4/17 Rheumatoid Arthritis - Corbett Flashcards
rheumatoid arthritis
overview
genetics/environmental factors
- most common persistent infl arthritis
- mean age of onset: 40s
- gender pref
- under 60? female predom (3-5x)
- over 60? equal
- family hx important
genetics
- ***HLA-DRB1 (major gene is 50-75% white) has shared epitope region → incr RA risk, greater jt damage
encironmental factors: smoking, silica
- alveolar macrophages respond to exposures by producing peptidyl arginine deiminase (PAD) → makes citrillinated peptides
CD4+ T cells activated, make cytokines → B cells activated → autoantibodies made
joint pathophys
key players
key changes x4
infl cells infiltrate synovial membrane → thickens, proliferates, becomes an inflammatory mass (pannus)
major player: CD4+ T cells stimulate…
-
B cells → produce IgM against IgG (rheumatoid ractor)
- immune complex formation starts here
-
macrophages → produce TNFalpha (regulates pro-infl cytokines)
- swelling and congestion of synovial mem
- destruction of bone, cartilage, soft tissue
PANNUS develops within joint
- prolif mass of infl tissue: erodes bone/cartilage
key changes in synovium:
- angiogenesis
- aynoviocyte prolif
- leukocyte infiltration
- cytokine synthesis (TNF)
RA and bone loss
- osteoclast activation at synovial insertion sites
- periarticular osteopenia : infl of bone marrow cavity → loss of trabecular bone
- accel osteoporosis
osteoarthritis vs rheumatoid arthritis
rheumatoid arthritis:
systemic illness
cytokine release leading to
- fatigue
- wt loss
- incr ESR
- incr CRP levels (C reactive protein - acute phase reactant)
WOULD NOT EXPECT TO SEE THIS WITH OSTEOARTHRITIS
RA hallmark fts
sx
course
how diff from OA
persistent symmetric polyarthritis (synovitis) affecting small joints of hands/feet
- larger synovial joints can be affected (hip uncommon)
- axial: upper cervical spine
- atlantoaxial disease of cervical spine → neuro dysfx and C1/C2 instability
- proximal MCP and PIP joints involved but DIP JOINTS ARE SPARED
insidious onset; fluctuating but progressive course
- past 3-6mo, remission uncommon
how diff from OA?
- stiffness in AM lasting about an hour, gets better with movement
- OA gets worse with movement
- constitutional sx: fever, fatigue, sweats, loss of app
RA: physical exam of joints
- swelling around joints
- joints are boggy, tender, warm
- soft, spongy texture with addt’l presence of fluid identified by fluctuant swelling
frequently involved: wrists, MCPs, PIPs
- fusiform swelling of hand (PIP)
hallmark features of RA
as disease progresses, destructive to joint → deformity, loss of fx
1. Boutonniere deformity
- non-reducible flexion at PIP with hyperext of DIP
2. swan-neck deformity of fingers
- hyperext of PIP with flexion of DIP
3. muscle atrophy
4. ulnar deviation
rheumatoid nodules
30-40% of RA pts
firm, nontender, oval/rounded subcut masses (up to 2cm diam), common on extensor surfaces
- central fibrinoid necrosis
- palisade of macrophages
- rim of granulation tissue
RA: extraarticular manifestations
-
cardiac
- MI, pericardial effusion, myocardial dysfx
-
pulmonary
- pleuritis, effusions, interstitial fibrosis, nodules
-
ocular
- keratoconjunctivitis sicca
- Sjogren’s syndrome
- rare: Felty syndrome (SANTA)
- splenomegaly
- anemia
- neutropenia
- thrombocytopenia
- arthritis (rheumatoid)
RA dx criteria
- joint involvement
-
serology: Rf, ACPA (anti-citrullinated peptide ab), ANA (anti-nuclear ab)
- 80% - Rf: serum IgM autoantibodies binding to Fc portion of IgG
- ACPA: indicative of more erosive disease involving more joints - more likely to be positive early than RF
- duration
- acute phase reactants (ESR or CRP)
long term prognosis of RA
- 10% spontaneous remission
- gradual worsening of diability
- 50+% unable to work 10 years after dx
- shortened life expectency
- systemic infl assoc with accel atherosclerosis
RA vs psoriatic arthritis vs seronegative spondyloarthropathy
joints, symmetry
RA: symmetric, small joints, hands/feet
psoriatic: asymmetric, large/small joints
seronegative spondyloarthritis: asymmetric, axial spine/SI joints, larger joints
three aims of tx: RA
- relief of sx
- aggressive strategy of disease mod: slow/stop progress, maintain/preserve fx
- support
- NSAIDs (incl COX2 specific inhibitors) - antiinfl, analgesic
- low-dose prednisone (bridge tx)
- intra-articular steroids during flare-ups
- DMARDs (disease modifying drugs) - slide
- biologicals if DMARDs unsuccessful
ddx for RA
symmetric join infl…
- RA or SLE
- no bone erosions, plus other manifestations of lupus
polyarthritis
- RA or connective tissue disorders (scleroderma, vasculitides)
types of arthritis summary/comparison
