Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.
A chronic metabolic disorder marked by hyperglycemia. DM results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and the developing fetus and the placenta during pregnancy. Type 1 or insulin-dependent DM has a prevalence of just 0.3 to 0.4%. Type 2 DM (formerly called adult-onset DM) has a prevalence in the general population of 6.6%. In some populations (such as older persons, Native Americans, African Americans, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM usually occurs in children, most of whom are active and thin, although extremely obese children are now being diagnosed with type 2 diabetes as well. See: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon
There is currently no cure for diabetes. The condition, however, can be managed so that patients can live a relatively normal life. Treatment of diabetes focuses on two goals: keeping blood glucose within normal range and preventing the development of long-term complications. Careful monitoring of diet, exercise, and blood glucose levels are as important as the use of insulin or oral medications in preventing complications of diabetes. In 2003, the American Diabetes Association updated its Standards of Care for the management of diabetes. These standards help manage health care providers in the most recent recommendations for diagnosis and treatment of the disease.
People with type 1 diabetes are unable to produce any insulin at all. People with type 2 diabetes still produce insulin, however, the cells in the muscles, liver and fat tissue are inefficient at absorbing the insulin and cannot regulate glucose well. As a result, the body tries to compensate by having the pancreas pump out more insulin. But the pancreas slowly loses the ability to produce enough insulin, and as a result, the cells don’t get the energy they need to function properly.
Not all people with diabetes need drug therapy. A healthy eating plan and exercise alone can be enough if the person makes significant lifestyle changes. Other signs, symptoms, and complications also may need treatment. For example, nutritional deficiencies should be corrected, heart or kidney disease may need to be treated, and vision must be checked for eye problems like diabetic retinopathy.
Talking to a counselor or therapist may help you cope with the lifestyle changes that come with a type 2 diabetes diagnosis. You may find encouragement and understanding in a type 2 diabetes support group. Although support groups aren't for everyone, they can be good sources of information. Group members often know about the latest treatments and tend to share their own experiences or helpful information, such as where to find carbohydrate counts for your favorite takeout restaurant. If you're interested, your doctor may be able to recommend a group in your area.
The woman’s weight may also play a role. Changing hormone levels and weight gain are part of a healthy pregnancy, but both changes make it more difficult for the body to keep up with its need for insulin. This may lead to gestational diabetes. As pregnancy progresses, the placenta also produces insulin-blocking hormones, which might result in a woman’s blood-glucose levels becoming elevated if there isn’t enough insulin to counter this effect.
Diabetes is a metabolic disorder that occurs when your blood sugar (glucose), is too high (hyperglycemia). Glucose is what the body uses for energy, and the pancreas produces a hormone called insulin that helps convert the glucose from the food you eat into energy. When the body either does not produce enough insulin, does not produce any at all, or your body becomes resistant to the insulin, the glucose does not reach your cells to be used for energy. This results in the health condition termed diabetes.
It is clearly established that diabetes mellitus is not a single disease but a genetically heterogeneous group of disorders that share glucose intolerance in common (4–7). The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder. Diabetes and glucose intolerance are not diagnostic terms, but, like anemia, simply describe symptoms and/or laboratory abnormalities that can have a number of distinct etiologies.
The problem with sugar, regardless of type, is the sheer amount of it that’s found in the Standard American Diet (SAD), which is the typical eating plan many people in the United States — as well as those in an increasing number of modernized countries — have developed a taste for. When consumed in excess, foods in this category can lead to heart disease, stroke, and other serious health issues. “Often, foods with added sugar also contain fat,” explains Grieger, noting that these components go hand in hand when it comes to the risk for insulin resistance, the hallmark of type 2 diabetes.
Jump up ^ Farmer, AJ; Perera, R; Ward, A; Heneghan, C; Oke, J; Barnett, AH; Davidson, MB; Guerci, B; Coates, V; Schwedes, U; O'Malley, S (27 February 2012). "Meta-analysis of individual patient data in randomised trials of self monitoring of blood glucose in people with non-insulin treated type 2 diabetes". The BMJ. 344: e486. doi:10.1136/bmj.e486. PMID 22371867.
For example, the environmental trigger may be a virus or chemical toxin that upsets the normal function of the immune system. This may lead to the body’s immune system attacking itself. The normal beta cells in the pancreas may be attacked and destroyed. When approximately 90% of the beta cells are destroyed, symptoms of diabetes mellitus begin to appear. The exact cause and sequence is not fully understood but investigation and research into the disease continues.
Despite our efforts, patients are still likely to suffer myocardial infarction. The Diabetes mellitus, Insulin Glucose infusion in Acute Myocardial Infarction (DIGAMI) study236,237 reported on treating subjects with acute myocardial infarction and either diabetes or raised random plasma glucose (i.e., not necessarily diabetic) with either an intensive insulin infusion and then a four-times daily insulin regimen or conventional treatment. Over a mean follow-up of 3.4 years, there was a 33% death rate in the treatment group compared with a 44% death rate in the control group, an absolute reduction in mortality of 11%. The effect was greatest among the subgroup without previous insulin treatment and at a low cardiovascular risk. Evidence is continuing to accumulate that the diabetic person should have a glucose/insulin infusion after a myocardial infarction.
^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
Glucagon is a hormone that causes the release of glucose from the liver (for example, it promotes gluconeogenesis). Glucagon can be lifesaving and every patient with diabetes who has a history of hypoglycemia (particularly those on insulin) should have a glucagon kit. Families and friends of those with diabetes need to be taught how to administer glucagon, since obviously the patients will not be able to do it themselves in an emergency situation. Another lifesaving device that should be mentioned is very simple; a medic-alert bracelet should be worn by all patients with diabetes.
Doctors can monitor treatment using a blood test called hemoglobin A1C. When the blood glucose levels are high, changes occur in hemoglobin, the protein that carries oxygen in the blood. These changes are in direct proportion to the blood glucose levels over an extended period. The higher the hemoglobin A1C level, the higher the person's glucose levels have been. Thus, unlike the blood glucose measurement, which reveals the level at a particular moment, the hemoglobin A1Cmeasurement demonstrates whether the blood glucose levels have been controlled over the previous few months.
FASTING GLUCOSE TEST. Blood is drawn from a vein in the patient's arm after a period at least eight hours when the patient has not eaten, usually in the morning before breakfast. The red blood cells are separated from the sample and the amount of glucose is measured in the remaining plasma. A plasma level of 7.8 mmol/L (200 mg/L) or greater can indicate diabetes. The fasting glucose test is usually repeated on another day to confirm the results.
A: There are two scenarios to consider here, pregnant patients who have diabetes and pregnant patients who have gestational diabetes. Gestational diabetes describes hyperglycemia discovered during pregnancy. This hyperglycemia often corrects itself after pregnancy, but women who experience gestational diabetes are at higher for developing type-2 diabetes later in life when compared to women who experience no hyperglycemia during pregnancy. Regardless of the type of diabetes a pregnant patient has, her physician will closely monitor her disease and its response to therapy. Proper glucose control is important not only for the health of the mother, but also her developing child.
In the exchange system, foods are divided into six food groups (starch, meat, vegetable, fruit, milk, and fat) and the patient is taught to select items from each food group as ordered. Items in each group may be exchanged for each other in specified portions. The patient should avoid concentrated sweets and should increase fiber in the diet. Special dietetic foods are not necessary. Patient teaching should emphasize that a diabetic diet is a healthy diet that all members of the family can follow.
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance
Type 1 diabetes is considered an autoimmune disease. With an autoimmune disease, your immune system – which helps protect your body from getting sick – is engaged in too little or too much activity. In Type 1 diabetes, beta cells, which are a kind of cell in the pancreas that produces insulin, are destroyed. Our bodies use insulin to take the sugar from carbohydrates we eat and create fuel. With Type 1 diabetes, your body does not produce insulin, and that's why you need to use insulin as part of your treatment.
What are symptoms of type 2 diabetes in children? Type 2 diabetes is becoming increasingly common in children, and this is linked to a rise in obesity. However, the condition can be difficult to detect in children because it develops gradually. Symptoms, treatment, and prevention of type 2 diabetes are similar in children and adults. Learn more here. Read now