Causes of Type 1 diabetes

List of causes of Type 1 diabetes

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Type 1 diabetes) that could possibly cause Type 1 diabetes includes:

• Haemochromatosis
• Polyendochrine syndromes - some rare syndromes cause multiple autoimmune diseases in various body glands
• Chronic pancreatitis - pancreas damage that can mimic diabetes.
• Cystic fibrosis
• Addison's disease

Longer list of causes of Diabetes-like symptoms: see full list of causes for Diabetes-like symptoms

Type 1 diabetes as a complication of other conditions:

Other conditions that might have Type 1 diabetes as a complication may, potentially, be an underlying cause of Type 1 diabetes. Our database lists the following as having Type 1 diabetes as a complication of that condition:

• Chronic Pancreatitis
• Hemochromatosis
• Pancreatitis
• Polyendocrine deficiency syndrome

Type 1 diabetes as a symptom:

Conditions listing Type 1 diabetes as a symptom may also be potential underlying causes of Type 1 diabetes. Our database lists the following as having Type 1 diabetes as a symptom of that condition:

• 18p minus syndrome
• Mental retardation - dysmorphism - hypogonadism - diabetes
• Pancreas agenesis, dorsal
• Pancreatic beta cell agenesis with neonatal diabetes mellitus
• Pyogenic arthritis - pyoderma gangrenosum - acne
• Pyogenic arthritis, pyoderma gangrenosum, and acne

What causes Type 1 diabetes?

Causes: Type 1 diabetes: Autoimmune attack against the pancreas's insulin-producing cells.
Type 1 diabetes is an autoimmune disease. An autoimmune disease results when the body's system for fighting infection (the immune system) turns against a part of the body. In diabetes, the immune system attacks the insulin-producing beta cells in the pancreas and destroys them. The pancreas then produces little or no insulin. Someone with type 1 diabetes needs to take insulin daily to live. (Source: excerpt from Diabetes Overview: NIDDK)
Article excerpts about the causes of Type 1 diabetes:

Understanding Autoimmune Disease: NIAID (Excerpt)

Type 1 diabetes mellitus results from autoimmune destruction of the insulin-producing cells of the pancreas. Insulin is required by the body to keep the blood sugar (glucose) level under control. High levels of glucose are responsible for the symptoms and the complications of the disease. However, most of the insulin-producing cells are destroyed before the patient develops symptoms of diabetes (Source: excerpt from Understanding Autoimmune Disease: NIAID)

Diabetes: NWHIC (Excerpt)

An autoimmune disease results when the body's system for fighting infection (the immune system) turns against a part of the body. In type 1 diabetes, the immune system attacks the insulin-producing beta cells in the pancreas and destroys them. The pancreas then produces little or no insulin, thereby preventing cells from taking up sugar from blood. (Source: excerpt from Diabetes: NWHIC)

What triggers Type 1 diabetes?

The following conditions are listed as possible triggers for Type 1 diabetes:

• Viruses - although unclear, various viruses have been mentioned as potential triggers.
  • Congenital rubella
  • Coxsackie B virus
  • Cytomegalovirus (CMV)
  • Adenovirus
  • Mumps virus
• Cow milk protein - certain unconfirmed theories exist about molecular mimicry between cow milk and pancreas islet cells.

Medical news summaries relating to Type 1 diabetes:

The following medical news items are relevant to causes of Type 1 diabetes:

• Children increasingly face adult diseases
• Diabetes: the simple facts
• Eating disorders can greatly increase the risk of complications in people with type 1 diabetes
• Gene mutation identified in autoimmune conditions
• International research aims to determine if cow's milk increases risk of type 1 diabetes
• Long-term offspring health may be affected by mother's diet during pregnancy
• More and more children are being diagnosed with type 1 diabetes
• New diagnostic technique for pre-diabetes
• Reason for increasing incidence of type 1 diabetes is a mystery
• Therapy to reduce allergies to cats
• More news »

Related information on causes of Type 1 diabetes:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Type 1 diabetes may be found in:

• Risk factors for Type 1 diabetes
• Genetics of Type 1 diabetes
• Hidden causes of Type 1 diabetes

Causes of Type 1 diabetes: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Type 1 diabetes.

Hyperglycemia: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Impaired fasting glucose

• 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

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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

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Source: In A Page: Pediatric Signs and Symptoms, 2007

Polydipsia: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Diabetes mellitus (type I and type II)
  –Hyperglycemia drives an osmotic diuresis that causes polyuria, which then leads to dehydration, increased thirst, and polydipsia
• Diabetes insipidus
  –Abnormal water balance due to vasopressin (ADH) deficiency or resistance, causing excretion of large amounts of dilute urine
• Central or neurogenic diabetes insipidus (vasopressin deficiency)
  –Congenital
  –Familial (autosomal dominant)
  –Acquired: Neurosurgery, tumor (e.g., craniopharyngioma), head trauma, infiltrative/inflammatory, infectious
  • Nephrogenic diabetes insipidus (decreased responsiveness of the kidneys to vasopressin)
    –Familial (X-linked dominant and recessive forms)
    –Acquired: Renal disease, obstructive uropathy, hypercalcemia/hypercalciuria
    –Hypokalemia, drug-induced (e.g., lithium, diuretics, ethanol, cisplatin)
    –Gestational DI: Increased clearance of ADH by placental vasopressinase, lower osmolar threshold for thirst and ADH release
  • Primary polydipsia
    –Compulsive water drinking
    –Dipsogenic DI
  • Primary hyperaldosteronism
  • Diabetes insipidus, diabetes mellitus, optic atrophy, and deafness (DIDMOAD) syndrome
  • Bartter syndrome
  • Hypertension (e.g., pheochomocytoma)
  • Neuroblastoma
  • Cystinosis
  • Congestive heart failure

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Source: In A Page: Pediatric Signs and Symptoms, 2007

Polydipsia: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

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, a decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.

Hypokalemia

Hypokalemia is an electrolyte imbalance that 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

Psychogenic polydipsia is an uncommon disorder that 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 a 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

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.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

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

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.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Diabetic complications during pregnancy: Causes
(Professional Guide to Diseases (Eighth Edition))

In diabetes mellitus, glucose is inadequately utilized either because insulin isn’t synthesized or because tissues are resistant to the hormonal action of endogenous insulin. 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 insulin’s effects; 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, females who are prediabetic or diabetic are unable to 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’s prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control, whereas the patient who’s insulin-dependent may need increased insulin dosage.

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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.

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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.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

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

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

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

Drug abuse and dependence: Causes
(Handbook of Diseases)

Drug abuse commonly results from a combination of low self-esteem, peer pressure, inadequate coping skills, and curiosity. There is also evidence of familial patterns of addiction.

Most people who are predisposed to drug abuse have few mental or emotional resources against stress, an overdependence on others, and a low tolerance for frustration. Taking the drug gives them pleasure by relieving tension, abolishing loneliness, allowing them to achieve a temporarily peaceful or euphoric state, or simply relieving boredom.

Drug dependence may follow experimentation with drugs in response to peer pressure. It may also follow the use of drugs to relieve physical pain, but this is uncommon.

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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.

» READ BOOK EXCERPT ONLINE »

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)

1. Diabetesmellitus
2. Diabetes insipidus
   1. Antidiuretichormone deficiency (central diabetes insipidus)
   2. Antidiuretic hormone resistance (nephrogenicdiabetes insipidus)
3. Primary polydipsia
   1. Compulsivewater drinking
   2. Hypothalamic thirst center defect

» READ BOOK EXCERPT ONLINE »

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