19961 - DIABETES INSIPIDUS Dr. Abdelaziz Elamin MD, PhD,...

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DIABETES INSIPIDUS Dr. Abdelaziz Elamin MD, PhD, FRCPCH Professor of Child Health consultant pediatric  endocrinologist Sultan Qaboos University Muscat, Oman. [email protected] .com
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DIABETES INSIPIDUS DI is a disorder resulting from deficiency of  anti-diuretic hormone (ADH) or its action and is  characterized by the passage of copious  amounts of dilute urine. It must be differentiated from other polyuric  states such as primary polydipsia & osmotic  duiresis. Central DI is due to failure of the  pituitary gland to secrete adequate ADH.  
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DIABETES INSIPIDUS /2 Nephrogenic DI results when the renal  tubules of the kidneys fail to respond to  circulating ADH.    The resulting renal concentration defect  leads to the loss of large volumes of dilute  urine. This causes cellular and  extracellular dehydration and  hypernatremia.
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THE POSTERIOR PITUITARY Is composed of nerve fibers that have their  cell bodies in the supraoptic & paraventricular  nuclei of the hypothalamus. The neurosecretory cells in these nuclei  synthesize Oxytocin & Vasopressin which  pass down the nerve fibres to be stored in &  released from the posterior pituitary.
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REGULATION OF ADH SECRETION ADH RELEASE IS STIMULATED BY: A PLASMA OSMOLALITY >280 mOsm/l A FALL IN PLASMA VOLUME EMOTIONAL FACTORS & STRESS SLEEP OTHER FACTORS
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Other ADH Stimulants CHOLINERGIC STIMULATION  a-ADRENERGIC STIMULATION ANGIOTENSIN II PROSTAGLANDIN E OPIATES NICOTINE HISTAMINE ETHER PHENOBARBITONE
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ADH SECRETION IS INHIBITED BY: ALCOHOL OROPHARYNGEAL WATER REFLEX b-DRENERGIC STIMULANTS ATRIAL NATRIURETIC FACTOR (ANF) PHENYTOIN
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ADH THE SUPRAOPTIC NUCLEUS (SON) IS 
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This note was uploaded on 02/23/2012 for the course PHARM 290 taught by Professor Staff during the Fall '10 term at Rutgers.

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19961 - DIABETES INSIPIDUS Dr. Abdelaziz Elamin MD, PhD,...

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