Framework Essay

1810 words - 8 pages

Therapeutic framework for Rheumatoid arthritis
1) Pathophysiology of the disease
Aetiology:
The exact cause of Rheumatoid arthritis is unknown. There is no single factor which is the cause of Rheumatoid arthritis; nonetheless, several factors seem to have a role in the development of Rheumatoid arthritis (Walker and Whittlesea, 2012). One of the risks of developing this condition is genetic factors (Symmons, 2013).
Many studies were done in order to understand the genetic factors which predispose to Rheumatoid arthritis. It has been found that “genetic factors contribute 53-65% of the risk” of developing Rheumatoid arthritis, particularly the HLA-DR4 allele which is associated with the tendency to develop the disease (Walker and Whittlesea, 2012). Several genes may contribute to the development and severity of the condition, but there is no single gene that is the cause of Rheumatoid arthritis (Symmons, 2013).
Similarly, no single environmental factor could be the cause of the condition. Some studies have demonstrated that cigarette smoking is a likely risk factor for development of Rheumatoid arthritis (Walker and Whittlesea, 2012).

Pathophysiology:
Rheumatoid arthritis is a chronic autoimmune systemic inflammatory disease. The condition affects the joints as well as a wide range of extra-articular organs. Some examples of the extra aritcular featured of the disease are summarized in ‘Figure a.’ The severity of the disease can vary from mild to severe (Walker and Whittlesea, 2012).
Rheumatoid arthritis is characterized by inflammation of the joints causing swelling, pain, stiffness and redness in the joints:
Inflammatory cells recruit to the joint, producing cytotoxic inflammatory mediators which lead to destruction of the joint tissue. Inflammatory cells involved in Rheumatoid arthritis include T-cells, B-cells, macrophages and plasma cells. These inflammatory cells produce cytokines including tumour necrosis factor, interleukin 1 and interleukin 6 leading to secretion of proteolytic enzymes by the synovium. Consequently, the synovial membrane becomes highly vascularized and hypertrophied, resulting in pannus formation. Then proliferation of fibroblasts and inflammatory cells occurs in the synovial membrane leading to cartilage destruction and bone erosion, causing deformity of the joints (Walker and Whittlesea, 2012). Rheumatoid arthritis is a progressive illness that has the potential to cause functional disability (Symmons, 2013; Walker and Whittlesea, 2012).

As Rheumatoid arthritis has no cure, goals of treatment are to relieve the pain, reducing stiffness in affected joints, prevent joint damage, minimize any disability caused by pain, joint damage or deformity and achieving disease remission (walker and Whittlesea, 2012). There are four main categories of drugs used in the management of Rheumatoid arthritis: non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, Disease-modifying anti-rheumatic drugs...

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