NR 507 Week 6 Recorded Disease Process Presentation
NR 507 Week 6 Recorded Disease Process Presentation
I really enjoyed your presentation and felt like I learned more about Addison’s disease. I was interested in this subject matter due to someone I know having this disease and wanting to understand more about her condition.
Discuss the risk factors and the connection to the etiology of the initial injury to the cell/tissue/organ
One of the things I found most interesting about Addison’s that I did not remember from nursing school was the most common cause of Addison’s being tuberculosis worldwide. Upon further research, I found that this is not common in further developed countries such as the United States, but in those underdeveloped countries (Burton, Cottrell, & Edwards, 2015, p. 488). Most often in established countries the cause is an autoimmune disease as you mentioned. Example of the autoimmune diseases would be type 1 diabetes, or Graves’ disease. Other risk factors include other chronic infections, removal of part of the adrenal gland, or polyendocrine deficiency syndrome. These autoimmune disorders cause breakdown of the adrenal cortex most often causing Addison’s disease.
Provide a brief diagnosis of how the disease is diagnosed
In your presentation you mentioned that diagnosis is made based on laboratory values to determine either primary or secondary adrenal insufficiency with high ACTH being primary and low ACTH being secondary. It is important to understand that the cortisol levels must be drawn in the morning to give a more accurate result. In my research, I found that patients are often misdiagnosed until they progress into Addisonian crisis due to providers focusing on other differential diagnoses based on the patient’s sign and symptoms (Burton, et. al, 2015, p.489). Once patients have become this ill, they usually present to the emergency department and the diagnosis is made based on presentation, laboratory values of hyperkalemia and hyponatremia, and then can be confirmed by morning cortisol levels. The delay in diagnosis was the most interesting.
Burton, C., Cottrell, E., & Edwards, J. (2015). Addison’s disease: identification and management in primary care. The British Jounral of General Practice, 65(638), 488-490. http://doi.org/10.3399/bjgp15X686713Links to an external site.
Analyze pathophysiologic mechanism associated with Addison’s Diseas:
Mediated destruction
Sanne van Haren, Hannah, Alex & Gijs (2018) indicated as did you that Addison’s Disease Caused by Tuberculosis. Just like Aspergillus Pneumonia, Addison’s disease is difficult to diagnose and treat. Fichna, Żurawek, Bratland, Husebye, Kasperlik-Załuska, Czarnocka & … Nowak. (2015) stated that Interleukin-2 subunit alpha (soluble receptor) reveals and confirms a direct connect between 21OH=directed reactivity and AAD, and 11.2 SNP. Fichna, Żurawek, Bratland, Husebye, Kasperlik-Załuska, Czarnocka & … Nowak. (2015) continued that Addison’s disease (AAD) has a direct connect to T-cell destruction of the adrenal cortex.
So there is lyphocytic infiltration of the adrenal gland, autoantibodies, 21 hydroxylase (21OH). It is also indicated that he etiology remains obscure but genetic and environmental factors can be significant. Your PowerPoint presentation was excellent. I read about genes influencing T-cell fate. Is this true about transcription factors STAT4, GATA3, interleukin-23 (IL23A: activates STAT4) and interferon-Gamma production aides in the production of interferon-Gamma by the memory CD4+ cells.
Relate research findings to the management of patients with complex pathophysiologic dysfunction of the adrenal cortex and how the hormones are all related. I can see the difficulty with the treatment in that rifampicin and steroids is part of the treatment, but low dose of steroids can be a problem with any long disorder, especially those who are immunocompromised. In addition, Aspergillus Pneumonia which is a rare opportunistic fungal infection would have a field day and be invasive to this type of individual. Any type of compromised disease would contribute to a host of problems later down the line. As with the disease that I had chosen, systemic considerations should be taken when it comes to signs and symptoms. For example, similarities exist with both diseases in that weight loss and gastrointestinal symptoms are common signs and symptoms for both. Clara, Joana, Marina, Fábio, Sara, Alexandre & … Teresa (2018) also agree that it is difficult to diagnose Addison’s disease in that this disease is rare and even gave a case about a teenager having multiple visits to the emergency room to which the teenager was treated with hydro cortisone and fludrocortisone and added that Addison’s disease has unspecific symptomatology.
References:
Clara, P., Joana, C., Marina, P., Fábio, B., Sara, L., Alexandre, F., & … Teresa, B. (2018).
Addison’s disease – the difficulty of diagnosis. Nascer E Crasser , Vol 27, Iss 1, Pp
39-42 (2018), (1), 39.
Fichna, M., Żurawek, M., Bratland, E., Husebye, E. S., Kasperlik-Załuska, A., Czarnocka,
B., & … Nowak, J. (2015). Interleukin-2 and subunit alpha of its soluble receptor in
autoimmune Addison’s disease–an association study and expression analysis.
Autoimmunity, 48, 2, 100-107. doi:10.3109/08916934.2014.976628
Sanne van Haren, N., Hannah, V., Alex, M., & Gijs, L. (2018). Addison’s Disease
Caused by Tuberculosis: Diagnostic and Therapeutic Difficulties. European
Journal of Case Reports In Internal Medicine (2018), doi:10.12890/2018_000911
