NR 507 Week 6: Recorded Disease Process Presentation Peer Review
Chamberlain University NR 507 Week 6: Recorded Disease Process Presentation Peer Review– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 6: Recorded Disease Process Presentation Peer Review assignment 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 NR 507 Week 6: Recorded Disease Process Presentation Peer Review
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 6: Recorded Disease Process Presentation Peer Review 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 NR 507 Week 6: Recorded Disease Process Presentation Peer Review
The introduction for the Chamberlain University NR 507 Week 6: Recorded Disease Process Presentation Peer Review 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 NR 507 Week 6: Recorded Disease Process Presentation Peer Review
After the introduction, move into the main part of the NR 507 Week 6: Recorded Disease Process Presentation Peer Review 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 NR 507 Week 6: Recorded Disease Process Presentation Peer Review
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 NR 507 Week 6: Recorded Disease Process Presentation Peer Review
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 NR 507 Week 6: Recorded Disease Process Presentation Peer Review
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
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Sample Answer 2 for NR 507 Week 6: Recorded Disease Process Presentation Peer Review
Risk factors
I agree with you that congenital malformations, pre-existing kidney, genetics, and infections are some of the risk factors for chronic renal disease.
Obesity, low birth weight, nephrotoxins, age, and ethnicity, are also risk factors associated with the disease (Kazancioğlu, 2013). According to Chang & Kramer, 2013, Glomerular hypertrophy and hyperfiltration increase capillary wall tension of the glomeruli and decreasing podocyte density. Obesity can also contribute to the pathogenesis of kidney damage through hypervolemia, adipokine disorders, inflammation, oxidative stress and endothelial dysfunction. Intrauterine growth restriction can also cause low nephron number that leads to intraglomerular hypertension and hyperfiltration in the available nephrons (Vikse, Irgens, Leivestad, Hallan, & Iversen, 2018). According to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI), the elderly population is more prone to develop chronic kidney disease (CKD) after several renal insults. Exposure to heavy metals, alcohol, and other drugs has linked to constant kidney disease progression (Falodia & Singla, 2013).
Treatment and prevention
You haven’t included nephrectomy anywhere in the treatment of chronic kidney disease. Nephrectomy is the surgical removal of the kidney to treat kidney cancer and other related kidney diseases. Partial and radical nephrectomy can be done to treat chronic renal disease. According to Charytoniuk et al., 2018, partial Nephrectomy is done on the diseased or injured portion of the kidney, and radical nephrectomy includes removing the entire organ together with a section of the tube leading to the bladder. Retroperitoneal robotic partial nephrectomy is, however, more effective in the treatment of chronic kidney disease due to reduced operative time and a shorter Length of stay as compared to trans peritoneal nephrectomy (Paulucci et al., 2018). Good job on your presentation.
References
Chang, A., & Kramer, H. (2013). CKD progression: a risky business. Nephrology Dialysis Transplantation, 27(7), 2607-2609. doi:10.1093/ndt/gfs095
Charytoniuk, T., Małyszko, M., Bączek, J., Fiedorczyk, P., Siedlaczek, K., & Małyszko, J. (2018). Progression to chronic kidney disease in patients undergoing nephrectomy for small renal masses: a price to pay for a therapeutic success? Postgraduate Medicine. doi:10.1080/00325481.2018.1511211
Falodia, J., & Singla, M. K. (2013). CKD epidemiology and risk factors. Clinical Queries: Nephrology, 1(4), 249-252. doi:10.1016/j.cqn.2012.09.004
Kazancioğlu, R. (2013). Risk factors for chronic kidney disease: an update. Kidney International Supplements, 3(4), 368-371. doi:10.1038/kisup.2013.79
Paulucci, D. J., Beksac, A. T., Porter, J., Abaza, R., Eun, D. D., Bhandari, A., … Badani, K. K. (2018). A Multi-institutional Propensity Score Matched Comparison of Transperitoneal and Retroperitoneal Partial Nephrectomy for cT1 Posterior Tumors. Journal of Laparoendoscopic & Advanced Surgical Techniques. doi:10.1089/lap.2018.0313
Sample Answer 3 for NR 507 Week 6: Recorded Disease Process Presentation Peer Review
Hello, I must commend you for a thorough presentation on the chronic renal disease.
Based on criteria numbers seven and eight.
Provide a brief description of the pharmacological and non-pharmacological interventions used to treat and manage the disease (#7).
You mentioned starting the patient on dialysis in stage four (4) chronic renal disease (CKD)
Comment and Feedback
As you rightly mentioned, stage four CKD is characterized by a glomerular filtration rate (GFR) of 15-29 milliliters/minute (ml/min). At this point, though the kidney functions had deteriorated significantly but the patient is not yet in kidney failure hence dialysis is usually not initiated at that stage. A recent multicenter prospective cohort study by Park et al. and other multiple studies showed that early initiation of dialysis with GFR of over 15ml/min was associated with higher mortality rate and it did not enhance patient survival rate (Park et al., 2017). It was shown that premature initiation of dialysis increases the loss of kidney residual function, which is harmful to the patient (Park et al., 2017). Dialysis is indicated in stage five when GFR is less than 15 ml/min and this is considered as end-stage renal disease or kidney failure (Kaplan, Fedorowicz, & Aird, 2018). The indication and timing of starting dialysis was recommended when there are life-threatening changes in fluid, electrolytes, and acid-base balance or when one or more of the following conditions exists in a CK D patient: Signs of serositis, life-threatening fluid and electrolyte balance, pruritus, uncontrollable blood pressure, cognitive impairment, malnutrition that is not responding to dietary intervention. These usually manifest when the GFR is between 5 to 10 ml/ per minute (Kaplan, Fedorowicz, Aird, & Trebbin, 2016).
In conclusion, the primary aim of treatment in CK D is to slow down the progression of kidney damage and avoid the loss of residual kidney functions and these could be undermined by premature initiation of dialysis (Kaplan, Fedorowicz, Aird, & Trebbin, 2016).
The implications for nurse practitioner practice #8
Question: what other healthcare professionals should be involved in the care of patients with a chronic renal disease?
Feedback: According to the Kidney Disease Outcomes Quality Initiatives (KDOQI) recommendations, stage 4 CK D patients (GFR 15-29 ml/min) should be provided with treatment options education for available renal replacement therapy modalities and be made aware that dialysis will be needed when the GFR drops below 10 to 15 ml/ minute with the manifestation of life-threatening symptoms (Kaplan, Fedorowicz, Aird, & Trebbin, 2016).
A team approach was highly recommended before and even after the initiation of dialysis both the American Society of Nephrology and Canadian Society of nephrology recommended against and the initiation in the absence of clinical indications and without an established shared decision-making process that involves the patients, their families, and nephrology healthcare team. A study shows that early referral to nephrologist was associated with a reduced mortality rate in CK D (Kaplan, Fedorowicz, Aird, & Trebbin, 2016).
Sample Answer 4 for NR 507 Week 6: Recorded Disease Process Presentation Peer Review
Thank you for your response and all of your kind words in regard to my presentation. I hope that my presentation allowed for a better understanding of renal disease and how as nurse practitioners we can provide the best care possible for these patients. I am so pleased with the questions you asked and was able to do some further research into this disease and gain some helpful knowledge because of them. Both questions you asked are addressed below.
Regarding this question, if a patient is told they will need dialysis, but they refuse, they have an approximate survival time of six months. What would you do to change the patient’s mind about dialysis?
For patients who are instructed to use dialysis for a treatment method, this can be scary and life changing. For patients that refuse at the initial instruction of dialysis it is essential to educate and ensure that he or she has an understanding of the outcome if refusal continues. One initial response, as was mentioned in the case you presented to me, the amount of time per week that the patient must set aside for the treatments. One important factor to mention to the patient is the possibility of performing the hemodialysis at home. In all cases it is not necessary to go to an outpatient setting to have dialysis performed. This option is often more acceptable to patients and allows them more independence than having to attend scheduled appointments. Another important fact that I did not mention in the presentation is the choice to do either hemodialysis or peritoneal dialysis. If the choice of peritoneal dialysis is made the patient will need to be aware a surgical procedure to place a abdominal catheter will be needed in order for treatments to take place. “During PD, sterile dialysate fluid is introduced in the patient’s peritoneal cavity and remains there for 6–8 hours while excess body fluid and toxins are filtered across the peritoneal membrane; at the completion of treatment, the dialysate fluid is drained from the peritoneal cavity” (Schub, Mennella, 2018, p. 1). This type of dialysis differs from hemodialysis because typically a catheter is placed in the chest until a graft can be established in the arm and then the blood is filtered rather than the peritoneal fluid. Again, it is important to educate the patient that both can be performed at home independently as long as compliance is achieved. After explaining all options of dialysis to the patient, inform the patient of the complications of not having dialysis such as electrolyte imbalances, fluid overload, toxin build up, and ultimately death. Healthcare is patient driven and ultimately it will be the patient’s decision whether or not he or she wants to have dialysis or not. The job of the healthcare provider is to educate and supply patients with the appropriate options and tools the live the best life possible living with this chronic disease.
If a patient does receive a kidney transplant, is there a lifetime medication regimen?
For patients with renal disease a kidney transplant is life changing and unless complications occur, will allow for a life without the disease. Patients who received a kidney transplant will be required to take medications for immunosuppression. The reasoning behind this is to prevent the body from rejecting the transplanted kidney. In the event of rejection, the patient will begin so show symptoms similar to that of infection and ultimately if not treated the patient can lose the transplanted kidney, enter into a state of shock, or even death. Drugs that are often times used in the immunosuppressive therapy are as follows: Rituxan, Rapamune, Prograf, Astagraf XL, Prednisone, CellCept, Nulojix, Cytoxan, Cyclosporine, Campath, Thymoglobulin, Imuran, and Simulect (Colaneri, 2014). These drugs are often times used in combination and it is imperative the patient does not miss a dose. Patients will also need to see the primary care provider to have blood drawn regularly in order to monitor levels such as with the medication Prograf. “immunosuppression should modify the immune system enough to prevent rejection, but not allow infection, malignancies, and other side effects” (Colaneri, 2014, p. 550). It is imperative to monitor transplant patients to ensure proper kidney health and the optimal life post-surgery.
References
Colaneri, J. (2014). An Overview of Transplant Immunosuppression – History, Principles, and Current Practices in Kidney Transplantation. Nephrology Nursing Journal, 41(6), 549-561.
Schub, T. B., & Mennella, H. A. (2018). Hemodialysis vs Peritoneal Dialysis. CINAHL Nursing Guide.
NR 507 Week 7 Discussion
- Compare and contrast the pathophysiology between Alzheimer’s disease and frontotemporal dementia.
Alzheimer’s disease and frontotemporal dementia are both neurodegenerative disorders (McCance & Huether, 2019). According to an article by Wilson et al. (2019), dementia disorders are classified based on the protein effects, including amyloid-b, tau, and alpha-synuclein. They are challenging to diagnose and untreatable. Alzheimer’s disease is the most common neurodegenerative dementia disorder that is caused by extracellular amyloid plaques that are made up of amyloid-b and intracellular neurofibrillary tangles. The neurofibrillary tangles are composed of hyperphosphorylated tau protein. The damage within the brain is widespread due to the plaques causing neuron death and damage.
Frontotemporal lobe dementia is a group of disorders that affects the frontal and temporal lobes of the brain. They are caused by aggregated tau involving frontal and temporal lobe degeneration. People with Alzheimer’s disease typically present with difficulty remembering details about their lives and may have problems with language, executive, and visuospatial functions. People with frontotemporal lobe dementia experience behavioral changes, aphasia, and loss of word comprehension. Frontotemporal lobe dementia is also damage specifically to frontal or temporal lobes in the brain and is not as noticeably widespread (Wilson et al., 2019).
Some critical differences between Alzheimer’s disease (AD) and frontotemporal dementia (FTD) are that FTD is more common during the ages 40 to 60 years old, and AD risk becomes more significant with aging. AD is associated with more memory loss, and FTD patients may experience memory loss as well. However, it is associated more with changes in behaviors and speech that are noticed first. Finally, hallucinations and delusions are common in AD but uncommon in FTD (Alzheimer’s Association, n.d.). Many symptoms overlap between AD and FTD but are not the primary signs of the specific neurodegenerative disorder.
- Identify the clinical findings from the case that supports a diagnosis of Alzheimer’s disease.
The clinical findings within the case that support a diagnosis of Alzheimer’s disease are the mini-mental state examination (MMSE) score of 12 out of 30 points, indicating moderate dementia, and the MRI showing hippocampal atrophy. Hippocampal atrophy is a hallmark clinical finding suggesting Alzheimer’s disease (Persson et al., 2022). The mini-mental state examination is a standard cognitive function test to assess the degree of dementia based on a scoring system (McCance & Huether, 2019). The patient is also experiencing memory loss, wandering, getting lost in familiar places, changes in mood, forgetfulness, making unsafe or irrational decisions, and requiring assistance with activities of daily living, like dressing. The patient also is older and has a family history of Alzheimer’s disease from his father. Age and genetics are risk factors for the development of Alzheimer’s disease (McCance & Huether, 2019).
- Explain one hypothesis that explains the development of Alzheimer’s disease.
The cause of Alzheimer’s disease is not entirely known, but it is clear that brain cells that process, store, and receive information break down and are destroyed. One hypothesis of the cause of Alzheimer’s disease is beta-amyloid dysfunction, which is a compound that is a byproduct of amyloid precursor protein. It is thought that the sticky substance builds up in the brain, making communication difficult between brain cells, and it eventually causes them to die and leads to atrophy throughout areas of the brain. It is thought that even in small amounts, the accumulation of beta-amyloid can be a cause of Alzheimer’s disease (Hillen, 2019).
- Discuss the patient’s likely stage of Alzheimer’s disease.
Alzheimer’s disease has multiple stages, and sometimes the symptoms overlap. In the early stages, the symptoms are very mild, including forgetting where an object was placed or a few words, but overall, the person can still function independently. The middle stages are the longest and are when the person begins to need more care as they are not safe to continue functioning independently due to having a moderate level of dementia. The symptoms are much more apparent, and their behavior may change to hostile or agitated when they cannot remember things. They may also refuse to perform activities of daily living, such as hygiene measures. They commonly forget personal information about themselves, such as their address, and get lost frequently and wander. Finally, in the late stage of Alzheimer’s disease, the symptoms are severe. The person is no longer able to communicate and eventually remember how to move, and they require total care (Alzheimer’s Association, n.d.).
This patient is likely in the middle stages of Alzheimer’s with moderate dementia. This is based on the inability to make safe and rational decisions, such as balancing the checkbook and letting strangers into the home to buy an already-owned security system, as stated by the wife. The patient is also wandering and getting lost in the neighborhood he has lived in for 35 years, becoming defensive and changing his behavior. He also needs more help with activities of daily living, such as dressing himself.
References
Alzheimer’s Association. (n.d.). Stages of Alzheimer’s. Retrieved on December 10, 2023, from https://www.alz.org/alzheimers-dementia/stagesLinks to an external site.
Alzheimer’s Association. (n.d.). Types of dementia. Retrieved on December 10, 2023, from https://www.alz.org/alzheimers-dementia/what-is-dementia/types-of-dementia/frontotemporal-dementiaLinks to an external site.
Hillen, H. (2019). The beta-amyloid dysfunction (BAD) hypothesis for Alzheimer’s disease. Frontiers in Neuroscience, 13, 1154–1154. https://doi.org/10.3389/fnins.2019.01154Links to an external site.
McCance, K.L. & Huether, S.E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences.
Persson, K., Edwin, T. H., Knapskog, A.-B., Tangen, G. G., Selbæk, G., & Engedal, K. (2022). Hippocampal atrophy subtypes of Alzheimer’s disease using automatic MRI in a memory clinic cohort: clinical implications. Dementia and Geriatric Cognitive Disorders, 51(1), 80–89. https://doi.org/10.1159/000522382
Wilson, H., Pagano, G., & Politis, M. (2019). Dementia spectrum disorders: lessons learnt from decades with PET research. Journal of Neural Transmission, 126(3), 233–251. https://doi.org/10.1007/s00702-019-01975-4