Flashcards in Rheumatoid Arthritis Deck (15):
Chronic progressive systemic autoimmune disease characterised by inflammatory polyarhtritis affecting peripheral joints, especially hands and feet.
Untreated initial synovial inflammation can lead to cartilage and bone erosion and joint destruction.
Rheumatoid factor and CCP Ab. Raised CRP and ESR (erythrocyte sedimentation rate).
Symptoms for at least 6 wk.
Genetic, hormones and environmental factors cause aberrant immune activation anf inflammation in joint.
Pro inflammatory outweigh anti. eg IL1, IL6, TNFa inflammatory cytokines.
CT disease eg SLE, scleroderma, sjorgrens.
Ca pyroP deposition.
Swollen, painful, stiff small joints. Worse in morning.
Rare- sudden onset widespread, recurring polyathritis, systemic illness, polymylagic onset, recurrent soft tissue problems.
Early- inflammation and swelling in hands and wrists, tenosynovitis, bursitis.
Later- joint damage and deformity, ulnar deviation, wrist subluxation, swan neck fingers, Z thumbs, ruptures hand extensor tendons. Larger joints can be involved.
Also rheumatoid nodules, lymphadenopathy, pleural and pericardial effusion, raynauds, CTS, vasculitis, alveolitis, bronchiolitis, peripheral neuropathy, splenomegaly, scleritis, OP, amyloiosis.
Disease modifying anti rheumatic drugs for chronic eg methotrexate, sulfalsalazine.
Biological DMARDs eg antiTNF, rituximab
Steroids, NSAIDs for acute. CS prevent mac IL1+6 production, and inhibit T activation.
CVS management, OP prevention, vaccines.
Swelling or tenderness in more than 3 joints
Arthritis of hands
Morning stiffness over 1 hour
Serology- positive RF and anti CCP Abs.
Acute phase reactants- CRP or ESR
Symptoms for over 6 weeks
Loss of joint space
Erosion of bone
Soft tissue swelling
Soft bones (osteopenia)
Late- subluxation ro carapl destruction.
US or MRI for synovitis and erosions.
Adverse lipid profile
Antiproliferative immunosuppressants eg azathioprine
Inhibits purine metabolism once cleaved to 6-MP.
Used lot in RA, enables steroid sparing.
AE- bm suppression, neutropenia, high risk malignancy and infection, hepatitis.
Monitor FBC and LFT
Test for TPMT metabolising enzyme levels first
Calcineurin inhibitors eg ciclosporin
Prevents T activation and signalling
Used in RA for patients with cytopenias as no effect on bm.
AE- HTN, nephrotoxic, increased lipid, hyperuricaemia, gingival hyperplasia.
Monitor BP and eGFR
avoid grapefruit and high K
Antimetabolites eg methotrexate
Not antifolate in RA MOA. Maybe inhibit purine metabolism and T activation.
Gold standard in RA
Low dose can combine with other DMARDs, NSAIDs, steroids.
AE-pneumonitis, hepatotoxicity, mucositis.
Monitor all bloods
DDI- binding competition with eg NSAID, phenytoin, tetracyclines, penicillin= increase myelosuppression.
DMARD eg sulfasalazine
T cell and neutrophil inhibition.
Some efficacy in RA
Vs methotrexate- not always require LT FBCs, few DDIs, not carcinogenic, safe in pregnancy.
AE- rash, low sperm count, mouth ulcer, fatigue, myelosuppression, heapatitis, nausea, headache.
Anti TNF eg infliximab
Used if fail to respond to 2 DMARDs for over 2 months at target dose. And only if evidence of clinically active RA.
Withdraw if AE or fail to respond by 6 month.
Dont escalate dose.
Reduce inflammation, angiogenesis and joint destruction.
AE- risk new malignancy if had one previously. Risk serious infections. TB reactivation.
B cell depletion eg rituximab
Use for severe RA where DMARD and anti TNF failed.
AE- hypogammaglobilin, infection, hypersensitivity or blocking immune response.