Ct-Ms - 2-23 - Ra

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Disease complex of RA

Back 1

Articular - more common in women. Synovial inflammation

Extra-articular - Men have it more than women. Due to immune complexes in places outside the synovium. (e.g. interstitial lung disease, which is the only one that continues to be on the rise)

Front 2

Big systemic sx associated with RA

Back 2

fatigue

Front 3

Timing of RA

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Abrupt. As opposed to OA which is a slow onset.

Front 4

Sx of RA

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symmetric joint stiffness, pain improving with exercise, worsening with rest.

Worst in the morning.

Hands feel weak and clumsy.

Front 5

Sites of RA

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in order of frequency

MCPs, PIPs, Wrists, MTPs

Front 6

Why is synovium targeted in RA?

Back 6

it is very pro-inflammatory

Front 7

Joints to focus on in physical exam for RA

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hands, feet, shoulders.

Front 8

Things to look for in pt when suspecting RA

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they wince before they shake your hand.

inability to oppose distal pulp space to base of digit.

these indicate MCP, PIP or flexor tendon inflammation.

Front 9

Mid-foot pain and stiffness

Back 9

limited differential which incl RA.

If metatarsalgia - (ball of foot) - Morton's neuroma or RA

If calcaneus (heel bone) - plantar fasciitis

Front 10

Main labs for RA

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RF and anti-CCP

Both very sensitive but CCP is very specific too!

Front 11

RF

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IgM against Fc of IgG

Front 12

Anti-citrullinated cyclic-peptide

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Post-translational conversion or arginine to citrulline.

Front 13

Does everyone make RF?

Back 13

Yes - but pts with RA make more and with higher IgG affinity.

High in babies because it increases IgG response.

Front 14

Anti-CCP

Back 14

also a bad predictor of outcome and a marker of shared epitope (a genetic test, basically)

Front 15

Does bone damage occur before sx present?

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Yes - because erosions are present at time of presentation.

Front 16

Why is early dx of RA very imp?

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Early stages of disease rapidly progresses and early treatment is very beneficial.

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Pathogen of RA

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T cells and B cells stimulate macrophages to make IL-6 (in humans) and TNF.

Overexp of TNF seems to give inflamm bowel disease and RA.

Getting rid of t cells and b cells will still give inflammation.

Front 18

Shared epitope theory in RA

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5 AAs in MHC2 beta chain is genetically acquired.

This presents citrullinated protein along with alpha chain for a CD4+ cell to recognize. But this specific beta chain makes the presentation occur for a longer amt of time. Due to enhanced binding of the peptide.

Front 19

Pts without anti-citrullinated Abs who have RA

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only 30% fall in this category and they have a better px.

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Major killer in RA

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ASCVD

This is highly predicted in pts with anti-CCP

Front 21

Are t cells needed for entire course of RA?

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No - eventually macrophages and fibroblasts cause IL-6 and TNF release and thus inflammation.

B cells in the germinal center are also proinflammatory.

Basically, the synovium changes to a lymph node over time.

Front 22

Most widely used tx for RA

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methotrexate - but can't use this during child-bearing years and in pts who drink alcohol.

Front 23

MTX vs. TNF-antag

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MTX is effective in managing sx but does not do as good of a job in halting bone erosions

Front 24

BeST trial

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Regardless of whether you use many drugs at once, keep changing drugs, or only use certain combos, the cost and effectiveness is the same.

Front 25

Extra-articular RA

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after the synovium is trashed and burnt out. not as common today because of better tx.

usually immune complex deposition leads to vascular compromise. it is RF dependent.

Front 26

Places to get extra-articular RA

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results in rheumatoid nodules, episcleritis/scleral disease, lung fibrosis/nodules/effusions, and vasculitis in nerves and digits of hand.

also carpal tunnel and atlantoaxial subluxation (bones in spinal column are compromised so with flexion there is spinal cord compression)

Front 27

Atlantoaxial subluxation

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dont do surgery with sedatives because they won't wake up as spinal cord is compressed.

need to do awake intubation.

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Key joint in RA for dx

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HANDS NEED TO BE INVOLVED!!!

feet are also important.

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Summary and realities

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The history/physical are key despite the fascinating insights provided by genetics and testing

The treatment of RA has been advanced as much as any autoimmune disease has ever been advanced

The lessons from RA therapeutics are likely to guide our treatment of all autoimmune diseases.