In people with type 1 diabetes, the symptoms often begin abruptly and dramatically. A serious condition called diabetic ketoacidosis, a complication in which the body produces excess acid, may quickly develop. In addition to the usual diabetes symptoms of excessive thirst and urination, the initial symptoms of diabetic ketoacidosis also include nausea, vomiting, fatigue, and—particularly in children—abdominal pain. Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity (see Acidosis), and the breath smells fruity and like nail polish remover. Without treatment, diabetic ketoacidosis can progress to coma and death, sometimes very quickly.
As with many conditions, treatment of type 2 diabetes begins with lifestyle changes, particularly in your diet and exercise. If you have type 2 diabetes, speak to your doctor and diabetes educator about an appropriate diet. You may be referred to a dietitian. It is also a good idea to speak with your doctor before beginning an exercise program that is more vigourous than walking to determine how much and what kind of exercise is appropriate.
The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.
Several tests are helpful in identifying DM. These include tests of fasting plasma glucose levels, casual (randomly assessed) glucose levels, or glycosylated hemoglobin levels. Diabetes is currently established if patients have classic diabetic symptoms and if on two occasions fasting glucose levels exceed 126 mg/dL (> 7 mmol/L), random glucose levels exceed 200 mg/dL (11.1 mmol/L), or a 2-hr oral glucose tolerance test is 200 mg/dL or more. A hemoglobin A1c test that is more than two standard deviations above normal (6.5% or greater) is also diagnostic of the disease.
Ketoacidosis, a condition due to starvation or uncontrolled diabetes, is common in Type I diabetes. Ketones are acid compounds that form in the blood when the body breaks down fats and proteins. Symptoms include abdominal pain, vomiting, rapid breathing, extreme lethargy, and drowsiness. Patients with ketoacidosis will also have a sweet breath odor. Left untreated, this condition can lead to coma and death.
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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.
A study by Dabelea et al found that in teenagers and young adults in whom diabetes mellitus had been diagnosed during childhood or adolescence, diabetes-related complications and comorbidities—including diabetic kidney disease, retinopathy, and peripheral neuropathy (but not arterial stiffness or hypertension)—were more prevalent in those with type 2 diabetes than in those with type 1 disease. [44]
Oral medications are available to lower blood glucose in Type II diabetics. In 1990, 23.4 outpatient prescriptions for oral antidiabetic agents were dispensed. By 2001, the number had increased to 91.8 million prescriptions. Oral antidiabetic agents accounted for more than $5 billion dollars in worldwide retail sales per year in the early twenty-first century and were the fastest-growing segment of diabetes drugs. The drugs first prescribed for Type II diabetes are in a class of compounds called sulfonylureas and include tolbutamide, tolazamide, acetohexamide, and chlorpropamide. Newer drugs in the same class are now available and include glyburide, glimeperide, and glipizide. How these drugs work is not well understood, however, they seem to stimulate cells of the pancreas to produce more insulin. New medications that are available to treat diabetes include metformin, acarbose, and troglitizone. The choice of medication depends in part on the individual patient profile. All drugs have side effects that may make them inappropriate for particular patients. Some for example, may stimulate weight gain or cause stomach irritation, so they may not be the best treatment for someone who is already overweight or who has stomach ulcers. Others, like metformin, have been shown to have positive effects such as reduced cardiovascular mortality, but but increased risk in other situations. While these medications are an important aspect of treatment for Type II diabetes, they are not a substitute for a well planned diet and moderate exercise. Oral medications have not been shown effective for Type I diabetes, in which the patient produces little or no insulin.
Morbidity and mortality stem from the metabolic derangements and from the long-term complications that affect small and large vessels, resulting in retinopathy, nephropathy, neuropathy, ischemic heart disease, and arterial obstruction with gangrene of extremities.2 The acute clinical manifestations can be fully understood in the context of current knowledge of the secretion and action of insulin.3 Genetic and other etiologic considerations implicate autoimmune mechanisms in the evolution of the most common form of childhood diabetes, known as type 1a diabetes.4,5 Genetic defects in insulin secretion are increasingly recognized and understood as defining the causes of monogenic forms of diabetes such as maturity-onset diabetes of youth (MODY) and neonatal DM and contributing to the spectrum of T2DM.6
Glucose is a simple sugar found in food. Glucose is an essential nutrient that provides energy for the proper functioning of the body cells. Carbohydrates are broken down in the small intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream, and is carried by the bloodstream to all the cells in the body where it is utilized. However, glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. Without insulin, the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. In certain types of diabetes, the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the midst of plenty". The abundant, unutilized glucose is wastefully excreted in the urine.
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
Information on mortality rates for type 1 diabetes mellitus is difficult to ascertain without complete national registers of childhood diabetes, although age-specific mortality is probably double that of the general population. [35, 36] Children aged 1-4 years are particularly at risk and may die due to DKA at the time of diagnosis. Adolescents are also a high-risk group. Most deaths result from delayed diagnosis or neglected treatment and subsequent cerebral edema during treatment for DKA, although untreated hypoglycemia also causes some deaths. Unexplained death during sleep may also occur and appears more likely to affect young males. [37]
All children with type 1 diabetes mellitus require insulin therapy. Most require 2 or more injections of insulin daily, with doses adjusted on the basis of self-monitoring of blood glucose levels. Insulin replacement is accomplished by giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is either long-acting (glargine or detemir) or intermediate-acting (NPH). The preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-acting (regular).

The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.
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.
"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas.
Type 2 diabetes, which is often diagnosed when a person has an A1C of at least 7 on two separate occasions, can lead to potentially serious issues, like neuropathy, or nerve damage; vision problems; an increased risk of heart disease; and other diabetes complications. A person’s A1C is the two- to three-month average of his or her blood sugar levels.
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