DI
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Chem. Symbol.
Chem. Symbol.
DI
la-di-da
lah-di-dah
(ˈlɑˈdiˈdɑ)Di
enUKDi
DI
DI
DI
DI
DI
Abbreviation for:date of injury
days of incubation
dead implant
deep inhalation
dental index
dentinogenesis imperfecta
detrusor instability
diabetes insipidus
diagnostic index
diagnostic imaging
diastolic interval
dietary intake
diffusion imaging
Director of Information
Dirofilaria immitis
disability index
disability insurance
disto-incisal
distraction index
dobutamine infusion
donor insemination
dorso-iliac
double immunodiffusion
drug induced
dyskaryosis index
DI
diabetes
(di?a-bet'ez) [Gr. diabetes, (one) passing through]brittle diabetes
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.
brittle diabetes mellitus
Brittle diabetes.bronze diabetes
Hemochromatosis.chemical diabetes
cystic-fibrosis-related diabetes
Abbreviation: CFRDPatient 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
endocrine diabetes
fibrocalculous pancreatic diabetes
gestational diabetes
Abbreviation: GDMGDM 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
iatrogenic diabetes
idiopathic diabetes
Type 1b diabetes.immune-mediated diabetes mellitus
Type 1 diabetes.diabetes insipidus
Abbreviation: DIEtiology
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: IDDMType 1 diabetes.
juvenile-onset diabetes
latent diabetes
latent autoimmune diabetes in adults
Abbreviation: LADAmaternally inherited diabetes and deafness
See: maternally inherited diabetes and deafnessmature-onset diabetes of youth
Abbreviation: MODY
diabetes mellitus
Abbreviation: DMType 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 Ketoacidosis | Hypoglycemia | |
|---|---|---|
| Onset | Gradual | Often sudden |
| 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 |
| Tremor | ||
| Muscle twitching | ||
| 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 | ||
| Irritability | ||
| Cardiovascular | Tachycardia | Variable |
| Orthostatic hypotension | ||
| Skin | Flushed, dry | Diaphoretic, pale |
| Respiratory | Air hunger | Variable |
| Acetone odor of breath | Increased respiratory rate | |
| Dyspnea | ||
| 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 |
non–insulin-dependent diabetes mellitus
Abbreviation: NIDDMType 2 diabetes. See: type 1 diabetes for table
pancreatic diabetes
phlorhizin diabetes
renal diabetes
secondary diabetes mellitus
steroid diabetes
strict control of diabetes
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.
tight control of diabetes
Strict control of diabetes.true diabetes
Diabetes mellitus.type 1 diabetes
| Type 1 | Type 2 | |
|---|---|---|
| Age at onset | Usually under 30 | Usually over 40 |
| Symptom onset | Abrupt | Gradual |
| Body weight | Normal | Obese—80% |
| HLA association | Positive | Negative |
| Family history | Common | Nearly universal |
| Insulin in blood | Little to none | Some usually present |
| Islet cell antibodies | Present at onset | Absent |
| Prevalence | 0.2–0.3% | 6% |
| Symptoms | Polyuria, polydipsia, polyphagia, weight loss, ketoacidosis | Polyuria, polydipsia, peripheral neuropathy |
| Control | Insulin, diet, and exercise | Diet, exercise, and often oral hypoglycemic drugs or insulin |
| Vascular and neural changes | Eventually develop | Will usually develop |
| Stability of condition | Fluctuates, may be difficult to control | May be difficult to control in poorly motivated patients |
type 1a diabetes mellitus
type 1b diabetes mellitus
type 2 diabetes
unstable diabetes mellitus
Brittle diabetes.diabetes insipidus
Abbreviation: DIEtiology
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.
DI
DI
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- nemoc
- nemo, captain
- nemocn
- nemocnica na okraji disku
- nemo cogitur rem suam vendere
- nemo contra factum suum venire potest
- nemod
- nemo damnum facit
- nemo dat
- nemo dat qui non habet
- nemo dat quod non habet
- nemo dat rule
- nemo debet esse judex in propria causa
- nemo debet ex aliena jactura lucrari
- nemo debet immiscere se rei alienae ad se nihil pertinenti
- nemo debet lucupletari ex aliena jactura
- nemo debet rem suam sine facto aut defectu suo amittere
- nemo de domo sua extrahi debet
- nemo est haeres viventes
- nemo ex alterius facto praegravari debet
- nemo ex consilio obligatur
- nemo ex suo delicto melioroem suam conditionem facere potest
- nemof
- nemo gene
- nemognathinae