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2808NRS Nursing
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2808NRS Nursing
0 Download4 Pages / 830 Words
Course Code: 2808NRS
University: Griffith University
MyAssignmentHelp.com is not sponsored or endorsed by this college or university
Country: Australia
Question:
For this task you need to create a single (1) slide (using PowerPoint) colour coded concept map and provide a word explanation, demonstrating analysis of the case study scenario emailed to you in week 1. A PowerPoint template file will be made available for you to customise based on your assigned case scenario.
? In your concept map you must include:1) Your Interpretation of the patient’s risk factors (from the case-study scenario) and determine how these risk factors relate to the diagnosed disease/disorder using evidence based literature;2) An outline of the links between the aetiology, cellular pathology and the pathophysiology of the diagnosed disease;3) A description of how the pathophysiology of the disease/disorder accounts for the patient’s clinical manifestations (described in the case-study scenario); and4) An analysis and interpretation including evidence-based research to suggest appropriate diagnostic assessments and treatment modalities for the patient’s diagnosis.
? In your 750 word written explanation you must:1) Explain the links between the patient’s risk factors and aetiology to account for the disease’s/disorder’s physiology.2) Describe how the disease’s/disorder’s pathophysiology manifests through the patient’s signs and symptoms (clinical manifestations).3) Justify your suggested diagnostic tests and treatment modalities listed in the concept map on their relevance and appropriateness for the diagnosed disease/disorder.
Answer:
The case study involves an 11-year-old female patient named Emilia, who has been diagnosed with autoimmune Type 1 diabetes mellitus. Emilia has a medical history of coeliac disease and tonsillectomy. Her family history included Type 1 diabetes mellitus (her father). Emilia presented to the hospital with chief complaint of worsening of vomiting and lethargy since twenty hours. Emilia was born in Finland and has recently moved to Australia. Her Physical examination revealed weakness, deep-rapid breathing and no response to verbal commandsType 1 DM is a disorder of the immune system in which the immune system destroys its own cells in the pancreas. The disease first manifests itself in adolescence or early age. In this disease, the pancreas cannot deliver any insulin – the hormone that controls glucose levels (Chiang, Kirkman, Laffel & Peters, 2014).Insulin production is insufficient to control blood glucose levels due to the permanent destruction of beta cells in the pancreas. This destruction progresses without any apparent time until the mass of these cell reductions reaches the extent that the measurement of the insulin delivered is insufficient (Kostic et al., 2015).Pathophysiology:The slow destruction of beta-cells in the pancreas, which is inevitably due to the onset of type 1 DM, is a consequence of the immune system response (Livingstone et al., 2015). The immune system working against body’s own cells can be activated by a natural factor presented to individuals who have hereditary deficiency.Risk factors:Despite the fact that systems of etiology of Type 1 diabetes are misty, it is thought to involve following risk factors:Genetic etiology – Some ethic groups, such as Scandinavians and Sardines, are likely to have more chances of Type 1 DM.Autoantigens – Proteins that are thought to have been discarded or detected in the normal turnover of pancreatic beta cells. Activation of TH1, TH2, B lymphocytes and CD8 cells occur. Autoantigens create an uncontrolled reaction leading to beta cell destruction.Clinical manifestationsGlucose does not move in cells because insulin is not there to do it. Rather, it develops in the blood and the cells begin to starve. This leads to high glucose, which can lead to symptoms such as:Dehydration: When there is increased sugar in the blood, patient dehydrates more. This is the body’s method of removing it. A lot of water comes out with urine, which drains the body (Onengut-Gumuscu et al., 2015).Weight loss: Glucose that goes out when urinating expels calories with it. This is the reason why many people with high glucose have glucose in urea. The lack of hydration further exerts influence.Diabetic ketoacidosis (DKA): If the body can not get enough glucose for fuel, it metabolizes the fat cells. This makes synthetic compounds called ketones (Bluestone et al., 2015).Other symptoms include:Polydipsia (excessive thirst), dry mouth, unexplained weight loss (despite the fact that patient eats and feels hungry), fatigue and deep rapid breathing.DiagnosisType 1 DM, blood glucose test. Test for glucose or ketone in urea.TreatmentMany people with type 1 diabetes live long and healthy life. The way of maintaining a healthy life is to maintain glucose levels within the range given by the specialist. Emilia needs to often undergo screening for insulin, nourishment and exercise to achieve this (Cherney et al., 2014).Emilia should be injected with insulin infusions to control glucose levels after consultation with a doctor.Changes in lifestyleExercise is a major element of the treatment of Type 1 DM. However, this does not include basic running exercise. Emilia must adjust the diet plan and dose of the insulin and the nutritional adjustment which will help in regulation of blood glucose level.
Reference list
Bluestone, J. A., Buckner, J. H., Fitch, M., Gitelman, S. E., Gupta, S., Hellerstein, M. K., … & Liu, W. (2015). Type 1 diabetes immunotherapy using polyclonal regulatory T cells. Science translational medicine, 7(315), 315ra189-315ra189.
Cherney, D. Z., Perkins, B. A., Soleymanlou, N., Maione, M., Lai, V., Lee, A., … & von Eynatten, M. (2014). Renal hemodynamic effect of sodium-glucose cotransporter 2 inhibition in patients with type 1 diabetes mellitus. Circulation, 129(5), 587-597.
Chiang, J. L., Kirkman, M. S., Laffel, L. M., & Peters, A. L. (2014). Type 1 diabetes through the life span: a position statement of the American Diabetes Association. Diabetes care, 37(7), 2034-2054.
Kostic, A. D., Gevers, D., Siljander, H., Vatanen, T., Hyötyläinen, T., Hämäläinen, A. M., … & Lähdesmäki, H. (2015). The dynamics of the human infant gut microbiome in development and in progression toward type 1 diabetes. Cell host & microbe, 17(2), 260-273.
Livingstone, S. J., Levin, D., Looker, H. C., Lindsay, R. S., Wild, S. H., Joss, N., … & McKnight, J. A. (2015). Estimated life expectancy in a Scottish cohort with type 1 diabetes, 2008-2010. Jama, 313(1), 37-44.
Onengut-Gumuscu, S., Chen, W. M., Burren, O., Cooper, N. J., Quinlan, A. R., Mychaleckyj, J. C., … & Achuthan, P. (2015). Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers. Nature genetics, 47(4), 381.
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