Writing brochure about a disease Essay Example

Autoimmune Diseases: Rheumatoid Arthritis

. In an autoimmune infection, the body immune system starts attacking its healthy tissues. In Rheumatoid Arthritis, the immune system mostly targets on the lining of joints where it causes inflammation and joints damage. Research indicates that RA primarily affects smaller joints such as those in hands. However, there still exists few chances of RA affecting large joints such as knees and hips. Turesson 2013 p.360)Rheumatoid arthritis (AR) is an autoimmune disease that is known for causing pain and swelling of body joints. The typical role of the body immune system is to protect the body from infection and maintain its health (

What is Rheumatoid Arthritis?

The HLA-DR molecules associated with Rheumatoid arthritis also carries the risk carries the shared epitope and confers the risk. Other HLA-DR4 molecules such as HLA-DR beta lacks the epitope and therefore do not confer the risk.

(Atsuhiko & Hideya 2012, P.78). Research indicates that there two main proteins involved in the Rheumatoid arthritis – a receptor and the corresponding binding protein. A protein molecule called CCL28 makes the body joints to become hypoxic once its overproduced in the joints. The protein expression CCL28 and sometimes CCR10 is modulated by tumor necrosis factor (TNF) -α. It’s the overexpression of CCL28 and CCR10 in Rheumatoid arthritis and their contribution to endothelial progenitor cells (EPCs) migration into RA joints cascades a potential therapeutic threat for Rheumatoid arthritis maintained through Toll-like receptor (TLR) activation

What are the molecular causes?

Autoimmune diseases; Rheumatoid arthritis.

, p.63). This process is activated by some cytokines, chemokines, and cell adhesion molecules. The pannus produces more enzymes which now aggravates to more areas while attracting the white cells at the same time. This inflammatory now goes to from affecting the bones into affecting other organs in other body parts.McInnes 2016The increased number of macrophages makes the makes the intimal lining hyperplastic. It’s hyperplastic which forms the pannus, an aggressive front which affects the bones structures (

In the inflamed Rheumatoid arthritis joint, the synovium is highly filled with CD4+ T Cells, macrophages and few B Cells.

, p.63). In Rheumatoid arthritis, the abnormal immune system creates destructive molecules which cause a slow and continuous inflammation of the synovium membrane. If no treatment approach is taken at this stage, the destruction of the cartilage continues and now at an accelerating speed. The fluid and the immune system cells gradually accumulate and form a pannus, a swelling which is composed of the thickened synovial tissue. (McInnes 2016The diseases process leading to Rheumatoid arthritis starts in the Synovium. This is the membrane which surrounds the body joints and creates a protective sac which contains synovial fluid. This fluid in additional to cushion joints forms a slippery tissue coats the ends of the bones

Rheumatoid arthritis disease process

. Strangfeld 2017, p.504There no a 100% cure for Rheumatoid arthritis. The aim of the Rheumatoid arthritis treatment now is to achieve the lowest possible level of RA activities (

Is there a cure for RA?

) The DMARDs are known as biological response modifiers since they are genetically engineered. The biologics work by interrupting with the various immune signal involved in the formation of synovium and damage of the joint tissue. Most of these drugs work by crippling the T cells which play a major role in the inflammation formation.Strangfeld, 2017Medications: some of the common Rheumatoid arthritis medication is disease-modifying antirheumatic drugs (DMARDs) which are used to slow the course of the disease (

What treatments are there for RA?

(3), pp.504-510.76, Annals of the rheumatic diseasesStrangfeld, A.,2017. Risk for lower intestinal perforations in patients with rheumatoid arthritis treated with tocilizumab in comparison to treatment with other biologic or conventional synthetic DMARDs.

(1), p.63.12, Nature Reviews. RheumatologyMcInnes, I.B., 2016. Cytokines in rheumatoid arthritis—shaping the immunological landscape.

(12), pp.2569-2582.210, Journal of Experimental MedicineScally, S.W., Petersen, J., Law, and McCluskey, J., 2013. A molecular basis for the association of the HLA-DRB1 locus, citrullination, and rheumatoid arthritis.

References

(2), pp.264-272.66, Arthritis & rheumatologyRincón, I., Battafarano, D.F., Restrepo, J.F., Erikson, J.M. and Escalante, A., 2014. Glucocorticoid Dose Thresholds Associated With All‐Cause and Cardiovascular Mortality in Rheumatoid Arthritis.

(3), pp.360-366.25, Current opinion in rheumatologyTuresson, C., 2013. Extra-articular rheumatoid arthritis.

Molecular Mechanisms of Rheumatoid Arthritis Revealed by Categorizing Subtypes of Fibroblast-Like Synoviocytes Katsuhiko Ishihara and Hideya Igarashi 2012.