RA Flashcards by Linda Chen

RA targets the

synovium and sometimes other internal organs

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what is the hallmark of RA

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

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what is the prognosis of RA

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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what causes RA?

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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chronic inflammation in RA leads to

presence of pannus
influx of inflammatory cells in synovial fluid
angiogenesis

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what is a pannus

thickened, inflamed joint lining

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onset of RA is usually

insidious- over weeks or months

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what is the distribution of RA

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

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list 3 sx of RA

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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what are the 4 complications of RA

CVD, infections, cancer, osteoporosis

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3 joints commonly affected by RA

PIP, MCP, MTP

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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

inflammamtory

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

noninflam

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which 2 lab findings point towards RA

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

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image findings on early RA

periarticular swelling, joint effusions

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image findings on intermed RA

uniform joint space narrowing and marginal erosions

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image findings in late RA

malalignment due to joint damage, periarticular osteopenia, and erosions

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what are 3 measuring scales for RA

ACR20
DAS28
HAQ

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describe the “window of opportunity” in RA

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

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describe the “T2T” approach in RA

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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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

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describe the step up tx approach in RA

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

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describe the combo approach in RA

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

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describe the step down approach in RA

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

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how often should RA tx be reassessed

q3mths

csDMARDs include

MTX, LF, SZZ, HCQ, chloroquine

tsDMARDs include

tofaciinib, baricitinib, upadacitinib

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

ASAP MTX

combination tx with csDMARDs should be considered in those with

Poor prognostic features Mod-high disease activity Recent onset disease

in combo tx, what is usually the anchor drug

MTX

DMARDs are the mainstay of RA tx because they

modify disease process, prevent/ reduce joint damage

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

csDMARDs should be initiated ___________, usually bridged with

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

MTX dose in RA

15-25mg qwk

how to adjust MTX dose based on renal

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

MTX onset and max eff

onset 2-4wks max 3-6mths

MTX MOA in chemo

inhibits dihydrofolate reductase = inhibits purine synthesis

MTX MOA in RA

Stimulates release of adenosine = anti inflam + inhibits neutrophils

what indicates that MTX is working in RA

increased MCV by 5pg/fL

list 3 common SEs of MTX

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)

which 2 agents can be used to tx MTX SEs

folic acid and dextromethorphan

folic acid can prevent MTX SEs like

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

dextromethorphan prevents MTX SEs including

malaise, fatigue, headaches, memory impairment

how does dex prevent MTX SEs

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)

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)

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

2, 4

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

LF onset and max eff

onset 6-8wks, max 3-6mths

LF common AEs

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

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

what is used for LF washout

cholestyramine

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

can you use alcohol on LF?

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

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

avoid SZZ use if CrCL

<30

SZZ onset and max eff

onset 8-12wks, max eff 6mths

SZZ is often used in combo with

MTX, HCQ

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

sulfonamide allergy only - salicylate allergy can be desensitized

common SZZ SEs include

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

HCQ onset and max eff

onset 12-16wks, max eff 6mths

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

avoid HCQ if CrCL

<30

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

2- risk of hypoglycemia

what are some first signs of HCQ eye toxicity

loss of red light perception

RFs for HCQ mediated eye toxicity

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

how to monitor for HCQ eye toxicity

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

what are 3 "other" DMARDs that are not often used anymore

gold salts minocycline azathioprine, cyclosporine, cyclophosphamide, mycophenolate

T or F: scDMARDs can increase the risk of infections

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

can scDMARDs be continued when pt needs surgery?

yes- usually

bDMARDs and txDMARDs are utilized in those

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

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

TNFi

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

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

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

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

how do bDMARDs work?

block specific pts of immune system- targeted therapy

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

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

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

TNFi onset and peak

onset 2wks peak 3-6mths

TNFi CIs

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

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

3, 5

abatacept MOA

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

onset and peak of abatacept

onset 2-4wks, peaks 3-6mths

abatacept is used in _____RA who ____

mod-severe RA who fail TNFi

abatacept may incerase the incidence of

AECOPD and pneumonia

tocilizumab and sarilumab are

IL6i

IL6- onset and peak

onset 2-4wks, peak 3-6mths

IL6i caries the rare but serious risk of

GI perforation is there is a hx of diverticulities

what increases the risk of GI perf with IL6i

hx of diverticulitis, NSAIDs, prednisone

how does IL6i interact with CYP enzymes

down regulates it

rituxumab class

B cell inhibitor

rituximab onset and peak in RA

onset 8wks, peak 4-6mths

rituximab is the preferred biologic in pts with

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

URTI is more common in the first year with ____

TNFi

allerguic reactions to RTX can be premedicated with

acetaminophen, cetirizine/ loratadine, +- metylprednisone

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

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

T or F: biosimilars are different in each batch

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

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

JAKi MOA

small molecule inhibitor of JAK induced cytokine production

Tofacitinib, upadacitinib, baricitinib are all

JAKi

onset and peak of JAKi

onset 2-4wks, peak 3-6mths

caution with JAKi

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

4 common SEs for JAKi

URTI, nasopharyngitis, HA, diarrhea

which JAKi has a signal with VTE

baricitinib = CV events and cancers under postmarketing surveillance

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

F- was slightly higher + crossed line of no effect

what should you do with bDMARDs and txDMARDs during infection?

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

how to prevent infection on bDMARDs/ tsDMARDs

vaccinate 4wks prior to initiation + avoid LIVE vaccines

should you hold b/ts DMARDs for a cold?

no- may consider if severe

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

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

what are steroids and NSAIDs used for in RA

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

are steroids and NSAIDs ever used in initial RA treatment?

yes

oral or IM steroids and NSAIDs in RA are useful for

managing sx in many joints

intraarticular steroids are useful in RA for

controlling residual synovitis in a single joint, tendon, bursa with less systemic toxicity when only 1-2 joints inflammed

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

relief onset in few days, lasts wks to months

what is a major pro of IA steroids

may help avoid steroid cycling

RA adjunct tx may include

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

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

which 3 NHPs may be used in RA

omega 3s calcium/ vit D

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

vaccine efficacy is most reduced with ___, ____, ____

MTX, prednisone, RTX

what are the vaccine guidelines for csDMARDs

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

what are the vaccine guidelines for bDMARDs and tsDMARDs

Inactivated vaccines considered safe Live vaccines CI

what to do with influenza vaccine and MTX

Hold methotrexate for 2 wks after vaccination only if disease allows

what to do with influenza vaccine and RTX

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

what to do with other nonlive attenuated vaccinations and RTX

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

what to do with MTX and other nonlive attenuated vaccines

continue as normal

RA Flashcards

(124 cards)