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.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
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.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Polydipsia:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Diabetes insipidus
This disorder characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Diabetes mellitus
Polydipsia is a classic finding with this disorder—a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur.
Hypercalcemia
As this disorder progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
Hypokalemia
This electrolyte imbalance can cause nephropathy, resulting in polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
Psychogenic polydipsia
This uncommon disorder causes polydipsia and polyuria. This condition may occur with any psychiatric disorder, but more common with schizophrenia. Signs of psychiatric disturbances, such as anxiety or depression, are typical. Other findings include headache, blurred vision, weight gain, edema, elevated blood pressure and, occasionally, stupor and coma. Signs of heart failure may develop with overhydration.
Renal disorders (chronic)
Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
Sheehan’s syndrome
Polydipsia, polyuria, and nocturia occur within this syndrome of postpartum pituitary necrosis. Other features include fatigue, failure to lactate, amenorrhea, decreased pubic and axillary hair growth, and reduced libido.
Sickle cell anemia
As nephropathy develops, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers, and bone deformities, such as kyphosis and scoliosis.
Thyrotoxicosis
This disorder infrequently causes polydipsia. Characteristic findings include tachycardia, palpitations, weight loss despite increased appetite, diarrhea, tremors, an enlarged thyroid, dyspnea, nervousness, diaphoresis, and heat intolerance. Exophthalmos may also occur.
Other causes
Drugs
Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Diabetic complications during pregnancy:
Causes
(Handbook of Diseases)
In diabetes mellitus, glucose is inadequately used either because insulin isn’t synthesized (as in type 1, insulin-dependent diabetes) or because tissues are resistant to the hormonal action of endogenous insulin (as in type 2, non–insulin-dependent diabetes).
Protective mechanisms
During pregnancy, the fetus relies on maternal glucose as a primary fuel source. Pregnancy triggers protective mechanisms that have anti-insulin effects: increased hormone production (placental lactogen, estrogen, and progesterone), which antagonizes the effects of insulin; degradation of insulin by the placenta; and prolonged elevation of stress hormones (cortisol, epinephrine, and glucagon), which raise blood glucose levels.
In a normal pregnancy, an increase in anti-insulin factors is counterbalanced by an increase in insulin production to maintain normal blood glucose levels. However, women who are prediabetic or diabetic can’t produce sufficient insulin to overcome the insulin antagonist mechanisms of pregnancy, or their tissues are insulin-resistant.
As insulin requirements rise toward term, the patient who is prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control. The insulin-dependent patient may need increased insulin dosage.
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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.
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Source: Handbook of Diseases, 2003
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.
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Source: Handbook of Diseases, 2003
Polydipsia:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Diabetes insipidus
Diabetes insipidus characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Diabetes mellitus
Polydipsia is a classic finding with diabetes mellitus — a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur. (See Associated disorder: Diabetes mellitus, page 514.)
CULTURAL CUE:Diabetes is the fourth leading cause of death in Black, Native American, Hawaiian, and Filipino women. Also, Blacks are at greater risk for developing diabetes than Whites.
Hypercalcemia
As hypercalcemia progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
Hypokalemia
An electrolyte imbalance — hypokalemia — can cause nephropathy, resulting in polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
Renal disorders (chronic)
Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
Sickle cell anemia
As nephropathy develops in patients with sickle cell anemia, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers and such bone deformities as kyphosis and scoliosis.
Other causes
Drugs
Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Polyuria and Polydipsia:
Principal Causes of Polyuria and Polydipsia
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
- Diabetesmellitus
- Diabetes insipidus
- Antidiuretichormone deficiency (central diabetes insipidus)
- Antidiuretic hormone resistance (nephrogenicdiabetes insipidus)
- Primary polydipsia
- Compulsivewater drinking
- Hypothalamic thirst center defect
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Polydipsia:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Diabetes insipidus.Diabetes insipidus characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Diabetes mellitus.Polydipsia is a classic finding with diabetes mellitus—a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur.
Hypercalcemia.As hypercalcemia progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
Hypokalemia.Hypokalemia can cause polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
Psychogenic polydipsia.Psychogenic polydipsia causes polydipsia and polyuria. It may occur with any psychiatric disorder, but is more common with schizophrenia. Signs of psychiatric disturbances, such as anxiety or depression, are typical. Other findings include headache, blurred vision, weight gain, edema, elevated blood pressure and, occasionally, stupor and coma. Signs of heart failure may develop with overhydration.
Renal disorders (chronic).Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
Sheehan's syndrome.Polydipsia, polyuria, and nocturia occur with Sheehan's syndrome, a disorder of postpartum pituitary necrosis. Other features include fatigue, failure to lactate, amenorrhea, decreased pubic and axillary hair growth, and a reduced libido.
Sickle cell anemia.With sickle cell anemia, as nephropathy develops, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers and bone deformities, such as kyphosis and scoliosis.
Other causes
Drugs.Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
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