Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that affects primarily the joints. The RA leads to destruction, mediated by cytokines, chemokines and metalloproteinases. Characteristically the peripheral joints (z. B. wrists, metacarpophalangeal joints) are affected symmetrically flammable, leading to a progressive destruction of the joint structures, usually accompanied by systemic symptoms. The diagnosis is based on specific clinical, laboratory and imaging criteria. The treatment consists of medication, physical activities and sometimes surgical interventions. Disease-modifying antirheumatic drugs help control the symptoms and slow the progression of the disease.

The RA has a prevalence of about 1%, women are affected more often 2 to 3 times. The disease can begin at any age, most often between the ages of 35 and 50 years, but also during childhood (see Juvenile idiopathic arthritis) or old age.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that affects primarily the joints. The RA leads to destruction, mediated by cytokines, chemokines and metalloproteinases. Characteristically the peripheral joints (z. B. wrists, metacarpophalangeal joints) are affected symmetrically flammable, leading to a progressive destruction of the joint structures, usually accompanied by systemic symptoms. The diagnosis is based on specific clinical, laboratory and imaging criteria. The treatment consists of medication, physical activities and sometimes surgical interventions. Disease-modifying antirheumatic drugs help control the symptoms and slow the progression of the disease. The RA has a prevalence of about 1%, women are affected more often 2 to 3 times. The disease can begin at any age, most often between the ages of 35 and 50 years, but also during childhood (see Juvenile idiopathic arthritis) or old age. Although the etiology of autoimmune processes in RA play an important role, the exact cause is still unknown, a multifactorial is likely. A genetic predisposition has been identified and located on a common epitope in HLA DR?1 -Genlokus of class II histocompatibility antigens (for whites). Unknown or unconfirmed environmental factors (eg., Viral infections, smoking) are likely to play a role in the initiation and maintenance of joint inflammation. Pathophysiology Prominent immunologic abnormalities include immune complexes formed by synovial lining cells and inflamed blood vessels. Plasma cells produce antibodies (such as rheumatoid factor [RF], anti cyclic citrullinated peptide antibody [anti-CCP].), Which contribute to these complexes; a destructive arthritis can jeoch occur in their absence. In the early stage of the disease macrophages migrate into the affected synovium; there exists an increased number of macrophages derived from synovial lining cells, as well as inflammation of the blood vessels. The synovium is characterized by a massive infiltration of lymphocytes, especially CD4 + T cells. Macrophages and lymphocytes in the synovium produce proinflammatory cytokines and chemokines such. B. TNF-alpha, granulocyte macrophage-colony stimulating factor (GM-CSF), various interleukins (IL) and interferon-?. The release of inflammatory mediators is believed to contribute to the systemic and joint manifestations. In chronically infected joints normally thin synovium proliferates and forms villous pleats. The synovial lining cells produce various substances such as collagenases and stromelysin that contribute to cartilage destruction, as well as IL-1 and TNF-?, which is also to stimulate cartilage destruction and osteoclast-mediated bone resorption, synovial inflammation and the production of anti-potentiating prostaglandins. Fibrin deposition, fibrosis and necrosis can also be detected. The hyperplastic synovial tissue (pannus) releases inflammatory mediators that erode cartilage, subchondral bone, the joint capsule and ligaments. Polymorphonuclear leukocytes (PMN) make an average of about 60% of the leukocytes into the synovial fluid. Approximately 30% of patients with RA to develop rheumatoid nodules. This is to granulomas, which consist of a central necrotic area with surrounding wall of histiocytic macrophages, enveloped by lymphocytes, plasma cells and fibroblasts. Nodes and vasculitis symptoms can also develop in visceral organs. Symptoms and signs The illness usually begins insidiously, often face systemic and joint symptoms at the beginning. Among the systemic symptoms include morning stiffness of the affected joints, fatigue and malaise in the afternoon, loss of appetite, generalized weakness and sometimes a mild fever. Pain, swelling and stiffness are the main joint symptoms. The disease progresses within the first 6 years v. a. in the first year, most progressive advance; 80% of patients develop persistent Gelenkabnormalit√§ten within 10 years. The disease course is unpredictable in individual patients. The joint symptoms typically occur symmetrically, morning stiffness lasts after getting up at least one hour, but it may, after each longer period of inactivity occur (so-called. Gelling). The affected joints are sensitive to pressure and have redness, warmth, swelling and restricted movement on. The main overall joints are affected: wrist and MCP joints of the index and middle finger (most affected) proximal interphalangeal metatarsophalangeal shoulders elbow hip knee hock With the exception of the distal interphalangeal (DIP) can be virtually affected every joint. In the area of ??the axial skeleton only the upper cervical spine is affected. The thickening of the synovium can be palpated. Often, the hinges are kept in flexion, so as to minimize the pain caused by the tension of the joint capsule. Fixed deformities, v. a. Flexion contractures may develop rapidly; Typical is an ulnar deviation where the extensor tendons slide over the MCP joints ulnar well gooseneck and boutonniere deformity (buttonhole and Schwanenhalsdeformit√§ten.). Due to the stretching of the joint capsule, a joint instability can arise. By compression of the median nerve can develop carpal tunnel syndrome from the Handgelenksynovitis. A popliteal Baker’s cysts can lead to swelling and tenderness of the lower leg, which may be confused with deep vein thrombosis. Swan neck Science Photo Library var model = {thumbnailUrl: ‘/-/media/manual/professional/images/c0095323_swans_neck_deformity_hands_with_rheumatoid_arthritis_science_photo_library_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media / manual / professional / images / c0095323_swans_neck_deformity_hands_with_rheumatoid_arthritis_science_photo_library_high_de ? .jpg lang = en & thn = 0 ‘, title:’ swan neck ‘, description:’ u003Ca id = “v38395270 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eEine Schwanennackendeformit√§t is characterized by extending the proximal interphalangeal and distal interphalangeal flexion of the u003c / p u003e u003c / div u003e. ‘credits’ Science Photo Library’

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