Rheumatoid Arthritis Flashcards

1
Q

which drugs are TNFa inhibitors

A

adalimumab
certolizumab
etanercept
golimumab
infliximab

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2
Q

which drugs are anti-IL-6

A

tocilizumab
sarcilumab

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3
Q

which drugs are anti IL-1

A

anakinra

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4
Q

which drugs are anti CD-20

A

rituximab

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5
Q

which drugs are JAK inhibitors

A

tofacitinib
baricitinib
upadacitinib

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6
Q

which drug binds to CD80/CD86 and inhibits T cell activation

A

abatacept

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7
Q

in RA, the inflammatory pathway is _____

A

multifactorial

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8
Q

role of T lymphocytes in RA?

A

stimulate the release of more inflammatory cytokines, matrix enzymes, osteoclasts, and B lymphocytes

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9
Q

how are T lymphocytes activated
(*note: which drug works here)

A

require 2 signals: stimulation by proinflammatory cytokines, binding of CD28 (on T cell) with CD80/86 on APC
abatacept works here

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10
Q

general role of proinflammatory cytokines in RA?

A

creates an imbalance, inflammation results

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11
Q

B lymphocytes are the _____ component

A

humoral

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12
Q

role of B lymphocytes in RA?

A

producing autoantibodies (antibodies directed against self; not pathogenic)

activation of complement system; stimulating further release of proinflammatory cytokines

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13
Q

what are autoantibodies associated with RA?

A

rheumatoid factor (RF) and anti-cyclic citrullinated protein antibody (ACPA)

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14
Q

______ is a transmembrane protein on B lymphocytes involved with their activation, proliferation, and differentiation
(*note: which drug works here)

A

CD20
rituximab

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15
Q

what is the role of janus kinase in RA?

A

regulates leukocyte maturation and activationi

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16
Q

when synovium becomes enlarged/thick, it is called ____

A

pannus

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17
Q

key notes of the clinical presentation of RA

A

morning stiffness >30 min
fatigue, weakness
joint pain at rest
synovitis/inflamed joints
soft and spongey

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18
Q

key notes of clinical presentation of OA

A

morning stiffness <30 min
crepitus
deep aching pain
pain aggravated with use
pain relieved by rest
hard and body (osteophytes)

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19
Q

which joints are involved in RA

A

more proximal joints: MCP, PIP

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20
Q

which joints are involved in OA

A

more distal joints: PIP, DIP

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21
Q

2 key points of value in differentiating RA from OA

A

symmetry, noninvolvement of DIP joints

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22
Q

what is a common extraarticular manifestation of RA

A

rheumatoid nodules

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23
Q

what are the extra-articular manifestations of RA

A

cardiac, rheumatoid nodules, pulmonary, vasculitis, ocular, hematologic, osteopenia

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24
Q

what are the KEY lab findings to RA (four)

A

ESR, CRP, RF, ACPA

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25
Q

what does seropositive mean

A

presence of RF or ACPA

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26
Q

what are the factors of a worse RA prognosis

A

seropositive, elevated ESR, extra-articular involvement (including nodules), poor functional status initially, bone erosion per X-ray, older age, female, genotype, cigarette smoking

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27
Q

2 requirements for RA diagnosis

A
  1. patient with at least one joint with definite clinical synovitis
  2. synovitis is not better explained by another disease (gout, SLE)
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28
Q

define remission in RA

A
  • not more than one tender or swollen joint
  • CRP<1
  • positive patient global assessment
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29
Q

you should initiate DMARDs within what time frame

A

3 months of diagnosis

30
Q

what are the nonbiologic DMARDs

A

methotrexate, leflunomide, hydroxychloroquine, sulfasalazine

31
Q

which nonbiologic DMARD is preferred

A

methotrexate

32
Q

which two nonbiologic DMARDs can never be combined together

A

methotrexate & leflunomide (liver toxicity)

33
Q

methotrexate can be used to _____ with biologics

A

reduce the formation of antibodies to biologics

34
Q

how is methotrexate dosed

A

weekly, oral or injectable
50% dose reduction when CrCL<50

35
Q

how to improve methotrexate tolerability at high doses

A

give the weekly dose split by 12 hours

36
Q

onset of nonbiologic DMARDs?

A

1-2 months

37
Q

absolute contraindication methotrexate/leflunomide

A

pregnancy/lactation

38
Q

relative contraindications methotrexate

A

acute bacterial infection, latent TB, chronic liver dx, CrCL<30, pleural/peritoneal effusions, immunodeficiency, leukopenia, thrombocytopenia

39
Q

adverse effects of methotrexate

A

stomatitis, n/d, increased liver enzymes, rash, alopecia, hematologic, pulmonary infiltrates

40
Q

how to reduce adverse effects of methotrexate

A

folic acid 5 mg/week or 1 mg/day

41
Q

methotrexate drug interactions

A

TMP/SMZ, PPI’s

42
Q

clinical pearls for leflunomide?

A

avoid pregnancy for TWO YEARS after stopping. cholestyramine or activated charcoal is recommended to help lower plasma levels of leflunomide more quickly

43
Q

which nonbiologic DMARD has a loading dose

A

leflunomide

44
Q

toxicity with leflunomide

A

hepatotoxicity (inc. with MTX), diarrhea, alopecia, rash, HA, peripheral neuropathy

45
Q

which nonbiologic DMARDs are typically used in early/less aggressive disease or as adjunct

A

hydroxychloroquine, sulfasalazine

46
Q

clinical pearl for hydroxychloroquine

A

complete an eye exam within the first year of treatment to monitor for macular damage, start an annual exam after 5 years

47
Q

adverse reactions of hydroxychloroquine

A

GI, derm, macular damage, potential QT prolongation

48
Q

which nonbiologic DMARDs CAN be used in pregnancy

A

hydroxychloroquine and sulfasalazine

49
Q

contraindications for sulfasalazine

A

platelets <50,000, liver disease, sulfa allergysi

50
Q

side effects for sulfasalazine

A

GI, derm, myelosuppression, LFTs, may cause urine to turn orange/yellow

51
Q

drug interactions with sulfasalazine

A

antibiotics, iron, warfarin

52
Q

all biologics are associated with an increased risk of ____

A

infection

53
Q

with all biologics, you need to screen for ___

A

TB, HepB/C

54
Q

with biologics, you need to avoid ____

A

live vaccines

55
Q

when switching biologics, how do you know when to give the new agent

A

initiate it when the patient is due for their previous biologic

56
Q

the onset of symptom relief is _____ with biologics

A

FASTER

57
Q

what are the first line biologics

A

TNF antagonists

58
Q

the time frame to MAX effect with TNF is ___, but there is a faster onset of symptom relief

A

3 months

59
Q

DO NOT USE TNF antagonists in ____

A

patients with moderate to severe heart failure (NYHA III/IV)

60
Q

which TNF is IV only and you have to go to an infusion center

A

infliximab (remicade)

61
Q

adverse effects TNF

A

reaction to injection/infusion, infections and malignancies, new onset/exacerbation multiple sclerosis

62
Q

use caution with use of abatacept in patients with ____

A

COPD

63
Q

abatacept adverse effects

A

site reaction, headache, URTI, nasopharyngitis, nausea, COPD worsening, infections and malignancies

64
Q

rituximab is first line for patients with ____

A

lymphoproliferative disorders

65
Q

how is rituximab dosed

A

2 infusions given 2 weeks apart, recovery of B cells can take months; give q16-24 weeks

66
Q

adverse effects rituximab

A

site reaction, URTIs, nasopharyngitis, UTI, bronchitis, bowel obstruction, blood cell disorders, CV events

67
Q

niche with IL-6

A

don’t typically need addition of methotrexate to improve efficacy

68
Q

JAK inhibitors dosage form

A

oral

69
Q

boxed warning JAK inhibitors

A

thromboembolism

70
Q

true/false: NSAIDs alter course of RA disease and prevent joint erosion

A

false

71
Q

what dose corticosteroids to use for RA

A

lowest dose as possible, <10 mg of prednisone or equivalent, short term to control flares or bridge