Diabetes: type 2 . This is also called impaired glucose tolerance. Initially individuals experience high blood glucose levels after eating and eventually this may lead to constant hyperglycaemia. The metabolic derangement is called insulin resistance because patients require higher levels of insulin to move glucose in the blood to the inside of cells such as muscles, the heart, the liver and the brain where it is needed for functioning of the cells. Insulin resistance is the main metabolic event leading to type 2 diabetes and the reduction of it should therefore also be the major aim of affected individuals and the treating physician or advising dietician. It is the most common form of diabetes and its incidence is rising in all population groups around the world. It is strongly associated with obesity, a sedentary lifestyle, and abnormal lipid levels. Those with a family history of the disease are more at risk than the general population. Symptoms are more those of a high glucose level than those of starving cells and include excessive thirst and urination, whereas weight loss is a late feature suggesting serious deficiency of insulin. The 2016 American Diabetes Association's (ADA's) standards of medical care in diabetes also indicate that a majority of patients with diabetes mellitus have hypertension. NA indicates not applicable. Eligibility data were not collected for nonrandomized screenees. All randomized participants were included in the analyses. The following represent additions to UpToDate from the past six months that were considered by the editors and authors to be of particular interest. Authors: Richards, Duncan; Aronson, Jeffrey Title: Oxford Handbook of Practical Drug Therapy, 1st Edition Copyright  It is treated, and can often be prevented, with a combination of lifestyle changes, diet and drugs – increased levels of exercise and a decrease in the intake of calories and especially lipids being the most important steps to improved health and longevity. There are many potential complications of type 2 diabetes if it is not correctly controlled (such as heart disease), since most organ systems in the body are affected by the disease. Alternative names. Non- insulin dependent diabetes (NIDDM) or adult onset diabetes – now rarely used. What is type 2 diabetes? Type 2 diabetes is the most common variety of diabetes. It is a disorder of carbohydrate metabolism in which the body effectively becomes resistant to the hormone insulin. ![]() Initially, the person with this disorder has impaired tolerance to glucose. This develops into high blood glucose levels after eating and eventually high blood glucose levels even when fasting. However, some people with type 2 diabetes remain relatively sensitive to insulin, while others have little or no insulin sensitivity. This difference affects treatment of the disease. In general, those type 2 diabetics who are not obese retain some sensitivity to insulin. What causes type 2 diabetes? The causes of type 2 diabetes are complex. Insulin resistance is the main metabolic abnormality leading to the development of type 2 diabetes. The most recent research suggests that type 2 diabetes can be seen as a consequence of a series of physiological disruptions, each of which makes the person vulnerable to subsequent disruption of normal glucose metabolism. Insulin resistance is common and is usually caused by obesity. There are effectively three stages in the development of type 2 diabetes: Insulin resistance, for which the body compensates by increasing the secretion of insulin to allow the liver and muscles to continue to function normally. Eventually the pancreas is unable to produce enough insulin to compensate for the insulin resistance. This leads to a sequence of impaired glucose tolerance, high blood glucose after eating (postprandial hyperglycaemia) and finally, high blood glucose levels even when fasting (fasting hyperglycaemia) and worsening postprandially. ![]() These high glucose levels are toxic not only to the large and small blood vessels but also to the cells producing insulin, the so- called beta- cells of the pancreas. This damage to the beta- cells leads to a decline in their function and eventually less insulin is produced as the disease progresses. ![]() The raised fasting and postprandial glucose levels result in complications which affect the small and large blood vessels of the body, and this contributes to renal failure, eye complications and more importantly, accelerated atherosclerosis leading to strokes and heart disease. The artherosclerotic complications are responsible for 8. Who gets type 2 diabetes and who is at risk? The percentage of the population with diabetes is highly variable among geographical regions and populations, so estimates are often inaccurate. A recent figure is 1. There are particular populations with a very high incidence of type 2 diabetes. For example, 4. 0% of Pima Indians in North America have type 2 diabetes. The South African Indian population also have amongst the highest incidence in the world. The risk factors for type 2 diabetes are: Obesity. Lack of exercise. An abnormal lipid profile. A family history of the disease. Who would be the typical person at risk for type 2 diabetes? The typical person would be: an overweight adultolder than 4. In women, persistent vaginal candida may be an early sign of type 2 diabetes, particularly in older women. How is type 2 diabetes diagnosed? Diabetes is diagnosed quite simply by measuring the levels of glucose in the blood. The normal levels are between 3,3 mmol/l and 5,9 mmol/l. The World Health Organisation defines diabetes as being when one or more of the following are present: Fasting blood glucose (blood glucose measured before breakfast) is over 6. Random blood glucose (blood glucose measured at any time) is over 1. Corresponding values for plasma glucose are 7. In some laboratories the glucose level is measured in plasma and not in blood and the concentration of glucose measured in plasma is 1. ![]() What is a glucose tolerance test? After an overnight fast, 7. Blood samples are taken in the fasting state and two hours after the glucose has been taken. It is used to diagnose glucose intolerance. When is glucose tolerance impaired? It is present when the fasting blood glucose is below 6. Corresponding values for plasma glucose are 7. Can type 2 diabetes be prevented? Type 2 diabetes is a disease of lifestyle in most cases, and can thus often be prevented. ![]() There is good evidence to show that controlling weight, getting plenty of exercise and eating a diet low in fats and high in complex carbohydrates – fruit and vegetables – lowers the risk of type 2 diabetes in most people. Many medical authorities recommend that anyone who has a family history of type 2 diabetes should have their blood glucose checked regularly, particularly once they are older than 4. Some doctors recommend that anyone over the age of 4. If impaired glucose tolerance is detected, then early prevention such as weight loss, exercise and a change of diet may well prevent or at least delay the onset of type 2 diabetes. How is type 2 diabetes treated? The mainstay of treatment in type 2 diabetes is lifestyle change – weight loss, a structured exercise programme and a diet low in fat and with plenty of fruit and vegetables. Any diabetic should consult a dietician early in the disease to work out the correct diet for their lifestyle. It is of utmost importance that individuals attempt to stop smoking, and if it is not possible to stop, reduce the habit to an absolute minimum. For prevention and management of diabetes complications in children and adolescents, please refer to Section 12 “Children and Adolescents.” In all patients with. Type 2 diabetes is a disease in which the person initially develops insulin resistance resulting in high glucose levels in the blood. This is also. ![]() However, recent research has shown that in most people, even the correct diet along with exercise will eventually not be sufficient to control their blood glucose and that drugs have to be used. The broad range of metabolic defects present often requires treatment with combinations of more than one drug. Furthermore, with time, as the ability of the pancreas to produce sufficient insulin wanes, increasing doses of medications and insulin injections may be required to control the blood sugar. The blood sugar levels should be reviewed by the patients doctor on a regular basis. The medications used for treating type 2 diabetes have the following aims: To regulate blood sugar levels. To prevent or treat complications due to type 2 diabetes. Medication to lower blood sugar levels Medications available to lower blood sugar can be divided into two groups, namely insulin, which can only be injected or delivered by glucose pump, and all other anti- diabetic medication except insulin. So, if you have been diagnosed with type 2 diabetes, how will your doctor start your medication? This is the step- by- step action plan for type 2 diabetics, based on 2. National Diabetes Advisory Board of SA. Step. 1: Lifestyle modification + metformin (for obese people, 1- 3 doses per day), or. Lifestyle modification + sulphonylureas (for non- obese people). If good blood glucose control is not achieved within 3 months (Hb. A1 > 7%), your doctor will proceed to step 2. A. Step 2. A: Add a second drug from a different class. The second drug may be one of the following: Metformin or sulphonylurea or basal insulin or pioglitazone (a thiazolidinedione). NOTE: Although not incorporated into the 2. Newer medications such as DPP- 4 inhibitors and incretin mimetics (see below) are more and more used as the second drug, while many experts advocate the use of insulin sooner rather than later. Step 2. B: If blood sugar levels are still not controlled within another 3 months, add a third drug from a different class. If blood sugar levels are still not controlled within another 3 months, your doctor will either start biphasic insulin or refer you to a specialist for intensive insulin therapy. Non- insulin medication options Most of these medications are available in tablet format (known as oral hypoglycaemic agents (OHAs), which literally means glucose- lowering medication taken by mouth). However, one of the newer generation anti- diabetic medications is only available as an injection. There is an increasing array of tablets that are now effective in lowering glucose levels in type 2 diabetics. They differ in their modes of action, side- effects, cost and dosing schedule. The choice of the most suitable one needs to be made on an individual basis after a full medical assessment. The main groups of oral blood glucose- lowering tablets are: A. Biguanides (e. g. C. Thiazolidinediones (relatively new)D. Alpha- glucosidase inhibitors (a recently developed class)E. Meglitinides (also new)F. Incretin mimetics (GLP- 1 agonists, also new)G. Diabetic Nephropathy. CLINICAL DIABETESVOL. Winter 2. 00. 0FEATURE ARTICLEDiabetic. Nephropathy. Timothy. C. Evans, MD, Ph. D, and Peter Capell, MDDiabetes is the most. United States today. Screening for the earliest. Diabetes is the most common cause. ESRD) in the United States today. Approximately. 4. ESRD, although the incidence is substantially higher in certain ethnic. This is thought to be a potentially preventable. Sensitive tests are available to identify patients with renal involvement early. For these. reasons, it is imperative that clinicians who care for patients with diabetes be. The pathophysiologic mechanisms of diabetic. The earliest. demonstrable abnormalities include intrarenal hypertension, hyperfiltration (increased. Clinically, the most important. Risk factors for development of diabetic. Key elements in the primary care of diabetes include. In general. the goal for glycemic control is a blood glucose level as close to normal (Hb. A1c. < 7%) as possible without causing dangerous hypoglycemia. Blood pressure control is at. Screening for diabetic nephropathy. DEFINITION OF TERMSFor purposes of. More. specifically, diabetic nephropathy is thought of in stages, the first being that. This may. progress to macroalbuminuria, or overt nephropathy (> 3. Later still, progressive renal functional decline characterized by decreased GFR. ESRD. Glucose combines with many proteins in. AGEs). The best known of these is glycosylated hemoglobin, a. Hemoglobin A1c (Hb. A1c) is a. specific member of this group and is useful as an indicator of average glycemia during the. The assay of Hb. A1c was standardized for the. Diabetes Control and Complications Trial (DCCT) and is now widely accepted as the standard. Other AGEs are presumed to contribute to the. EPIDEMIOLOGYDiabetes and its. United States today. Costs of caring for. Diabetic nephropathy accounts for 3. ESRD in the United States today. Patients with type 1 diabetes are at highest. There is evidence that the incidence of renal failure in type 1 diabetes. The. incidence of renal complications in type 2 diabetes, however, may be increasing. In the San Antonio Heart Study,9 the incidence of new- onset type 2 diabetes. Among non- Hispanic whites, the several- fold increased incidence was borderline. P = 0. 0. 7). Since type 2 diabetes accounts for at least 9. ESRD exceeds. those with type 1 diabetes overall. The prevalence of microalbuminuria in patients with. Hypertension. occurs in 5. Concomitant nephropathy in patients with diabetes and hypertension results in a 3. Important clinical concomitants of diabetic. Nearly all patients with diabetic. This has important implications for. The. reverse is not as frequently true. That is, a much lower percentage of patients with. Diabetic renal disease is also closely. The presence of microalbuminuria is a powerful. Thus, the presence of diabetes, especially. In addition to direct. ETIOLOGYA variety of. By definition, hyperglycemia is a. Most significant, however, is the presence. Genetics and Ethnicity. Although a sizable. ESRD. In. addition to the risks of poor glycemic control and hypertension, a subset of patients may. Familial. clustering of patients with nephropathy may result from similarly poor glycemic or blood. Diabetic siblings of patients with diabetes and. There is a strong concordance of. In a. study of Brazilian families with two or more diabetic members, the presence of diabetic. Postulates have been advanced linking diabetic. In a study of 8. 9. Moreover, the parents of patients with. Familial clustering and the beneficial effects. ACE) inhibition on diabetic nephropathy have also led to. Increased levels of ACE. ACE gene. 2. 0 In a study of type 1 patients with. ESRD compared with type 1 patients with diabetes for at least 1. DD genotype at the ACE locus increased the risk of. ESRD is known to be more prevalent in certain. Native Americans, Mexican Americans, and African Americans—than in. Caucasian Americans. Certainly, there is reason for special vigilance for early signs of. Hyperglycemia. It is well. Nephropathy is uncommon in patients with Hb. A1c consistently. At the very least, glucose is a meaningful. DCCT2. 3 and other treatment trials that demonstrate decreased. Other hyperglycemia- dependent metabolic. AGEs and. polyols. AGEs are the result of nonenzymatic covalent attachment of glucose to proteins. Proteins of many types are affected by this process, and. AGEs have been shown to correlate with microalbuminuria. In a study of low- and high- molecular- weight AGEs in subjects with. AGE content in arterial wall collagen was fourfold higher in. Diabetic patients with ESRD had twice as much tissue AGE as. Circulating AGEs were elevated in patients with diabetes. Flux through the polyol pathway beginning with. Clinical trials of aldose reductase inhibitors. Hypertension. Hypertension is. In the glomerulus, an early. Renal. responsiveness to the renin- angiotensin system may be abnormal in the diabetic kidney. For these reasons, agents that help to correct the abnormal intraglomerular pressures are. ACE inhibitors. specifically decrease the efferent arteriolar pressure, thereby decreasing intraglomerular. Particularly after microalbuminuria is present. Analysis of a number of risk factors showed a 1. PATHOPHYSIOLOGYThe key. With. renal damage, there is progressive thickening of the basement membrane, pathologic change. AGEs, accumulation of polyols via the aldose. C. 2. 2,3. 0,3. 1 Passage of. The renal hemodynamic abnormality is similar in. An early physiologic abnormality is glomerular. This is accompanied by the onset of microalbuminuria, the first practical evidence of. This is a critical time in the evolution of diabetic renal. A clinically asymptomatic period of decline. Once overt nephropathy (macroalbuminuria). GFR of. 2. The rate of decline depends on type of diabetes, genetic. Hypertension is. the single most important cause of progression and point of successful intervention in. Later stages may also be accompanied by clinically significant. Eventually, the characteristic clinical. SCREENINGIt has become clear over time that once overt nephropathy has developed, treatment is a. Though not all patients with early renal. ESRD, the likelihood is much greater among. Ideally, it would be useful to be able to predict which patients. ESRD before onset, but there is currently no way to definitively identify. Consequently, a high priority in the care of patients. For this reason, regular screening. Among the earliest changes demonstrable in. This is accompanied by. Eighty. percent of type 1 diabetes patients with microalbuminuria will progress to overt. Of those, 5. 0% will develop ESRD within 1. Among patients with. Standard urinalysis dipsticks are not. If protein is detectable on a standard urinalysis dipstick. In. type 1 diabetes, annual screening should begin after puberty and 5 years after initial. In type 2 diabetes, because of the likelihood that diabetes has been present. Despite the importance of microalbuminuria. In a study. of more than 1,0. However, only 1. 7% screened type 1. Several methods are available for screening and. The gold standard is the 2. Somewhat more convenient for the patient is the albumin/creatinine ratio on a. Measuring albumin. Clinicians should remember that there is a. Thus, measurement on collections of less than 2. There is also considerable variation from day to day, so three. Median survival after the onset of nephropathy has. Benefits accrue not only in younger patients. Both glycemic control and rigorous control of. Identification of patients with microalbuminuria selects a. Studies in both type 1 and type 2. ACE inhibitors leads to decreased albumin excretion and may. The importance of prevention cannot be. Once overt nephropathy is present, progression cannot be halted. It is much more effective to screen for early nephropathy with sensitive. Additional targets of potential intervention. AGEs, the polyol pathway, and systemic and intrarenal. Earlier trials of inhibitors of the. Glycemic Control. Tight glycemic. control has been shown in several studies to decrease the risk of microvascular disease in. In the DCCT, intensive glucose. In the United. Kingdom Prospective Diabetes Study (UKPDS), there was a 3. The DCCT benefit in type 1 diabetes was. Hb. A1c (9. 0. In the UKPDS. Hb. A1c (7. 9. This suggests. Furthermore, it suggests that this benefit can be attained in patients. Glycemic control remains critical in stabilizing. As noted above, not only was. DCCT, but. also secondary progression from microalbuminuria to macroalbuminuria was slowed. A similar result was found in the Steno studies. Very persuasive was a study. All patients had lesions of diabetic nephropathy, from mild to advanced, at the time of. At 5 years after. At 1. 0 years, however, albumin excretion had returned to normal. In general, the goal for glycemic control is. Specific goals outlined by the American. Diabetes Association (ADA) for optimum glycemic control include preprandial blood glucose. In the. enalapril- treated group during this 4- year period, however, albumin excretion decreased. There was no change in creatinine. Hb. A1c in either group, suggesting that the. ACE inhibitor was independent of its systemic antihypertensive. The debate is expanding to include normotensive. ACE inhibitors in preventing diabetic. In a double- blind. After 6 years, microalbuminuria developed in 1. During this period, creatinine clearance decreased at a rate of 2. Hb. A1c. decreased slightly in both groups, and blood pressure remained normal. If confirmed and. Currently most evidence and published guidelines. ACE inhibitors as first- choice antihypertensives in patients with diabetes. The extent of blood- pressure lowering, however, rather than the class of antihypertensive. Blood pressure. < 1. Hg is associated with preserved renal function. Calcium- channel blocking agents have been shown to have beneficial effects,3. ACE inhibition and calcium- channel blockade have shown positive. Evidence is accumulating that.
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