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Disease Prevention Pathophysiology Paper

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Disease Prevention Paper
HCS/436
April 29, 2014
Maria Libano

Disease Prevention and description about the kidneys There is a common saying that “the body is a one way street”, therefore any alteration can hinder the flow and may cause damage to vital body systems and organs. The kidneys which are bean-shaped structure primary function are elimination of waste and toxins out of the body and blood filtration. Each kidney contains almost one million nephrons, which is a major aspect of the functional unit of the kidney which filters blood and urine production through the network of capillaries tubules in the glomerulus. The tubules ensure that the glomerulus filters the substances that are essential including protein and that waste exit to the bladder to the urethra. The kidneys participate in different life-sustaining duties of the body including removal of waste and any excess fluid in the body, maintenance of salt and minerals in the blood, blood pressure regulation, producing of erythropoietin through renin by stimulating red blood cells, and can also aid in the production of vitamin D. When the glomerulus is not able to meet the daily demand from the kidneys by the human body as a result of damaged, it can hinder the function causing protein and blood loss in the urine, accumulation of waste product because it can no longer filter, which will then lead to edema in the extremities, fatigue, and elevated blood pressure as a result of inflammation is named glomerulonephritis. Glomerulonephritis disease destroys the kidney and the ability to eliminate waste and extra fluids from the body to be excreted. Globally, it is the second most common disease. The cause of the disease, the pathophysiological aspect of glomerulonephritis including inflammatory response, common clinical presentation and manifestation, therapeutic regimen and treatment with diagnosis and further the risk and prevention of the disease will be elaborated. Etiology and Pathophysiology The etiology of the disease is idiopathic and can either be primary or secondary. The primary cause is as a result of an autoimmune disease or the disease occurs by itself and secondary which may be different number of autoimmune disease like diabetes or lupus, metabolic diseases, malignant from tumors, and complicating systemic infection diseases. These diseases can be triggered resulting in immune-mediated injury and exhibit humoral and cellular components. The immune response when the disease is present causing the glomerulus unable to filter waste and toxins in the kidneys. When the inflammatory cells such as lymphocytes and macrophage accumulate and antibody deposition is absence. With humoral immune response, it can lead to immune deposit formation and the glomeruli activating the complement. Deposited antibodies within the glomerulus circulate and react with the glomerular basement membrane diseases, trapped antigen within the glomerulus, or immune complexes in systemic circulation of the body. This can result in injury from inflammatory mediators (growth factors, vasoactive agent) release and activate a complex form of events that will ultimately affect the functional and structural characteristic of some of the glomerular immune disease. Clinical Presentation The four most common types of clinical presentation include acute glomerulonephritis, rapid progressive glomerulonephritis (RPGN), Berger disease, and chronic glomerulonephritis. Acute glomerulonephritis or postinfectious acute glomerulonephritis is common strep throat and skin infection like impetigo, common in children in developing countries or impoverished surrounding in developed country. One of the most common finding is the color of the urine will be coffee color or smoky brown color. Berger disease or “IgA nephropathy (IgAN) is considered to be the most common form of glomerulonephritis in the world” (Kawasaki, 2011 p. 1), caused by a viral infection appears to be triggering the upper respiratory tract or gastrointestinal and deposit IGA in the mesangium. As abnormal IgA continue to increase, IgA complexes are formed and produced causing injury to the mesangium which can lead to renal failure. RPGN also known as crescentric glomerulonephritis appears as a lesion which comprises of a crescent-shaped deposits accumulating in the Bowman’s space from deposits from epithelial cells, macrophages, and fibrin. The Goodpasture syndrome which is part of the RPGN results from combining glomerulonephritis with bleeding from the alveolar and the appearance of anti-glomerular basement membrane antibodies. This causes patient to manifest pulmonary problems such as shortness of breath. Chronic glomerulonephritis which implies that the disease is progressing to renal failure, the need for dialysis and eventually a kidney transplant. The continuous fibrotic change in the membrane causes the lesion to proliferate and dominated by sclerotic injury. Clinical Manifestation and Diagnosis Also, common clinical manifestations associated with disease are hematuria, proteinuria, decrease glomerular filtration rate, edema from fluid retention, high blood pressure and fatigue may arise from anemia or failed kidney. The clinical presentation has specific renal diseases and symptoms may vary depending on the existing condition. Diagnosis is made depending on the disease the signs and symptoms present, presentation, history, and lab test including urinalysis. In addition, according to Chen, et al, “Glomerulonephritis can be classified as antibody (Ab)-related and non-Ab–related based on different diagnostic characteristics” (2010 p 1). Therapeutic Treatment and Interventions Treatment of the disease depends on the underlying condition, the different type of symptoms present and the severity of the disease, if it is acute or chronic, and the characteristic of the diagnosis. The major focus for treatment is to protect the kidneys and avoid further damage. In acute cases of glomerulonephritis, especially with strep throat will improve by itself and no treatment will be required. While high blood pressure is a common clinical manifestation of glomerulonephritis, it is essential to control it and maintain a normal reading so that kidney function will not decline. Angiotensin converting enzymes (ACE) inhibitors will be utilized for blood pressure management. Corticosteroids and medication to suppress the body immune system can be used to control inflammation. Another way to reduce inflammation is through plasmapheresis, which is a procedure to extract the fluid part of the blood that have antibodies and replace with fluids that do not have antibodies present like intravenous fluids or plasma that is donated. The rationale behind this is to prevent proteins that are automatically present in the blood not to attack an individual own tissue and remove toxins from the blood. Also, lifestyle adjustment and food regimen choices like limit salt intake, reduce potassium and protein food consumption, monitor liquid intake, weight management, blood sugar control for individual with diabetes, and quit smoking. The benefit of these lifestyle change and food adjustments can minimize toxins build up in the blood and further prevent renal failure in a relatively long period of time. In addition, a support group may assist an individual in coping with the stress of the disease by getting support from other people that have experience the illness. Risk Factors and Prevention Individuals with respiratory infection from having a strep throat or gastrointestinal infections from the past may trigger recurrent episodes of symptoms like hematuria. Hepatitis B and hepatitis C can also have a triggering effect of antigen antibodies deposition are circulating in the blood vessels can cause thickening of the basement membrane. This can thereby activate the complement and further damage the glomeruli or otherwise refer to as membranoproliferation “Membranoproliferative glomerulonephritis (MPGN also called mesangiocapillary glomerulonephritis) is a lesion not a disease” (Fervenza & Glassock, 2012 p. 1). This membranoproliferation can also be present with person with infective endocarditis and skin infection. Also, lupus and human immune virus patient are at risk. The risk to prevent glomerulonephritis is not high, but measures can be taken to reduce risk and control the disease including take control of one’s health by managing weight, exercise, control blood pressure, blood sugar, can prevent and lessens a person’s likelihood against damage kidneys from hypertension or diabetic neuropathy. Also, if a person has strep throat or a skin infection like impetigo seek medical treatment immediately and follow up with treatment regimen prevent complication that may lead to glomerulonephritis. Glomerulonephritis prevention and care is essential because the disease can be temporary and the kidneys will not be affected or it can progress further and impede the functions of the kidney, causing chronic renal failure, and that will lead to end-stage renal failure. The individual may need to start dialysis and kidney transplant may be needed. Conclusion The kidneys which are bean-shaped structure participate in different life-sustaining duties of the body including filtration of blood and elimination of waste and toxins from the body. The glomerulus is a network of capillaries that ensure the filtration process, with a one way flow in the kidneys. Any alteration or injury to the kidneys can impede the flow or damage vital body system and organs. This can result in glomerulonephritis and if essential care and prevention is not taken immediately, it may lead to renal failure and progress to end-stage kidney failure.

Reference
Chen, J., Hwang, J., Chang, L., Wu, C., & Lin, Y. (2010). Attributes of antiangiogenic

factor plasminogen kringle 5 in glomerulonephritis. Archives Of Pathology & Laboratory Medicine, 134(12), 1804-1812. doi:10.1043/2009-0490-OAR.1

Copstead, L. C., & Banasik, J. L. (2010). Pathophysiology (5th ed.). St. Louis, MO:

Saunders Elsevier.

Fervenza, F., Sethi, S., & Glassock, R. (2012). Idiopathic membranoproliferative

glomerulonephritis: does it exist?. Nephrology, Dialysis, Transplantation: Official Publication Of The European Dialysis And Transplant Association - European Renal Association, 27(12), 4288-4294. doi:10.1093/ndt/gfs288

Kawasaki, Y. (2011). Mechanism of onset and exacerbation of chronic

glomerulonephritis and its treatment. Pediatrics International: Official Journal Of The Japan Pediatric Society, 53(6), 795-806. doi:10.1111/j.1442-200X.2011.03469.x

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