NURS 6501 WEEK 2 CASE STUDY ANALYSIS
Walden University NURS 6501 WEEK 2 CASE STUDY ANALYSIS– Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 WEEK 2 CASE STUDY ANALYSISassignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 WEEK 2 CASE STUDY ANALYSIS depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
The introduction for the Walden University NURS 6501 WEEK 2 CASE STUDY ANALYSIS is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
After the introduction, move into the main part of the NURS 6501 WEEK 2 CASE STUDY ANALYSIS assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
Introduction
The presented scenario involves a 42-year-old man who seeks medical attention due to pain, redness, and swelling of his right calf. He developed the symptoms after he injured his leg while trimming his yard with a string trimmer. In addition, he experienced fever, shivers, and an increase in redness and edema. This study aims to look into the potential causes of the patient’s symptoms and the genetic factors that may be associated with the disease’s development.
Explanation of the Patient’s Symptoms
In this scenario, the patient presented with pain, redness, swelling in his right calf, fever, and shivers. These signs and symptoms can be attributed to cellulitis, a bacterial skin infection. Cellulitis is a prevalent bacterial infection of the epidermis that causes redness, swelling, and pain in the affected area that if left untreated, it can spread and cause severe health problems (Thakrar & Sultan, 2021).
The patient’s accidental cut on his leg while using a string trimmer in his yard was the primary cause of this condition. The cut allowed bacteria from the surrounding environment to enter the deeper layers of the epidermis. Following the injury, the patient cleaned the wound with water from the garden tap. This approach, however, may not have eliminated all germs from the wound, allowing for bacterial colonization and eventual illness. Covering the incision with a huge Band-Aid might have encouraged the spread of germs by giving a warm, moist environment to thrive. The immune system responded to the infection as the bacteria proliferated and disseminated throughout the patient’s tissues over time. Typical inflammatory signs like pain, redness, and swelling result from the localized immune response. Inflammation manifests outwardly due to the production of inflammatory mediators and the subsequent recruitment of immune cells to the site of infection. In addition, the emergence of fever and chills indicates that the infection has spread to other body parts. This suggests that the microbes had spread beyond the primary injury site and may have entered the bloodstream. Infections that spread throughout the body often cause a stronger immune response, and one of the most noticeable signs of this is a high body temperature or fever.
Genes Associated with Disease Development
Several genes associated with immune response and susceptibility to infection may affect the patient’s disease development. While genetics is commonly linked to congenital disabilities, it also plays a role in influencing an individual’s reaction to sickness and other environmental circumstances. Toll-like receptors (TLRs) are a group of genes that may be associated with the development of cellulitis (Tartey & Takeuchi, 2017). TLRs are a group of proteins responsible for recognizing specific patterns of pathogens and initiating immune responses. The capacity of TLR genes to identify and respond to particular bacterial infections can be affected by genetic differences. For instance, a mutation in the TLR2 gene has been linked to an increased susceptibility to certain bacterial cutaneous infections, including cellulitis.
Cytokines, which are immune-response-regulating signaling molecules, are also implicated in the development of cellulitis. Mutations in the genes that code for cytokines, like interleukins (ILs) and tumor necrosis factor (TNF), might alter the body’s ability to produce and respond to these molecules. Gene variants affecting TNF-alpha have been linked to changes in inflammatory response and infection susceptibility.
Human leukocyte antigen (HLA) genes, which present foreign antigens to immune cells, may also contribute to the development of cellulitis. Variations in HLA genes are associated with decreased susceptibility to infection by various microorganisms. A higher risk of contracting skin infections is linked to a specific HLA allele. Moreover, genes implicated in maintaining the integrity of the skin barrier can affect susceptibility to skin infections, such as cellulitis. Impairment of skin barrier function and increased susceptibility to skin infections have been related to mutations in genes like filaggrin that are crucial for skin barrier function.
It is essential to observe that genetic variations may not induce cellulitis directly. Environmental variables amplify these innate vulnerabilities, including bacterial exposure and an open wound. Cellulitis is caused by a complex set of pathways, and knowing which genes make you more likely to get sick is a big step toward understanding those mechanisms. This information might be potentially useful in the future and might lead to developing individualized treatment plans or preventative measures for people at a higher risk of acquiring cellulitis.
Process of Immunosuppression and Its Effects on Body Systems
Immunosuppression describes the diminished immune response that results from the purposeful or accidental suppression of the immune system. Genetic mutations, medications, or chronic diseases may cause immunosuppression. It has extensive consequences for health, as it impacts many different bodily functions. Immunosuppression can result when a gene involved in immune system function is damaged. Mutations in the genetic code can impair immune cell identification and signaling, alter the generation and activity of immune components, and also interfere with the normal functioning of the immune system (Wadhawan & Gupta, 2023). These changes impair the immune system’s capacity to produce a strong defense against pathogens, leaving the individual more susceptible to infections. Additionally, this condition can also be caused by medications prescribed to treat particular conditions. Immunosuppressive drugs, such as corticosteroids or immunosuppressants, treat autoimmune diseases or prevent organ transplant rejection. They might hinder immune cell activation, lower the generation of defensive molecules, or interfere with the communication between immune cells, resulting in a weakened immune response.
Immunosuppression can also be caused by chronic diseases such as HIV/AIDS, certain types of cancer, or autoimmune disorders. Due to disruptions in immune cell activity, these disorders weaken the body’s natural defenses against infection. It has far-reaching consequences that go beyond the immune system. Individuals with a compromised immune response are more susceptible to infections, including opportunistic infections that a robust immune system would normally be able to control with relative ease. Furthermore, it hinders the body’s ability to eliminate infections, resulting in protracted or recurring infections effectively. In addition, wound healing may be impaired, and infections may progress more swiftly, leading to severe complications. Healthcare professionals must remember that an immunocompromised patient is more likely to get infections. Preventive measures, such as good hygiene and immunizations, should be considered. Effective and timely treatment of infections is essential for minimizing complications and maximizing outcomes. It may be important to consult with infectious disease specialists to devise individualized treatment programs and keep a close eye on the patient’s progress. Prompt diagnosis, active treatment, and vigilant monitoring are important to manage infections and prevent subsequent consequences successfully.
Sample Answer 2 for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
The NURS 6501 WEEK 2 CASE STUDY ANALYSIS features a 24-year-old male patient who comes to the clinic with significant dandruff on his head and pitting of his fingernails. He also has morning joint soreness, which diminishes somewhat once he gets ready for work. He has tried many dandruff shampoos but has received no alleviation from his problems. A negative rheumatoid factor was found in the laboratory testing. The rate of erythrocyte sedimentation increased somewhat. The NURS 6501 WEEK 2 CASE STUDY ANALYSIS paper examines the patient’s situation and explains the immunosuppressive process and its influence on the human body.
Reasons behind the Patient’s Symptoms
The patient may have psoriatic arthritis based on the symptoms of finger pitting, scalp dandruff, and morning joint discomfort (Coates et al., 2022). Psoriatic arthritis is a chronic inflammatory disease that predominantly affects the joints and skin. They are triggered by environmental stimuli such as infection or mechanical stress. The body’s production of IL-23, a critical cytokine, is crucial in the progression of these disorders (Soomro et al., 2023). Dendritic cells and macrophages both generate IL-23. Due to impaired barrier function or changes in the microbiota, the gastrointestinal tract might be the source of IL-23. Psoriatic arthritis is characterized by enthesitis rather than synovitis, the prevailing pathological lesion in rheumatoid arthritis. Psoriatic arthritis often affects the distal interphalangeal joints, but rheumatoid arthritis does not.
Genes Associate
Researchers are now investigating the etiology of psoriatic arthritis, precisely the differential vulnerability among persons with psoriasis. The contribution is anticipated to be impacted by an intricate interaction of genetic and environmental factors. A considerable percentage, varying between 33 and 50 percent, of those who have received a diagnosis of psoriasis-related arthritis exhibit a familial pattern, wherein at least one sibling or parent has also been diagnosed with the condition (Curry et al., 2023). Psoriatic arthritis has been linked to several genes on chromosome six’s human leukocyte antigens locus. The immune function is intricately associated with this specific site. In addition, other non-HLA genes have been identified as having a potential involvement in immune function (Helliwell et al., 2023).
Immunosuppression
Immunosuppression is a physiological state in which the immune system’s capacity to effectively react to exogenous antigens, such as the surface antigens on malignant cells, is compromised. According to Xiao et al. (2023), immunosuppression may result from the destruction of immune cell effector cells or the blocking of intracellular pathways essential for identifying antigens and other immune system reactions. Continued suppression of the immune system raises the probability of acquiring cancer. Immunocompromised individuals may experience evasion of immune surveillance by possibly malignant cells that arise spontaneously or have been modified by carcinogens, which operate via mechanisms such as genotoxicity or various modes of action associated with oncogenic viruses (Schett et al., 2022). As a result, the improved capacity of these cells to survive and multiply dramatically contributes to the development of tumors. Psoriatic arthritis patients undergo immunosuppression due to immune failure during periods of active illness or the use of immunosuppressive medicines during remission, leaving them vulnerable to infections.
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NURS 6501 WEEK 2 CASE STUDY ANALYSIS Conclusion
The patient in the case study has symptoms consistent with a diagnosis of psoriatic arthritis. In rare people, psoriatic arthritis may occur before the beginning of psoriasis. In some people, psoriatic arthritis might occur without any visible psoriasis lesions. Chronic psoriasis and psoriatic arthritis are examples of autoimmune diseases brought on by a dysfunctional immune system.
References
Coates, L. C., Soriano, E. R., Corp, N., Bertheussen, H., Callis Duffin, K., Campanholo, C. B., Chau, J., Eder, L., Fernández-Ávila, D. G., FitzGerald, O., Garg, A., Gladman, D. D., Goel, N., Helliwell, P. S., Husni, M. E., Jadon, D. R., Katz, A., Laheru, D., Latella, J., & Leung, Y.-Y. (2022). Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA): updated treatment recommendations for psoriatic arthritis 2021. Nature Reviews Rheumatology. https://doi.org/10.1038/s41584-022-00798-0
Curry, P. D. K., Morris, A. P., Barton, A., & Bluett, J. (2023). Do genetics contribute to TNF inhibitor response prediction in Psoriatic Arthritis? The Pharmacogenomics Journal, 23(1), 1–7. https://doi.org/10.1038/s41397-022-00290-8
Helliwell, P. S., Coates, L. C., & Gladman, D. D. (2023). Psoriatic Arthritis. Springer EBooks, pp. 97–104. https://doi.org/10.1007/978-3-031-23488-0_8
Schett, G., Rahman, P., Ritchlin, C., McInnes, I. B., Elewaut, D., & Scher, J. U. (2022). Psoriatic arthritis from a mechanistic perspective. Nature Reviews Rheumatology. https://doi.org/10.1038/s41584-022-00776-6
Soomro, M., Hum, R., Barton, A., & Bowes, J. (2023). Genetic Studies Investigating Susceptibility to Psoriatic Arthritis: A Narrative Review. Clinical Therapeutics, 45(9), 810–815. https://doi.org/10.1016/j.clinthera.2023.07.003
Xiao, Q., Mears, J., Nathan, A., Ishigaki, K., Baglaenko, Y., Lim, N., Cooney, L. A., Harris, K. M., Anderson, M. S., Fox, D. A., Smilek, D. E., Krueger, J. G., & Raychaudhuri, S. (2023). Immunosuppression causes dynamic changes in the expression of QTLs in psoriatic skin. Nature Communications, 14(1), 6268. https://doi.org/10.1038/s41467-023-41984-2
Sample Answer 3 for NURS 6501 WEEK 2 CASE STUDY ANALYSIS
This paper examines a case study of a 49-year-old male patient. The patient has rheumatoid arthritis. He has come to the clinic with a chief complaint of fever. The patient currently uses medications, including atorvastatin 40 mg at night, methotrexate 10 mg every Friday morning, and prednisone 5 mg. He reports a fever for about a week and admits to sweats and chills. He also has hemoptysis, fatigue, and chest pain. The patient works as a grain inspector at a large farm cooperative. An extensive work-up led to the client being diagnosed with invasive aspergillosis. Therefore, the purpose of this essay is to examine the reasons for the client presenting with the above symptoms, genes associated with the development of the disease, the immunosuppression process, and its effect on the body systems.
Why the Patient Presented with the Described Symptoms
The patient developed the above symptoms because of the combination of the prolonged use of immunosuppressive drugs and environmental exposures from his occupation. Methotrexate and prednisone are two drugs that increase the risk of immunosuppression when used over a long period. Corticosteroids such as prednisone work by inhibiting the body’s inflammatory responses. They also repress the activity of key immunomodulatory transcription factors such as NF-kB and AP-1 factors, which play a crucial role in strengthening the body’s immune systems (Luo et al., 2021). Prolonged use of these drugs weakens the immunity, which predisposes patients to opportunistic infections, including invasive aspergillosis.
The patient in the case study has also been using methotrexate. Methotrexate is a drug that inhibits dihydrofolate reductase, an enzyme involved in the reduction of folate to tetrahydrofolate. The effects of methotrexate include suppression of the immune responses and inflammatory processes. Methotrexate suppresses the immune system through processes such as inhibition of pyrimidine and purine syntheses and the blockage of transmethylation reactions. These inhibitions cause the release of adenosine, uncoupling of nitric oxide synthase, and inhibition of NF-kB signaling, JAK-STAT signaling, and regulation of long noncoding RNAs (Valer et al., 2021). The changes cause immunosuppression, hence, the increased risk of opportunistic infections.
The immunosuppression from the use of corticosteroids and methotrexate, coupled with environmental exposure to Aspergillus bacteria caused invasive Aspergillosis. The patient in the case study reports that he works as a grain inspector at a large farm cooperative. His workplace could have predisposed him to Aspergillus, a fungus that causes Aspergillosis in immunocompromised individuals. The fungus causes three types of bronchopulmonary aspergillosis, including invasive, chronic, and allergic aspergillosis (Fosses Vuong et al., 2024). Patients with invasive aspergillosis experience symptoms, including fever, dyspnea, hemoptysis, increased sputum production, and pleuritic chest pain.
Genes That May be Associated with the Development of the Disease
Invasive aspergillosis has genetic predispositions. Studies have revealed the presence of specific genes increases the risk of an individual being affected by the disease. The research by Cb et al. (2020) demonstrated a strong association between polymorphisms within CX3CR1 and ART2 genes and the risk of invasive aspergillosis. Carriers of CX3CR1rs9823718, CX3CR1rs7631529A, and ARNT2rs137421G alleles had an increased risk of developing invasive aspergillosis (Cb et al., 2020). In another research, the C allele of IL10rs1800896 was linked with an increased risk of invasive aspergillosis in 36 patients out of 357 patients enrolled in the study (Tanpaibule et al., 2020). Tanpaibule et al. (2020) asserted in their study that epigenetic events such as those leading to DNA methylation alter gene expression, histone modification, and interaction between genotypes, environment, and microbes, which increase the risk of invasive aspergillosis in patients. Furthermore, the authors argue that deficiency in the PTX3 gene, downregulation of CD50 and CD80 molecules, and variations in STAT1 and STAT3 genes increase the risk of invasive aspergillosis (Tanpaibule et al., 2020).
Process of Immunosuppression and the Effect it has on Body Systems
Immunosuppression refers to the reduced ability of the body’s immune system to respond to foreign antigens. The process of immunosuppression begins with the body’s exposure to substances or environments that kill immune effector cells. The exposure also inhibits the intracellular pathways that are involved in antigen recognition and activation of immune responses. Factors such as exposure to oncogenic viruses, ionizing and ultraviolet radiation, infections, including HIV, use of some medications, and infection by parasites can cause immunosuppression. Immunosuppression affects the ability of the body’s systems to defend themselves against foreign antigens. The risk of opportunistic infections and cancer development in immunosuppressed individuals is high. In some cases, the mortality rate is high among immunocompromised patients (Rice, 2019). Immunosuppression also affects the ability of the body systems to recover from an infection. As a result, immunosuppressed patients are likely to stay longer in the hospital as compared to those with normal immunity.
Conclusion
In summary, the patient developed the described symptoms due to the combined effects of immunosuppression and environmental exposure to opportunistic infections. Several genes play a role in the development of invasive aspergillosis in immunocompromised individuals. Immunosuppression develops from an individual’s exposure to factors that lower the body’s immunity to respond to foreign antigens. Immunosuppression has adverse patient and health outcomes.
References
Cb, L., M, M.-B., Jm, S.-M., J, B., C, C., J, S., M, L., J, S.-C., Lm, C., L, A.-F., Ma, L.-N., L, F., Jm, A., L, P., E, L.-F., M, A.-R., L, P., Sm, G., M, L., … J, S. (2020). Polymorphisms within the ARNT2 and CX3CR1 genes are associated with the risk of developing invasive Aspergillosis. Infection and Immunity, 88(4). https://doi.org/10.1128/IAI.00882-19
Fosses Vuong, M., Hollingshead, C. M., & Waymack, J. R. (2024). Aspergillosis. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK482241/
Luo, J., Beattie, J. A., Fuentes, P., Rizvi, H., Egger, J. V., Kern, J. A., Leung, D. Y. M., Lacouture, M. E., Kris, M. G., Gambarin, M., Santomasso, B. D., Faleck, D. M., & Hellmann, M. D. (2021). Beyond Steroids: Immunosuppressants in steroid-refractory or resistant immune-related adverse events. Journal of Thoracic Oncology, 16(10), 1759–1764. https://doi.org/10.1016/j.jtho.2021.06.024
Rice, J. M. (2019). Immunosuppression. In R. A. Baan, B. W. Stewart, & K. Straif (Eds.), Tumour Site Concordance and Mechanisms of Carcinogenesis. International Agency for Research on Cancer. http://www.ncbi.nlm.nih.gov/books/NBK570319/
Tanpaibule, T., Jinawath, N., Taweewongsounton, A., Niparuck, P., & Rotjanapan, P. (2020). Genetic risk surveillance for invasive aspergillosis in hematology patients: a prospective observational study. Infectious Diseases and Therapy, 9(4), 807–821. https://doi.org/10.1007/s40121-020-00331-4
Valer, J. B., Curra, M., Gabriel, A. de F., Schmidt, T. R., Ferreira, M. B. C., Roesler, R., Evangelista, J. M. C., Martins, M. A. T., Gregianin, L., & Martins, M. D. (2021). Oral mucositis in childhood cancer patients receiving high-dose methotrexate: Prevalence, relationship with other toxicities and methotrexate elimination. International Journal of Paediatric Dentistry, 31(2), 238–246. https://doi.org/10.1111/ipd.12718
- Explain why you think the patient presented the symptoms described.
Based on the patient’s symptoms and medical history, it is likely that the patient is experiencing an infection caused by the fungus Aspergillus, known as invasive aspergillosis. This infection is particularly common in immunocompromised patients, such as those with rheumatoid arthritis who are taking immunosuppressive medications like methotrexate and prednisone.
The patient’s fever, chills, and sweats are common symptoms of an infection, as the body’s immune system attempts to fight off the invading pathogen. The fatigue may also be a result of the body’s immune response, as well as the patient’s underlying rheumatoid arthritis. The chest pain associated with coughing and hemoptysis (coughing up blood) are concerning symptoms that suggest the infection may have spread to the lungs, which is a common complication of invasive aspergillosis.
The patient’s occupation as a grain inspector at a large farm cooperative may also be a contributing factor to the development of invasive aspergillosis, as Aspergillus is commonly found in soil and decaying plant matter. It is possible that the patient was exposed to the fungus through his work environment.
In summary, the patient’s symptoms are consistent with an infection caused by Aspergillus, which is particularly common in immunocompromised patients like those with rheumatoid arthritis. The patient’s occupation may also have contributed to his exposure to the fungus.
- Identify the genes that may be associated with the development of the disease.
Aspergillosis is a fungal infection caused by the Aspergillus fungus. The development of invasive aspergillosis is multifactorial and involves both host and environmental factors. Genetic factors may also play a role in the development of the disease.
Several genes have been identified that may be associated with the development of invasive aspergillosis. These include:
- CARD9: This gene encodes a protein that is involved in the immune response to fungal infections. Mutations in this gene have been associated with an increased risk of developing invasive aspergillosis.
- CLEC7A: This gene encodes a protein that is involved in the recognition of fungal pathogens by the immune system. Mutations in this gene have been associated with an increased risk of developing invasive aspergillosis.
- IL1B: This gene encodes a cytokine that is involved in the inflammatory response to fungal infections. Polymorphisms in this gene have been associated with an increased risk of developing invasive aspergillosis.
- TLR2: This gene encodes a protein that is involved in the recognition of fungal pathogens by the immune system. Polymorphisms in this gene have been associated with an increased risk of developing invasive aspergillosis.
It is important to note that the development of invasive aspergillosis is likely to be influenced by multiple genetic factors, as well as environmental and host factors. Further research is needed to fully understand the genetic basis of this disease.
- Explain the process of immunosuppression and the effect it has on body systems.
Immunosuppression is a process of reducing or suppressing the immune system’s activity. This can be done intentionally, such as in the case of organ transplantation, or unintentionally, such as in the case of autoimmune diseases like rheumatoid arthritis. Immunosuppressive medications like methotrexate and prednisone are commonly used to treat autoimmune diseases by reducing the activity of the immune system.
However, immunosuppression can have significant effects on the body systems. The immune system plays a crucial role in protecting the body from infections and diseases. When the immune system is suppressed, the body becomes more susceptible to infections, and the infections can be more severe and difficult to treat. This is because the immune system is not able to mount an effective response to the invading pathogens.
Immunosuppression can also lead to an increased risk of developing certain types of cancers, such as lymphoma and skin cancer. This is because the immune system plays a critical role in identifying and destroying abnormal cells that can lead to cancer.
Furthermore, immunosuppressive medications can have adverse effects on other body systems. For example, long-term use of corticosteroids like prednisone can lead to osteoporosis, muscle weakness, and increased risk of infections. Methotrexate can cause liver damage and increase the risk of infections. Atorvastatin, a cholesterol-lowering medication, can cause muscle pain and weakness.
In the case of the patient with rheumatoid arthritis, the immunosuppressive medications he was taking likely contributed to his increased susceptibility to invasive aspergillosis, a fungal infection that can be life-threatening in immunocompromised individuals. The patient’s symptoms of fever, chills, sweats, fatigue, chest pain, coughing, and hemoptysis are all consistent with invasive aspergillosis.
In conclusion, immunosuppression can have significant effects on the body systems, including an increased risk of infections, certain types of cancers, and adverse effects on other body systems. It is important for healthcare providers to carefully monitor patients who are taking immunosuppressive medications and to promptly identify and treat any infections that may occur
Reference:
Dandachi, D., Wilson Dib, R., Fernández-Cruz, A., Jiang, Y., Chaftari, A. M., Hachem, R., & Raad, I. (2018). Invasive pulmonary aspergillosis in patients with solid tumours: risk factors and predictors of clinical outcomes. Annals of medicine, 50(8), 713–720. https://doi.org/10.1080/07853890.2018.1518581
Teixeira da Silva, F., Romano, M., Esteves, A., Carvalho, J., & Ferreira, M. (2020). Invasive Pulmonary Aspergillosis in an (Apparently) Immunocompetent Patient. Cureus, 12(9), e10238. https://doi.org/10.7759/cureus.10238
(Grulich et al., 2007; Schulz, 2009; Wieland et al., 2014),
Ben-Baruch A. Inflammation-associated immune suppression in cancer: the roles played by cytokines, chemokines and additional mediators. Semin Cancer Biol. 2006;16:38-52.,
NURS 6501 Week 3 Cardiovascular Disorders
Concept Map Template
Primary Diagnosis: Myocarditis
- Describe the pathophysiology of the primary diagnosis in your own words. What are the patient’s risk factors for this diagnosis?
Pathophysiology of Primary Diagnosis | |
Acute myocarditis is characterized by inflammation of the heart muscle. Upon the virus entering the myocardial cells, an inflammatory response is triggered. This entry initiates a natural immune reaction within the initial week, succeeded by a response of adaptive immunity within the subsequent one to four weeks (Schultheiß et al., 2021). Heart muscle changes and inflammation that last for a long time cause cardiac enlargement and cardiomyopathy in the chronic stage. Interleukin and DAMP are released when the virus damages cells. These facilitate the attraction of inflammatory cells from the innate immune system. In addition, stressors like pain or anxiety activate the medullary cells involved in monocytopoiesis. Myeloid progenitor cells are being released. The pro-inflammatory cells are encouraged to proliferate from the spleen. Pro-inflammatory cells go into the damaged myocardium, where interferon-gamma release promotes further recruitment. Ventricular dysfunction, remodeling, and chronic inflammation result from an overreaction to viral heart damage. | |
Causes | Risk Factors (genetic/ethnic/physical) |
Acute myocarditis causes can be categorized as infectious or non-infectious. Typically, no identifiable cause is found in the majority of cases (Schultheiß et al., 2021). Viral infection is the primary cause identified in most patients. The most prevalent cardiotropic viruses leading to myocarditis are Coxsackie and echoviruses. Additional viral pathogens comprise the adenovirus, poliovirus, Parvovirus B19, hepatitis B and C, HIV, Epstein-Barr virus, and more. | Factors that increase the risk of myocarditis include age, gender, body response to inflammation, genetic predisposition, and excessive alcohol consumption beyond recommended limits (Schultheiß et al., 2021). Whites make up the largest proportion of patients brought to the hospital with myocarditis, followed by Blacks, then Hispanics, Native Americans, and culminating with Asians.
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- 2. What are the patient’s signs and symptoms for this diagnosis? How does the diagnosis impact other body systems and what are the possible complications?
Signs and Symptoms – Common presentation | How does the diagnosis impact each body system? Complications? |
Acute myocarditis may manifest in a wide range of ways, from showing no symptoms or moderate fever to developing cardiogenic shock and rapid cardiac death. The appearance might be either sudden or gradual in beginning and development. No specific clinical signs are indicative of a particular disease. Patients may exhibit symptoms such as fever, fatigue, dyspnea, orthopnea, palpitations, presyncope, syncope, and/or chest pain. The chest pain from acute myocarditis may resemble pericarditis discomfort or at times be intense central pain similar to acute coronary syndrome pain. A recent acute febrile illness, such as a respiratory tract infection, may be identified in at least 60% of patients (Palaskas et al., 2020). | A noteworthy physical examination is performed on individuals who have decompensated heart failure. Pulmonary rales, peripheral edema, and an S3 gallop are all seen on this examination. When auscultation is performed on individuals who have pericardial involvement, a frictional pericardial rub could be heard (Tschöpe et al., 2020). The pansystolic murmur of mitral regurgitation is a condition that may occur in patients who have ventricular dilatation. Patients could also exhibit signs and symptoms of the systemic disorders that are the root cause of myocarditis. For example, patients with sarcoidosis might have lymphadenopathy, patients with eosinophilic myocarditis might have a maculopapular rash, and patients with acute rheumatic fever might have erythema margenatum, chorea, polyarthralgia, and subcutaneous nodules. Patients who have been infected with diphtheria may have symptoms related to their nervous system. |
- 3. What are other potential diagnoses that present similarly to this diagnosis (differentials)?
Acute myocarditis can be differentially diagnosed from Acute coronary syndrome, Coronary vasospasm, and Stress cardiomyopathy. The term “acute coronary syndrome” is used to describe a collection of disorders that include unstable angina, STEMI, and NSTEMI. ACS is a prevalent condition that accounts for a significant portion of mortality in individuals over the age of 35 (Tschöpe et al., 2020). Coronary artery vasospasm refers to the constriction of the coronary arteries leading to potential complete or near-complete occlusion of the vessel. This vasospastic illness might manifest as acute coronary syndrome, stable angina, or acute ischemia at any point in the angina spectrum (Tschöpe et al., 2020). CAVS is a complex condition that does not align with conventional risk factors for coronary artery disease. Finally, excessive mental or physical stress causes stress cardiomyopathy, which causes quick and severe reversible heart malfunction. The condition resembles a heart attack, showing alterations in the electrocardiogram and echocardiogram, yet there is no blockage in the coronary arteries (Ammirati & Moslehi, 2023).
- 4. What diagnostic tests or labs would you order to rule out the differentials for this patient or confirm the primary diagnosis?
Endomyocardial biopsy is considered the most reliable method for diagnosing myocarditis. According to the consensus scientific statement, evidence of abrupt heart failure lasting less than two weeks with preserved ventricular dimensions but disrupted hemodynamics is the class I indication for electromyography. Patients with dilated ventricles, tachyarrhythmias and bradyarrhythmias, newly developed heart failure lasting two weeks to three months, and failure to respond to medication within one to two weeks might consider EMB. Additional signs consist of anthracycline toxicity, idiopathic restrictive cardiomyopathy, and unexplained arrhythmias. Further diagnostic tests may involve leukocytosis or, in some cases, eosinophilia, increased levels of C-reactive protein, interleukin, or interferon. Additional lab findings include increased erythrocyte sedimentation rate, elevated troponin-I or T levels, and EKG frequently displaying nonspecific ST changes (Seidman & McManus, 2022).
- 5. What treatment options would you consider? Include possible referrals and medications.
Supportive care is the primary approach to managing acute myocarditis. The management process involves the following phases. Heart failure management includes medications used to treat heart failure regardless of its etiology. Beta-blockers, renin-angiotensin-aldosterone inhibitors, sodium-glucose co-transporter-2 inhibitors, mineralocorticoid receptor antagonists, and diuretics are the major drugs utilized (Palaskas et al., 2020). Acute myocarditis may develop into a complex condition accompanied by arrhythmias of the ventricles or atrium, or heart block. Beta-blockers should be given to people with tachyarrhythmia who have steady blood pressure and no signs of peripheral hypoperfusion. Amiodarone and dofetilide are potential treatments for persistent ventricular arrhythmias. Immunosuppressive treatment is not recommended for regular usage due to lack of therapeutic benefit, save for individuals with systemic autoimmune or granulomatous inflammatory disorders.
Any fever-related or systemic disease causing new symptoms such as difficulty breathing during physical activity or while lying down, heart palpitations, excessive fatigue, or bouts of fainting should be assessed by a specialist. Diagnosis and patient management need a multidisciplinary team consisting of a cardiologist, cardiac imaging specialist, cardiac interventionist, heart failure expert, and cardiac rehabilitation specialist (Seidman & McManus, 2022).
References
Ammirati, E., & Moslehi, J. (2023). Diagnosis and treatment of acute myocarditis. JAMA, 329(13), 1098. https://doi.org/10.1001/jama.2023.3371
Palaskas, N., Lopez‐Mattei, J., Durand, J. B., Iliescu, C., & Deswal, A. (2020). Immune Checkpoint inhibitor myocarditis: Pathophysiological characteristics, diagnosis, and treatment. Journal of the American Heart Association, 9(2). https://doi.org/10.1161/jaha.119.013757
Schultheiß, H., Baumeier, C., Aleshcheva, G., Bock, C., & Escher, F. (2021). Viral Myocarditis—From pathophysiology to treatment. Journal of Clinical Medicine, 10(22), 5240. https://doi.org/10.3390/jcm10225240
Seidman, M. A., & McManus, B. M. (2022). Myocarditis. In Elsevier eBooks (pp. 553–575). https://doi.org/10.1016/b978-0-12-822224-9.00005-0
Tschöpe, C., Ammirati, E., Bozkurt, B., Caforio, A. L., Cooper, L. T., Felix, S. B., Hare, J. M., Heidecker, B., Heymans, S., Hübner, N., Kelle, S., Klingel, K., Maatz, H., Parwani, A. S., Spillmann, F., Starling, R. C., Tsutsui, H., Seferović, P., & Van Linthout, S. (2020). Myocarditis and inflammatory cardiomyopathy: Current evidence and future directions. Nature Reviews Cardiology, 18(3), 169–193. https://doi.org/10.1038/s41569-020-00435-x
Tschöpe, C., Ammirati, E., Bozkurt, B., Caforio, A. L., Cooper, L. T., Felix, S. B., Hare, J. M., Heidecker, B., Heymans, S., Hübner, N., Kelle, S., Klingel, K., Maatz, H., Parwani, A. S., Spillmann, F., Starling, R. C., Tsutsui, H., Seferović, P., & Van Linthout, S. (2020). Myocarditis and inflammatory cardiomyopathy: Current evidence and future directions. Nature Reviews Cardiology, 18(3), 169–193. https://doi.org/10.1038/s41569-020-00435-x