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Your search term(s) "diabetes insipidus" returned 12 results.

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Endocrine Emergencies. IN: Gardner, D.; Shoback, D., eds. Greenspan’s Basic and Clinical Endocrinology. 8th ed. Columbus, OH: McGraw Hill. 2007. pp 868-893.

This chapter about endocrine emergencies is from a textbook about endocrinology that describes the scientific principles and clinical management of patients with endocrine-related diseases and disorders. The author notes that acute or chronic failure of an endocrine gland can occasionally result in catastrophic illness and even death. The chapter focuses on crises involving the thyroid, anterior pituitary, or adrenal glands; diabetes mellitus; and abnormalities in calcium, sodium, and water balance. Topics discussed include myxedema coma, thyroid storm, thyrotoxic periodic paralysis, amiodarone-induced thyrotoxicosis, acute adrenal insufficiency, pituitary apoplexy, diabetic ketoacidosis, nonketotic hyperosmolar coma, hypercalcemic crisis, acute hypocalcemia, hyponatremia, and diabetes insipidus. A list of abbreviations is provided. 3 figures. 12 tables. 41 references.

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Hypothalamic-Pituitary Disorders. IN: Camacho, P.M.; Gharib, H.; Sizemore, G.W., eds. Evidence-Based Endocrinology. 2nd ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2007. pp 1-29.

This chapter on hypothalamic-pituitary disorders is from a concise, reference-based handbook that is intended to help busy clinicians with endocrine-related diagnostic and therapeutic decisions required in their practices. Using a modification of the McMaster criteria, the contributors to the text have critically assessed and graded studies, assisting readers in quickly evaluating the articles that have led to practice recommendations. Topics covered in this chapter include evaluation of the hypothalamic-pituitary axis, imaging of the hypothalamic-pituitary system, pituitary tumors, hypopituitarism, disorders of the prolactin system, acromegaly, Cushing disease, diabetes insipidus, and the syndrome of inappropriate antidiuretic hormone secretion. For each disease state included, the authors discuss etiology, epidemiology, pathophysiology, diagnosis, and treatment considerations. The chapter includes an outline and an extensive, annotated list of references. 3 tables. 78 references.

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Posterior Pituitary (Neurohypophysia). IN: Gardner, D.; Shoback, D., eds. Greenspan’s Basic and Clinical Endocrinology. 8th ed. Columbus, OH: McGraw Hill. 2007. pp 157-170.

This chapter about the posterior pituitary is from a textbook about endocrinology that describes the scientific principles and clinical management of patients with endocrine-related diseases and disorders. The author describes the posterior pituitary as the distal axon terminals of the hypothalamic magnocellular neurons that make up the neurohypophysis. Vasopressin and oxytocin are nonapeptides that are synthesized in the cell bodies of these neurons. The author reviews normal anatomy and physiology of hormone synthesis and release from the posterior pituitary and discusses modified normal physiologic states, vasopressin-insufficient diabetes insipidus, pathologic lesions producing diabetes insipidus, primary polydipsia and polyuria, imaging of the neurohypophysis, nephrogenic diabetes insipidus, excess vasopressin and the syndrome of inappropriate antidiuretic hormone (SIADH), and the role of oxytocin in parturition and lactation. The chapter includes numerous black-and-white photographs and illustrations; a list of abbreviations is provided. 6 figures. 2 tables. 28 references.

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Disorders of the Neurohypophysis. IN: Jameson, J.L., ed. Harrison's Endocrinology. Columbus, OH: McGraw Hill. 2006. pp 57-70.

This chapter on disorders of the neurohypophysis is from a textbook that offers a comprehensive, practical look at the field of endocrinology. The neurohypophysis, or posterior pituitary gland, produces arginine vasopressin––AVP, also known as antidiuretic hormone––and oxytocin. The author reviews the action, synthesis and secretion, metabolism, and role in thirst of vasopressin. The author discusses oxytocin, diabetes insipidus, adipsic hypernatremia, and excess vasopressin secretion and action hyponatremia. AVP deficiency causes diabetes insipidus, characterized by the production of large amounts of dilute urine. Excessive or inappropriate AVP production predisposes to hyponatremia if water intake is not reduced in parallel to urine output. Oxytocin stimulates postpartum milk letdown in response to suckling. Oxytocin may help to initiate or facilitate labor by stimulating contraction of uterine smooth muscle. The chapter includes full-color illustrations. 5 figures. 4 tables. 6 references.

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Evaluation and Treatment of Constipation in Infants and Children. American Family Physician. 73(3): 479-480. February 1, 2006.

This article reviews the evaluation and treatment of constipation in infants and children, a problem that is usually functional and the result of stool retention. However, the authors encourage family physicians to be alert for indications of the presence of an uncommon but serious organic cause of constipation, such as Hirschsprung's disease, also called congenital aganglionic megacolon; pseudo-obstruction; spinal cord abnormality; hypothyroidism; diabetes insipidus; cystic fibrosis; gluten enteropathy; or congenital anorectal malformation. Functional constipation is treated with disimpaction using oral or rectal medication. Polyethylene glycol is effective and well-tolerated, but a number of alternatives are also available. After disimpaction, children may need to be on a maintenance program for months to years because relapse of functional constipation is common. Education of the family and, when possible, the child is important for improving functional constipation. Cow's milk may promote constipation in some children, so a trial period of withholding milk may be considered. Adding fiber to the diet is another recommended strategy. The authors conclude that, despite treatment, only 50 to 70 percent of children with functional constipation demonstrate long-term improvement. Two patient care algorithms are provided. 2 figures. 6 tables. 18 references.

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History of Diabetes Insipidus. Endless Water. 11(1): 1-2. Winter 2006.

This newsletter article offers information about the history of diabetes insipidus, a condition characterized by increased production of urine due to a lack of urinary concentration (water diuresis). The author describes the search for the cause of diabetes insipidus (DI) and the discovery that the cause of polyuria in DI was a lack of one or more substances produced by the pituitary gland. The author also discusses the problem of DI in people with schizophrenia, nephrogenic DI, gestational DI, and the different types of treatments that are used for each type of DI. This article is the first in a series of articles about DI; additional articles consider diagnostic and treatment strategies for patients with DI.

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Neonatal Kidney Problems. IN: Hogg, R., ed. Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. pp 53-66.

This chapter about neonatal kidney problems is from a textbook that presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The author reviews maturation during fetal life, postnatal maturation, symptoms and signs of renal disease in the neonate, gross hematuria, malformation syndromes, diagnostic tests used to confirm kidney and urologic disorders in the neonate, blood pressure and hypertension, renal function during neonatal respiratory disorders, acute renal failure (ARF), acquired diseases, and drugs and the neonatal kidney, including drugs administered to the mother during pregnancy. Acquired diseases discussed include urinary tract infection; renal venous thrombosis; cortical, medullary, and papillary necrosis; Bartter’s syndrome; nephrogenic diabetes insipidus; and oligonephropathy. The chapter includes black-and-white illustrations and photographs and concludes with an extensive list of references. 6 figures. 16 tables. 24 references.

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Renal Tubular Disorders. IN: Hogg, R., ed. Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. pp 165-180.

This chapter about renal tubular disorders is from a textbook that presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The author notes that hereditary renal tubular transport disorders can lead to profound problems in the homeostasis of electrolytes, minerals, or organic solutes in the body and thus can be associated with significant morbidity. However, not all tubular disorders are associated with significant clinical abnormalities. Most patients with renal tubular disorders present in the neonatal period or the 1st year of life. The author summarizes the general characteristics of hereditary tubular transport disorders, reviews some aspects of the pathophysiology and genetic aspects of a few of the diseases, describes the clinical features of the tubulopathies, and briefly summarizes the therapy of some of the disorders that are seen in children. Specific disorders considered include classic cystinuria, hereditary isolated glycosuria, Dent’s disease, proximal renal tubular acidosis, Bartter’s and Gitelman’s syndromes, Liddle syndrome, pseudohypoaldosteronism type 1, distal renal tubular acidosis, and nephrogenic diabetes insipidus. The author concludes that molecular genetics and molecular biology studies have led to the identification of numerous renal tubular disease-causing mutations, have provided important insight into the defective molecular mechanisms underlying various tubulopathies, and have greatly increased the understanding of the physiology of renal tubular transport. 9 figures. 2 tables. 55 references.

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Renal Tubulointestitial Diseases. IN: Nilsson, K.R.; Piccini, J.P., eds. Osler Medical Handbook. Philadelphia, PA: Saunders. 2006. pp. 731-740.

The renal tubulointerstitial diseases are a heterogeneous group of disorders with characteristic features that may include sterile pyuria and white blood cell casts, parenchymal concentrating defects resulting in polyuria and nephrogenic diabetes insipidus, and tubular defects such as renal tubular acidosis (RTA). This chapter on renal tubulointerstitial diseases is from a handbook that provides the essentials of diagnosis and treatment, as well as the latest in evidence-based medicine, for residents working bedside, in-patient care. The chapter begins with a presentation of essential Fast Facts and concludes with Pearls and Pitfalls useful to the practicing internist. The body of the chapter is divided into sections: Epidemiology, Clinical Presentation, Diagnosis, and Management. Specific topics covered in this chapter include acute interstitial nephritis (AIN), a condition that can be caused by drugs, infection, and immunologic disease; acute tubular necrosis (ATN), the most common cause of in-hospital acute renal failure (ARF), often caused by medications, iodinated contrast dye, and hypotension; patients at high risk for contrast nephropathy, including those with preexisting renal dysfunction, diabetes mellitus, multiple myeloma, and advanced age; and the problem of rhabdomyolysis leading to ARF via intratubular obstruction and ATN. The chapter concludes with a list of references, each labeled with a 'strength of evidence' grade to help readers determine the type of research available in that reference source. 2 figures. 1 table. 18 references.

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What Goes Wrong in Diabetes Insipidus?. Endless Water. 11(2): 1-3, 9. Spring 2006.

This article familiarizes readers with diabetes insipidus (DI), a condition characterized by excessive urination and thirst. The author provides some brief background information about the way people normally regulate the amount of water in their body and explains how defects in different parts of this regulatory system result in the abnormalities associated with the different types of DI. An inability to produce normal amounts of the antidiuretic hormone vasopressin is known as pituitary DI. A deficiency of vasopressin due to increased degradation by the placenta is gestational DI. A deficiency of vasopressin caused by excessive intake of water or other fluids is primary polydipsia or dipsogenic DI. An inability of the kidney to respond normally to vasopressin is called nephrogenic DI. This article is one in a series of patient education newsletter articles on DI.

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Causes of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review American Journal of Kidney Diseases. 45(4): 626-637. April 2005.

In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). This review article summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. The reviewers identified and considered 155 studies published between 1957 and March 2004; these studies described 30 risk factors for NDI. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. Of the 155 studies, 58 studies provided a ‘definite’ diagnosis of NDI; 83 studies, a ‘probable’ diagnosis; and 14 studies, a ‘possible’ diagnosis. Nine factors were considered definite causes of NDI; 15 factors were probable causes; and 6 factors considered possible causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. The authors conclude that most risk factors for reversible NDI were medications, and their identification and removal resulted in resolution of the condition. 5 tables. 110 references.

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Helping Your Family Cope with Your Diabetes. Endless Water. 10(3): 1-3, 8-9. Fall 2005.

Coping with a long-term medical condition is complex for both caregivers and the patient. This article explores how a long-term or chronic condition such as diabetes insipidus (DI) can affect not only the patient's medical status, but also the patient's family's social life, emotional stability, financial resources, and physical health. The author encourages readers to learn as much as they can about their disease and to help family members educate themselves as well. Readers are referred to the Diabetes Insipidus Foundation website as well as other resources for more information (www.diabetesinsipidus.org). The article offers practical strategies for patients as they adjust to a new diagnosis of DI: be realistic and take changes slowly; do not forget to have fun to reduce stress, understand one's own coping process, and try to cultivate a positive attitude and a sense of humor. Readers are also encouraged to learn and use communication strategies to help with clear understanding and supporting each family member. A final section addresses financial concerns that may arise when dealing with a chronic illness. 8 references.

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