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DM

Abbreviation for adamsite; diabetes mellitus; diastolic murmur; dopamine.

dM

Abbreviation for decimorgan.

DM

diabetes mellitus; diphenylamine chlorarsine.

DM

abbreviation for diabetes mellitus.

DM

Diabetes mellitus, also, doctor of medicine–MD is used in the US

DM

Abbreviation for Adamsite;
dexamethasone;
diabetes mellitus;
dopamine.

diabetes

(di?a-bet'ez) [Gr. diabetes, (one) passing through]
A general term for diseases marked by excessive urination and elevated blood sugar, esp. diabetes mellitus (DM).

brittle diabetes

DM that is exceptionally difficult to control. The disease is marked by alternating episodes of hypoglycemia and hyperglycemia. Frequent adjustments of dietary intake and insulin dosage are required.

Etiology

Diabetes may be brittle when insulin is not well absorbed; insulin requirements vary rapidly; insulin is improperly prepared or administered; the Somogyi phenomenon is present; the patient has coexisting anorexia or bulimia; the patient's daily exercise routine, diet, or medication schedule varies; or physiological or psychological stress is persistent.

Synonym: brittle diabetes mellitus

brittle diabetes mellitus

Brittle diabetes.

bronze diabetes

Hemochromatosis.

chemical diabetes

1. Asymptomatic DM, a stage in which no obvious clinical signs and symptoms of the disease are present but blood glucose measurements are abnormal.
2. Type 2 DM occurring in an obese child or adolescent. The syndrome is sometimes referred to as “mature onset diabetes of youth” (MODY).

cystic-fibrosis-related diabetes

Abbreviation: CFRD
DM arising in patients with cystic fibrosis (CF). It is the most common complication of CF other than those conditions that affect the lungs. It is caused by destruction of islet cells (the cells in the pancreas that make insulin) as well as a decrease in sensitivity of the liver and muscles to the actions of insulin. The disease usually first becomes clinically obvious in young adults.

Patient Care

Although CFRD can be diagnosed with fasting glucose blood tests or hemoglobin A1c levels, many experts recommend using an oral glucose tolerance test. Fifteen to thirty percent of patients with CF are affected by their 20th birthday, and perhaps as many as half have the disease by age 30. CFRD is associated with more severe lung disease than is experienced by patients with CF and normal glucose tolerance. Oral hypoglycemic agents, insulin, and exercise are the primary methods of treatment. Caloric restriction, a cornerstone of treatment for other forms of diabetes, is relatively contraindicated because of the need for aggressive nutritional supplementation in CF patients.

double diabetes

A colloquial term for hybrid diabetes, also called type 3 diabetes or type 1 and a half diabetes.

endocrine diabetes

DM caused by diseases of the ovaries, pituitary, thyroid, or adrenal glands.

fibrocalculous pancreatic diabetes

A rare form of DM caused by chronic tropical pancreatitis and destruction of insulin-producing islet cells.

gestational diabetes

Abbreviation: GDM
DM that begins during pregnancy owing to changes in glucose metabolism and insulin resistance.

GDM affects a large percentage of pregnant American women, ranging from about 1.5 to 14 %, depending on the ethnic group studied. Although gestational diabetes usually subsides after delivery, women with GDM have a 45% risk of recurrence with the next pregnancy and a significant risk of developing type 2 diabetes later in life.

Diagnosis

Although many diabetic specialists recommend universal screening for GDM, it is agreed by all diabetologists that women at risk for GDM (women over age 25 who are overweight at the start of pregnancy; have a previous history of gestational diabetes; have had a previous infant weighing 9 lb or more at birth; have a history of a poor pregnancy outcome, glycosuria, or polycystic ovary syndrome; or who are from families or ethnic groups with a high incidence of type 2 DM) should undergo oral glucose tolerance testing as soon as possible to assess blood glucose levels while fasting and after meals. Testing should be repeated at 24 to 28 weeks' gestation if the first screening is negative.

Treatment

A calorically restricted diet, regular exercise, and metformin or insulin are used to treat GDM.

Patient care

Blood glucose self-monitoring is essential to management, and patients should be taught to monitor glucose levels four times each day, obtaining a fasting level in the morning, followed by three postprandial levels (1 hr after the start of each meal). Blood glucose levels at 1 hr after beginning a meal are considered the best predictor for subsequent fetal macrosomia. Target blood glucose levels are 90 mg/dL or less (fasting) and 120 to 140 mg/dL postprandially. The patient and her partner should be instructed that food, stress, inactivity, and hormones elevate blood glucose levels and that exercise and insulin lower them. They will need to learn about both pharmacological (measuring and injecting insulin) and nonpharmacological (menu management and physical activity) interventions to maintain a normal glycemic state (euglycemia) throughout the pregnancy, while ensuring adequate caloric intake for fetal growth and preventing maternal ketosis. Women who have no medical or obstetrical contraindicting factors should be encouraged to participate in an approved exercise program, because physical activity increases insulin receptor sensitivity. Even performing 15 to 20 min of “armchair exercises” daily (while reading or watching television) can help the pregnant woman reduce hyperglycemia without increasing the risk of inducing uterine contractions. If euglycemia is not achieved by nutrition therapy and exercise within 10 days, insulin is started. Pregnant women require three to four times the amount of insulin needed by a nonpregnant woman. Human minimally antigenic insulin should be prescribed. Often one dose of long-acting insulin at bedtime is sufficient, with rapid-acting insulins, i.e., regular insulin, insulin aspart recombinant (Novolog), or insulin lispro recombinant (Humalog) used to aid optimal glycemic control. Insulin glargine (Lantus), once used for gestational diabetes, is no longer recommended for pregnant women. Because stress can significantly raise blood glucose levels, stress management is a vital part of therapy. The woman’s feelings about her pregnancy and diabetes as well as her support system should be carefully assessed. Coping strategies should be explored. The patient is taught about deep breathing and relaxation exercises and encouraged to engage in activities that she enjoys and finds relaxing. She and her partner should learn to recognize interaction tensions and ways to deal with these to limit stress in their environment.

Maternal complications associated with GDM include pregnancy-induced hypertension, eclampsia, and the need for cesarean section delivery.

hybrid diabetes

A form of DM that has characteristics of both types 1 and 2. The patient may have episodes of diabetic ketoacidosis but marked insulin resistance and an obese body type.

iatrogenic diabetes

DM due to administration of drugs such as corticosteroids or dextrose infusions.

idiopathic diabetes

Type 1b diabetes.

immune-mediated diabetes mellitus

Type 1 diabetes.

diabetes insipidus

Abbreviation: DI
Excessive urination caused either by inadequate amounts of circulating vasopressin (antidiuretic hormone) in the body (hypothalamic DI) or by failure of the kidney to respond to antidiuretic hormone (nephrogenic DI). Urinary output is often massive, e.g., 5 to 15 L/day, which may result in dehydration in patients who cannot drink enough liquid to replace urinary losses, e.g., those with impaired consciousness. The urine is dilute (specific gravity is often below 1.005), and typically the patient's serum sodium level and osmolality rise as free water is eliminated as urine. If water deficits are not matched or the urinary losses are not prevented, death will result from dehydration.

Etiology

DI usually results from hypothalamic injury (such as brain trauma or neurosurgery) or from the effects of certain drugs (such as lithium or demeclocycline) on the renal resorption of water. Other representative causes include sickle cell anemia (in which renal infarcts damage the kidney's ability to retain water), hypothyroidism, adrenal insufficiency, inherited disorders of antidiuretic hormone production, and sarcoidosis.

Symptoms

The primary symptoms are urinary frequency, thirst, and dehydration.

Treatment

When DI is a side effect of drug therapy, the offending drug is withheld. DI caused by failure of the posterior pituitary gland to secrete antidiuretic hormone is treated with synthetic vasopressin.

Patient care

Fluid balance is monitored. Fluid intake and output, urine specific gravity, and weight are assessed for evidence of dehydration and hypovolemic hypotension. Serum electrolyte and blood urea nitrogen levels are monitored.

The patient is instructed in nasal insufflation of vasopressin (desmopressin acetate, effective for 8 to 20 hr, depending on dosage), the oral tablet form being more useful for bedtime or administration of subcutaneous or intramuscular vasopressin (effective for 2 to 6 hr). The length of the therapy and the importance of taking medications as prescribed and not discontinuing them without consulting the prescriber are stressed. Hydrochlorothiazide can be prescribed for nephrogenic DI not caused by drug therapy; amiloride may be used in nephrogenic DI caused by lithium administration. Meticulous skin and oral care are provided; use of a soft toothbrush is recommended; and petroleum jelly is applied to the lips and an emollient lotion to the skin to reduce dryness and prevent skin breakdown. Adequate fluid intake should be maintained.

Both the patient and family are taught to identify signs of dehydration and to report signs of severe dehydration and impending hypovolemia. The patient is taught to measure intake and output, to monitor weight daily, and to use a hydrometer to measure urine specific gravity. Weight gain should be reported because this may signify that the medication dosage is too high. Recurrence of polyuria may indicate dosing that is too low. The patient should wear or carry a medical ID tag and have prescribed medications with him or her at all times. Both patient and family need to know that chronic DI will not shorten the lifespan, but lifelong medications may be required to control the signs, symptoms, and complications of the disease. Counseling may be helpful in dealing with this chronic illness.

insulin-dependent diabetes mellitus

Abbreviation: IDDM
Type 1 diabetes.

juvenile-onset diabetes

A dated term for type 1 diabetes.

latent diabetes

DM that manifests itself during times of stress such as pregnancy, infectious disease, weight gain, or trauma. Before the stress, no clinical or laboratory findings of diabetes are present. There is a very strong chance that affected people will eventually develop overt type 2 DM.

latent autoimmune diabetes in adults

Abbreviation: LADA
A form of type 1 diabetes usually diagnosed after 30 years of age, in which there are serum antibodies against insulin, pancreatic islet cells, or the protein products of those cells. Most patients affected by LADA eventually require insulin therapy, like patients with type 1 DM.

maternally inherited diabetes and deafness

See: maternally inherited diabetes and deafness

mature-onset diabetes of youth

Abbreviation: MODY
Type 2 DM that presents during childhood or adolescence, typically as an autosomal dominant trait in which there is diminished but not absent insulin production by the pancreas. Children with this form of DM are not prone to diabetic ketoacidosis.
Enlarge picture
WELL-CONTROLLED DIABETES MELLITUS: Daily blood sugar abstracted from the records of a patient whose DM is well controlled (hemoglobin A1c=6.4). The average capillary blood glucose level is 104 mg/dL, and the standard deviation is 19. Sixty-five percent of the readings are between 90 and 140 mg/dL; the lowest blood sugar is 67 mg/dL (on April 15) and the highest is about 190 (on March 21).

diabetes mellitus

Abbreviation: DM
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

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.

Etiology

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.

Symptoms

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.

Diagnosis

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.

Treatment

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).

Prognosis

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.

Patient care

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.

Diabetic KetoacidosisHypoglycemia
OnsetGradualOften sudden
HistoryOften acute infection in a diabetic or insufficient insulin intakeRecent insulin injection, inadequate meal, or excessive exercise after insulin
Previous history of diabetes may be absent
MusculoskeletalMuscle wasting or weight lossWeakness
Tremor
Muscle twitching
GastrointestinalAbdominal pains or cramps, sometimes acuteNausea and vomiting
Nausea and vomiting
Central nervous systemHeadacheConfusion, delirium, or seizures
Double or blurred vision
Irritability
CardiovascularTachycardiaVariable
Orthostatic hypotension
SkinFlushed, dryDiaphoretic, pale
RespiratoryAir hungerVariable
Acetone odor of breathIncreased respiratory rate
Dyspnea
Laboratory valuesElevated blood glucose (> 200 mg/dL)Subnormal blood glucose (0–50 mg/dL)
Glucose and ketones in blood and urineAbsence of glucose and ketones in urine unless bladder is full

non–insulin-dependent diabetes mellitus

Abbreviation: NIDDM
Type 2 diabetes. See: type 1 diabetes for table

pancreatic diabetes

Diabetes associated with destruction of the exocrine and endocrine functions of the pancreas, such as occurs in chronic or recurrent pancreatitis.

phlorhizin diabetes

Glycosuria caused by administration of phlorhizin.

renal diabetes

Renal glycosuria, marked by a low renal threshold for glucose. Glucose tolerance is normal and diabetic symptoms are lacking.

secondary diabetes mellitus

DM that results from damage to the pancreas (e.g., after frequent episodes of pancreatitis) or from drugs such as corticosteroids (which increase resistance to the effects of insulin).

steroid diabetes

Hyperglycemia caused by the use of exogenously administered corticosteroids, e.g., prednisone, methylprednisolone, or dexamethasone.

strict control of diabetes

Regulation of blood glucose to normal or nearly normal levels, both before and after meals. Tight control of blood sugar has been shown to improve the survival of patients in intensive-care units and to prevent long-term complications of DM, e.g., blindness, nerve damage, and kidney failure.

Patients with meticulously controlled DM typically have a hemoglobin A1c level of 6.5 to 7.0 or lower, fasting blood sugars that are less than 110 mg/dL, and after-meal blood sugar readings that are 140 mg/dL or less.

Synonym: tight control of diabetes

tight control of diabetes

Strict control of diabetes.

true diabetes

Diabetes mellitus.

type 1 diabetes

DM that usually has its onset before the age of 25 years, in which the essential abnormality is related to absolute insulin deficiency. It was formerly known as juvenile diabetes.
See: table
Type 1Type 2
Age at onsetUsually under 30Usually over 40
Symptom onsetAbruptGradual
Body weightNormalObese—80%
HLA associationPositiveNegative
Family historyCommonNearly universal
Insulin in bloodLittle to noneSome usually present
Islet cell antibodiesPresent at onsetAbsent
Prevalence0.2–0.3%6%
SymptomsPolyuria, polydipsia, polyphagia, weight loss, ketoacidosisPolyuria, polydipsia, peripheral neuropathy
ControlInsulin, diet, and exerciseDiet, exercise, and often oral hypoglycemic drugs or insulin
Vascular and neural changesEventually developWill usually develop
Stability of conditionFluctuates, may be difficult to controlMay be difficult to control in poorly motivated patients

type 1a diabetes mellitus

The most common form of type 1 DM. It is caused by autoimmune destruction of the beta cells of the pancreas and inadequate insulin production. In type 1a DM, antibodies against insulin, islet cells of the pancreas, or glutamic acid decarboxylase is often present in the blood. The patient is prone to develop diabetic ketoacidosis if he or she is not treated with insulin.

type 1b diabetes mellitus

A relatively less common form of type 1 DM (seen in only about 10% of type 1 diabetics) in which autoimmune antibodies against insulin, pancreatic beta cells, or their protein products are not found in the blood. Beta cells are nonetheless destroyed (by unknown means), and the patient develops hyperglycemia or ketoacidosis unless he or she receives insulin.
Synonym: idiopathic diabetes

type 2 diabetes

A type of DM that occurs predominantly in adults. The insulin produced is sufficient to prevent ketoacidosis but insufficient to meet the total needs of the body, and resistance to the effects of insulin on peripheral tissues is often present. This type of diabetes in nonobese patients can usually be controlled by diet and oral hypoglycemic agents (e.g., sulfonylurea drugs or metformin). Eventually, insulin therapy is often required. In some patients the condition can be controlled by careful diet and regular exercise. Synonym: non–insulin-dependent diabetes mellitus See: type 1 diabetes for table

unstable diabetes mellitus

Brittle diabetes.
Enlarge picture
WELL-CONTROLLED DIABETES MELLITUS: Daily blood sugar abstracted from the records of a patient whose DM is well controlled (hemoglobin A1c=6.4). The average capillary blood glucose level is 104 mg/dL, and the standard deviation is 19. Sixty-five percent of the readings are between 90 and 140 mg/dL; the lowest blood sugar is 67 mg/dL (on April 15) and the highest is about 190 (on March 21).

diabetes mellitus

Abbreviation: DM
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

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.

Etiology

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.

Symptoms

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.

Diagnosis

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.

Treatment

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).

Prognosis

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.

Patient care

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.

Diabetic KetoacidosisHypoglycemia
OnsetGradualOften sudden
HistoryOften acute infection in a diabetic or insufficient insulin intakeRecent insulin injection, inadequate meal, or excessive exercise after insulin
Previous history of diabetes may be absent
MusculoskeletalMuscle wasting or weight lossWeakness
Tremor
Muscle twitching
GastrointestinalAbdominal pains or cramps, sometimes acuteNausea and vomiting
Nausea and vomiting
Central nervous systemHeadacheConfusion, delirium, or seizures
Double or blurred vision
Irritability
CardiovascularTachycardiaVariable
Orthostatic hypotension
SkinFlushed, dryDiaphoretic, pale
RespiratoryAir hungerVariable
Acetone odor of breathIncreased respiratory rate
Dyspnea
Laboratory valuesElevated blood glucose (> 200 mg/dL)Subnormal blood glucose (0–50 mg/dL)
Glucose and ketones in blood and urineAbsence of glucose and ketones in urine unless bladder is full
See also: diabetes

dystrophy

(dis'tro-fe) [ dys- + -trophy]
A disorder caused by defective nutrition or metabolism. dystrophic (dis-tro'fiik), adjective

adiposogenital dystrophy

Fröhlich syndrome.

asphyxiating thoracic dystrophy

Jeune syndrome.

Becker muscular dystrophy

See: Becker muscular dystrophy

Bietti crystalline dystrophy

See: Bietti crystalline dystrophy

cone-rod dystrophy

A form of retinitis pigmentosa in which central visual loss occurs first. Common symptoms include progressive visual loss followed by the loss of color perception, and eventually peripheral visual loss and night blindness. The visual loss is not correctable with standard lenses. See: retinitis pigmentosa

congenital hereditary endothelial dystrophy

Abbreviation: CHED
An eye disorder in which the corneal endothelium becomes cloudy, resulting in myopia.

corneal dystrophiy

Any of several inherited disorders in which the cornea becomes cloudy, hazy, or speckled, resulting in variable degrees of visual loss.

corneoretinal dystrophy

Bietti crystalline dystrophy.

distal muscular dystrophy

Abbreviation: DD
One of several rare forms of muscular dystrophy in which the forearm, hand, calf, and foot muscles are primarily affected as opposed to the muscles of the shoulders or pelvic girdle. Its onset is usually in adults between the ages of 40 and 60. Synonym: distal myopathy

Duchenne muscular dystrophy

See: Duchenne, Guillaume B. A.

Emery-Dreifuss muscular dystrophy

See: Emery-Dreifuss muscular dystrophy

facioscapulohumeral muscular dystrophy

A hereditary, progressive muscular dystrophy with onset in childhood or adolescence. It is marked by atrophic changes in the muscles of the shoulder girdle and face, inability to raise the arms above the head, myopathic facies, eyelids that remain partly open in sleep, and inability to whistle or purse the lips.

Treatment

Therapy is supportive; e.g., orthopedic devices can be used to prevent functional losses at the shoulder girdle. The patient should be encouraged to maintain as full and normal a life as possible and to avoid prolonged bed rest.

macular dystrophy

Any inherited, progressive degeneration of the macula lutea retinae marked by progressive central visual loss beginning in childhood or adolescence. Representative forms of macular dystrophy include Best disease and Stargardt disease. See: macula lutea retinae

muscular dystrophy

Any of nine distinct genetic syndromes that affect muscular strength and action, some of which first become obvious in infancy, whereas others manifest in adolescence or young adulthood. The syndromes are marked by either generalized or localized muscle weakness, difficulties with walking or maintaining posture, muscle spasms, and sometimes neurological, behavioral, cardiac, or other functional limitations. Detailed information about the disease can be obtained from the Muscular Dystrophy Association website at www.mdausa.org.

myotonic dystrophy

Abbreviation: DM
An autosomal dominant disorder caused by the repeated expansion of the trinucleotide sequence cytosine-thymidine-guanine (CTG)) in the DNA of chromosome 19. It is the most commonly inherited of the muscular dystrophies.

oculopharyngeal muscular dystrophy

Abbreviation: OPMD
A rare form of muscular dystrophy in which muscles that control the eyelids and swallowing are primarily affected. Ptosis and dysphagia beginning in the patient's late 40s or early 50s are characteristic symptoms. Weakness in the limbs often follows. The disease occurs most often in French-Canadian or Hispanic kindreds.

progressive muscular dystrophy

Spinal muscular atrophy.

pseudohypertrophic muscular dystrophy

Duchenne muscular dystrophy.

reflex sympathetic dystrophy

An abnormal response of the nerves of the face or of an extremity, marked by pain, autonomic dysfunction, vasomotor instability, and tissue swelling. Although the precise cause of the syndrome is unknown, it often follows trauma, stroke, neuropathy, or radiculopathy. In about one third of all patients, the onset is insidious. Affected patients often complain of burning pain with any movement of an affected body part, excessive sensitivity to light touch or minor stimulation, temperature changes (heat or cold) in the affected limb, localized sweating, localized changes of skin color, or atrophic changes in the skin, nails, or musculature. Synonym: algodystrophy; complex regional pain syndrome, type 1; shoulder-hand syndrome; Sudeck disease

Treatment

Early mobilization of the body part with multimodality therapy may improve the symptoms of reflex sympathetic dystrophy. Drug therapies often include prednisone or other corticosteroids and narcotic analgesics; trancutaneous electrical stimulation, physical therapy, or nerve blocks may also prove helpful.

rod-cone dystrophy

A form of retinitis pigmentosa in which rod degeneration precedes cone degeneration. Night blindness is usually the first symptom, followed by peripheral visual loss.

Schnyder crystalline dystrophy

See: Schnyder crystalline dystrophy

twenty-nail dystrophy

Longitudinal ridging and fragmentation of all the fingernails and toenails. It is a characteristic finding in lichen planus.

vitelliform dystrophy

Vitelliform macular dystrophy.

vitelliform macular dystrophy

An autosomal dominant retinal disease in which central visual acuity is diminished when lipofuscin accumulates under the macula. When the disease occurs in childhood, it is called Best disease.

vulvar dystrophy

Lichen sclerosus et atrophicus.

myotonic dystrophy

Abbreviation: DM
An autosomal dominant disorder caused by the repeated expansion of the trinucleotide sequence cytosine-thymidine-guanine (CTG)) in the DNA of chromosome 19. It is the most commonly inherited of the muscular dystrophies.
See also: dystrophy

DM

Abbrev. for Doctor of Medicine.

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

DM

1. dry matter.
2. one of the arsenical smokes used in crowd control. A sternutator and causes lacrimation, sneezing and vomiting. Called also adamsite.
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