Complications in Patients with Type 2 Diabetes - Term Paper Example

Running head: DIABETES Complications in patients with type 2 diabetes Your first and last name here The name of the institution here Introduction It is well known that diabetes represents a risk factor as morbidity and mortality of arteriosclerosis and the diseases related to it, mainly coronary artery disease and cerebrovasculary disease. 30-40% of the patients on hemodialysis or peritoneal dialysis suffer from diabetic neuropathy, while the main cause of blindness is diabetic retinopathy. Statistics show that lifespan is reduced 20-30% in patient with diabetes, and diabetes in the developed countries is still the forth cause of mortality. Cardiovascular diseases are the cause of death in 75% of the patients with diabetes, while in patients with type I diabetes, diabetic neuropathy is the leading cause with around 30% (WHO, 2009). The statistics provided by the World Health Organization (WHO, 2009) are, to say at least, defeating. It is estimated that 220 million people suffer from diabetes, and that in 2005 alone, 1.1 million people have died from the disease worldwide, and the alarming statistics show that the number of deaths from diabetes will double by 2030. It is also important to mention that 80% of diabetic deaths occur in underdeveloped and developing countries, and that half of diabetes deaths occur in patients under the age of 70%. Diabetic deaths are also more prevalent in women that in men, with 55%. One should also mention the serious economic impact that diabetes has on a nation’s budget. It is estimated that the cost of treating diabetes and its related illnesses has reached 4100 billion in the US, and, even more drastically, China will suffer a loss of $558 billion during the period of 2006-2015 because of diabetes (WHO, 2009). While diabetes represents a singular chronic condition related to the metabolism of carbohydrates, through the disruption of insulin secretion and/or effect, it can have a multiple etiology. The most prominent and well known are diabetes type I and II, but other forms include gestational diabetes, diabetes related to the genetic defects of the beta cells of the pancreas, of insulin action, diseases of the exocrine pancreas and several other diseases that influence the condition of the pancreas. The most prominent of the previously mentioned is type II diabetes and it represents one of the key metabolic issues in modern medicine. The pathophysiological process the development of type II diabetes is largely unknown, however, there is a clear indication of the etiology behind type II diabetes. A large prospective study performed on 84,941 female nurses from 1980 to 1996 has shown that lack of exercise, a high-fat diet, smoking, and abstinence from alcohol are associated with a significantly increased risk of diabetes (Hu et al., 2001). In essence, type II diabetes represents insulin resistance with relative insulin deficit or predominately insulin defect in secretion with or without insulin resistance. Unlike, type I diabetes, there are no antibodies against beta cells of the pancreas in type II diabetes. This diabetes appears amongst the adult population and the clinical characteristic of the illness is the slow, incremental climb with minute elevations of glycemia during fasting, and high glycemia after a meal. This is the main reason why the vascular complications of the disease are discovered too late. It should be mentioned that type II diabetes has a tendency towards macrovascular complications. As we have previously mentioned, most of the patients with type II diabetes are obese, with the adipose tissue mostly located in the abdominal region. The tendency towards ketoacidosis is very rare and usually develops during stressful situations. With age, patients with type II diabetes have a tendency to develop non-ketotic hyperosmolaric condition or coma. The function of the beta cells is maintained, but the secretion is insufficient to compensate for the resistance towards the insulin, or the action of the insulin is normal, but the secretion is insufficient. It is also known that the reduction of the body mass leads to an improvement of the glycimic status (Fauci et al, 2008). When diagnosing diabetes, it should be know that the current WHO diagnostic criteria for diabetes should be maintained – fasting plasma glucose ≥ 7.0mmol/l (126mg/dl) or 2–h plasma glucose ≥ 11.1mmol/l (200mg/dl). Usually an oral glucose tolerance test (OGTT0 should be used in individuals with fasting plasma glucose 6.1-6.9mmol/l (110–125mg/dl) to determine glucose tolerance status (WHO, 2009). There are many complications of diabetes, of which we will mention are the diabetic foot, brought on by vascular issues and diabetic nephropathy, which are the two most serious dangers in a patient with diabetes and extensive hyperlipidemia. The diabetic foot as a result of vascular issues The diabetic foot can present with a variety of problems, but the most important clinically are ulceration, amputation and Charcot neuroarthropathy. These will be the focus of this chapter. Many diabetic complications have a great impact on the foot and it is therefore not surprising that diabetic foot problems account for more hospital inpatient days than any other diabetic problems. Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration and may act alone, together or in combination with other factors such as microvascular disease, biomechanical abnormalities, limited joint mobility and increased susceptibility to infection. A thorough understanding of the contributory factors that lead to foot ulceration and amputation is essential for successful treatment of established pathology. Perhaps more importantly, as the role of education and appropriate footwear in preventing ulceration and amputation is now established, accurate identification of high-risk patients on whom these services can be focused is vital (Cossentino et al 2009). Atherosclerotic vascular disease is probably present (at least in a subclinical form) in all patients with long-duration diabetes. Like other forms of macrovascular disease, peripheral vascular disease (PVD) is more common in diabetes. Using clinical techniques of palpation of foot pulses, a study found a 25–50% excess of PVD in people with diabetes, but using Doppler pressures, PVD can be found in up to 3 times as many diabetic as nondiabetic people (Bauer, 2000). The distribution of vascular disease in the lower limb is thought to be different in diabetes, with more frequent involvement of vessels below the knee. This is somewhat similar to the distal pattern of disease that is often seen in the coronary circulation, and may partly explain the fact that PVD is frequently asymptomatic in people with diabetes, and may present with ischaemic foot ulceration or gangrene, with no previous claudication (Piaggesi A. et al., 2003). Distal disease may allow a reasonable blood supply to be maintained to the large muscles involved in walking, whilst critically impairing the supply to the ski of the feet. Co-existent neuropathy and exercise limitation due to other diseases may also mask the symptoms of PVD. Thus, regular screening by physical examination is necessary to identify people with PVD (Valk, G.D. et al, 2003). Diabetic Nephropathy Diabetic nephropathy is the leading known cause of end-stage renal disease (ESRD) in the United States. It accounts for an estimated 28,000 new cases of ESRD per year. However, most if not all future ESRD from diabetic nephropathy is preventable. Diabetic nephropathy affects 20% to 40% of patients with type I diabetes 20 years after onset. Although a lower percentage (less than 20%) of patients with type II diabetes have nephropathy, still about one-half of patients with ESRD and diabetes have type II diabetes. Although diabetes accounts for more than 40% of cases of ESRD in the United States, patients with diabetes consume 75% of ESRD costs, principally because the renal disease is associated with other complications. Data from Denmark suggest that the increased mortality risk for type I diabetes may be confined to patients with nephropathy. The risk of nephropathy increases with duration of diabetes to 25 to 30 years' duration (after which this complication rarely begins) and with family history of essential hypertension. Some authorities contend the appearance of diabetic nephropathy is the result of the combination of diabetes and genetic predisposition to hypertension (Fauci et al, 2008) . The course of diabetic nephropathy is slow. It once was thought that there was a long silent period in which no changes were demonstrated. Now, through demonstration of an increased albumin excretion rate, so-called microalbuminuria (urine albumin levels of 30 to 300 mg per 24 hours), it is possible to identify diabetic nephropathy during this period, a stage known as incipient diabetic nephropathy. During this stage, there may be hyperfiltration or blood pressure elevation as well. This is followed by the development of clinical-grade proteinuria (urine albumin levels more than 300 mg per 24 hours, also detectable with standard reagent dipstick tests for protein), which defines the presence of overt diabetic nephropathy and is usually accompanied by the appearance of hypertension (Remuzzi, G. et al, 2002). Advanced diabetic nephropathy is defined by a progressive decline in renal function (declining glomerular filtration rate (GFR) measured according to decreases in creatinine clearance and increases in serum levels of blood urea nitrogen and creatinine), progressive proteinuria, and hypertension. Progression to ESRD is recognized with the appearance of uremia, the nephrotic syndrome, and the need for renal replacement therapy (transplantation or dialysis) (Abboud, H. et al. 2010). Glycemic control has been shown to be important in slowing the evolution of diabetic nephropathy. The has been shown that intensive therapy yields a 39% reduction in development of microalbuminuria and a 54% reduction in development of clinical-grade proteinuria. It was also shown that glycemic control resulted in a 33% reduction in microalbuminuria after 12 years of follow-up study (Nishiyama, A. et al, 2008).. Pancreatic transplantation accompanied by normoglycemia has been shown to prevent the recurrence of diabetic nephropathy in kidney grafts. Other interventions also may slow the appearance or progression of nephropathy, particularly aggressive, effective control of coexisting hypertension, which slows the rate of decline in GFR in early or advanced nephropathy. Dramatic slowing has been achieved with ACE inhibitors. For patients with microalbuminuria, the European Microalbuminuria Captopril Study showed a 66% reduction in rate of progression to clinical-grade proteinuria with an ACE inhibitor. Among patients with proteinuria, it was found that with an ACE inhibitor there was a 48% reduction in the rate of doubling of serum creatinine level and a 50% reduction in the rate of death, dialysis, or transplantation (Nishiyama, A. et al, 2008). Angiotensin receptor blockers probably share these effects. Use of calcium channel blockers also has reduced the rate of microalbuminuria. Restriction of dietary protein may delay the decline in GFR that occurs with diabetic nephropathy. Aldose reductase inhibitors may decrease or prevent an increase in albumin excretion rate. Cross-link blockers, such as aminoguanidine, have been effective in slowing renal disease in animal models of diabetes and are in clinical trials as therapy for diabetes among humans. In a provocative but uncontrolled study, pentoxifylline was found to decrease albumin excretion rate. It may be possible to prevent diabetic nephropathy with a strategy that includes careful glycemic control and aggressive control of coexisting hypertension. Routine urinalysis should be performed yearly for adults. Postpubertal patients who have had diabetes for 5 years should undergo annual measurement of either albumin excretion rate in a timed urine collection specimen (24 hours or overnight) or albumin-to-creatinine ratio. If abnormal albumin or protein excretion is detected, serum creatinine or urea nitrogen concentrations should be measured and GFR assessed. There should be appropriate use of dietary protein restriction, early use of ACE inhibitors, and potential use of other emerging strategies (Abboud, H. et al. 2010). As renal disease progresses, careful attention should be paid to all aspects of the medical renal plan, particularly that aimed at prevention of renal osteodystrophy. Protein intake for patients with evidence of nephropathy should be no more than 0.8 g per kilogram per day, or approximately 10% of daily calories. The presence of diabetes is not a contraindication to dialysis, as once was asserted. Chronic ambulatory peritoneal dialysis has been advocated by some authorities, but experience is limited. The most effective therapy for ESRD due to diabetes is renal transplantation, which often is performed at an earlier stage than with other forms of renal disease because of the accelerated catabolism that occurs when diabetes and uremia coexist. These patients ideally should undergo simultaneous renal and pancreatic transplantation, which reduces the risk of recurrent nephropathy in the transplanted kidney and takes advantage of the need for immunosuppression to prevent renal allograft rejection to allow reversal of the hyperglycemic state by the pancreatic graft (Remuzzi, G. et al, 2002).. References: 1. Bauer E. Sumpio. (2000). Foot Ulcers. New England Journal of Medicine, volume 343:787-793 2. Cosentino, F., Ryden, L., Francia, P., Mellbin, L. G. (2009). ESC Textbook of Cardiovascular Medicine. London: Wiley-Blackwell publishing. 3. Diabetes-Key Facts. (2009). World Health Organization. Accessed March 15, 2010. http://www.who.int/mediacentre/factsheets/fs312/en/. 4. Fauci A. et al. (2008). Harrison’s Principles of Internal Medicine. New York: McGraw-Hill Professional. 5. Giuseppe Remuzzi, Arrigo Schieppati, and Piero Ruggenenti, M.D (2002). Nephropathy in Patients with Type 2 Diabetes. New England Journal of Medicine, volume 346:1145-1151 6. Hanna Abboud, and William L. Henrich. (2010). Stage IV Chronic Kidney Disease. New England Journal of Medicine, volume 362:56-65 7. Mogensen CE and Cooper ME (2004). Diabetic renal disease: from recent studies to improved clinical practice. Diabetic Medicine, vol 21: 4–17. 8. Nishiyama A, Nakagawa T, Kobori H, Nagai Y, Okada N, Konishi Y, Morikawa T, Okumura M, Meda I, Kiyomoto H, Hosomi N, Mori T, Ito S, Imanishi M. (2008). Strict angiotensin blockade prevents the augmentation of intrarenal angiotensin II and podocyte abnormalities in type 2 diabetic rats with microalbuminuria. Journal of Hypertension, volume 26(9):1849-59. 9. Piaggesi A, Viacava P, Rizzo L, Naccarato G, Baccetti F, Romanelli M, Zampa V, Del Prato S. (2003). Semiquantitative analysis of the histopathological features of the neuropathic foot ulcer: effects of pressure relief. Diabetes Care vol 26: 3123–3128. 10. Siebenhofer A, Plank J, Horvath K, Berghold A, Sutton AJ, Sommer R & Pieber TR. (2004). Angiotensin receptor blockers as anti-hypertensive treatment for patients with diabetes mellitus: meta-analysis of controlled double-blind randomised trials. Diabetic Medicin vol. 21: 18–25. 11. Valk GD, Kriegsman DM, Assendelft WJ. (2003) Patient education for preventing diabetic foot ulceration: a systematic review. Endocrinol. Metab. Clin. N. Amer. 2003; 31:633-658. 12. World Health Organization. (2009). Definition and diagnosis of diabetes mellitus and intermediate hyperglycaemia. Geneva: WHO Document Production. Read More