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Diabetes: Cardiovascular Risk Factor - Essay Example

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Thi essay "Diabetes: Cardiovascular Risk Factor" is about John, whose name and identity will remain undisclosed due to ethical reasons. John is a middle-aged HGV driver with type 2 diabetes mellitus. He is overweight and has a family history of diabetes…
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Diabetes: Cardiovascular Risk Factor
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Diabetes as a Cardiovascular Risk Factor - A Case Study Introduction: This case study is about John, whose and identity will remainundisclosed due to ethical reasons. John is a middle-aged HGV driver with type 2 diabetes mellitus. He is overweight and has a family history of diabetes. Due to his profession, he is constantly on the move, and it is very difficult for him to control diet and have regular medications that he had been prescribed by his physician. This is being manifested by his poor glycaemic control in terms of his raised HbA1c in the range of 10%. Over the top of it, as expected, he has raised cholesterol and triglycerides. To complicate matter further, he is hypertensive and a smoker too. He has been told repeatedly by his physician to control diet and to remain on regular medications to minimise the aggravated risk factors of cardiovascular disease due to his diabetes in this particular scenario, and even though he is on metformin for his blood sugars, his glycosylated haemoglobin is not showing any trend to show lower values. There are indeed reasons for such things happening to him, and there are both physical and social factors for such poor results that if continued will have long-term implications on his health conditions, and this case study intends to analyze all those factors involved in his case to formulate a management plan customized for him (Adler, AI, 2003). As in the case of John, prolonged exposure to hyperglycemia is recognized as the primary causal factor in the pathogenesis of complications associated with diabetes mellitus. Hyperglycaemia and poor control of blood sugars in his case would induce a large number of alterations in the vascular tissue that would promote accelerated atherosclerotic process consequentially. These effects are often irreversible and they lead to progressive endothelial cell dysfunction. Once established, they progress over time, and reversal of hyperglycemia to normoglycaemic ranges would not reverse the pathology back to normal. Moreover, in his case associated overweight, dyslipidaemia, and hypertension, all independently promote atherosclerosis that is known to be a single most important pathological event to precipitate a cardiovascular accident, the prognosis of which becomes far less encouraging in the backdrop of his family history of and his diabetic disease (Blendea MC, McFarlane SI, Isenovic ER, Gick G, Sowers JR., 2003). One of the important mechanisms responsible for the accelerated atherosclerosis in diabetes is the nonenzymatic reaction between glucose and proteins or lipoproteins in arterial walls. Glucose forms chemically reversible early glycosylation products with reactive amino groups of proteins. Diabetes mellitus (DM) increases coronary heart disease (CHD) mortality. Reduction of serum cholesterol levels, arterial pressure control, quitting smoking, weight control, diabetes improvement, and physical activity (Frayn KN., 2001) improve the endothelium-dependent response. Both type 1 and type 2 diabetic patients have mostly been described under enhanced oxidative stress, and both conditions are known to be powerful and independent risk factors for coronary heart disease, stroke, and peripheral arterial disease. Coronary artery disease and glucose metabolism alterations in diabetes mellitus have raised to the idea that atherosclerosis and diabetes may share common antecedents. In his case, with his development of diabetes with a genetic background and probable environmental antecedents, there is a higher chance of complications that would need interventions to prevent calamities (Bloomgarden, ZT., 2005). John's problem is not isolated. Diabetes, both type 1 and type 2, is increasing in prevalence and it is estimated that three million individuals in the UK will have type 2 disease by 2010. John is middle aged overweight male, and as predictable, this would have a concomitant risk factor for cardiovascular disease. It is worrying in his case since type 2 diabetes mellitus increases the risk of all manifestations of vascular disease. The particular association of high triglycerides, impaired glucose control, genetic factor, metabolic derangements, environmental factors, all predispose to increased risk of death in case of John, due to cardiovascular disease, and over and above that, he is on metformin that has its attendant complications of hypoglycaemia if diet is not taken care of (Aronson D, Rayfield EJ, 2002). Heart disease is well recognised as a chronic complication of diabetes, and is the major cause of morbidity and mortality in patients from middle-age onwards. With his type 2 diabetes, his associated risk factors for heart disease such as hypertension and obesity, the risk of heart disease increases further. Hyperglycaemia and high lipids in his blood has pushed his metabolism off the balance. From that point of view, his disease of type 2 diabetes mellitus is just not diabetes or state of inappropriately controlled hyperglycemia, with his overweight stature, high serum lipids, and hypertension and smoking, he can be considered suffering from a spectrum disorder associate with potentially great cardiovascular risk (Fuller JH, Stevens LK, Wang SL., 2001). His obesity with type 2 diabetes, places him in the category where perhaps insulin resistance is the cause for his persistent hyperglycemia indicated by protractedly elevated glycosylated hemoglobin. Insulin resistance, if it be the cause of his problem, makes things further worrisome since insulin resistance is associated with many risk factors, and they typically include almost all that John has. These are central obesity, a dyslipidaemia characterized by high trigkeycerides and low HDL cholesterol, high blood pressure, and many others (Fisher M., 2003). The point that John is having insulin resistance is very significant from the point of view of his management. In pathogenic terms insulin resistance is a principal feature of type 2 diabetes and precedes the clinical development of the disease by 10-20 years. Insulin resistance is caused by the decreased ability of peripheral target tissues to respond properly to normal insulin levels. In John's case, Initially, increasing pancreatic insulin secretion must have been able to counteract insulin resistance and thus normal glucose homoeostasis could be maintained. Eventually, with his age and obesity, the peripheral demands had increased, and on the face of it, glucose concentrations have risen, and the plasma glucose concentration have risen beyond the cut-off point, and time to time control over a period of time has also been affected beyond acceptable levels as indicated by glycosylated haemoglobin of 10%. His obesity has further worsened the picture (Goldin A, Beckman JA, Schmidt AM, Creager MA, 2006). With increasing obesity, in particular visceral obesity, fat cells become enlarged and apparently less responsive to insulin, i.e. insulin resistant. Examining how this is going to increase his burden of disease in terms of cardiovascular risk factors, a simple increase in the mass of visceral fat tissue in obese individuals would in itself enhance free fatty acid (FFA) release. Excess release of FFAs into the portal circulation drives excess hepatic triglyceride accumulation and synthesis, in the form of very-low-density lipoprotein (VLDL) particles, with a resultant increase in plasma triglyceride concentrations (Greenberg AS, Obin MS., 2006). His hypertension is a risk factor for atherosclerosis. In the United Kingdom Prospective Diabetes Study (UKPDS), more than a third of patients at diabetes diagnosis were hypertensive. His hypertension can be viewed as pathogenic to his cardiovascular system. This would lead to atherogenesis working in synergy with the high triglycerides, and increased shearing forces on the preexistent plaques in the arterial wall would lead to plaque instability and further atherogenesis (UK Prospective Diabetes Study (UKPDS) Group, 1998). John has been put on metformin for his glycaemic control. Metformin controls plasma glucose. Due to his erratic food habit due to his profession, he was needed to be placed on an agent which even in large dosage would not produce hypoglycaemia. Metformin reduces glucose levels primarily by decreasing hepatic glucose production and by increasing insulin action in muscle and fat. The physician has advised him to stop or miss a dose if he is on a long drive, has a probability that he cannot have food for a longer period of time. His HbA1c is high, and with a maximum dose of 2.5 mg per day, this drug lowers HbA1c by about 2%, thus restoring the blood sugar levels within the acceptable higher range. He is overweight, and metformin does not promote weight gain, and this is an agent particularly suitable to reduce his plasma triglycerides. It is expected that John with regular use of metformin would register a 15 to 20% reduction in his plasma triglycerides. There is a strong consensus that any hypoglycaemic therapy that reduces HbA1c levels would also reduce microvascular complications of diabetes mellitus. In contrast to other agents, metformin is also known to reduce macrovascular complications of diabetes mellitus type 2. Another benefit of metformin is that if with an irregular life style, the HbA1c tends to increase in case of John despite full dose of metformin therapy, the management can be tailored to the requisite level by combining metformin to other agents including insulin therapy. There is now abundant evidence that insulin-sensitising therapies appear to offer benefits beyond just glucose lowering. Metformin is an insulin-sensitizing agents and is well accepted as a therapy that goes very well with insulin for therapy of type 2 diabetes as in the case of John. It has also demonstrable positive effects on FFAs, HDL-cholesterol, and other inflammatory parameters of diabetes mellitus. Moreover, metformin in comparison to other oral hypoglycaemic agents confers greater benefits on cardiovascular risks. The other aspect in the management that must be targeted is attenuation of other associated risk factors that have developed in John. It is clear that by targeting glucose alone without attention to the many other risk factors in diabetes, CVD risk will be only modestly attenuated. Much stronger CVD risk reduction is clearly observed when patients with diabetes have, in addition to glucose control, their lipids and blood pressures and obesity targeted (Grant, PJ., 2003). Department of Health has a framework in place that centres around the need for the diabetic people, focused on integrated care to deliver the best possible outcomes for these patients. According to this framework, John's management would need to focus on prevention of coronary artery disease. For him, the most important modifiable risk factor is action to tackle overweight and obesity that could be central for his prevention strategies. The forms of intervention, thus would be establishment of good control of diabetes, obesity management, and control of hypertension and lipid abnormalities will also contribute to a better outcome. It is evident that better care of John would need his involvement into the care process, since it demands lifestyle modification. Therefore, the care plan must be agreed upon, and he would need to maintain a personal diabetes record. Structured education programmes are important tools, and John must be persuaded to attend those. These would enable him to understand the importance of a diet programme, and he might as well be convinced about the absolute necessity to alter his health habits and lifestyles, since the implications of poor control of blood sugars would only then be known by him, from which he can make an informed decision about how to go about it. John would need psychological support to do this so he can participate himself in maintaining his target blood glucose levels within normal limits, an HbA1c level of 7.5% (Department of Health, 2001). This, according to the service delivery framework would need an integrated care. This need works across service boundaries with clear accountability involving a multidisciplinary team. Apart from clinical care, the social aspect of the disease would need to be addressed in equal extent. It would necessitate involvement of John in his own care. The committed staff from primary and specialist care would serve as the backbone of the improvements of care. But care in the community is also involved in it to ensure all round healthcare relationship between the client and the care team. Staff across primary, community, and specialist care would need to ensure that they have the range of competences to support greater self management by John himeslf. The confidence of John in the care team is essential so he can understand that the care plan centres around his needs. It is also important for him to understand that the care team is skillful, educated, and professionally trained to deliver quality care underpinned by service protocols, and is working as a part of a team, all with complementary skills (NICE, 2006). The management strategy according to this framework and knowledge gathered from this case study would follow the following parameters. There must be a specialist assessment to know the extent of his cardiovascular disease and the disease of diabetes. A structured education programme must be arranged to educate John, and the importance of dietary measures to control overweight, hypertriglyceridaemia, and to improve blood sugar control must be highlighted by the care team who would work centering him and his needs. He must be supported psychologically and encouraged to participate in the planning of his care. The importance of regular diabetic diet and physical exercise must be stressed, and a diet plan would be made in consideration of his behaviour and occupation. Control of his hypertension, socioeconomic factors associated with it would be attended, and medications to improve his glycaemic control would be used. For his profession, insulin would be a poor choice, hence it would be reserved. He would be educated on hypoglycaemia and measures and precautions to avoid those, but it is expected that with control of his weight, his insulin resistance would improve, hence with the existing dose of metformin, he would achieve appropriate glycaemic control. He should be monitored for lipids, hypertension, and HbA1c in regular intervals, and it is expected that his risk for developing cardiovascular disease will be less, specially when along with these he will be controlling his smoking as promised by him (Hansson GK, 2005). Reference List Adler AI (2003). Managing diabetes: what to do about cardiovascular disease. Diabetes Research and Clinical Practice 61 (Suppl 1): S3-8. Aronson D, Rayfield EJ, (2002). How hyperglycemia promotes atherosclerosis: molecular mechanisms. Cardiovasc Diabetol;1:1. Blendea MC, McFarlane SI, Isenovic ER, Gick G, Sowers JR (2003). Heart disease in diabetic patients. Current Diabetic Report 3: 223-229. Bloomgarden ZT (2005). Inflammation, atherosclerosis, and aspects of insulin action. Diabetes Care 28: 2312-19. Department of Health, (2001). National Service Framework for Diabetes: Standards. London. Department of Health. Fisher M (2003). Diabetes: can we stop the time bomb Heart 89 (Suppl 2): 28-30. Frayn KN (2001). Adipose tissue and the insulin resistance syndrome. Proceedings of the Nutrition Society 60: 375-80. Fuller JH, Stevens LK, Wang SL (2001). Risk factors for cardiovascular mortality and morbidity: the WHO multinational study of vascular disease in diabetics. Diabetologia 44: 554-64. Goldin A, Beckman JA, Schmidt AM, Creager MA, (2006). Advanced glycation end products: sparking the development of diabetic vascular injury. Circulation;114:597-605. Grant PJ (2003). Beneficial effects of metformin on haemostasis and vascular function in man. Diabetes and Metabolism 29: 6S44-52. Greenberg AS, Obin MS (2006). Obesity and the role of adipose tissue in inflammation and metabolism. American Journal of Clinical Nutrition 83: 461S-465S. Hansson GK, (2005). Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med;352: 1685-1695. NICE, (2006). NICE and Diabetes. A summary of relevant guidelines. UK Prospective Diabetes Study (UKPDS) Group (1998). Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 352: 837-53. Read More
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