Divided into folowing types-
1)Deficient prodn of ADH
i)Primary defi (neurogenic, pituitary, cranial) due 2 agenesis/destrction of neurohypophysis
ii)Secondary defi due to inhibition of ADH secretion
2)Deficient action of ADH (neurogenic diabetes insipdus)
**Etio:-
1) Primary defi of ADH
-severe head injury
-neoplasms
craniopharyngioma, pituitary adenoma
-granulomas
sarcoidosis, histiocytosis
-infections
chronic meningitis, viral encephalitis
-inflamatory
hypophysitis
-vascular
Sheehan's syndrome
-Genetic defects
-Idiopathic
2) Secondary defi of ADH
-Psychogenic polydipsia
-Dipsogenic polydipsia
-Iatrogenic
3) Nephrogenic diabts insipidus
-Drugs
lithium, demeclocycline
-Metabolic
hypercalcemia, hypokalaemia
-Obstructive uropathy
-Amyoidosis
-Vascular causes
sickl cel anamia, acute tubular necrosis
-Genetic
-Idiopathic
**C/F
Polyuria, excesiv thirst & polydipsia r d cardinal symptoms
Daily urine output may reach as high as 10-15 litres
**Diagno
-Urine clear, & of low sp gravity. Osmolality low, usualy less dan plasma
-Serum sodium is borderline high indicating water loss
-Water deprivation test
diagno of cranial DI dpends on demo dat a rise of plasma osmolality induced by widholding fluids is nt acompnied by a normal rise in d osmolality / sp gravity of urine, but wen vasopresin is givn, such a rise does occur. Later test is necesary 2 shw dat kidny is capable of concentrating urine whch it cant do in nephrogenic DI
-MRI of pituitary & hypothalamus
**Rx
-Desmopressin(DDAVP) 10-20microgm intranasaly once/twice a day
-Chlorpropamide enhances renal responsiveness 2 vasopressin
-Carbamazepine can b used
-Thiazide diuretics in nephrogenic DI
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