Rheumatoid Arthritis (RA) PDF

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St John's Institute of Dermatology, KCL, London, UK

Dr. Roaa Salim

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rheumatoid arthritis inflammatory arthritis medical presentation healthcare

Summary

This is a presentation on rheumatoid arthritis (RA). It covers the definition, epidemiology, pathophysiology, clinical characteristics, diagnostic methods, and management strategies of the condition. The presentation concludes with an overview of surgical interventions for managing RA.

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Rheumatoid Arthritis (RA) Dr. Roaa Salim F.I.B.M.S (Rheumatology) Learning objectives At the vend of this lecture thev student should be able to know : Definition and Epedimiology of RA Pathophysiology of RA Clinical feature of RA Diagnostic criteria of RA Investigations of RA Managemento...

Rheumatoid Arthritis (RA) Dr. Roaa Salim F.I.B.M.S (Rheumatology) Learning objectives At the vend of this lecture thev student should be able to know : Definition and Epedimiology of RA Pathophysiology of RA Clinical feature of RA Diagnostic criteria of RA Investigations of RA Managementof RA Prognosis of RA Definition and Epidemiology of RA Rheumatoid arthritis (RA) is a common form of inflammatory arthritis, It is a chronic disease characterized by exacerbations and remissions occurring throughout the world and in all ethnic groups. Archibald Garrod coined the term “rheumatoid arthritis” in 1890. The prevalence of RA is approximately 0.8%–1.0% in Europe and South Asia. female-to-male ratio of 3:1. Pathophysiology and causes of RA combination of Genetic and environmental factors is important. higher rate of RA in monozygotic compared with dizygotic twins increased frequency of disease in first-degree relatives of patients. The strongest association is with variants in the HLA region mostly HLA DR4 cigarette smoking is the strongest environmental risk factor and is associated with more severe disease and reduced responsiveness to treatment. The disease is characterized by infiltrations of synovium with lymphocytes, plasma cells, dendritic cells and macrophages. Pathophysiology and causes of RA The Prostaglandins and There is activation of T macrophages nitric oxide produced cells to produce cytokines produce several within inflamed and activation of B cells pro-inflammatory synovium cause to produce cytokines, vasodilatation, autoantibodies, including including TNF-α, resulting in swelling RF and ACPA. IL-1 and IL-6 and pain. Muscles adjacent to A key pathogenic factor in inflamed joints atrophy and bone erosions and may be infiltrated with periarticular osteoporosis is lymphocytes. osteoclast activation Clinical feature Joint pain and swelling of the small joints of the hands, feet and wrists in a swelling and tenderness of symmetrical fashion , Large joint can be the affected joints. History : Examination deformities may develop affected later. : with long-standing Morning stiffness often last 1 hour or uncontrolled disease more. Radial deviation of the wrist ,ulnar deviation of Rheumatoid Nodules MCP joint , swan neck deformity can be seen on (hyperextension of PIP),boutonniere extensor surface in deformity(flexion of PIPS), also feet deformity advance disease. can occur Systemic features Anorexia. weight loss. fatigue. Osteoporosis is a common complication. muscle-wasting. Extra articular manifestations most common in patients with long-standing seropositive ( Rheumatoid factor and anti citrullinated peptide positive ) and erosive disease. Investigations The diagnosis of RA is essentially clinical. investigations are useful in confirming the diagnosis and assessing disease activity The ESR and CRP are usually raised, but may be normal. Tests for anticitrullinated cyclic peptide( ACPA) are positive in about 70% of cases and are highly specific for RA. Rheumatoid factor (RF )is also positive in about 70% of cases ,but not specific. Ultrasound and MRI of the joints can be used but not routinely. Plain X-rays of the hands, wrist and feet are usually normal in early RA, but periarticular osteoporosis and marginal joint erosions may be observed with more advanced disease. Diagnostic Criteria Managment The treatment goal is to: suppress inflammation. control symptoms. prevent joint damage. maintain function. a combination of pharmacological and non-pharmacological therapies used. Pharmacological therapy Non biologic DMARD Prompt initiation of Conventional Disease modifying antirheumatic cDMARD therapy is indicated in all patients as this improves outcome. Methotrexate (MTX) : an initial dose of 15 mg weekly with folic acid 5 mg weekly is the most effective first line treatment for RA ,Most common side effect is GIT problem. sulfasalazine and HCQ are other c DMARD can be used alone or in combination with MTX. Supportive treatment Steroid can be started to control symptoms at the same time with cDMARD but steroid should be stopped at 12 weeks. Nonsteroidal anti inflammatory drugs((NSAID) can be used until DMARD work. Pharmacological therapy Biologic DMARD If disease activity remains high despite c DMARD it is usual to progress to biologic or tsDMARD therapy. The most commonly used first-line biologic in RA is anti tumor necrotic factor (anti-TNF-α) therapy like Infliximab , Adalimumab ,Etanercept ,most important side effect is infection IL- 6 inhibitor like Tocilizumab. IL -1 antagonist like Anakinra. Target synthetic DMARD (t sDMARD) like Tofacitinib. Rituximab anti CD20 used after failure of other biologics. non-pharmacological therapy Occupational therapy as aiding tools. Use of splints for active inflamed joint. psychologist support are all important for RA patients. Education for patients and there families. Surgery Synovectomy can be helpful in joints that have failed to respond adequately to systemic therapy and intra-articular injections. Joint arthroplasty may be required where secondary OA evolves. Disease course Disease flares can occur from Transient flares can be time to time even in patients who treated with local joint or are established on DMARD and deep IM ‘depot’ steroid injections or a short course biologic therapy. of oral prednisolone. If a sustained flare Joint destruction and occurs, a change in complication of DMARD and/or biologic inflammation can occur should be. considered. Complication of RA Ischemic heart disease increase 2 to 3 times over the general population, is one of the leading cause of death. Infections especially pneumonia and septic arthritis. Interstitial lung disease and COPD. Lymphoma and leukemia are increased 2 to 3 fold ,lung cancer increased. Renal disease due to amyloidosis and gastrointestinal hemorrhage from NSAID also increased. Osteoporosis and secondary osteoarthritis. Vasculitis and felty syndrome. Rheumatoid Arthritis in pregnancy Many patients with rheumatoid arthritis go into remission during pregnancy. methotrexate should be discontinued for ≥ 3 months and leflunomide discontinued for ≥ 24 months before trying to conceive. Paracetamol: the oral analgesic of choice during pregnancy. Oral non-steroid anti inflammatory drugs and selective cyclo-oxygenase (COX-2) inhibitors: can be used from implantation to 20 weeks’ gestation. Rheumatoid Arthritis in pregnancy Glucocorticoids: may be used to control disease flares. DMARDs that may be used: sulfasalazine, azathioprine and hydroxychloroquine. DMARDs that must be avoided: methotrexate, leflunomide, cyclophosphamide and mycophenolate. breastfeeding: methotrexate, leflunomide and cyclophosphamide are contraindicated Poor prognostic feature Persistent Long disease Poor functional Persistently moderate to duration prior to status and low elevated ESR severe disease treatment. education. or CRP. activity. Extra articular (RF,anticcp) postive Early erosion on x feature specialy and high titer RF,HLA ray. rheumatoid nodules DR 4 and vasculitis. Question 45 years old female presented with joint pain and swelling ,morning stiffness more than 1 hour for 2 month duration with fatigue ,on examination of her joints there is tenderness and swelling of small joints of both hand in symetrical fashion : What is the most likely diagnosis ? What is the investigation you recommend ? What is the first line treatment for her condition? References Davidson’s 24 th edition. Secrets Rheumatology.

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