Pathophysiology of Rheumatoid Arthritis

Pathophysiology of Rheumatoid Arthritis

In Rheumatoid arthritis, an autoimmune reaction mainly occurs in the synovial tissue. Phagocytosis produces enzymes in the joints. These enzymes will break down collagen resulting in edema, proliferation of the synovial membrane and pannus formation eventually. Pannus will destroy cartilage and bone erosion. The result is the disappearance of the joint surface that would interfere with joint motion. Muscles will also be affected due to the muscle fibers will experience degenerative changes with the disappearance of muscular elasticity and strength of muscle contraction (Smeltzer & Bare, 2002).

The early inflammatory synovial joints such as edema, vascular congestion, fibrin exudate and cellular infiltration. Ongoing inflammation, synovial becomes thickened, especially in the joint articular cartilage of joints. In this joint pannus of granulation form, or a cover that covers the cartilage. Pannus into the bone sub- chondria. Advanced granulation tissue due to inflammation caused disruption in articular cartilage nutrition. Cartilage becomes necrotic.

The rate of erosion of joint cartilage determine the level of disability. When the cartilage damage was extensive adhesion occurs between the joint surfaces, due to fibrous tissue or bone together (ankylosis). Damage to cartilage and bone causing tendons and ligaments so weak and can cause subluxation or dislocation of the joints. Invasion of bone sub chondrial can cause local osteoporosis.

The duration of rheumatoid arthritis varies among individuals characterized by the absence of attacks and attack. While some people recover from the first attack and then not attacked again. However, in a minority of individuals occurs characterized by rapidly progressive joint damage that occurs continuously and diffuse vasculitis (Long, 1996).