Rheumatoid Arthritis Flashcards
Definition
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.
Symmetrical deforming.
Rheumatoid factor and CCP Ab. Raised CRP and ESR (erythrocyte sedimentation rate).
Symptoms for at least 6 wk.
Aetiology
Genetic, hormones and environmental factors cause aberrant immune activation anf inflammation in joint.
Pro inflammatory outweigh anti. eg IL1, IL6, TNFa inflammatory cytokines.
Differentials
Infection CT disease eg SLE, scleroderma, sjorgrens. Seronegative spondyloarthropathies. Ca pyroP deposition. Gout Polymyalgia rheumatica. Haemochromatosis Paraneoplastic syndrome OA
Symptoms
Swollen, painful, stiff small joints. Worse in morning.
Rare- sudden onset widespread, recurring polyathritis, systemic illness, polymylagic onset, recurrent soft tissue problems.
Signs
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.
Management
Disease modifying anti rheumatic drugs for chronic eg methotrexate, sulfalsalazine. Biological DMARDs eg antiTNF, rituximab Cyclophosphamide cytotoxic Steroids, NSAIDs for acute. CS prevent mac IL1+6 production, and inhibit T activation. Physio Splints Surgery CVS management, OP prevention, vaccines.
Diagnosis
Swelling or tenderness in more than 3 joints Arthritis of hands Symmetrical arthritis Rheumatoid nodules Morning stiffness over 1 hour Serology- positive RF and anti CCP Abs. Acute phase reactants- CRP or ESR Symptoms for over 6 weeks XR- LESS 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.
Corticosteroid ADRs
Weight gain Fat redistribution Striae Growth retardation OP Avascular necrosis Glucose intolerance Adverse lipid profile Infection risk Cataracts
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.
Explanation
- RA happens when your own immune system attacks your joints, leading to inflammation and damage. Genetic, hormonal and enviromental factors are involved.
- it can damage cartilage which is the smooth padding in your joints, as well as the bone itself. This will eventually lead to deformity, usually especially in the hands, and loss of movement in affected joints.
- lifestyle?
- drugs are available that will dampen down the immune response that is causing the damage. As well as drugs to relieve any pain. Also physiotherapy and use of supporting splints can help. Surgery is an option if none of those treatments work.
