Assignment: Foundational Concepts of Cellular Pathophysiology NURS 6501
Assignment: Foundational Concepts of Cellular Pathophysiology NURS 6501
Module 1: Foundational Concepts of Cellular 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.
Having Trouble Meeting Your Deadline?
Get your assignment on Assignment: Foundational Concepts of Cellular Pathophysiology NURS 6501 completed on time. avoid delay and – ORDER NOW
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.
Struggling to Meet Your Deadline?
Get your assignment on Assignment: Foundational Concepts of Cellular Pathophysiology NURS 6501 done on time by medical experts. Don’t wait – ORDER NOW!
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
What’s Happening This Module?
This course is composed of eight (8) separate modules. Each module consists of an overarching topic and each week within the module includes specific subtopics for learning. As you work through each module, you will draw upon the knowledge you gain by completing various Knowledge Checks and Case Study Assignments.
Module 1: Foundational Concepts of Cellular Pathophysiology is a 2-week module, Weeks 1 and 2 of the course. In this module, you will examine fundamental concepts of cellular processes and the alterations that lead to various diseases. You will evaluate the genetic environment and its impact on these diseases. You will also evaluate the impact of patient characteristics, including racial and ethnic variables, on physiological functioning.
What do I have to do?
When do I have to do it?
Review your Learning Resources
Days 1–7, Weeks 1 and 2
Discussion: Alterations in Cellular Processes
Post by Day 3 of Week 1 and respond to your colleagues by Day 6 of Week 1.
Module 1 Assignment: Case Study Analysis
You are encouraged to work on your Module 1 Assignment throughout the module. However, this Assignment is not due until Day 7 of Week 2.
Go to the Week’s Content
Week 1
Week 2
Click here to ORDER NOW FOR AN ORIGINAL PAPER ASSIGNMENT: Assignment: Foundational Concepts of Cellular Pathophysiology NURS 6501
Week 1: Cellular Processes and the Genetic Environment
One of the more common biology analogies refers to cells as the “building blocks” of life. This rightfully places an emphasis on understanding cells, cellular behavior, and the impact of the environment in which they function.
Such an understanding helps explain how healthy cell activity contributes to good health. Just as importantly, it helps explain how breakdowns in cellular behavior and alterations to cells lead to health issues.
This week, you examine cellular processes that are subject to alterations that can lead to disease. You evaluate the genetic environments within which these processes exist as well as the impact these environments have on disease.
Learning Objectives
Students will:
Evaluate cellular processes and alterations within cellular processes
Evaluate the impact of the genetic environment on disease
Learning Resources
Required Readings (click to expand/reduce)
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Chapter 1: Cellular Biology; Summary Review
Chapter 2: Altered Cellular and Tissue Biology: Environmental Agents (pp. 46-61; begin again with Manifestations of Cellular Injury pp. 83-97); Summary Review
Chapter 3: The Cellular Environment: Fluids and Electrolytes, Acids, and Bases
Chapter 4: Genes and Genetic Diseases (stop at Elements of formal genetics); Summary Review
Chapter 5: Genes, Environment-Lifestyle, and Common Diseases (stop at Genetics of common diseases); Summary Review
Chapter 7: Innate Immunity: Inflammation and Wound Healing
Chapter 8: Adaptive Immunity (stop at Generation of clonal diversity); Summary Review
Chapter 9: Alterations in Immunity and Inflammation (stop at Deficiencies in immunity); Summary Review
Chapter 10: Infection (pp. 289–303; stop at Infectious parasites and protozoans); (start at HIV); Summary Review
Chapter 11: Stress and Disease (stop at Stress, illness & coping); Summary Review
Chapter 12: Cancer Biology (stop at Resistance to destruction); Summary Review
Chapter 13: Cancer Epidemiology (stop at Environmental-Lifestyle factors); Summary Review
Justiz-Vaillant, A. A., & Zito, P. M. (2019). Immediate hypersensitivity reactions. In StatPearls. Treasure Island, FL: StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/
Credit Line: Immediate Hypersensitivity Reactions – StatPearls – NCBI Bookshelf. (2019, June 18). Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/. Used with permission of Stat Pearls
Required Media (click to expand/reduce)
Module 1 Overview with Dr. Tara Harris
Dr. Tara Harris reviews the structure of Module 1 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Discussion and Assignment. (4m)
Immunity and Inflammation
Khan Academy (2010, February 24). Inflammatory response | Human anatomy and physiology | Health & medicine [Video file]. Retrieved from https://www.youtube.com/watch?v=FXSuEIMrPQk
Note: The approximate length of the media program is 14 minutes.
Soo, P. (2018, July 28). Pathophysiology Ch 10 alterations in immune function [Video file]. Retrieved from https://www.youtube.com/watch?v=Jz0wx1-jTds
Note: The approximate length of the media program is 37 minutes.
Acid-Base Balance #1
MedCram. (2012, April 28). Medical acid base balance, disorders & ABGs explained clearly [Video file]. Retrieved from https://www.youtube.com/watch?v=4wMEMhvrQxE
Note: The approximate length of the media program is 13 minutes.
Acid-Base Balance #2
MedCram. (2012, April 29). Medical acid base balance, disorders & ABGs explained clearly | 2 of 8 [Video file]. Retrieved from https://www.youtube.com/watch?v=GmEeKVTpOKI
Note: The approximate length of the media program is 15 minutes.
Hyponatremia
MedCram. (2017, December 23). Hyponatremia explained clearly (remastered) – Electrolyte imbalances [Video file]. Retrieved from https://www.youtube.com/watch?v=bLajK5Vy55M
Note: The approximate length of the media program is 15 minutes.
Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children
In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapters 3, 7, and 8 that relate to alterations in immunity, hyponatremia, and acid/base balance.
Note: To access the online resources included with the text, you need to complete the FREE online registration that is located at https://evolve.elsevier.com/cs/store?role=student
To Register to View the Content
Go to https://evolve.elsevier.com/cs/store?role=student
Enter the name of the textbook, Pathophysiology: The Biologic Basis for Disease in Adults and Children, or ISBN 9780323654395 (name of text without the edition number) in the Search textbox.
Complete the registration process.
To View the Content for This Text
Go to https://evolve.elsevier.com/
Click on Student Site.
Type in your username and password.
Click on the Login button.
Click on the plus sign icon for Resources on the left side of the screen.
Click on the name of the textbook for this course.
Expand the menu on the left to locate all the chapters.
Navigate to the desired content (checklists, videos, animations, etc.).
Note: Clicking on the URLs in the APA citations for the Resources from the textbook will not link directly to the desired online content. Use the online menu to navigate to the desired content.
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
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
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