Diabetes Types 1 & 2 PDF

Type 1 Diabetes Type 1 diabetes accounts for approximately 5% of all diabetes cases. In the past, type 1 diabetes was called juvenile-onset diabetes mellitus or insulin-dependent diabetes mellitus (IDDM). However, these terms have fallen out of favor because type 2 diabetes is becoming more common...

Type 1 Diabetes Type 1 diabetes accounts for approximately 5% of all diabetes cases. In the past, type 1 diabetes was called juvenile-onset diabetes mellitus or insulin-dependent diabetes mellitus (IDDM). However, these terms have fallen out of favor because type 2 diabetes is becoming more common in children, and many people with type 2 diabetes use insulin to manage their diabetes. In general, type 1 diabetes develops during childhood or adolescence, and symptom onset is relatively abrupt. That being said, type 1 diabetes can develop during adulthood. The primary defect in type 1 diabetes is destruction of pancreatic β cells---the cells responsible for insulin synthesis and release into the bloodstream. Insulin levels are reduced early in the disease and usually fall to zero later. β cell destruction is the result of an autoimmune process (i.e., the patient\'s immune system inappropriately wages war against its own β cells). The trigger for this immune response is not entirely known, but genetic, environmental, and infectious factors likely play a role. Type 2 Diabetes Type 2 diabetes is the most prevalent form of diabetes, accounting for 90% to 95% of all diagnosed cases. In the past, type 2 diabetes was called non--insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes mellitus. As discussed previously for type 1 diabetes, these terms are no longer clinically useful because insulin is commonly used by people with type 2 diabetes and type 2 diabetes can occur in all age groups. The disease most commonly begins in middle age and progresses gradually. In contrast to type 1 diabetes, type 2 diabetes carries little risk for ketoacidosis. However, type 2 diabetes does carry the same long-term risks as type 1 diabetes (see later). Symptoms of type 2 diabetes usually result from a combination of insulin resistance and impaired insulin secretion. In contrast to patients with type 1 diabetes, those with type 2 diabetes are capable of insulin synthesis. In fact, early in the disease, insulin levels tend to be normal or slightly elevated, a state known as hyperinsulinemia. However, although insulin is still produced, its secretion is no longer tightly coupled to plasma glucose level: release of insulin is delayed, and peak output is subnormal. More important, the target tissues of insulin (liver, muscle, adipose tissue) exhibit insulin resistance: for a given blood insulin level, cells in these tissues are less able to take up and metabolize the glucose available to them. Insulin resistance appears to result from three causes: reduced binding of insulin to its receptors, reduced receptor numbers, and reduced receptor responsiveness. Over time, hyperglycemia leads to diminished pancreatic β cell function, and hence insulin production and secretion eventually decline as the β cells work harder to overcome insulin resistance within the tissues. Although the underlying causes of type 2 diabetes are not entirely known, there is a strong familial association, suggesting that genetics play a role. This possibility was reinforced by a study that implicated the gene for insulin receptor substrate-2 (IRS-2), a compound that helps mediate intracellular responses to insulin. Diabetes and Pregnancy Although insulin therapy has greatly improved outcomes, successful management of the diabetic pregnancy remains a challenge. Three factors contribute to the problem. First, the placenta produces hormones that antagonize insulin\'s actions. Second, production of cortisol, a hormone that promotes hyperglycemia, increases threefold during pregnancy. Both factors increase the body\'s need for insulin. And third, because glucose can pass freely from the maternal circulation to the fetal circulation, hyperglycemia in the mother will stimulate excessive secretion of insulin in the fetus. The resultant hyperinsulinism can have multiple adverse effects on the fetus. Successful management of diabetes during pregnancy demands that proper glucose levels be maintained in both the mother and fetus; failure to do so may be teratogenic or may otherwise harm the fetus. Achieving glucose control requires diligence on the part of the mother and her prescriber. Some experts on diabetes in pregnancy advise that blood glucose levels must be monitored six to seven times a day. Insulin dosage and food intake must be adjusted accordingly. Gestational diabetes is defined as diabetes that appears in the pregnant patient during pregnancy and then subsides rapidly after delivery. Gestational diabetes is managed in much the same manner as any other diabetic pregnancy: blood glucose should be monitored and then controlled with diet and insulin. In most cases the diabetic state disappears almost immediately after delivery, permitting discontinuation of insulin. However, if the diabetic state persists beyond parturition, it is no longer considered gestational and should be rediagnosed and treated accordingly. In women taking an oral drug for type 2 diabetes, current practice is to discontinue the oral drug and switch to insulin. The only exception is the oral agent metformin, which is often satisfactory for managing type 2 diabetes in pregnancy. Women who discontinue oral medications can resume oral therapy after delivery. Diagnosis Diagnosis of diabetes was once made solely by measuring blood levels of glucose. However, hemoglobin A1c---a test that provides an estimate of glycemic control over the previous 2 to 3 months is now considered a standard test as well. Tests Based on Blood Levels of Glucose Excessive plasma glucose is diagnostic of diabetes. Several tests may be used: a fasting plasma glucose (FPG) test, a casual plasma glucose test, and an oral glucose tolerance test (OGTT). To make a definitive diagnosis, the patient must be tested on two separate days, and both tests must be positive. Any combination of two tests (e.g., two FPG tests; one FPG test and one OGTT) may be used. Fasting plasma glucose test. To determine FPG levels, blood is drawn at least 8 hours after the last meal. In normoglycemic individuals, FPG levels are less than 100 mg/dL. If FPG glucose levels are 126 mg/dL or higher, diabetes is present. Random plasma glucose test. For this test, blood can be drawn at any time, without regard to meals. Fasting is not required. Of note, the test can be performed in the office, using a finger-stick blood sample and the same type of test device used by patients at home. A plasma glucose level that is 200 mg/dL or greater suggests diabetes. However, to make a definitive diagnosis, the patient must also display classic signs of diabetes: polyuria, polydipsia, and rapid weight loss. Ketonuria may also be present, but only if blood glucose is extremely high. Oral glucose tolerance test. This test is often used when diabetes is suspected but could not be definitively diagnosed by measuring fasting or casual plasma glucose levels. The OGTT is performed by giving an oral glucose load (equivalent to 75 g of anhydrous glucose) and measuring plasma glucose levels 2 hours later. In individuals who do not have diabetes, 2-hour glucose levels will be less than 140 mg/dL. Diabetes is suggested if 2-hour plasma glucose levels are 200 mg/dL or greater. The OGTT test is more expensive and time consuming than the alternatives and is not used routinely. Hemoglobin A1c As described later under "Monitoring Treatment," levels of hemoglobin A1c, or simply A1c, reflect average blood glucose levels over the previous 2 to 3 months. Accordingly, if a patient\'s A1c is high, we know that the patient\'s glucose levels have been high for a relatively long time. In other words, we know that the patient has diabetes. An A1c value of 6.5% or higher is considered diagnostic. It is important to note that the A1c test is not necessarily accurate in all patients because some people have conditions that can affect hemoglobin levels, thus skewing the results of this test. Among these are pregnancy, chronic kidney or liver disease, recent severe bleeding or blood transfusion, and certain blood disorders, including thalassemia, iron deficiency anemia, and anemia related to vitamin B12 deficiency. Increased Risk for Diabetes (Prediabetes) Increased risk for diabetes (sometimes referred to as prediabetes) is a state defined by impaired FPG (between 100 and 125 mg/dL) or impaired glucose tolerance (2-hour OGTT result of 140 to 199 mg/dL). These values are below those that define diabetes but are too high to be considered normal. People with "prediabetes" are at increased risk for developing type 2 diabetes and cardiovascular disease (CVD)---but not the microvascular complications associated with diabetes (i.e., retinopathy, nephropathy, neuropathy). The risk for CVD can be reduced by dietary modifications, increased physical activity, and, if indicated, use of appropriate drugs to control blood lipids and blood pressure. The risk for progression to diabetes may be reduced by diet and exercise and possibly by certain oral antidiabetic drugs (such as metformin). It is important to note that many people who meet the criteria for prediabetes never go on to develop diabetes---even if they do not modify their lifestyle, and even if they do not take antidiabetic drugs. Hence, although prediabetes indicates an increased risk for diabetes, it by no means guarantees that diabetes will occur. Overview of Treatment The primary goal of treating type 1 or type 2 diabetes is prevention of long-term complications. To minimize complications, treatment must keep glucose levels as close to "normal" as safely possible. In addition, treatment must keep blood pressure and blood lipids within an acceptable range. In both type 1 and type 2 diabetes, proper diet and adequate physical activity are central components of management. Type 1 Diabetes Preventing complications of diabetes requires a comprehensive plan directed at glycemic control and reduction of cardiovascular risk factors. Glycemic control is accomplished with an integrated program of diet, self-monitoring of blood glucose (SMBG), physical activity, and insulin replacement. Of importance, glycemic control must be achieved safely, that is, adequately controlling glycemia while minimizing the risk for hypoglycemia. Insulin replacement. Among patients with type 1 diabetes, survival requires daily dosing with insulin. Before insulin replacement became available, people with type 1 diabetes invariably died within a few years after disease onset. The cause of death was usually ketoacidosis. It is essential to coordinate insulin dosage with carbohydrate intake. If carbohydrate intake is too great or too small with respect to insulin dosage, hyperglycemia or hypoglycemia will result. Although insulin is the cornerstone to the management of type 1 diabetes, the use of other medications as add-on therapy to insulin is currently under study. Managing hypertension and dyslipidemia. An angiotensin-converting enzyme (ACE) inhibitor (e.g., lisinopril) or an angiotensin II receptor blocker (ARB; e.g., losartan) can reduce the risk for diabetic nephropathy, a long-term consequence of poor glycemic control. These same drugs are preferred agents for managing diabetic hypertension. The current goal, as set by the American Diabetes Association (ADA), is to keep blood pressure at or less than 140/90 mm Hg, with lower systolic blood pressure targets (\