Rumathoid arthiritis Flashcards

1
Q

What are the key features of RA?

A
Polyarthirits-more than 1 joint
1 joint in mono arthiritis
tend to be symetrical
manifest with morning stiff-unlike OA
may lead to joint damage and destruction if unckecked

exrta diseases can happen from it-rheumathoid nodules, rare-vasculatits, eposcleritis
test for rheumathoid factor-IgM againt IgG

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2
Q

Who gets RA? Is it genetic?

A

1% of population-more in women

Important genetic component-not mendelian-usually HLA bases
Smoking contributes to RA risk

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3
Q

What joints are commonly affected by RA?

A
Metacarpophalengeal joints
proxmal interphalangeal
Wrists
Knees
Ankles
Metatarsalphalangeal joint

Hands and feet

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4
Q

What classic deforminties do you see?

A

Boutonniere-deforminity-hyper flexion of POP
Swan neck deformities-hyperflexion at PIP joint and distal IP
Xray-sorta like a dislocation-shift off from ulnar line

affects synovium lining: Extensor tenosynovitis-bumps on back of hand
Olecranon busritis
PIP join synovitis

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5
Q

What are rheumathoid nodules?

A

Usually happen just distal of elbow-like a bump
Fibrinoid necrosis with histiocytes and connective tissue on top
happen in bad disease (30%)

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6
Q

What is rheumathoid factor?

A

Its an IgM against an IgG
Form an immune complexes that activate complement and activate inflammation

present in 70% of patient–seropositive
10-15% become seropositive over 10 years
seronegative are better

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7
Q

appart from rheumathoid factor, what is another diagnostic test

A

Arginine can be made to citruline (not naturally occuring AA)
AB against citruline are common in RA-test for that
maybe because of smoking causing citrullination

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8
Q

What HLA modification causes rhumathoid arthiritis suceptibility?

A

Individuals that are susceptible tend to carry a conserve AA sequence (epitope)-HLA DRbeta chain-DR1,6,10 can containthat shared epitode
Its role is to present Ag to CD4 T cells
The sequence binds more readily to citruiline

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9
Q

What are the systemic consequences/extra articular features of RA? Why?

A

malais, weight loss, fever, night sweats (often thought as infection, cancer,)
More uncommon-vasculitis, occular inflammatopm
Neuropathies
Amyloidosis=high serum myeloid that deposits in organs and cause failure
Lung diseases-internal nodules
Felty;s syndrome-triad of spelomegaly, leukopenia and RA

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10
Q

What are the Xray findings that are found in RA?

A

Early on-nothing-want it to keep it there
Start with osteopenia-bone is lighter on Xray-thinner bone/less dense bone-caused by metalloproteases activity
Later-erosions of margins, blurry of the joins, loss of joint space, irregular
later-deformities and destruction-resorbtion

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11
Q

What can you find inside a synovial joijt?

A

Synovium around-1/3 cell deep with phagocytes and fibroblast cells producign hyaluronic acid, type 1 collagebn
Fluid-high hyluronic acid-viscous
And cartilage-typeII collagen and proteoglycan

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12
Q

How does the synovium change in RA?

A

Neovascularisation and lymphangiogenesis
Inflammatory cells use the new places to come to tissue
Deficite of regulation and constant upregulation –TNFalpha drives RA a lot (pro-inflam-cytokine, chemokine release, leukocyte accumulation, angiogenesise, osteoclast activation

=> TNF a is a great therapeutic target

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13
Q

What are the 3 main ideas for curing RA?

A

Blockign TNFa and
Biological therapy-use AB to block AB, or block IL6 or other factors. IL1 doesnt seem to work in RA
other is cytokine blockade-deplete B cells in RA by administering AB againt B cell surface AG

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14
Q

What is the management of RA?

A

Physio, OH, hydrotherapy,-remake muscle and keep joint healthy (for more avdances)

DOesnt matter the drug but treat EARLY and AGRESSIVLy

classically; first line;metotrexate and hyxroxycoroquine/sulfosarasine–immune modulators
classes are DMARDs-disease mododifying anti RA drugs

other is steroids-for rapid control, biological therapies

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15
Q

What are DMARDS in RA?

A

Disease modifying anti RA drugs-
Not currative-usually prevent damage tho
have to take it for a long time and will lead to remission if stopped

4 classic: Methotrexate-first line-but can upset liver
Suplhasalazine-
Hydroxycoloquine-
1st three are common
Leflunomide-rarer
Janus kinase inhbit-new
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16
Q

What are the biological therapies available for RA?

A
Anti TNFa AB
etanarecept-decoy TNFa receptor-reduce its action 
B cell depletion-Rituximab vs CD20
Modulation of T cell costimulation
Inhbition of IL6 -Anti IL6 AB
17
Q

What are the downsides of AB therapy?

A

Very expensive-limited for severe diseases

Risk can incluse increased infection risks
TNF inhbit-mycobarterial
Bdepletion-hepB reactivation