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- QUESTION
In clinical settings, some of the most common questions that patients ask are Why do I have this? What caused this disorder? Will it ever go away? These emotional questions can be difficult to ask and to answer. However, for patients to come to terms with their diagnoses and adhere to treatment plans, they must have an understanding of factors that might have caused, or continue to impact, their disorders. As an advanced practice nurse, it is important that you are able to explain disorders, associated alterations and symptoms, and changes that might occur within your patients’ bodies.
To Prepare
Review this week’s media presentation with Dr. Terry Buttaro. Reflect on the importance of developing an in-depth understanding of pathophysiology.
Select a disorder from the following list:
Adrenal insufficiency (Addison’s disease)
Atherosclerosis
Cholelithiasis (gallstones)
Colon cancer
Cystic fibrosis
Hemophilia
Nephrolithiasis (kidney stones)
Osteoporosis
Parkinson’s disease
Tuberculosis
Select one of the following patient factors: genetics, gender, ethnicity, age, or behavior. Reflect on how that factor might impact your selected disorder, as well as potential associated alterations and symptoms.
Identify the pathophysiology of the associated alterations, including the normal and altered cellular function. Consider both intra- and extra-cellular changes that occur.
By Day 3
Post a brief description of a patient scenario involving the disorder and the factor you selected. Explain how the factor might impact your selected disorder, as well as potential associated alterations and symptoms. Finally, explain the pathophysiology of the associated alterations, including changes in cellular function.Main Posting:
Response to the discussion question is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources.--Outstanding Performance 44 (44%) - 44 (44%)
Excellent Performance 40 (40%) - 43 (43%)
Competent Performance 35 (35%) - 39 (39%)
Proficient Performance 31 (31%) - 34 (34%)
Room for Improvement 0 (0%) - 30 (30%)
Main Posting:
Writing--Outstanding Performance 6 (6%) - 6 (6%)
Excellent Performance 5.5 (5.5%) - 5.5 (5.5%)
Competent Performance 5 (5%) - 5 (5%)
Proficient Performance 4.5 (4.5%) - 4.5 (4.5%)
Room for Improvement 0 (0%) - 4 (4%)
Main Posting:
Timely and full participation--Outstanding Performance 10 (10%) - 10 (10%)
Excellent Performance 0 (0%) - 0 (0%)
Competent Performance 0 (0%) - 0 (0%)
Proficient Performance 0 (0%) - 0 (0%)
Room for Improvement 0 (0%) - 0 (0%)
First Response:Post to colleague's main post that is reflective and justified with credible sources.--
Outstanding Performance 9 (9%) - 9 (9%)
Excellent Performance 8.5 (8.5%) - 8.5 (8.5%)
Competent Performance 7.5 (7.5%) - 8 (8%)
Proficient Performance 6.5 (6.5%) - 7 (7%)
Room for Improvement 0 (0%) - 6 (6%)
First Response:
Writing--Outstanding Performance 6 (6%) - 6 (6%)
Excellent Performance 5.5 (5.5%) - 5.5 (5.5%)
Competent Performance 5 (5%) - 5 (5%)
Proficient Performance 4.5 (4.5%) - 4.5 (4.5%)
Room for Improvement 0 (0%) - 4 (4%)
First Response:
Timely and full participation--Outstanding Performance 5 (5%) - 5 (5%)
Excellent Performance 0 (0%) - 0 (0%)
Competent Performance 0 (0%) - 0 (0%)
Proficient Performance 0 (0%) - 0 (0%)
Room for Improvement 0 (0%) - 0 (0%)
Second Response:
Post to colleague's main post that is reflective and justified with credible sources.--Outstanding Performance 9 (9%) - 9 (9%)
Excellent Performance 8.5 (8.5%) - 8.5 (8.5%)
Competent Performance 7.5 (7.5%) - 8 (8%)
Proficient Performance 6.5 (6.5%) - 7 (7%)
Room for Improvement 0 (0%) - 6 (6%)
Second Response:
Writing--Outstanding Performance 6 (6%) - 6 (6%)
Excellent Performance 5.5 (5.5%) - 5.5 (5.5%)
Competent Performance 5 (5%) - 5 (5%)
Proficient Performance 4.5 (4.5%) - 4.5 (4.5%)
Room for Improvement 0 (0%) - 4 (4%)
Second Response:
Timely and full participation--Outstanding Performance 5 (5%) - 5 (5%)
Excellent Performance 0 (0%) - 0 (0%)
Competent Performance 0 (0%) - 0 (0%)
Proficient Performance 0 (0%) - 0 (0%)
Room for Improvement 0 (0%) - 0 (0%)
| Subject | Nursing | Pages | 6 | Style | APA |
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Answer
The Influence of Genetics on Tuberculosis
Tuberculosis is one of the leading communicable diseases whose pathophysiology has a genetic influence. One person dies every 15 seconds due to the disease and 8 million individuals tend to develop active form of the disease every year. One infected person can infect about 10-15 other individuals thought the respiratory route. In addition, the global incidence of the disease rises by 0.4% per year (World Health Organization (WHO), 2018). Tuberculosis develops after one is infected by Mycobacterium tuberculosis; however, some individuals do not develop the signs and symptoms of the disease. Symptoms of the disease include weight loss, persistent cough, coughing blood, fever, and sweating at night. It is spread from one person to another through aerosols as one coughs and sneezes (WHO, 2018).
Tuberculosis is diagnosed with tuberculin-skin reaction or Mantoux test, chest X-ray, and microscopic analysis of mucous for the M. tuberculosis (WHO, 2018). Immune reaction of an infection facilitates diagnosis of the disease regardless of whether the disease shows signs and symptoms or not. Another immune based diagnostic test for tuberculosis is the positive interferon-γ response assay. Both Mantoux test and positive interferon-γ response assay are important for diagnosing latent Mycybacterium tuberculosis infection (Stein, 2011). Treatment and prognosis may vary from one person to another (WHO, 2018).
Host genetics is a significant modifier of disease risk (Rudko et al., 2016). Studies have shown that there is a Mendelian predisposition of some individuals to severe form of the disease (Abel et al., 2017; Rudko et al., 2016; Stein, 2011). Host genetics influences the drug treatment and disease susceptibility (Abel et al., 2017). For instance, the NRAMP1 (SLC11A1) gene in humans confers resistance of macrophages to infection by protozoa and bacteria. NRAMP1 gene has important pleiotropic effects on microphage activation. It includes regulation of interleukin-1β, CXC chemokine KC, tumor necrosis factor α, major histocompatibility complex class II, oxidative burst, L-arginine flux, and inducible nitric oxide synthase. Mutation at amino acid 169 resulting in substitution of Asp with Gly protein production of the NRAMP1 gene contributes to susceptibility to the disease (Blackwell et al., 2011). Mutation of the NRAMP1 gene may increase the susceptibility of development of the severe form of the disease (Stein, 2011). Similarly, a study by Baghdadi et al. (2013) established that children with a complete deficiency of IL-12Rβ1 tend to develop severe form of the disease.
Similar, the genetic factors of the causative bacteria can impact treatment. Some strains have developed resistance to multiple agents, thus, the name multidrug-resistant M. tuberculosis. Subsequently, the rise of multidrug resistance strains compounded by generally inaccessible and limited diagnostic and treatment services for the disease accounts for the rise of drug-resistant strains and high incidence of the disease in Asia, sub-Saharan Africa, and eastern Europe (Zumla et al., 2015). An increased understanding of the relationship between genetics and genetics facilitates discovery and development of tuberculosis therapeutics and vaccines (Stein, 2011).
In conclusion, tuberculosis manifestation may vary in individuals, perhaps due to genetic implications. Mutation in the NRAMP1 gene and/or complete absence of IL-12β1 is some of the key risk factors for development of severe tuberculosis. Besides, genetics, especially immune reaction to the infection is important in diagnosis of the disease. Immune response to the infection is the basis of tests such as Mantoux test and positive interferon-γ response assay. In addition, genetic mutation in M. tuberculosis confers it with drug resistance capability; hence, complicating the treatment process since some agents may be rendered ineffective. Genetics is an important determinant of tuberculosis manifestation, diagnosis, and treatment.
References
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Abel, L., Fellay, J., Haas, D.W., Schurr, E., Srikrishna, G., Urbanoswki, M., et al. (2017). Genetics of human susceptibility to active and latent tuberculosis: present knowledge and future perspectives. The Lancet, 18(3), E64-E75. DOI: https://doi.org/10.1016/S1473-3099(17)30623-0. Baghdadi, E.J., Grant, A.V., Sabri, A., Azbaoui, S., Zaidi, H., Cobat, A., Schurr, E., Boisson-Dupuis, S., Casanova, J.L., & Abel, L. (2013). [Human genetic of tuberculosis]. Pathol Biol (Paris), 61(1) 11-6. DOI: 10.1016/j.patbio.2013.01.004. Blackwell, J.M., Goswami, T., Evans, C.A.W., Sibthorpe, D., Papo, N., White, J.K., Searle, et al. (2011). SLC11A1 (formerly NRAMP1) and disease resistance. Cell Microbiol., 3(12), 773-784. Rudko, A.A., Bragina, E.Y., Puzyrev, V.P., & Freidin, M.B. (2016). The genetics of susceptibility to tuberculosis: Progress and challenges. Asian Pacific Journal of Tropical Disease, 6(9), 680-684. https://doi.org/10.1016/S2222-1808(16)61109-X Stein, C.M. (2011). Genetic epidemiology of tuberculosis susceptibility: impact of study design. PLoS Pathog 7(1): e1001189. https://doi.org/10.1371/journal.ppat.1001189 WHO. (2018). Genomics resource center: Genes and human disease. Retrieved on Jan 06, 2019 from, https://www.who.int/genomics/public/geneticdiseases/en/index4.html Zumla, A., George, A., Sharma, V., Herbert, N., Ilton, M., Oxley, A., et al. (2015). The WHO 2014 global tuberculosis report – further to go. The Lancet, 3(1), E10-E12.
Appendix
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