Rheumatoid arthritis

Rheumatoid arthritis(infectious polyarthritis) is a chronic disease with progressive deorganization of the connective tissue of the articular membranes and cartilages which cause its deformation.

Pathology. Musculoskeletal system. Rheumatoid arthritis causes a broad spectrum of morphologic alterations; the most severe are manifested in the joints. Initially the synovium becomes edematous, thickened, and hyperplastic transforming its smooth contour to one covered by delicate and bulbous fronds. A dense perivascular inflammatory infiltrate composed of lymphoid follicles, plasma cells, and macrophages fills the synovial stroma. The vascularity is increased with

superficial hemosiderin deposits and scattered giant cells. Aggregates of organizing fibrin cover portions of the synovium and float in the joint space as «rice bodies». Neutrophils accumulate in the synovial fluid and cluster along the surface but usually do not penetrate deep to the synoviocytes. The fluid, although turbid and increased in volume, forms a poor mucin clot on exposure to acetic acid. The inflamed and hyperemic synovium creeps over the articular surface forming a pannus and causes erosion of the underlying cartilage.The mediators released by the inflammatory cells and synoviocytes result in osteoclastic activity, allowing the synovium to penetrate into the bone forming juxta-articular erosions, subchondral cysts, and osteoporosis. After the cartilage has been destroyed, the fibrocellular pannus bridges the opposing bones, forming a fibrous ankylosis that eventually ossifies ultimately resulting in bony ankylosis.

Tendinoligamentous involvement frequently accompanies arthritis. The inflamed synovial sheaths cause irreversible damage or even rupture of the tendons and ligaments. Occasionally the inflammation extends into the adjacent muscles.

Skin. Rheumatoid nodules are the most common cutaneous manifestation. They occur in regions that are subjected to pressure, including the ulnar aspect of the forearm, elbows, occiput, and lumbosacral area. Less commonly they form in the lungs, spleen, pericardium,

myocardium, heart valves, aorta, and other viscera. Rheumatoid nodules are firm, and round to oval and in the skin arise in the subcutaneous tissue. Microscopically they have a central zone of fibrinoid necrosis surrounded by a prominent rim of epithelioid histiocytes and numerous lymphocytes and plasma cells.

Blood vessels. Patients with severe erosive disease, rheumatoid nodules, and high titers of rheumatoid factor are at risk of developing vasculitic syndromes. Rheumatoid vasculitic is potentially catastrophic, and the different types vary according to the size and nature of the affected vessels. Frequently segments of small arteries, such as vasa nervorum and digital arteries, are obstructed by endarteritis obliterans and medial necrosis resulting in peripheral neuropathy, ulcers, and gangrene. The involvement is similar to that in polyarteritis nodosa except that in rheumatoid arthritis the kidneys are not involved. Leukocytoclastic venulitis produces purpura cutaneous ulcers, and nail bed infarcts.

Visceral changes: nonspecific inflammation, rheumatoid nodules, and vasculitic can affect virtually all organ systems, especially the eyes, lungs, and heart.

Complications: luxations and subluxations of the small joints, limited mobility, ankylosis, osteoporosis, renal amyloidosis.

The death is caused by uremia.