Rheumatoid Arthritis: Pathophysiology, Aetiology and Treatment

This report provides a comprehensive overview of Rheumatoid Arthritis (RA), a systemic inflammatory disease characterized by chronic joint inflammation and synovial hypertrophy. It delves into the pathophysiology, highlighting the roles of mononuclear phagocytes, fibroblasts, neutrophils, and CD4 T cells, as well as the impact of abnormal cytokine production. The report also explores the aetiology of RA, discussing genetic, environmental, immunological, hormonal, and lifestyle factors. It examines the populations most affected, including the influence of cigarette smoking, hormonal changes, and dietary factors. Furthermore, the report emphasizes the clinical problem and its relevance to nursing practice, detailing the financial costs, statistical prevalence, and workload implications of RA. It concludes with a discussion of best practices, including lifestyle assessment, patient education, nutritional assessment, pharmacological management, pain reduction, and the assessment of clinical manifestations, all supported by citations in CDU APA 6th format.

Running head: RHEUMATOID ARTHRITIS
RHEUMATOID ARTHRITIS
Name of the Student
Name of the university
Author’s note

1RHEUMATOID ARTHRITIS
1. Background of the problem
Pathophysiology
Rheumatoid arthritis is a systemic inflammatory disease. Some external triggers
autoimmune reactions giving rise to chronic joint inflammation and synovial hypertrophy (Baker
et al. 2015). The synovial joint hyperplasia leads to uncontrolled inflammation and causes
destruction of bones and cartilages. The mononuclear phagocytes, fibroblasts, neutrophils and
the CD4 T cells play a major role in the pathophysiology of Rheumatoid arthritis. Abnormal
production of the cytokines leads to joint inflammation (Schett & Gravallese, 2012).
Aetiology
The aetiology of RA is still not known clearly. The environmental, genetic, immunologic,
hormonal and other life style factors may impact the development of the disease (Gibofsky,
2014). It has been found that 50 % of RA is formed due to genetic factors. Infectious agents like
Mycoplasma, rubella and Ebstein-Barr virus also contribute to RA. Hormones like
hyperprolactinemia can be a risk factor for RA (Choy, 2012).
Persons affected most
Cigarette smoking and passive smoking has been associated with the development of
Rheumatoid arthritis (Di Giuseppe et al. 2013). Changes in the hormonal environment in
females, during pregnancy or under contraception, have also contributed to RA. Recent studies
have also indicated towards the role of diets in RA. High consumption of red meat and caffeine
have also contributed towards RA (Scott, 2012).

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2. Self-reflection
While reflecting on the choice of the topic I have used 5R’s of reflection. My choice of topic is
Rheumatoid arthritis. I have brainstormed through the databases for finding the relevant articles
for R.A and the extensive literature search has helped me to understand about the environmental,
genetic and the other predisposing factors that lead to RA. The critical reasoning has helped me
to understand that R.A is an auto-immune disease that is painful and affects the mobility of
individuals and affects their quality of life. This has provided the rationale for choosing the topic.
About 3.9 million of the Australians are suffering with R.A that can grow to 5.4 million by the
end of 2030. I have tried to relate the pathophysiology of the diseases with the etiology and
probable symptom of the disease. In order to prepare proper treatment plans for the patients in a
cost effective way, it is necessary to understand the pathogenesis, their linkage with the clinical
condition and how the drugs can prevent them. The knowledge of the pathophysiology has
helped me to understand that an integrated approach is required to treat RA that requires both
pharmacological as well as non-pharmacological approach.
3. Importance and relevance of the clinical problem/practice to nursing
Financial cost- R.A costs $5.5 billion of the health care system in Australia, which can grow
to $7.6 billion by 2030 (Gibofsky, 2014).
Statistics- About 3.9 million of the Australians are suffering with R.A that can grow to 5.4
million by the end of 2030 (Gibofsky, 2014).
Workload- Too much physical workload such as bending and lifting of the heavy weights can
lead to RA.

3RHEUMATOID ARTHRITIS
All these factors contribute to the development of a proper nursing regimen.
4.
Best Practice Citation in CDU APA 6th format
Life style assessment (Di Giuseppe et al., 2015)
Patient education (Gibofsky, 2014), (Vaghef-Mehrabany et al., 2014)
Nutritional assessment (Baker et al., 2012)
Pharmacological management (Fleischmann et al., 2012), (Kostoglou-
Athanassiou et al., 2012), (Scott, 2012).
Reduction of the pain and comfort (Gibofsky, 2014), (Singh et al., 2016)
To assess the clinical manifestations (Schett & Gravallese, 2012), (Choy, 2012),

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References
Baker, J. F., Baker, D. G., Toedter, G., Shults, J., Von, J. F., & Leonard, M. B. (2012).
Associations between vitamin D, disease activity, and clinical response to therapy in
rheumatoid arthritis. Clinical and experimental rheumatology, 30(5), 658-664.
http://europepmc.org/abstract/med/22776409
Choy, E. (2012). Understanding the dynamics: pathways involved in the pathogenesis of
rheumatoid arthritis. Rheumatology, 51(suppl_5), v3-v11.
https://doi.org/10.1093/rheumatology/kes113
Di Giuseppe, D., Orsini, N., Alfredsson, L., Askling, J., & Wolk, A. (2013). Cigarette smoking
and smoking cessation in relation to risk of rheumatoid arthritis in women. Arthritis
research & therapy, 15(2), R56. https://doi.org/10.1186/ar4218
Fleischmann, R., Kremer, J., Cush, J., Schulze-Koops, H., Connell, C. A., Bradley, J. D., ... &
Kanik, K. S. (2012). Placebo-controlled trial of tofacitinib monotherapy in rheumatoid
arthritis. New England Journal of Medicine, 367(6), 495-507. DOI:
10.1056/NEJMoa1109071
Gibofsky, A. (2014). Epidemiology, pathophysiology, and diagnosis of rheumatoid arthritis: A
Synopsis. The American journal of managed care, 20(7 Suppl), S128-35.
http://europepmc.org/abstract/med/25180621

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Kostoglou-Athanassiou, I., Athanassiou, P., Lyraki, A., Raftakis, I., & Antoniadis, C. (2012).
Vitamin D and rheumatoid arthritis. Therapeutic advances in endocrinology and
metabolism, 3(6), 181-187. doi/abs/10.1177/2042018812471070
Schett, G., & Gravallese, E. (2012). Bone erosion in rheumatoid arthritis: mechanisms, diagnosis
and treatment. Nature Reviews Rheumatology, 8(11), 656. doi:10.1038/nrrheum.2012.153
Scott, D. L. (2012). Biologics‐based therapy for the treatment of rheumatoid arthritis. Clinical
Pharmacology & Therapeutics, 91(1), 30-43. https://doi.org/10.1038/clpt.2011.278
Singh, J. A., Saag, K. G., Bridges, 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.
https://doi.org/10.1002/art.39480
Vaghef-Mehrabany, E., Alipour, B., Homayouni-Rad, A., Sharif, S. K., Asghari-Jafarabadi, M.,
& Zavvari, S. (2014). Probiotic supplementation improves inflammatory status in patients
with rheumatoid arthritis. Nutrition, 30(4), 430-435.
DOI: https://doi.org/10.1016/j.nut.2013.09.007