Case Study Analyze 42-year-old female, Assignments of Nursing

Download Case Study Analyze 42-year-old female and more Assignments Nursing in PDF only on Docsity!

CASE STUDY ANALYSIS

This case study delves into analyzing and diagnosing a 42-year-old female presenting with increased fatigue, joint pain over the last few weeks that is worse in the mornings, and chills. Her vital signs are within normal parameters except for a temperature of 100 F. The patient has a history of similar episodes, with a prior elevated erythrocyte sedimentation rate (ESR) and negative antinuclear antibody (ANA). This paper will explore the possible causes of the patient's symptoms, associated genetic factors, and the implications of immunosuppression on the body. Symptoms Explanation The patient history and clinical presentation in the scenario are indicative of a diagnosis of seronegative rheumatoid arthritis. Rheumatoid arthritis (RA) is a severe inflammatory and systemic autoimmune disease affecting the joints (Bullock et al., 2018). Based on the patient's markers, this can be classified as seropositive or seronegative (Paknikar et al., 2021). The patient's symptoms of increased fatigue, occasional chills, and worsening joint pain are exacerbated in the mornings and partially relieved by ibuprofen. These symptoms suggest the patient has an autoimmune disorder, likely RA (NICE, 2018). Additionally, a history of elevated ESR and febrile with a temperature of 100°F may indicate an ongoing inflammation. Researchers have argued that the anti-cyclic citrullinated peptide antibody (ACPA) is an effective marker for diagnosing RA (Choi & Lee, 2018). However, a negative ANA should not rule out the diagnosis of RA as a person may have low levels of rheumatoid factor (RF) and ACPA in their blood, and or the ACPA may not be present or undetectable, which allows the diagnosis of seronegative RA (Perniola et al., 2023).

Genes of the disease This multifactorial disease RA, genes disposition is based on shared epitope (SE) alleles, such as HLA-DRB101 and DRB104; other HLA alleles, such as HLA-DRB113 and DRB115, which have been linked to the disease for decades (Kurkó et al., 2013). Furthermore, SE alleles, primarily S2 and S3P, have been associated with seropositive RA (Dedmon, 2020). Moreover, non-HLA gene single nucleotide polymorphisms (SNPs) relevant to RA are PTPN22, IL23R, TRAF1, CTLA4, IRF5, STAT4, CCR6, and PADI4 (Kurkó et al., 2013). The gene makeup of HLA and non-HLA may differentiate ACPA seropositive and seronegative RA (Dedmon, 2020). These genetic variants contribute to dysregulation of the immune response, leading to autoantibody production and tissue inflammation. The process of immunosuppression and the effect it has on body systems. According to Jang et al. (2022), once the disease is triggered, cytokines/chemokines are produced in large amounts in the joints, activating more immune cells' migration into the tissue. Immunosuppressive effects cause the production of the T and B cells. The B cells aid in diagnostic and prognostic markers due to the self-reactive immunoglobulin G (IgG). Moreover, hyperplasia of the synovial membrane occurs, and synoviocytes proliferate and cause inflammation. The synovial fluid increases, which narrows the joint space, causing mobility issues, pain, and swelling. Various medications are used for immunosuppression in RA, including disease-modifying antirheumatic drugs (DMARDs), corticosteroids, and biologic agents (Choi & Lee, 2018). Immunosuppressive therapy aids in mitigating patients' symptoms.

Conclusion The patient's clinical presentation, medical history, and examination findings suggest RA, specifically seronegative RA, due to the negative ANA. Genetic factors contribute to the diagnosis and treatment of the disease. Immunosuppressive therapy plays a significant role in managing symptoms by migrating the inflammatory response.

References Bullock, J., Rizvi, S. a. A., Saleh, A., Ahmed, S., Duc, P., Ansari, R. A., & Ahmed, J. (2018). Rheumatoid arthritis: A brief overview of the treatment. Medical Principles and Practice , 27 (6), 501–507. https://doi.org/10.1159/ Choi, S., & Lee, K. (2018). Clinical management of seronegative and seropositive rheumatoid arthritis: A comparative study. PLOS ONE , 13 (4), e0195550. https://doi.org/10.1371/journal.pone. Dedmon, L. E. (2020). The genetics of rheumatoid arthritis. Rheumatology , 59 (10), 2661–2670. https://doi.org/10.1093/rheumatology/keaa Jang, S. S., Kwon, E., & Lee, J. J. (2022). Rheumatoid arthritis: Pathogenic roles of diverse immune cells. International Journal of Molecular Sciences , 23 (2), 905. https://doi.org/10.3390/ijms Kurkó, J. E., Besenyei, T., Laki, J., Glant, T. T., Mikecz, K., & Szekanecz, Z. (2013). Genetics of Rheumatoid Arthritis — A Comprehensive review. Clinical Reviews in Allergy & Immunology , 45 (2), 170–179. https://doi.org/10.1007/s12016-012-8346- NICE. (2018, July 11). Recommendations | Rheumatoid arthritis in adults: management | Guidance | NICE. https://www.nice.org.uk/guidance/ng100/chapter/Recommendations Paknikar, S. S., Crowson, C. S., Davis, J. M., & Thanarajasingam, U. (2021). Exploring the role of antinuclear antibody positivity in the diagnosis, treatment, and health outcomes of patients with rheumatoid arthritis. ACR Open Rheumatology , 3 (6), 422–426. https://doi.org/10.1002/acr2. Perniola, S., Chimenti, M. S., Spinelli, F. R., Frediani, B., Foti, R., Ferrigno, S., Garufi, C., Cassone, G., Venerito, V., Atzeni, F., Caporali, R., Conti, F., Favalli, E. G., Iannone, F.,

Sebastiani, M., Ferraccioli, G., Lapadula, G., & Gremese, E. (2023). Rheumatoid Arthritis from Easy to Complex Disease: From the “2022 GISEA International Symposium.” Journal of Clinical Medicine , 12 (8), 2781. https://doi.org/10.3390/jcm