Walden NURS 6501 Week 1 Discussion Advanced Pathophysiology
Walden NURS 6501 Week 1 Discussion Advanced Pathophysiology
An infection by a disease causing microorganisms often lead to alteration in the cellular responses. The alteration in the cellular responses result in the development of signs and symptoms that guide the development of diagnoses and treatment plans. The cellular responses also reflect the active role that innate and acquired immunity plays in preventing individuals from a disease. The management of diseases relies on the use of interventions such as prescription of pharmacological agents. Patient factors must be considered in the prescription of drugs to minimize the risk of adverse events. Therefore, this paper examines a case study to evaluate the role of genetics, presentation of signs and symptoms and influence of age on the selected patient assignment.
The Role of Genetics in the Disease
Recurrent sore throat is a common health problem in children. Streptococcus group A bacteria causes this health problem and is often associated with genetics (Zupin et al., 2016). Accordingly, the existence of genetic variations in the HLA region have been linked to the recurrence in sore throat. The variations in the HLA region of the genes have been shown to cause gene mediated interaction with the bacteria causing sore throat (Tian et al., 2017). The genetic variation in the HLA region has also been shown to alter the normal innate as well as acquire defense systems towards the bacterial infection (Pearce et al., 2020). The influence of genetics in sore throat can also be seen in the recurrence of the disease in twins. The recurrence of sore-throat related infections such as tonsillitis in identical twins is almost similar while the rate of recurrence varies in dizygotic twins. Due to this, scholars argue that about 60% of sore throat recurrence in children is associated with environmental exposures while the rest occurs due to environmental exposure. Similar findings can be seen in the study by Bager et al., (2018) where the researchers found the recurrence of severe tonsillitis to be highly linked to genetic factors. The authors found that the influence of genetics on the development of severe tonsillitis did not depend on patient’s age and sex. Therefore, genetics play a role in the recurrence of the sore throat infections.
Why Patient is presenting with the Specific Symptoms
The signs and symptoms that the patient presented with to the hospital is attributed to the changes in the cellular response processes. The invasion of the body with Streptococcus group A bacteria stimulates immune response that is characterized by the secretion of pus as well as reddening and inflammation of the tonsils. The production of pus arises from the release of inflammatory cells in response to the infection to fight the bacteria. As a result, the clinical symptoms of sore throat develop due to the accumulation of the fibronectin-binding proteins in the pharynx. The symptoms that the patient reported following ingestion of amoxicillin were attributed to allergic reactions to antibiotics. The symptoms show that the ingestion of amoxicillin led to the stimulation of the immune system to release IgE. The release of IgE increased the secretion of inflammatory cells such as interleukins and cytokines. The result of these processes is that massive inflammation occurred leading to vomiting, nausea, fast heart rate, difficulty in breathing, wheezing, swelling of the face and lips and shock. These symptoms are the signs or allergic response to an allergen such as drug or environmental pollutant.
Physiologic Response to Stimuli
A number of signs and symptoms in the case study demonstrate the patient’s response to stimuli. The signs and symptoms include the reddening of the posterior pharynx alongside the enlargement of the tonsils 3+. The assessment also revealed posterior and anterior cervical adenopathy, which imply immune response to the infection. A rapid strep test also confirmed the positive diagnosis of streptococcus group A bacteria (Volavšek, 2016). These symptoms were experienced due to the patient’s acquired and innate response to the infection.
Cells and Cellular Mediators
The cellar mediators that were involved in the response to the infection include prostaglandins E2m chemokines, leukotriene B4, eicosanoids, antimicrobial peptides, and cytokines that enhanced the inflammatory processes. The cells that were involved in the response include macrophages, neutrophils, epithelial, mast, and dendritic cells. The mediated actions of these cells and the cellular response mechanisms led to the development of the signs and symptoms of the disease as well as recovery from it (Kırmusaoğlu, 2018). The response to infection by the cells also led to the symptoms seen in the allergic reaction to amoxicillin.
Effect of Age on Response
The response to Streptococcus group A bacterial infections vary with age. Unlike children, adults are least likely to be affected by the infection. The symptoms of the infection are also less severe in adults than in children. The differences in the response is attributed to the influence of immune system development in adults than in children (Chanmugam et al., 2016). Therefore, healthcare providers should make treatment decisions with a consideration of the age of the patients to minimize the risk of adverse drug events.
References
Bager, P., Corn, G., Wohlfahrt, J., Boyd, H. A., Feenstra, B., & Melbye, M. (2018). Familial aggregation of tonsillectomy in early childhood and adolescence. Clinical Epidemiology, 10, 97–105. https://doi.org/10.2147/CLEP.S148575
Chanmugam, A. S., Bissonette, A., Rothman (MD), R., Desai, S. V., & Putman, S. B. (2016). Infectious Diseases Emergencies. Oxford University Press.
Kırmusaoğlu, S. (2018). Bacterial Pathogenesis and Antibacterial Control. BoD – Books on Demand.
Pearce, S., Bowen, A. C., Engel, M. E., Lande, M. de la, & Barth, D. D. (2020). The incidence of sore throat and group A streptococcal pharyngitis in children at high risk of developing acute rheumatic fever: A systematic review and meta-analysis. PLOS ONE, 15(11), e0242107. https://doi.org/10.1371/journal.pone.0242107
Tian, C., Hromatka, B. S., Kiefer, A. K., Eriksson, N., Noble, S. M., Tung, J. Y., & Hinds, D. A. (2017). Genome-wide association and HLA region fine-mapping studies identify susceptibility loci for multiple common infections. Nature Communications, 8(1), 599. https://doi.org/10.1038/s41467-017-00257-5
Volavšek, M. (2016). Head and Neck Pathology. Springer International Publishing.
Zupin, L., Angelelli, F., Grasso, D., & Crovella, S. (2016). Lactoferrin gene polymorphisms in Italian patients with recurrent tonsillitis. International Journal of Pediatric Otorhinolaryngology, 88. https://doi.org/10.1016/j.ijporl.2016.07.002
Alterations in Cellular Processes
occur for many reasons. But some, such as cystic fibrosis and Parkinson’s Disease, occur because of alterations that prevent cells from functioning normally.
Understanding of signals and symptoms of alterations in cellular processes is a critical step in diagnosis and treatment of many diseases. For the Advanced Practice Registered Nurse (APRN), this understanding can also help educate patients and guide them through their treatment plans.
For this Discussion, you examine a case study and explain the disease that is suggested. You examine the symptoms reported and explain the cells that are involved and potential alterations and impacts.
To prepare:
By Day 1 of this week, you will be assigned to a specific scenario for this Discussion. Please see the “Course Announcements” section of the classroom for your assignment from your Instructor.
By Day 3 of Week 1
Post an explanation of the disease highlighted in the scenario you were provided. Include the following in your explanation:
The role genetics plays in the disease.
Why the patient is presenting with the specific symptoms described.
The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
The cells that are involved in this process.
How another characteristic (e.g., gender, genetics) would change your response.
Read a selection of your colleagues’ responses.
By Day 6 of Week 1
Respond to at least two of your colleagues on 2 different days and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not
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You must proofread your paper. But do not strictly rely on your computer’s spell-checker and grammar-checker; failure to do so indicates a lack of effort on your part and you can expect your grade to suffer accordingly. Papers with numerous misspelled words and grammatical mistakes will be penalized. Read over your paper – in silence and then aloud – before handing it in and make corrections as necessary. Often it is advantageous to have a friend proofread your paper for obvious errors. Handwritten corrections are preferable to uncorrected mistakes.
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Kidney transplant is an effective treatment for patients suffering from end-stage renal disease. However, some patients develop adverse effects including kidney rejection. The management of kidney transplant rejection depends on the type and patient factors. Therefore, this paper examines why a patient with acute kidney transplant developed the described symptoms, genes associated with kidney transplant rejection and process of immunosuppression.
Why the Patient Presented the Symptoms Described
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The patient presented symptoms that include gaining weight, decreased urinary output, fatigue, and running temperatures up to 101 F. The patient gained weight because of the increased body fluid volume level. The kidneys excrete excess fluids from the body. Impaired kidney function as seen in the case study affects the regulation of fluids in the body, hence, its accumulation and weight gain. The decline in renal function also impaired normal urine output. This led to reduced urine production, as seen in the case study. The rejection altered the normal renal function in the excretion process, leading to oliguria. The kidneys also eliminate toxins from the body. This includes excess ammonia in urine. Impaired kidney problems affect the elimination of these toxins, which lead to symptoms such as fatigue, poor concentration, acidosis, and anemia. Therefore, this explains the patient’s experience of fatigue. Patients with end-stage renal disease and those with kidney transplant rejection problems also experience immunosuppression (Rauen et al., 2020). This predisposes them to infections, hence, the fever that the patient has.
Genes Associated with the Development of the Disease
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Genes have been linked with kidney transplant rejection. They include cytochrome p450 2EI (CYP2EI), CYP3A5, cytotoxic T-lymphocyte associated protein 4 (CTLA4), C-X-C motif chemokine ligand 8 (CXL8), epoxy hydrolase 2, coagulation factor II thrombin, and coagulation factor V genes. In addition, Forkhead box P3, Fc fragment of IgG receptor IIA, major histocompatibility complex class II, I, DO alpha, and interleukin 1 beta, 2, 2-receptor subunit beta genes also play a role in the development of the rejection in kidney transplant. Genes such as interleukin genes are inflammatory cytokines that inhibits inflammatory processes once a person received an allograft. On the other hand, this gene also downgrades the maturation of antigens and cells that develops host’s immunity following the transplant (Arnold et al., 2022; Spicer & Runkel, 2019; van Vugt et al., 2022). Other genes such as ATP-binding genes increase the body’s resistance towards drugs used in suppressing the immune system following the transplant.
Process of Immunosuppression
Immunosuppression refers to the state in which the ability of the body to fight infections is reduced. The immune system is lowered to a level that it cannot counteract any disease causing organisms from invading the body. The causes of immunosuppression include the use of medications that are used in conditions such as cancer. The other cause is conditions that depress the immune system such as cancer and HIV. Treatments for cancer such as radiotherapy and chemotherapy also cause immunosuppression. The effects of immunosuppression are varied. They include increasing the vulnerability of patients to infections. It also increases costs that patients incur due to frequent hospitalizations (Gupta et al., 2021). Prolonged infections also affect the patients’ quality of life. Patients may also die in cases where the immune system is severely compromised.
Conclusion
In conclusion, the patient presented the symptoms because of reduced renal functioning. Genes are involved in the development of kidney transplant rejection. The rejection may result in immunosuppression, which has negative effects on health.
References
Arnold, M.-L., Heinemann, F. M., Oesterreich, S., Wilde, B., Gäckler, A., Goldblatt, D., Spriewald, B. M., Horn, P. A., Witzke, O., & Lindemann, M. (2022). Correlation of Fc Receptor Polymorphisms with Pneumococcal Antibodies in Vaccinated Kidney Transplant Recipients. Vaccines, 10(5), Article 5. https://doi.org/10.3390/vaccines10050725
Gupta, R., Woo, K., & Yi, J. A. (2021). Epidemiology of end-stage kidney disease. Seminars in Vascular Surgery, 34(1), 71–78. https://doi.org/10.1053/j.semvascsurg.2021.02.010
Rauen, T., Wied, S., Fitzner, C., Eitner, F., Sommerer, C., Zeier, M., Otte, B., Panzer, U., Budde, K., Benck, U., Mertens, P. R., Kuhlmann, U., Witzke, O., Gross, O., Vielhauer, V., Mann, J. F. E., Hilgers, R.-D., Floege, J., Floege, J., … Hilgers, R.-D. (2020). After ten years of follow-up, no difference between supportive care plus immunosuppression and supportive care alone in IgA nephropathy. Kidney International, 98(4), 1044–1052. https://doi.org/10.1016/j.kint.2020.04.046
Spicer, P., & Runkel, L. (2019). Costimulatory pathway targets for autoimmune and inflammatory conditions: Clinical successes, failures, and hope for the future. Expert Opinion on Investigational Drugs, 28(2), 99–106. https://doi.org/10.1080/13543784.2019.1557146
van Vugt, L. K., Schagen, M. R., de Weerd, A., Reinders, M. E., de Winter, B. C., & Hesselink, D. A. (2022). Investigational drugs for the treatment of kidney transplant rejection. Expert Opinion on Investigational Drugs, 31(10), 1087–1100. https://doi.org/10.1080/13543784.2022.2130751