Diabetes has been coined the “silent killer” because the symptoms are so easy to miss. Over 24 million people in America have diabetes, so this is no tiny issue. Kids years ago hardly ever knew another child with diabetes, but such is no longer the case. Approximately 1.25 million children in the United States living with diabetes, which is very telling for state of health in America in 2016 when children are having to endure a medical lifestyle at such a young age.


According to the National Institutes of Health, the reported rate of gestational diabetes is between 2% to 10% of pregnancies. Gestational diabetes usually resolves itself after pregnancy. Having gestational diabetes does, however, put mothers at risk for developing type 2 diabetes later in life. Up to 10% of women with gestational diabetes develop type 2 diabetes. It can occur anywhere from a few weeks after delivery to months or years later.
Several common medications can impair the body's use of insulin, causing a condition known as secondary diabetes. These medications include treatments for high blood pressure (furosemide, clonidine, and thiazide diuretics), drugs with hormonal activity (oral contraceptives, thyroid hormone, progestins, and glucocorticorids), and the anti-inflammation drug indomethacin. Several drugs that are used to treat mood disorders (such as anxiety and depression) also can impair glucose absorption. These drugs include haloperidol, lithium carbonate, phenothiazines, tricyclic antidepressants, and adrenergic agonists. Other medications that can cause diabetes symptoms include isoniazid, nicotinic acid, cimetidine, and heparin. A 2004 study found that low levels of the essential mineral chromium in the body may be linked to increased risk for diseases associated with insulin resistance.

observations The onset of type 1 diabetes mellitus is sudden in children. Type 2 diabetes often begins insidiously. Characteristically the course is progressive and includes polyuria, polydipsia, weight loss, polyphagia, hyperglycemia, and glycosuria. The eyes, kidneys, nervous system, skin, and circulatory system may be affected by the long-term complications of either type of diabetes; infections are common; and atherosclerosis often develops. In type 1 diabetes mellitus, when no endogenous insulin is being secreted, ketoacidosis is a constant danger. The diagnosis is confirmed by fasting plasma glucose and history.
Recently, battery-operated insulin pumps have been developed that can be programmed to mimic normal insulin secretion more closely. A person wearing an insulin pump still must monitor blood sugar several times a day and adjust the dosage, and not all diabetic patients are motivated or suited to such vigilance. It is hoped that in the future an implantable or external pump system may be perfected, containing a glucose sensor. In response to data from the sensor the pump will automatically deliver insulin according to changing levels of blood glucose.
observations The onset of type 1 diabetes mellitus is sudden in children. Type 2 diabetes often begins insidiously. Characteristically the course is progressive and includes polyuria, polydipsia, weight loss, polyphagia, hyperglycemia, and glycosuria. The eyes, kidneys, nervous system, skin, and circulatory system may be affected by the long-term complications of either type of diabetes; infections are common; and atherosclerosis often develops. In type 1 diabetes mellitus, when no endogenous insulin is being secreted, ketoacidosis is a constant danger. The diagnosis is confirmed by fasting plasma glucose and history.
Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver of pregnancy. These cause DI by impairing hepatic clearance of circulating vasopressinase. It is important to consider these diseases if a woman presents with diabetes insipidus in pregnancy, because their treatments require delivery of the baby before the disease will improve. Failure to treat these diseases promptly can lead to maternal or perinatal mortality.
Lithium-induced nephrogenic DI may be effectively managed with the administration of amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics. Clinicians have been aware of lithium toxicity for many years, and traditionally have administered thiazide diuretics for lithium-induced polyuria and nephrogenic diabetes insipidus. However, amiloride has recently been shown to be a successful treatment for this condition.[16]
There is no known preventive measure for type 1 diabetes.[2] Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet.[2] Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%.[74] Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish.[75] Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes.[75] Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.[76]
The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.
At the end of the test, a health care provider will compare the patient's blood sodium, vasopressin levels, and urine concentration to determine whether the patient has diabetes insipidus. Sometimes, the health care provider may administer medications during the test to see if they increase a patient's urine concentration. In other cases, the health care provider may give the patient a concentrated sodium solution intravenously at the end of the test to increase the patient's blood sodium level and determine if he or she has diabetes insipidus.
Hypoglycemia, or low blood sugar, can be caused by too much insulin, too little food (or eating too late to coincide with the action of the insulin), alcohol consumption, or increased exercise. A patient with symptoms of hypoglycemia may be hungry, cranky, confused, and tired. The patient may become sweaty and shaky. Left untreated, the patient can lose consciousness or have a seizure. This condition is sometimes called an insulin reaction and should be treated by giving the patient something sweet to eat or drink like a candy, sugar cubes, juice, or another high sugar snack.
When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria).[64] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[62] In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).[65]
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.

If you have type 2 diabetes and your body mass index (BMI) is greater than 35, you may be a candidate for weight-loss surgery (bariatric surgery). Dramatic improvements in blood sugar levels are often seen in people with type 2 diabetes after bariatric surgery, depending on the procedure performed. Surgeries that bypass a portion of the small intestine have more of an effect on blood sugar levels than do other weight-loss surgeries.
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
The blood vessels and blood are the highways that transport sugar from where it is either taken in (the stomach) or manufactured (in the liver) to the cells where it is used (muscles) or where it is stored (fat). Sugar cannot go into the cells by itself. The pancreas releases insulin into the blood, which serves as the helper, or the "key," that lets sugar into the cells for use as energy.
Though it may be transient, untreated GDM can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.[54]
Patients with type 1 DM, unless they have had a pancreatic transplant, require insulin to live; intensive therapy with insulin to limit hyperglycemia (“tight control”) is more effective than conventional therapy in preventing the progression of serious microvascular complications such as kidney and retinal diseases. Intensive therapy consists of three or more doses of insulin injected or administered by infusion pump daily, with frequent self-monitoring of blood glucose levels as well as frequent changes in therapy as a result of contacts with health care professionals. Some negative aspects of intensive therapy include a three times more frequent occurrence of severe hypoglycemia, weight gain, and an adverse effect on serum lipid levels, i.e., a rise in total cholesterol, LDL cholesterol, and triglycerides and a fall in HDL cholesterol. Participation in an intensive therapy program requires a motivated patient, but it can dramatically reduce eye, nerve, and renal complications compared to conventional therapy. See: insulin pump for illus.
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