RA Flashcards

1
Q

RA targets the

A

synovium and sometimes other internal organs

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2
Q

what is the hallmark of RA

A

persistent symmetric synovial proliferation and tenderness of multiple joints- esp in the hands and feet

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3
Q

what is the prognosis of RA

A

poor, with progressive joint damage and deformity
Acute/ chronic pain
Erosions on X ray = deformities
Long term disabilities
Reduced life expectancy

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4
Q

what causes RA?

A

External trigger leads to autoimmune reactions in genetically susceptible individual with rheumatoid factor (RF) and/or anti citrullinated protein antibody (ACPA)

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5
Q

chronic inflammation in RA leads to

A

presence of pannus
influx of inflammatory cells in synovial fluid
angiogenesis

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6
Q

what is a pannus

A

thickened, inflamed joint lining

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7
Q

onset of RA is usually

A

insidious- over weeks or months

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8
Q

what is the distribution of RA

A

initially oligoarticular, progressing to polyarthritis, can affect almost any joint + symmetrical in presentation
most common in hands and feet

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9
Q

list 3 sx of RA

A

morning stiffness (gelling) for >1hr, symmetrical swelling and tenderness = reduced grip strength + inability to make fist, reduced function, systemic (fatigue, poor sleep, low energy, weight loss, low grade fever)
anemia, keratoconjunctivitis sicca, carpal tunnel sx/ tarsal tunnel sx, rheumatoid nodules and baker’s cysts

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10
Q

what are the 4 complications of RA

A

CVD, infections, cancer, osteoporosis

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11
Q

3 joints commonly affected by RA

A

PIP, MCP, MTP

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12
Q

is this inflammatory of noninflammatory arthritis? the pt has pain at rest and with activity, soft tissue swelling, and morning stiffness that lasts an hour

A

inflammamtory

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13
Q

is this inflammatory of noninflammatory arthritis? the pt has pain with activity and bony joint swelling, there is no local erythema or warmth

A

noninflam

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14
Q

which 2 lab findings point towards RA

A

rheumatoid factor
ACPA
CRP elevated
increased WBCs and platelets, decreased Hb

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15
Q

image findings on early RA

A

periarticular swelling, joint effusions

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16
Q

image findings on intermed RA

A

uniform joint space narrowing and marginal erosions

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17
Q

image findings in late RA

A

malalignment due to joint damage, periarticular osteopenia, and erosions

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18
Q

what are 3 measuring scales for RA

A

ACR20
DAS28
HAQ

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19
Q

describe the “window of opportunity” in RA

A

timeframe within which there is disproportionate response to therapy, resulting in LT sustained benefits

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20
Q

describe the “T2T” approach in RA

A

Early aggressive tx (regular reassessment, making changes individually) tailored to the disease activity of an individual pt aimed at achieving remission critical for optimizing LT results

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21
Q

why do guidelines start to use monotx or the T2T approach in RA?
1. because monotx is just as effective as combo
2. because methotrexate must first be trialed before being combined with another agent to determine pt tolerability
3. because monotx works better than combo tx
4. because monotx achieves remission in 1/3 -1/2 patients anyways and may be more cost effective
5. because there is no rush to control the disease early, as it takes weeks to months to progress

A

4

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22
Q

describe the step up tx approach in RA

A

initial monotx, add DMARDs q3-6mths prn (used in North America)

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23
Q

describe the combo approach in RA

A

initial combo tx, add/ switch DMARDs q3-6mths prn

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24
Q

describe the step down approach in RA

A

initial biologic DMARD and/or prednisone in combination, add/ switch DMARDs q3-6mths prn (usually not used due to expenses)

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25
Q

how often should RA tx be reassessed

A

q3mths

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26
Q

csDMARDs include

A

MTX, LF, SZZ, HCQ, chloroquine

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27
Q

tsDMARDs include

A

tofaciinib, baricitinib, upadacitinib

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28
Q

DMARDs should be introduced ___, ____ is the preferred agent with respect to efficacy and safety in initial tx of RA

A

ASAP
MTX

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29
Q

combination tx with csDMARDs should be considered in those with

A

Poor prognostic features
Mod-high disease activity
Recent onset disease

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30
Q

in combo tx, what is usually the anchor drug

A

MTX

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31
Q

DMARDs are the mainstay of RA tx because they

A

modify disease process, prevent/ reduce joint damage

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32
Q

DMARDs are
1. immune modulating
2. antiinflammatory
3. immunosuppressive
4. all of the above

A

1

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33
Q

csDMARDs should be initiated ___________, usually bridged with

A

soon after disease onset
bridge with short course of prednisone or NSAIDs

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34
Q

MTX dose in RA

A

15-25mg qwk

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35
Q

how to adjust MTX dose based on renal

A

Reduce dose by 50% if CrCL 10-50mL/min (some avoid if <30)

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36
Q

MTX onset and max eff

A

onset 2-4wks
max 3-6mths

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37
Q

MTX MOA in chemo

A

inhibits dihydrofolate reductase = inhibits purine synthesis

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38
Q

MTX MOA in RA

A

Stimulates release of adenosine = anti inflam + inhibits neutrophils

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39
Q

what indicates that MTX is working in RA

A

increased MCV by 5pg/fL

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40
Q

list 3 common SEs of MTX

A

mouth/ nose ulcers (3-10% tx w/ folic acid), N/V, loss of appetite (>10% tx w/ folic acid), fatigue, malaise 24-48hrs after dose (tx w/ dextromethorphan)

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41
Q

which 2 agents can be used to tx MTX SEs

A

folic acid and dextromethorphan

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42
Q

folic acid can prevent MTX SEs like

A

mouth/ nose ulcers, hair loss, ALT/ AST elevation

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43
Q

dextromethorphan prevents MTX SEs including

A

malaise, fatigue, headaches, memory impairment

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44
Q

how does dex prevent MTX SEs

A

blocks neurostimulation of homocysteine (↑ due to MTX ant of folic acid) at NMDA receptor in brain = avoids headache, lethargy, malaise, memory impairment/fogginess from homocysteine (10mL BID on day of + day after MTX)

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45
Q

how should you advise a patient that has forgotten to take a dose of MTX
1. take one dose ASAP, then take the next dose at the same time you usually do next week
2. take one dose ASAP, then if the usual time is <4 days away, push to next week, if >4 days = take on usual day
3. if <2 days to next dose, skip and take next dose
4. if <4 days to next dose, skip and double next dose
5. take one dose ASAP, then take next dose a 6-7 days after (can take 1 day early every week to get back to previous schedule)
6. take one dose ASAP, then take next dose 5-7 days after (can take 2 days early per week get back to previous schedule)

A

5

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46
Q

which of the following is not CI in pregnancy
1. MTX
2. SSZ
3. LF
4. HCQ

A

2, 4

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47
Q

which of the following should not be used with MTX
1. NSAIDs
2. penicillins
3. pantoprazole
4. trimethoprim
5. quinolones

A

4

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48
Q

LF onset and max eff

A

onset 6-8wks, max 3-6mths

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49
Q

LF common AEs

A

diarrhea, ↓ hair, ↑ liver enzyme, mouth/ nose ulcers, N/V, ↓ appetite, HA

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50
Q

interstitial lung disease is a rare SE of
1. LF
2. MTX
3. HCQ
4. CA

A

1

51
Q

what is used for LF washout

A

cholestyramine

52
Q

LF should be stopped ____ before conception
1. 1yr
2. 2 yrs
3. 2 yrs + washout
4. doesn’t have to be, is safe in preg

A

2

53
Q

can you use alcohol on LF?

A

yes, 1-2/wk but caution if also on MTX

54
Q

which does not require renal adjustment
1. MTX
2. LF
3. SZZ
4. HCQ

A

2

55
Q

avoid SZZ use if CrCL

A

<30

56
Q

SZZ onset and max eff

A

onset 8-12wks, max eff 6mths

57
Q

SZZ is often used in combo with

A

MTX, HCQ

58
Q

SZZ CIs
1. sulfonamdie allergy
2. salicylate allergy
3. both

A

sulfonamide allergy only - salicylate allergy can be desensitized

59
Q

common SZZ SEs include

A

nausea, dyspepsia, diarrhea (use enteric coated tablet), photosensitivity (sunscreen), rash, HA, dizziness

60
Q

HCQ onset and max eff

A

onset 12-16wks, max eff 6mths

61
Q

what is the mildest and best tolerated DMARD
1. MTX
2. LF
3. SZZ
4. HCQ

A

4

62
Q

avoid HCQ if CrCL

A

<30

63
Q

caution should be used with HCQ if the pt has a hx of
1. depression
2. diabetes
3. HPTN
4. dyslipidemia

A

2- risk of hypoglycemia

64
Q

what are some first signs of HCQ eye toxicity

A

loss of red light perception

65
Q

RFs for HCQ mediated eye toxicity

A

> 60yrs, hx ocular diseases, renal/ liver dysfunction

66
Q

how to monitor for HCQ eye toxicity

A

baseline, 5yrs (if no RFs/ sx), annual if high risk (older, sx)
V extensive, pictures taken, dilation (must check if optometrist doing this)

67
Q

what are 3 “other” DMARDs that are not often used anymore

A

gold salts
minocycline
azathioprine, cyclosporine, cyclophosphamide, mycophenolate

68
Q

T or F: scDMARDs can increase the risk of infections

A

F- but may last longer or seem worse- only d/c DMARD if severe/ on MD advice

69
Q

can scDMARDs be continued when pt needs surgery?

A

yes- usually

70
Q

bDMARDs and txDMARDs are utilized in those

A

with inadequate response to at least 2 csDMARDs (mono/combo) after 3mths at target dose

71
Q

what is usually the initial advanced therapy one could use after csDMARD failure

A

TNFi

72
Q

what is primary failure to TNFi? what should be done?

A

No response to TNFi: switch to alt bDMARD or tsDMARD, do not retry another TNFi

73
Q

what is secondary failure to TNF? what should be done?

A

ail TNFi after years = switch to alt TNFi, other b/tsDMARD

74
Q

how do bDMARDs work?

A

block specific pts of immune system- targeted therapy

75
Q

bDMARDs have
1. increased damage
2. reduced sc and CV risk
3. increased CV risk
4 .increased infection risk

A

4

76
Q

T or F: when using bDMARDs, MTX should still be included

A

T- MTX still anchor to improve effectiveness + to avoid antibody formatio nto the biologic proteins

77
Q

TNFi onset and peak

A

onset 2wks
peak 3-6mths

78
Q

TNFi CIs

A

HF (NYHA class III-IV), MS (personal hx maybe also 1st degrees relatives), active cancer (caution: hx of lymphoma or skin), may also trigger lupus like sx, psoriasis

79
Q

pick all that apply, whcih of the following must be used with MTX
1. adalimumab
2. certolizumab
3. golimumab
4. etanercept
5. infliximab

A

3, 5

80
Q

abatacept MOA

A

T cell costimulation modulator- mimics CTLA4 = prevents CD28 from binding to CD80/86 = enables T regulatory activity to continue = lower T cell immune mediated cascade by blocking 2nd signal = decreases inflammation

81
Q

onset and peak of abatacept

A

onset 2-4wks, peaks 3-6mths

82
Q

abatacept is used in _____RA who ____

A

mod-severe RA who fail TNFi

83
Q

abatacept may incerase the incidence of

A

AECOPD and pneumonia

84
Q

tocilizumab and sarilumab are

A

IL6i

85
Q

IL6- onset and peak

A

onset 2-4wks, peak 3-6mths

86
Q

IL6i caries the rare but serious risk of

A

GI perforation is there is a hx of diverticulities

87
Q

what increases the risk of GI perf with IL6i

A

hx of diverticulitis, NSAIDs, prednisone

88
Q

how does IL6i interact with CYP enzymes

A

down regulates it

89
Q

rituxumab class

A

B cell inhibitor

90
Q

rituximab onset and peak in RA

A

onset 8wks, peak 4-6mths

91
Q

rituximab is the preferred biologic in pts with

A

B cell lymphoma, latent TB infection, MS, concomitant vasculitis or overlap syndromes

92
Q

URTI is more common in the first year with ____

A

TNFi

93
Q

allerguic reactions to RTX can be premedicated with

A

acetaminophen, cetirizine/ loratadine, +- metylprednisone

94
Q

T or F: bDMARDs increase the risk of solid tumors and lymphoma

A

F- MTX and bDMARDS may be associated with a small risk

95
Q

T or F: biosimilars are different in each batch

A

T

96
Q

what is required to compare the biosimilar to the reference product?

A

at least 1 clinical study to see that there are no clinically meaningful differences between biosim and originator

97
Q

JAKi MOA

A

small molecule inhibitor of JAK induced cytokine production

98
Q

Tofacitinib, upadacitinib, baricitinib are all

A

JAKi

99
Q

onset and peak of JAKi

A

onset 2-4wks, peak 3-6mths

100
Q

caution with JAKi

A

risk of GI perforation of hx diverticulitis (RF: NSAIDs, prednisone)

101
Q

4 common SEs for JAKi

A

URTI, nasopharyngitis, HA, diarrhea

102
Q

which JAKi has a signal with VTE

A

baricitinib = CV events and cancers under postmarketing surveillance

103
Q

T or F: tofacitinib met noninferiority compared to TNFi for risk of CVD

A

F- was slightly higher + crossed line of no effect

104
Q

what should you do with bDMARDs and txDMARDs during infection?

A

hold until 48hrs after abx complete/ sx resolved (including for topical infections)

105
Q

how to prevent infection on bDMARDs/ tsDMARDs

A

vaccinate 4wks prior to initiation + avoid LIVE vaccines

106
Q

should you hold b/ts DMARDs for a cold?

A

no- may consider if severe

107
Q

what to do with b/ts DMARDs in the perioperative times

A

hold per and post op to decrease risk of infection + ensure appropriate healing
Timing dependent on bDMARD and the operation

108
Q

what are steroids and NSAIDs used for in RA

A

managing flares, as bridging tx while awaiting DMARD onset, sx control if no other options exist

109
Q

are steroids and NSAIDs ever used in initial RA treatment?

A

yes

110
Q

oral or IM steroids and NSAIDs in RA are useful for

A

managing sx in many joints

111
Q

intraarticular steroids are useful in RA for

A

controlling residual synovitis in a single joint, tendon, bursa with less systemic toxicity

when only 1-2 joints inflammed

112
Q

how long does it take IA steroids to kick in? how long does it last?

A

relief onset in few days, lasts wks to months

113
Q

what is a major pro of IA steroids

A

may help avoid steroid cycling

114
Q

RA adjunct tx may include

A

analgesics (APAP,. Opioids, cannabis), antiinflammatories; NSAIDs (PO/ topical), NHPs

115
Q

T or F: if NSAIDs, opioids, and cannabis have not relieved RA pain within a month, it is unlikely to work ever

A

T

116
Q

which 3 NHPs may be used in RA

A

omega 3s
calcium/ vit D

117
Q

should an RA patient use immune boosters like gingseng and echinacea to prevent infection

A

no

118
Q

vaccine efficacy is most reduced with ___, ____, ____

A

MTX, prednisone, RTX

119
Q

what are the vaccine guidelines for csDMARDs

A

Inactivated vaccines considered safe
Some live vaccines considered safe- MMR booster

120
Q

what are the vaccine guidelines for bDMARDs and tsDMARDs

A

Inactivated vaccines considered safe
Live vaccines CI

121
Q

what to do with influenza vaccine and MTX

A

Hold methotrexate for 2 wks after vaccination only if disease allows

122
Q

what to do with influenza vaccine and RTX

A

Continue rituximab, give influenza vaccine on schedule (delay subseq rit dose F2wks if disease state allows)

123
Q

what to do with other nonlive attenuated vaccinations and RTX

A

Time vaccination for when next rituximab dose is due, then hold rituximab for at least 2 wks after vaccination

124
Q

what to do with MTX and other nonlive attenuated vaccines

A

continue as normal