DMARDs

disease modifying antirheumatic drug

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2
Q

better disease outcome

A

referral to rheumatologist

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3
Q

non-biologic DMARDs

A

hydroxychloroquine
leflunomide
methotrexate
sulfalazine

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4
Q

hydroxychloroquine

A

non-biologic DMARD

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5
Q

leflunomide

A

non-biologic DMARD

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6
Q

methotrexate

A

non-biologic DMARD

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7
Q

sulfasalazine

A

non-biologic DMARD

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8
Q

rarely used DMARDs

A

azathioprine
cyclosporine
gold salts
minocycline

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9
Q

adalimumab

A

TNF-a blocker - biologic DMARD

mAb

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10
Q

certolizumab

A

TNF-a blocker - biologic DMARD

mAb

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11
Q

etanercept

A

TNF-a blocker - biologic DMARD

recombinant fusion protein**

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12
Q

golimumab

A

TNF-a blocker - biologic DMARD

mAb

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13
Q

infliximab

A

TNF-a blocker - biologic DMARD

mAb

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14
Q

anti-CD20 mAb

A

rituximab

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15
Q

T cell Fc-fusion

A

abatacept

domain of CTLA-4 receptor

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16
Q

anti-IL-6 mAb

A

tocilizumab

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17
Q

prevention of recurrent gout

A

allopurinol
febuxostat
pegloticase
probenecid

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18
Q

initial tx of rheumatoid arthritis

A

MTX or leflunomide

HCQ or sulfalazine - safer - if milder disease

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19
Q

NSAIDs

A

adjunct of pain relief for rheumatoid arthritis

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20
Q

corticosteroids

A

short term - for severe acute sx

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21
Q

biologic therapy for RA

A

after inadequate response to non-biologics

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22
Q

TNF-a inhibitors

A

no study to compare if one is more effective than another

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23
Q

etanercept

A

common first choice biologic

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24
Q

MOA methotrexate

A

inhibit dihydrofolate reductase

  • impaired DNA synthesis
  • causes cell death
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25
Q

MTX dosage

A

high - chemo
low - RA tx

high has myelosuppression - not a worry with RA tx and low dose

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26
Q

response time MTX

A

4-6 weeks to several months

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27
Q

adverse of methotrexate

A

nausea, upset stomach, diarrhea, stomatitis**, alopecia, fever, rash, HA, fatigue

elevation of hepatic enzymes - but cirrhosis rare - should monitor levels**
-screen those at risk for hepatitis, no alcohol

myelosuppression if high dose

28
Q

supplement with methotrexate

A

folic acid or leucovorin

reduce adverse effects

29
Q

MOA leflunomide

A

prodrug converted to active A77-1726

inhibits dihydroorotate dehydrogenase - reduced ribonucleotide synthesis and G1 arrest

inhibit B and T cell proliferation

30
Q

response time leflunomide

A

6-12 weeks

31
Q

adverse of leflunomide

A

diarrhea

elevated liver enzymes

32
Q

category X pregnancy

A

leflunomide and methotrexate

33
Q

MOA hydroxychloroquine

A

poorly understood - T cell suppression, decreased leukocyte chemotaxis, inhibit DNA/RNA synthesis, all possible causes

34
Q

response time hydroxychloroquine

A

3-6 months

35
Q

ocular toxicity

A

with hydroxychloroquine

need to monitor eyes**

36
Q

MOA sulfasalazine

A

poorly understood - possibly decreased IgA and IgM rheumatoid factor production - suppression of T cell and B cell prolifeation, etc.

metabolized to 5-aminosalicylic acid

37
Q

response time sulfasalazine

A

1-3 months

38
Q

prevent rejection of transplant organs

A

azathioprine

rare used DMARD

39
Q

pregnant transplant patient

A

cyclosporine

rare used DMARD

40
Q

drug induced lupus

A

with minocycline

rare used DMARD

41
Q

MOA TNF-a inhibitors

A

prevent binding of TNF-a to TNF receptors

-down-regulation of macrophages and T cells

42
Q

biologic DMARD response time

A

1-2 weeks

faster than non-biologics**

43
Q

biologic DMARDs

A

monotherapy - or combo (usually with MTX)

44
Q

adverse of biologic DMARD

A

cytopenia
-monitor CBC**

opportunistic infection** - bacterial sepsis and TB

heart failure association

45
Q

before starting biologic DMARD

A

screen for latent TB**

46
Q

rare demyelinating disease

A

infliximab

47
Q

NSAID MOA

A

inhibit COX - decreased prostaglandins

48
Q

DMARD induction, transition to different DMARD, and during disease flare of RA

A

use NSAIDs

not acetaminophen - poor anti-inflammatory

49
Q

adverse NSAIDs

A

GI ulcers and bleeds

can give ranitidine (H2 histamine antagonist)

50
Q

less GI toxicity

A

with celecoxib - COX2 selective

51
Q

third trimester pregnancy

A

no NSAIDs**

52
Q

adverse of corticosteroids

A

osteoporosis, weight gain, fluid retention, cataracts, glaucoma, poor wound healing, hyperglycemia, HTN, adrenal suppression

should give Ca and Vit D supplements

53
Q

first line for acute gout

A

NSAIDs

inhibit urate crystal phagocytosis

54
Q

aspirin and gout

A

NO - because inhibit urate excretion at low doses

55
Q

glucocorticoids

A

used in severe gout

56
Q

colchicine MOA

A

binds tubulin and prevents polymerization - inhibit leukocyte migration and phagocytosis

57
Q

decrease urate synthesis

A

xanthine oxidase inhibitor - allopurinol

58
Q

increased renal excretion of urate

A

uricosuric agent - probenecid

59
Q

colchicine

A

should not be repeated within 14 days - to avoid toxicity cumulation

60
Q

allopurinol MOA

A

purine analog that inhibits xanthine oxidase
-decreased uric acid production

decreased recurrence of gout regardless of pathology

61
Q

allopurinol

A

preferred for gout during periods between acute episodes

62
Q

reduce dose of chemotherapy purines

A

if patient on allopurinol

63
Q

febuxostat MOA

A

non-purine inhibitor of xanthine oxidase

64
Q

probenacid MOA

A

organic acid - acts at anionic transport site of renal tubules to reduce reabsorption of uric acid

tx of hyperuricemia with gout - when tophi present

65
Q

adverse of probenacid

A

increased likelihood of renal stone formation

MSK Exam 2 Spring 2015 (10 decks)

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