Diabetes mellitus is a complex of metabolic conditions that results to the accumulation of high levels of blood sugar over a prolonged period. The disease occurs when either the pancreas fails to produce insulin or produce insufficient insulin, or due to the failure of body cells in responding to the already produced insulin. The disease poses costly burdens on individual, social and economic levels, and the global burden is elevating in each new day. In addition, the asymptomatic nature and insidious onset of the condition make many individuals remain undiagnosed at the early stage posing them high risks of developing disastrous complications. This paper pays high attention to the natural history, clinical manifestations, prognosis, etiology and the pathogenesis of diabetes mellitus.
The oldest description of this condition as a polyuric state was in ancient Egypt on 1550 BC. During the 2nd century, Aretaeus of Cappadocia clinically described the disease as a condition of passing through of urine. In the 5th and the 6th centuries, Indian physicians discovered that the urine of polyuric patients was characterized by sweet and honey-like taste, which attracted insects such as ants. These physicians also identified the distinction between two types of diabetes: one in old and fat individuals and the other in thin people who rapidly die. In the 17th century, the sweetness in the urine was rediscovered by Thomas Willis, who also remarked concerning change of lifestyle after recognizing that the diabetes prevalence increased due to high intake of unalloyed wine (Polonsky, 2012). A century later, physician Matthew Dobson discovered that the urinary sweetness was caused by sugar that was linked to the elevation of blood sugar.
At the onset of 18th century, physician john Rollo became the first person to describe the condition as diabetes mellitus (honey) as a way of distinguishing it from diabetes insipidus (tasteless). During the 19th century, French physiologist, Claude Bernard, discovered that sugar was stored as glycogen in the liver and that the transfixion of medulla in normal rabbits resulted to high levels of blood sugar. In the same century, Paul Langerhans discovered pancreas islets as the endocrine tissue of the pancreas, and then linked pancreas and diabetes mellitus (Polonsky, 2012).
Diabetes mellitus is linked with high mortality and mortality in most individuals. Approximately 60% of patients with diabetes mellitus rarely do they develop serious complications over the long term, but most experience end-stage renal condition, blindness and in some cases early death. However, the risk of end-stage renal disease and proliferative retinopathy is two times high in men than in women when the condition occurs before the age of 15 years. Although end-stage renal disease one of the serious complication of the disease, its incidence rates are moderately low ranging from 2.2% at 20 years to 7.8% at 30 years after diagnosis (American Diabetes Association, 2013).
Moreover, patients with mild diabetic nephropathy have the risk of developing cardiovascular disease. In addition, 60% of diabetic patients have elevated prevalence of developing small-fiber neuropathy. However, the severity of diabetes mellitus depends on how well the patient manages his or her risk of complications. For type 1 diabetes, patients can live 10-20 years through the administration of long-term coordinated care management. Type 2 diabetes requires patients to have integrated medication in order to control their blood sugar. Moreover, to some extent, diabetic patients must be depended on dialysis due to kidney failure. However, 60% of mortality cases occur due to heart attack, kidney disease and other diabetes-related short-term and long-term complications (American Diabetes Association, 2013).
Diabetes mellitus occurs due to the production of insufficient insulin (either totally or virtually to the body needs), inability of the cells to utilize insulin properly and efficiently or due to the production of defective insulin. The absolute lack of insulin is a destructive process that affects insulin-producing cells in the pancreas resulting to type 1diabetes. Insulin is made by pancreas, which has a cluster of cells referred to as islets. Beta cells within the islets have the role of processing insulin and then releasing it into the blood. When these beta cells fail to produce enough insulin, glucose levels accumulate in the blood leading to diabetes. The high elevation of glucose in the blood starves body cells of energy (American Diabetes Association, 2013).
However, beta cells fail to produce sufficient insulin due to various factors. The first factor is due to destruction by t-cells. At this point, the t-cells consider beta cells as antigens and thus attacking them leading to the reduction of beta cells that in the long run leads to inadequate production of insulin. Genetic susceptibility is linked to causing t-cells attack beta cells. Some gene variants carry codes of making proteins on the white blood cells that are referred to as human leukocyte antigens (HLA) (American Diabetes Association, 2013). The HLA genes produce proteins that assist the body to recognize a cell as part of the body or not.
After the destruction of beta cells through autoimmunity, the presence of insulitis, also known as the lymphocytic infiltration of the islets becomes evident in newly diagnosed patients. The result is an increase of glucose in the blood; a condition referred as hyperglycemia and intense ketonuria. When the blood sugar level remains high over time, kidney usually hits the threshold level of reabsorption. The resulting impact is the excretion of glucose in the urine (glycosuria). Moreover, the osmotic pressure of the urine is increased causing an inhibition of the reabsorption of water by the kidney and hence elevated levels of urine production and high loss of body fluids (Kitabchi et al. 2009).
Patients with diabetes mellitus have high elevated levels of blood sugar (hyperglycemia) that is approximately 180mg/100ml or even higher. An average blood sugar level ranges from 70 to 100mg/100ml though this range fluctuates throughout the day. High level of glucose is evident in the urine of diabetic patients due to the failure of the kidney to conduct reabsorption of blood sugar. Osmotic pressure of the blood also increases causing high and frequent production of urine that in the long run results to excessive thirst (polydipsia). The elevated levels of glucose loss result in weight loss, weakness, increased appetite (polyphagia) and fatigue (Kitabchi et al. 2009). In addition, patients with hyperglycemia have high risks to infections such as urinary tract and vaginal infections. Other manifestations include poor eyesight, numbness of the feet and hands, slow healing of sores, dry skin among others.
It is, therefore, evident that diabetes mellitus is caused by production of insufficient insulin or the failure of the body cells to respond to the already produced insulin. Moreover, the condition has numerous adverse complications such as hyperglycemia and kidney failure. However, there is a possibility of diabetic patients to survive more years even after being diagnosed with the condition especially through administration of long-term coordinated care management.
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