Rheumatoid Arthritis (RA) is a pervasive disorder of the autoimmune system that affects roughly 1% of the global population (Allan, 2015) . The actual cause of RA remains indefinite; nevertheless, the genesis of the disease appears to stem from the interface between individuals of genetic predisposition, triggers from the environment, and by chance. RA is embodied by inflammatory mechanisms that in the joint’s synovium that are dysregulated that in the results in damaging of both bony and cartilaginous parts of the joint leading to pain and incapacity. Allan (2015) states systemic inflammation linked with RA is concomitant with an array of extra-articular comorbidities, counting cardiovascular illnesses, leading to a high number of deaths in RA patients. Also, RA is also allied to several psychological disorders. Early detection of RA is essential to initiate effective management before the irreversible pathological alterations kick in.
Pathophysiology
The synovitis, inflammation, and joint impairment that typify RA that is active are the outcome multifaceted autoimmune and swelling process that entails constituents of both adaptive and innate immune system (Demoruelle et al., 2015) . In a vulnerable person, the combination of genes and the environment leads to a deficiency intolerance of individual proteins that has a residue of citrulline. These proteins are derived when residues of arginine undergo a post-translational alteration to citrulline by a deiminase enzyme peptidylarginine. Patients having mutual epitopes produce citrullinated peptides that cease to be identified as “self” by the immune system, which in the end creates ACPAs against them (Demoruelle et al., 2015) . Assessment of magnetic resonance imaging (MRI) and data from synovial biopsy from healthy persons with MRI and biopsy record from RA patients indicates that the systemic autoantibody making pave the way for inflammation and formation of adhesion elements in the synovium, suggesting that probably a secondary occurrence is needed to trigger the participation of the synovium in RA.
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Synovitis results from a consequence of infiltration of leukocyte into the synovium. The build-up of white blood cells (WBC) in the synovium does not originate from local cellular propagation but instead from the migration of WBC from secluded areas of development in response to the manifestation of chemokines and adhesion molecules by triggered endothelial cells of synovial microvessels (Allan, 2015) . The inflamed synovium interior becomes hypoxic, probably due to increase in the number of synovial cells with decrease in the flow of synovial capillary as an aftermath of heightened fluid capacity in the synovium (Quiñonez-Flores et al., 2016) . In the synovium, hypoxia concomitantly initiates angiogenesis through the inducement of development of facets that incite the formation of vessels, for example, vascular endothelial growth factor.
According to CDC (2019) activation of the immune system and progression of RA is a multifaceted process that entails interaction among components present in both innate and adaptive immunity pathways. The manner of communication depends on the action of local cytokine and chemokine milieus of the synovium in which they occur. The significance of the path for the adaptive immune system is shown by the availability of dendritic cells, HLA class II molecules, and co-stimulatory molecules. Dendritic cells (DCs) function as antigen presenting cells to T cells found within the synovium and also function as a component of the T cell activation mechanism. For T cells to be activated two signals are required (Singh et al. 2016). The first being presentation of antigens to receptors of the T-cell and the second signal, the costimulatory message, necessitates communication of CD80/86 a cell surface protein on the dendritic cell with a protein CD28 found on the T cell.
Besides, adaptive humoral immunity has an essential duty in RA pathogenesis. The influence of B cells to autoimmune disorders may be capable of mediation via numerous processes. Shortcomings in checkpoints of B cell tolerance can lead to the emergence of B cells that are autoreactive that function to present antigen that may lead to T cells being activated. B cells are capable of releasing cytokine that is both pro- and anti-inflammatory. Besides, B cells can also act as antibody-producing cells (Quiñonez-Flores et al., 2016) . Either together or in separate, these processes can interject to the pathogenesis of RA. Further support of the role of B cells in RA can be seen in the management of RA when agents that function to destroy particular B-cell population are used such as Rituximab.
Innate immune system cells, such as Macrophages (MQs), natural killer cells and mast cells are found within the synovial membrane, while neutrophils are present within the synovial fluid. MQs are integral synovitis effectors that function via phagocytosis; presentation of antigen; and the production of pro-inflammatory cytokines; prostanoids, an enzyme that degrades matrix, and reactive oxygen species (Allan, 2015) . TLRs receptors on monocytes, MQs, DCs function to trigger immune and inflammatory response upon contact with an immunogenic spur, for instance, microbial pathogen.
Activated TLRs leads to the quick manifestation of pro-inflammatory cytokines that solicits an immune response triggering lymphocytes, monocytes, and neutrophils. MQs and DCs amass processed antigen and travel to tissues of peripherally lymphoid in which presentation of antigen to adaptive immune system cells occurs leading to triggering of cellular immunity and release of antibodies (Demoruelle et al., 2015) . Usually, combined actions of adaptive and innate immunity are adequate to destroy the pathogen resulting in termination of the immune response. However, in RA the inflammatory response does not undergo cessation following the elimination of pathogen but persist chronically activated.
Teaching Plan for a Newly Diagnosed RA Patient
Patient X has been working as a sale manager for 30 years. She is currently retired, and she started feeling the pangs of standing for long hours while she was working. Repeatedly, she feels the sensation of pain around the knees and swelling and redness were evident around the area. A similar feeling began spreading to her elbows, shoulders, and hips. After a medical check-up and thorough laboratory examination, she was diagnosed with RA.
RA patients require optimal care which combines integrated methods of both non-pharmacologic and pharmacologic approaches. Non-pharmacologic approaches include diet, exercise, surgery, physical therapy, massage, stress reduction (Dediu et al., 2015). Patient X, therefore, will start on non-pharmacologic approaches starting with healthcare behavior changes. Rest and exercise: People with RA require sufficient balance of rest and exercise, more res when the disease is active while more training when it is not (Halls et al., 2017). Rest reduces active joint inflammation and pin to minimize fatigue. Exercise helps maintain strong and healthy bones and muscles conserving mobility of the joint and sustaining flexibility.
Practicing a healthful diet is also crucial for RA patients. Food should include basic daily requirements and rich in proteins, vitamins, and iron for repair and tissue building. Some individuals should avoid alcoholic drinks, especially when undergoing treatment to prevent drug-alcohol interaction, especially when using methotrexate (Dediu et al., 2015). Therapy is also essential. A recognized program with physical and occupational therapy is used to enlighten patients on joint protection, simplification of duties, pacing undertakings, and range of motion. Recommendations to societal agencies, for example, the Arthritis Foundation can help RA patients to access more support.
Pharmacologic approaches may be divided into three; these include Early RA which includes NSAIDs COX-2 treatments which block the inflammatory enzyme. Methotrexate is currently widely used and accepted medication due to its capacity to deter both destructions of the joint and long term disability. Finally, analgesics may be prescribed. Moderate RA medications include cyclosporine is include to magnify the effects of methotrexate. Corticosteroids may also be used for patients with unremitting pain and swelling. Also, Rituximab, Abatacept, and Anakinra are used (Singh et al., 2016). Surgery management includes reconstructive surgery, synovectomy, arthroplasty, arthrodesis, and tenorrhaphy.
Patient X late diagnosis has been made for RA. Therefore, the best plan of care for her will be first starting episodes of exercise to strengthen the muscles and to keep her active. RA has already spread into various body parts such as hips and elbows, hence treatment will major on pharmacologic approach where I will prescribe for her Methotrexate, and monitor her progress, before continuing to other medication such as corticosteroids when RA is unremitting. I will also give her advice on diet change by reducing excess intake of proteins, calories, and calcium. Correctional surgery will be the last option.
References
Allan. G. (2015). Epidemiology, Pathophysiology, and Diagnosis of Rheumatoid Arthritis: A Synopsis. Retrieved April 18, 2019, from https://www.ajmc.com/journals/supplement/2014/ace017_may14_ra-ce/ace017_may14_ra-ce_gibofsky1_s128
Angelotti, F., Parma, A., Cafaro, G., Capecchi, R., Alunno, A., & Puxeddu, I. (2017). One year in review 2017: Pathogenesis of rheumatoid arthritis. Clin Exp Rheumatol , 35 (3), 368-78.
Dediu, G. N., Crismaru, I., Bajan, M., Ionescu, G., Ilie, M., Udrea, G., ... & Bartos, D. (2015). THE NON-PHARMACOLOGIC TREATMENT OF RHEUMATOID ARTHRITIS. Romanian Journal of Rheumatology , 24 (2).
Demoruelle, M. K., Harrall, K. K., Ho, L., Purmalek, M. M., Seto, N. L., Rothfuss, H. M., ... & Kelmenson, L. B. (2017). Anti-citrullinated protein antibodies are associated with neutrophil extracellular traps in the sputum in relatives of rheumatoid arthritis patients. Arthritis & Rheumatology , 69 (6), 1165-1175.
Halls, S., Law, R. J., Jones, J. G., Markland, D. A., Maddison, P. J., & Thom, J. M. (2017). Health professionals' perceptions of the effects of exercise on joint health in rheumatoid arthritis patients. Musculoskeletal Care , 15 (3), 196-209.
Quiñonez-Flores, C. M., González-Chávez, S. A., Del Río Nájera, D., & Pacheco-Tena, C. (2016). Oxidative stress relevance in the pathogenesis of rheumatoid arthritis: a systematic review — Biom ed research international , 2016 .
Rheumatoid Arthritis (RA) | Arthritis | CDC. (2019). Retrieved from https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html
Singh, J. A., Saag, K. G., Bridges Jr, S. L., Akl, E. A., Bannuru, R. R., Sullivan, M. C., ... & Curtis, J. R. (2016). 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis & Rheumatology , 68 (1), 1-26.
