Diabetes insipidus Flashcards
Diabetes insipidus
Lack of ADH or lack of response to ADH
Prevents kidneys from being able to concentrate the urine leading to polyuria and polydipsia
Types of diabetes insipidus
Nephrogenic or cranial
Causes of cranial
Idiopathic
Post head injury
Pituitary surgery
Craniopharyngiomas
Infiltrative (histiocytes, sarcoidosis)
Wolfram’s syndrome
Haemochromatosis
Brain infections
Wolfram’s syndrome
Diabetes insipidus
Diabetes mellitus
Optic atrophy
Deafness
Causes of nephrogenic
Genetic (more common affects the ADH receptor, less common gene encodes aquaporin 2 channel)
Hypercalcaemia
Hypokalaemia
Lithium
Democlocyline
Tubulo-interstial disease (obstruction, sickle-cell, pyelonephritis)
Presentation
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatreamia
Investigations
Low urine osmolality
High serum osmolality
Water deprivation test
Water deprivation test method
Patients avoid taking any fluids for 8 hours
Urine osmolality measured and synthetic ADH administered
8 hours later urine osmolality measured again
Water deprivation test nephrogenic diabetes results
Patient unable to respond to ADH
Diluting their urine with excessive water secretion by the kidneys
Urine osmolality will be low initially and remain low even after synthetic ADH given
Water deprivation test cranial diabetes results
Kidneys still capable of responding to ADH
Urine osmolality initially low as continues to be diluted by excessive water secretion
When synthetic ADH given, kidneys respond by reabsorbing water and concentrating the urine so urine osmolality will be high
Water deprivation test primary polydipsia
8 hours of water deprivation will cause urine osmolality to be high even before the synthetic ADH is given
(high urine osmolality after 8 hours of water deprivation indicates no diabetes insipidus)
Management
If possible treat underlying cause
Desmopressin in cranial
Thiazides and low salt/ protein diet for nephrogenic
Desmopressin in higher doses for nephrogenic under close monitoring
