Diabetes Insipidus And Inappropriate ADH Syndrome PDF

DIABETES INSIPIDUS AND INAPPROPIATE ADH SYNDROME 1)Diabetes Insipidus: Excretion of a large volume of urine(diabetes)that is hypotonic, dilute and tasteless(insipid) Patients present with polyuria (urine output exceeding 3 L/day) Caused by either decreased synthesis and secretion of vaso...

DIABETES INSIPIDUS AND INAPPROPIATE ADH SYNDROME 1)Diabetes Insipidus: Excretion of a large volume of urine(diabetes)that is hypotonic, dilute and tasteless(insipid) Patients present with polyuria (urine output exceeding 3 L/day) Caused by either decreased synthesis and secretion of vasopressin or decreased end-organ response to vasopressin  Vasopressin (ADH) is the water retaining hormone and along with thirst is the primary regulator of osmolality Vasopressin acts on V2 receptors in principal cells in the collecting duct to stimulate the expression of intracellular water channels, aquaporin-2 Vasopressin is produced in hypothalamus and stored in posterior pituitary  Causes of diabetes insipidus: 1)Solid tumors and hematologic malignancies:the most common solid tumor to produce diabetes insipidus is craniopharyngioma.Lymphoma or infiltration of the hypothalamus with leukemia are rare causes of diabetes insipidus  2)Trauma or surgery 3)Granulomatous and infectious disease: Langerhans cell histiocytosis, wegener granulomatosis, sarcoidosis, tuberculosis and other infections 4)lymphocyctic infundibulohypophysitis: 5)cerebral anoxia/death 6)Decreased end organ response to vasopressin(Nephrogenic diabetes insipidus) Nephrogenic diabetes insipidus: 1)Congenital nephrogenic DI: a)X linked recessive mutation of the V2 receptor b)Autosomal recessive mutation of the aquaporin-2 water channels 2)Acquired nephrogenic DI:hypercalcemia,potassium deficiency, lithium,demeclocycline  Diagnosis is made by dehydration test İmaging of the hypothalamus is an important tool in DI. MR may reveal thickening of the stalk and absence of the posterior pituitary bright spot  Hypothalamic DI is best treated by the vasopressin analogue desmopressin In nephrogenic DI any offending drug or electrolyte abnormality that might produce acquired nephrogenic DI should be stopped and corrected  SYNDROME OF INAPPROPIATE ANTIDIURETIC HORMONE The pathophysiology of SIADH begins with uncontrolled secretion of vasopressin Hypoosmolality and hyponatremia occur Thirst is not adequately suppressed so fluid intake continues  Vasopressin limits the excretion of water in the urine.continued ingestion of water produces an expansion of extracellular and intracellular volume.the body attempts to bring the extracellular fluid volume back to normal by natriuresis This natriuresis decreases total body water and total body sodium  Symptoms of hyponatremia: When hyponatremia develops rapidly and is severe(serum sodium level < 120 mEq/L), patients are at risk for cerebral edema with herniation of the brain stem Hyponatremia is usually considered chronic if hyponatremia has developed slowly and persisted for greater than 48 hours  Diagnosis:decreased plasma osmolality, clinical euvolemia,increased urinary sodium excretion and absence of other causes of euvolemic hypoosmolality such as hypothyroidism, adrenal insufficiency or diuretic use  Three main etiologies of SIADH are: A)ectopic production of vasopressin by cancer B)drug-induced SIADH :SSRI, tricyclic antidepressants,carbamazapine, desmopressin C)central nervous system disorders and pulmonary disorders  Treatment: In chronic hyponatremia that is asymptomatic the safest therapy is restriction of free water When hyponatremia occurs rapidly and severe and symptomatic , discontinuing the administration of any hypotonic fluid and administration of hypertonic NACL should be promptly considered  The tetracycline derivate demeclocycline is known to cause nephrogenic DI and has been used to treat chronic SIADH The most specific treatment for SIADH is to block the V2 receptors in the kidney (conivaptan, Tolvaptan)