diabetes mellitus(redirected from Diabetes melitus)
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Types of diabetes mellitus
Causes and symptoms
- are obese (more than 20% above their ideal body weight)
- have a relative with diabetes mellitus
- belong to a high-risk ethnic population (African-American, Native American, Hispanic, or Native Hawaiian)
- have been diagnosed with gestational diabetes or have delivered a baby weighing more than 9 lbs (4 kg)
- have high blood pressure (140/90 mmHg or above)
- have a high density lipoprotein cholesterol level less than or equal to 35 mg/dL and/or a triglyceride level greater than or equal to 250 mg/dL
- have had impaired glucose tolerance or impaired fasting glucose on previous testing
- fenugreek (Trigonella foenum-graecum) has been shown in some studies to reduce blood insulin and glucose levels while also lowering cholesterol
- bilberry (Vaccinium myrtillus) may lower blood glucose levels, as well as helping to maintain healthy blood vessels
- garlic (Allium sativum) may lower blood sugar and cholesterol levels
- onions (Allium cepa) may help lower blood glucose levels by freeing insulin to metabolize them
- cayenne pepper (Capsicum frutescens) can help relieve pain in the peripheral nerves (a type of diabetic neuropathy)
- gingko (Gingko biloba) may maintain blood flow to the retina, helping to prevent diabetic retinopathy
Treatment of pituitary diabetes insipidus consists of administration of vasopressin. A synthetic analogue of vasopressin (DDAVP) can be administered as a nasal spray, providing antidiuretic activity for 8 to 20 hours, and is currently the drug of choice. Patient care includes instruction in self-administration of the drug, its expected action, symptoms that indicate a need to adjust the dosage, and the importance of follow-up visits. Patients with this condition should wear some form of medical identification at all times.
The American Diabetes Association sponsored an international panel in 1995 to review the literature and recommend updates of the classification of diabetes mellitus. The definitions and descriptions that follow are drawn from the Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. The report was first approved in 1997 and modified in 1999. Although other terms are found in older literature and remain in use, their use in current clinical practice is inappropriate. Epidemiologic and research studies are facilitated by use of a common language.
The Expert Committee notes that most cases of diabetes fall into two broad categories, which are called Type 1 and Type 2. There are also other specific types, such as gestational diabetes and impaired glucose homeostasis. See table for definitions of types of diabetes mellitus.
The typical symptoms of diabetes mellitus are the three “polys:” polyuria, polydipsia, and polyphagia. Because of insulin deficiency, the assimilation and storage of glucose in muscle adipose tissues, and the liver is greatly diminished. This produces an accumulation of glucose in the blood and creates an increase in its osmolarity. In response to this increased osmotic pressure there is depletion of intracellular water and osmotic diuresis. The water loss creates intense thirst and increased urination. The increased appetite (polyphagia) is not as clearly understood. It may be the result of the body's effort to increase its supply of energy foods even though eating more carbohydrates in the absence of sufficient insulin does not meet the energy needs of the cells.
Fatigue and muscle weakness occur because the glucose needed for energy simply is not metabolized properly. Weight loss in type 1 diabetes patients occurs partly because of the loss of body fluid and partly because in the absence of sufficient insulin the body begins to metabolize its own proteins and stored fat. The oxidation of fats is incomplete, however, and the fatty acids are converted into ketone bodies. When the kidney is no longer able to handle the excess ketones the patient develops ketosis. The overwhelming presence of the strong organic acids in the blood lowers the pH and leads to severe and potentially fatal ketoacidosis.
The metabolism of body protein when sufficient amounts of insulin are not available causes an elevated blood urea nitrogen. This first occurs because the nitrogen component of protein is discarded in the blood when the body metabolizes its own proteins to obtain the glucose it needs.
Persons with diabetes are prone to infection, delayed healing, and vascular disease. The ease with which poorly controlled diabetic persons develop an infection is thought to be due in part to decreased chemotaxis of leukocytes, abnormal phagocyte function, and diminished blood supply because of atherosclerotic changes in the blood vessels. An impaired blood supply means a deficit in the protective defensive cells transported in the blood. Excessive glucose allows organisms to grow out of control.
Another manifestation of diabetes mellitus is visual disturbance due to increased osmolarity of the blood and accumulation of fluid in the eyeball, which changes its shape. Once the diabetes is under control, visual problems should abate. Persistent vaginitis and urinary tract infection also may be symptoms of diabetes in females.
Visual impairment and blindness are common sequelae of uncontrolled diabetes. The three most frequently occurring problems involving the eye are diabetic retinopathy, cataracts, and glaucoma. photocoagulation of destructive lesions of the retina with laser beams can be used to delay further progress of pathologic changes and thereby preserve sight in the affected eye.
Another area of pathologic changes associated with diabetes mellitus is the nervous system (diabetic neuropathy), particularly in the peripheral nerves of the lower extremities. The patient typically experiences a “stocking-type” anesthesia beginning about 10 years after the onset of the disease. There may eventually be almost total anesthesia of the affected part with the potential for serious injury to the part without the patient being aware of it. In contrast, some patients experience debilitating pain and hyperesthesia, with loss of deep tendon reflexes.
Other problems related to the destruction of nerve tissue are the result of autonomic nervous system involvement. These include impotence, orthostatic hypotension, delayed gastric emptying, diarrhea or constipation, and asymptomatic retention of urine in the bladder.
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.
The protocol for therapy is determined by the type of diabetes; patients with either type 1 or type 2 must pay attention to their diet and exercise regimens. Insulin therapy may be prescribed for patients with type 2 diabetes as well as any who are dependent on insulin. In most cases, the type 2 diabetes patient can be treated effectively by reducing caloric intake, maintaining target weight, and promoting physical exercise.
Diet. In general, the diabetic diet is geared toward providing adequate nutrition with sufficient calories to maintain normal body weight; the intake of food is adjusted so that blood sugar and serum cholesterol levels are kept within acceptable limits. Overweight diabetic patients should limit caloric intake until target weight is achieved. In persons with type 2 diabetes this usually results in marked improvement and may eliminate the need for drugs such as oral hypoglycemic agents.
The patient, physician, nurse, and dietician must carefully evaluate the patient's life style, nutritional needs, and ability to comply with the proposed dietary prescription. There are a variety of meal planning systems that can be used by the patient with diabetes; each has benefits and drawbacks that need to be evaluated in order to maximize compliance. Two of the most frequently used ones are the exchange system (see accompanying table) and the carbohydrate counting system.
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.
The carbohydrate counting system focuses on matching the unit of insulin to the total number of grams of carbohydrate in food eaten. This system is the most accurate method for calculating insulin to food intake.
It is especially important that persons with diabetes who are taking insulin not skip meals; they must also be sure to eat the prescribed amounts at the prescribed times during the day. Since the insulin-dependent diabetic needs to match food consumption to the available insulin, it is advantageous to increase the number of daily feedings by adding snacks between meals and at bedtime.
Exercise. A program of regular exercise gives anyone a sense of good health and well-being; for persons with diabetes it gives added benefits by helping to control blood glucose levels, promoting circulation to peripheral tissues, and strengthening the heart beat. In addition, there is evidence that exercise increases the number of insulin receptor sites on the surface of cells and thus facilitates the metabolism of glucose. Many specialists in diabetes consider exercise so important in the management of diabetes that they prescribe rather than suggest exercise.
Persons with diabetes who take insulin must be careful about indulging in unplanned exercise. Strenuous physical activity can rapidly lower their blood sugar and precipitate a hypoglycemic reaction. For a person whose blood glucose level is over 250 mg/dl, the advice would be not to exercise at all. At this range, the levels of insulin are too low and the body would have difficulty transporting glucose into exercising muscles. The result of exercise would be a rise in blood glucose levels.
Insulin Therapy. Exogenous insulin is given to patients with diabetes mellitus as a supplement to the insufficient amount of endogenous insulin that they produce. In some cases, this must make up for an absolute lack of insulin from the pancreas. Exogenous insulin is available in various types. It must be given by injection, usually subcutaneously, and because it is a potent drug, the dosage must be measured meticulously. Commonly, regular insulin, which is a fast-acting insulin with a short span of action, is mixed with one of the longer-acting insulins and both types are administered in one injection.
Human insulin (Humulin) is produced by recombinant DNA technology. This highly purified biosynthetic insulin reduces the incidence of allergic reactions and the changes in subcutaneous tissues (lipodystrophy) at sites of injection.
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.
Oral Agents. Oral antidiabetic drugs (see hypoglycemic agents) are sometimes prescribed for patients with type 2 diabetes who cannot control their blood glucose with diet and exercise. These are not oral forms of insulin; they are sulfonylureas, chemically related to the sulfonamide antibiotics. Patients receiving them should be taught that the drug they are taking does not eliminate the need for a diet and exercise program. Only the prescribed dosage should be taken; it should never be increased to make up for dietary indiscretions or discontinued unless authorized by the physician.
1. Monitoring of blood glucose status. In the past, urine testing was an integral part of the management of diabetes, but it has largely been replaced in recent years by self monitoring of blood glucose. Reasons for this are that blood testing is more accurate, glucose in the urine shows up only after the blood sugar level is high, and individual renal thresholds vary greatly and can change when certain medications are taken. As a person grows older and the kidney is less able to eliminate sugar in the urine, the renal threshold rises and less sugar is spilled into the urine. The position statement of the American Diabetes Association on Tests of Glycemia in Diabetes notes that urine testing still plays a role in monitoring in type 1 and gestational diabetes, and in pregnancy with pre-existing diabetes, as a way to test for ketones. All people with diabetes should test for ketones during times of acute illness or stress and when blood glucose levels are consistently elevated.
2. Home glucose monitoring using either a visually read test or a digital readout of the glucose concentration in a drop of blood. Patients can usually learn to use the necessary equipment and perform finger sticks. They keep a daily record of findings and are taught to adjust insulin dosage accordingly. More recent glucose monitoring devices can draw blood from other locations on the body, such as the forearm.
3. Pathophysiology of diabetes mellitus, including functions of the pancreas and the long-term effects of uncontrolled diabetes.
4. Insulin administration (if appropriate), including types of insulin and syringes, rotation of sites of injection, injection techniques, and pump therapy instructions.
5. Signs and symptoms ofhyperglycemiaandhypoglycemia, and measures to take when they occur. (See accompanying table.) It is important for patients to become familiar with specific signs that are unique to themselves. Each person responds differently and may exhibit symptoms different from those experienced by others. It should be noted that the signs and symptoms may vary even within one individual. Thus it is vital that the person understand all reactions that could occur. When there is doubt, a simple blood glucose reading will determine the actions that should be taken.
6. Oral antidiabetic agents, including information about drug-drug interactions, proper administration, and potential side effects.
7. Personal hygiene and activities of daily living, including general skin care, foot care, treatment of minor injuries to avoid infection, a formal exercise program as well as exercise at school or at work, recreational activity, and travel.
8. Identification tag and card and needed medical information.
9. Information on what to do on “sick days” when nausea, vomiting, or respiratory infection can interfere with the usual meals and exercise.
10. Importance of keeping appointments and staying in touch with a health care provider for consultation and assessment. Periodic evaluation of the binding of glucose to hemoglobin (glycosylated hemoglobin or hemoglobin A1C testing) can give information about the effectiveness of the prescribed regimen and whether any changes need to be made. The ADA position statement on tests of glycemia in diabetes recommends routine testing for all patients with diabetes. It should be a part of the initial assessment of the patient, with subsequent measurements every three months to determine if the patient's metabolic control has been reached and maintained.
di·a·be·tes mel·li'·tus (DM),
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
diabetes mellitus(mə-lī′təs, mĕl′ĭ-)
diabetes mellitus (DM)
diabetes mellitusEndocrinology A chronic condition which affects ±10% of the general population, characterized by ↑ serum glucose and a relative or absolute ↓ in pancreatic insulin production, or ↓ tissue responsiveness to insulin; if not properly controlled, the excess glucose damages blood vessels of the eyes, kidneys, nerves, heart Types Insulin dependent–type I and non-insulin dependent–type II diabetes Symptoms type 1 DM is associated with ↑ urine output, thirst, fatigue, and weight loss (despite an ↑ appetite), N&V; type 2 DM is associated with, in addition, non-healing ulcers, oral and bladder infections, blurred vision, paresthesias in the hands and feet, and itching Cardiovascular MI, stoke Eyes Retinal damage, blindness Legs/feet Nonhealing ulcers, cuts leading to gangrene and amputation Kidneys HTN, renal failure Neurology Paresthesias, neuropathy Diagnosis Serum glucose above cut-off points after meals or when fasting; once therapy is begun, serum levels of glycosylated Hb are measured periodically to assess adequacy of glucose control Management Therapy reflects type of DM; metformin and triglitazone have equal and additive effects on glycemic control Prognosis A function of stringency of glucose control and presence of complications. See ABCD Trial, Brittle diabetes, Bronze diabetes, Chemical diabetes, Gestational diabetes, Insulin-dependent diabetes, Metformin, MODY diabetes, Nephrogenic diabetes insipidus, Non-insulin-dependent diabetes mellitus, Pseudodiabetes, Secondary diabetes, Starvation diabetes, Troglitazone.
di·a·be·tes mel·li·tus(DM) (dī-ă-bē'tēz me-lī'tŭs)
See also: Type 1 diabetes, Type 2 diabetes
diabetes mellitusAbbreviation: DM
Type 1 DM usually presents as an acute illness with dehydration and often diabetic ketoacidosis. Type 2 DM is often asymptomatic in its early years. The American Diabetes Association (1-800-DIABETES) estimates that more than 5 million Americans have type 2 DM without knowing it.
Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.
Classic symptoms of DM are polyuria, polydipsia, and weight loss. In addition, patients with hyperglycemia often have blurred vision, increased food consumption (polyphagia), and generalized weakness. When a patient with type 1 DM loses metabolic control (such as during infections or periods of noncompliance with therapy), symptoms of diabetic ketoacidosis occur. These may include nausea, vomiting, dizziness on arising, intoxication, delirium, coma, or death. Chronic complications of hyperglycemia include retinopathy and blindness, peripheral and autonomic neuropathies, glomerulosclerosis of the kidneys (with proteinuria, nephrotic syndrome, or end-stage renal failure), coronary and peripheral vascular disease, and reduced resistance to infections. Patients with DM often also sustain infected ulcerations of the feet, which may result in osteomyelitis and the need for amputation.
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.
DM types 1 and 2 are both treated with specialized diets, regular exercise, intensive foot and eye care, and medications.
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.
Some patients with type 2 DM can control their disease with a calorically restricted diet (for instance 1600 to 1800 cal/day), regular aerobic exercise, and weight loss. Most patients, however, require the addition of some form of oral hypoglycemic drug or insulin. Oral agents to control DM include sulfonylurea drugs (such as glipizide), which increase pancreatic secretion of insulin; biguanides or thiazolidinediones (such as metformin or pioglitazone), which increase cellular sensitivity to insulin; or a-glucosidase inhibitors (such as acarbose), which decrease the absorption of carbohydrates from the gastrointestinal tract. Both types of diabetics also may be prescribed pramlintide (Symlin), a synthetic analog of human amylin, a hormone manufactured in the pancreatic beta cells. It enhances postprandial glucose control by slowing gastric emptying, decreasing postprandial glucagon concentrations, and regulating appetite and food intake; thus pramlintide is helpful for patients who do not achieve optimal glucose control with insulin and/or oral antidiabetic agents. When combinations of these agents fail to normalize blood glucose levels, insulin injections are added. Tight glucose control can reduce the patient’s risk of many of the complications of the disease. See: illustration
Prevention of Complications
Patients with DM should avoid tobacco, actively manage their serum lipid levels, and keep hypertension under optimal control. Failure to do so may result in a risk of atherosclerosis much higher than that of the general public. Other elements in care include receiving regular vaccinations, e.g., to prevent influenza and pneumococcal pneumonia).
Diabetes is a chronic disease whose symptoms can be ameliorated and life prolonged by proper therapy. The isolation and eventual production of insulin in 1922 by Canadian physicians F. G. Banting and C. H. Best made it possible to allow people with the disease to lead normal lives.
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.
Home blood glucose self-monitoring is indispensable in helping patients to adjust daily insulin doses according to test results and to achieve optimal long-term control of diabetes. Insulin or other hypoglycemic agents are administered as prescribed, and their action and use explained to the patient. With help from a dietitian, a diet is planned based on the recommended amount of calories, protein, carbohydrates, and fats. The amount of carbohydrates consumed is a dietary key to managing glycemic control in diabetes. For most men, 60 to 75 carbohydrate g per meal are a reasonable intake; for most women, 45 to 60 g are appropriate. Saturated fats should be limited to less than 7% of total caloric intake, and trans-fatty acids (unsaturated fats with hydrogen added) minimized. A steady, consistent level of daily exercise is prescribed, and participation in a supervised exercise program is recommended.
Hypoglycemic reactions are promptly treated by giving carbohydrates (orange juice, hard candy, honey, or any sugary food); if necessary, subcutaneous or intramuscular glucagon or intravenous dextrose (if the patient is not conscious) is administered. Hyperglycemic crises are treated initially with prescribed intravenous fluids and insulin and later with potassium replacement based on laboratory values.
Regular ophthalmological examinations are recommended for early detection of diabetic retinopathy. The patient is educated about diabetes, its possible complications and their management, and the importance of adherence to the prescribed therapy. The patient is taught the importance of maintaining normal blood pressure levels (120/80 mm Hg or lower). Control of even mild-to-moderate hypertension results in fewer diabetic complications, esp. nephropathy, cerebrovascular disease, and cardiovascular disease. Limiting alcohol intake to approximately one drink daily and avoiding tobacco are also important for self-management. Emotional support and a realistic assessment of the patient's condition are offered; this assessment should stress that, with proper treatment, the patient can have a near-normal lifestyle and life expectancy. Long-term goals for a patient with diabetes should include achieving and maintaining optimal metabolic outcomes to prevent complications; modifying diet and lifestyle to prevent and treat obesity, dyslipidemia, cardiovascular disease, hypertension, and nephropathy; improving physical activity; and allowing for the patient’s nutritional and psychosocial needs and preferences. Assistance is offered to help the patient develop positive coping strategies. It is estimated that 23 million Americans will be diabetic by the year 2030. The increasing prevalence of obesity coincides with the increasing incidence of diabetes; approx. 45% of those diagnosed receive optimal care according to established guidelines. According to the CDC, the NIH, and the ADA, about 40% of Americans between ages 40 and 74 have prediabetes, putting them at increased risk for type 2 diabetes and cardiovascular disease. Lifestyle changes with a focus on decreasing obesity can prevent or delay the onset of diabetes in 58% of this population. The patient and family should be referred to local and national support and information groups and may require psychological counseling.
|History||Often acute infection in a diabetic or insufficient insulin intake||Recent insulin injection, inadequate meal, or excessive exercise after insulin|
|Previous history of diabetes may be absent|
|Musculoskeletal||Muscle wasting or weight loss||Weakness|
|Gastrointestinal||Abdominal pains or cramps, sometimes acute||Nausea and vomiting|
|Nausea and vomiting|
|Central nervous system||Headache||Confusion, delirium, or seizures|
|Double or blurred vision|
|Skin||Flushed, dry||Diaphoretic, pale|
|Acetone odor of breath||Increased respiratory rate|
|Laboratory values||Elevated blood glucose (> 200 mg/dL)||Subnormal blood glucose (0–50 mg/dL)|
|Glucose and ketones in blood and urine||Absence of glucose and ketones in urine unless bladder is full|
diabetes mellitus; DM multiaetiology metabolic disease due to reduced/absent production of pancreatic insulin, and/or insulin resistance by peripheral tissue insulin receptors; characterized by reduced carbohydrate metabolism and increased fat and protein metabolism, leading to hyperglycaemia, increasing glycosuria, water and electrolyte imbalance, ketoacidosis, coma and death if left untreated; chronic long-term complications of DM include nephropathy, retinopathy, neuropathy and generalized degenerative changes in large and small arteries; treatment (with insulin/oral hypoglycaemic agents/diet) aims to stabilize blood glucose levels to the normal range (difficult to achieve fully; patients may tend to hyperglycaemia or hypoglycaemia due to mismanagement of glycaemic control); Tables D4-D7
di·a·be·tes mel·li·tus(dī-ă-bē'tēz mel'i-tŭs)
n a metabolic disorder caused primarily by a defect in the production of insulin by the islet cells of the pancreas, resulting in an inability to use carbohydrates. Characterized by hyperglycemia, glycosuria, polyuria, hyperlipemia (caused by imperfect catabolism of fats), acidosis, ketonuria, and a lowered resistance to infection. Periodontal manifestations if blood sugar is not being controlled may include recurrent and multiple periodontal abscesses, osteoporotic changes in alveolar bone, fungating masses of granulation tissue protruding from periodontal pockets, a lowered resistance to infection, and delay in healing after periodontal therapy. See also blood glucose level(s).
insulin-dependent (IDDM), juvenile-onset diabetes, brittle diabetes, and
non insulin-dependent (NIDDM), maturity-onset diabetes, adult-onset diabetes, ketosis-resistant diabetes, and
n a condition of glycosuria caused by inhibition of phosphorylation of phlorizin. It is not related to an endocrine disturbance.
Patient discussion about diabetes mellitus
Q. My 7yr has Diabetes. She been Diabetic for about 5 weeks and we can't get numbers at a good spot. she aether way to low (30- 60 scary when she gets like this) and to high (300 - 400) We been looking at what she eating calling the physician. he been play with here shots but nothing working. Its when she at school is were the nuber are mostly going up an down. we been trying to work with the school but she the only one in the hole school that has Diabetes. what to do ?
Keep an eye on her, but don't make it sound like such a big deal.
Q. how diabetes is caused
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Q. my grandmother was diabetic ... and i learned that diabetic is genetic ... should i be concern for me or or for one of my family reletives ... she suffered a lot and she died of it .. if a blood tests shows high amount of sugar in my blood , does i mean i am diabetic ?More discussions about diabetes mellitus