Causes of Impaired glucose tolerance
Impaired glucose tolerance Causes: Book Excerpts
Impaired glucose tolerance as a complication of other conditions:
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Impaired glucose tolerance as a symptom:
Conditions listing Impaired glucose tolerance
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Impaired glucose tolerance as a symptom of that condition:
Medical news summaries relating to Impaired glucose tolerance:
The following medical news items are relevant to causes of Impaired glucose tolerance:
Related information on causes of Impaired glucose tolerance:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Impaired glucose tolerance may be found in:
Causes of Impaired glucose tolerance: Online Medical Books
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for more information about the causes of Impaired glucose tolerance.
Hyperglycemia:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Medications
–Corticosteroids are a common cause
–Common medications include growth
hormone, estrogen (including oral contraceptives), nicotinic acid, salicylates and NSAIDs, thiazide and loop diuretics, phenytoin, and epinephrine - Diabetes mellitus type I
–Diabetic ketoacidosis -
Diabetes mellitus type II
-
Pancreatic disease
–Acute or chronic pancreatitis
–Pancreatectomy
–Pancreatic carcinoma
–Hemochromatosis
–Cystic fibrosis
-
Increased counter-regulatory hormones associated with acute disease
–Myocardial infarction
–Stroke or other neurologic disease
–Renal insufficiency
–Hepatic insufficiency
-
Acromegaly
-
Cushing's syndrome
-
Pheochromocytoma
-
Hyperthyroidism (thyroid storm)
-
Glucagonoma
-
Gestational diabetes
-
Amyloidosis
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Hyperglycemia:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Type I diabetes mellitus
–Most common form of diabetes in children
–Prevalence: 1.9/1,000
–Autoimmune-mediated destruction of
pancreatic islets (β-cells)
–Absolute insulin deficiency
–Often presents with ketosis and DKA
- Type II diabetes mellitus
–Increasing prevalence in children, especially
among obese
–In children, onset usually in mid-puberty
–More frequent in blacks, Hispanics, Pacific
Islanders, Asians, and Native Americans (Pima Indians)
–Strong association with family history of type II diabetes
–Insulin resistance and inadequate insulin secretion results in relative insulin deficiency
-
Maturity-onset diabetes of the young (MODY)
–Infrequent
–Autosomal dominant disease
–Onset usually between 9 and 25 years old
–Genetic defects in enzymes or nuclear
transcription factors involved in islet cell development or the regulation of insulin secretion
-
Drug- or chemical-induced diabetes
–Glucocorticoids, β-adrenergic agonists, phenytoin, asparaginase, cyclosporine, tacrolimus, vacor, pentamidine, diazoxide, nicotinic acid, thyroid hormone, thiazides
-
Other endocrinopathies: Cushing disease, acromegaly, pheochromocytoma
-
Exocrine pancreatic diseases
–Cystic fibrosis
–Hemochromatosis
-
Pancreatectomy
-
Physiological stress (trauma, infection)
-
Infections
–CMV
–Congenital rubella
-
Genetic syndromes: Prader-Willi syndrome, Down syndrome, Turner syndrome, Klinefelter syndrome, Wolfram syndrome
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Diabetes insipidus:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Diabetes insipidus results centrally from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture, or head trauma that damages the neurohypophyseal structures. It can also result nephrogenically from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial. (Note: Pituitary diabetes insipidus shouldn’t be confused with nephrogenic diabetes insipidus, a rare congenital disturbance of water metabolism that results from renal tubular resistance to vasopressin.)
Normally, the hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable. The absence of vasopressin in diabetes insipidus allows the filtered water to be excreted in the urine instead of being reabsorbed.
Nephrogenic diabetes insipidus involves a defect in the parts of the kidneys that reabsorb water back into the bloodstream. It occurs less commonly than central diabetes insipidus. Nephrogenic diabetes insipidus may occur as an inherited disorder in which male children receive the abnormal gene that causes the disease on the X chromosome from their mothers. Nephrogenic diabetes insipidus may also be caused by diseases of the kidney (such as polycystic kidney disease) and the effects of certain drugs (such as lithium and amphotericin B).
Diabetes insipidus is rare, affecting 1 in 25,000 people. Males and females are affected equally.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Diabetes mellitus:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
DM affects an estimated 6% of the population of the United States, about half of whom are undiagnosed. Incidence is greater in females and rises with age. Type 2 accounts for 90% of cases.
In type 1 diabetes, pancreatic beta-cell destruction or a primary defect in beta-cell function results in failure to release insulin and ineffective glucose transport. Type 1 immune-mediated diabetes is caused by cell-mediated destruction of pancreatic beta cells. The rate of beta-cell destruction is usually higher in children than in adults. The idiopathic form of type 1 diabetes has no known cause. Patients with this form have no evidence of autoimmunity and don’t produce insulin.
In type 2 diabetes, beta cells release insulin, but receptors are insulin-resistant and glucose transport is variable and ineffective. Risk factors for type 2 diabetes include:
❑ obesity (even an increased percentage of body fat primarily in the abdominal region); risk decreases with weight and drug therapy
❑ lack of physical activity
❑ history of GDM
❑ hypertension
❑ Black, Hispanic, Pacific Islander, Asian American, Native American origin
❑ strong family history of diabetes
❑ older than age 45
❑ high-density lipoprotein cholesterol of less than 35 or triglyceride of greater than 250
❑ Seriously impaired glucose tolerance (IGT) test.
ELDER TIP As the body ages, the cells become more resistant to insulin, thus reducing the older adult’s ability to metabolize glucose. In addition, the release of insulin from the pancreatic beta cells is reduced and delayed. These combined processes result in hyperglycemia. In the older patient, sudden concentrations of glucose cause increased and more prolonged hyperglycemia.
The “other specific types” of DM result from various conditions (such as a genetic defect of the beta cells or endocrinopathies) or from use of or exposure to certain drugs or chemicals. GDM is considered present whenever a patient has any degree of abnormal glucose during pregnancy. This form may result from weight gain and increased levels of estrogen and placental hormones, which antagonize insulin.
Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage in the fat deposits. Insulin deficiency compromises the body tissues’access to essential nutrients for fuel and storage.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Hereditary fructose intolerance:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Transmitted as an autosomal recessive trait, hereditary fructose intolerance results from a deficiency in the enzyme fructose-1-phosphate aldolase. The enzyme operates at only 1% to 10% of its normal biological activity, thus preventing rapid uptake of fructose by the liver after ingestion of fruit or foods containing cane sugar.
In some European countries, hereditary fructose intolerance may have an incidence as high as 1 in 20,000 people.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Diabetes insipidus:
Causes
(Handbook of Diseases)
Pituitary diabetes insipidus results from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture, or head trauma that damages the neurohypophyseal structures. It can also result from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial.
The hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into the general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable.
In pituitary diabetes insipidus, the absence of vasopressin allows the filtered water to be excreted in the urine instead of being reabsorbed. In renal diabetes insipidus, the kidney doesn’t respond to vasopressin, which is usually present in high concentrations.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Diabetes mellitus:
Causes
(Handbook of Diseases)
The effects of diabetes mellitus result from insulin deficiency. Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or resistance compromises the body tissues’access to essential nutrients for fuel and storage.
Type 1A results from autoimmune beta-cell destruction, resulting in insulin deficiency. Type 1B leaves these immunologic markers but results in insulin deficiency and kerosis.
Other risk factors include the following:
❑ Obesity contributes to the resistance to endogenous insulin.
❑ Physiologic or emotional stress can cause prolonged elevation of stress hormone levels (cortisol, epinephrine, glucagon, and growth hormone). This raises blood glucose levels, which, in turn, places increased demands on the pancreas.
❑ Pregnancy causes weight gain and increases levels of estrogen and placental hormones, which antagonize insulin.
❑ Some medications can antagonize the effects of insulin, including thiazide diuretics, adrenal corticosteroids, and hormonal contraceptives.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
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