22. Diabetes insipidus Flashcards
etiology of diabetes insipidous ?
Central diabetes insipidus (CDI); most common form: caused by insufficient or absent hypothalamic synthesis or secretion of antidiuretic hormone (ADH) from the posterior pituitary
Primary (∼ ⅓ of cases)
Most cases are idiopathic.
Secondary (∼ ⅔ of cases) Brain tumors (especially craniopharyngioma) and cerebral metastasis (most common: lung cancer and leukemia/lymphoma)
Neurosurgery: usually after the removal of large adenomas
Traumatic brain injury,
pituitary bleeding, subarachnoid hemorrhage
Pituitary ischemia (e.g., Sheehan syndrome, ischemic stroke)
Infection (e.g., meningitis)
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Nephrogenic diabetes insipidus (NDI);
caused by defective ADH receptors in the distal tubules and collecting ducts
Hereditary (mutation in ADH receptor; very rare)
Acquired
multiple myeloma
Adverse effect of medications (lithium, demeclocycline)
Renal disease (e.g., autosomal dominant polycystic kidney disease, renal amyloidosis)
Pregnancy - increased metabolism of vasopressin in pregnancy due to the placenta making an enzyme
clinical features of diabetes insidious ?
Polyuria with dilute urine
Nocturia → restless sleep, daytime sleepiness
abscise of this the diagnosis of DI unlikely
Polydipsia (excessive thirst)
In cases of low water intake → severe dehydration (altered mental status, lethargy, seizures, coma) and hypotension
what is the diagnosis of DI ?
central and nephrogenic DI
mild hypernatremia
ADH decreased in central
ADH - normal or increased in nephrogenic
plasma osmolality - high
urine osmolality - low
urine specific gravity less than 1.005
After obtaining baseline lab values, patients stop drinking water for 2–3 hours before the first measurement
After 2–3 hours without drinking water
Test urine volume and osmolality every hour
Test sodium and plasma osmolality every two hours
Water deprivation continues until one of the following occurs:
Urine osmolality rises and reaches a normal value→ DI ruled out and primary polydipsia confirmed
No change in urine osmolality despite a rising plasma osmolality
administer desmopressin (a synthetic ADH analog)
Monitor urine osmolality testing every 30 minutes for 2 hours
In CDI: Urine osmolality rises after desmopressin administration (renal ADH receptors are intact).
In NDI: Urine osmolality remains low after desmopressin administration (defective renal ADH
what is the treatmnet for DI ?
Central diabetes insipidus
Desmopressin: synthetic vasopressin without vasoconstrictive effects
Administration: intranasal, subcutaneous, or oral
Important side effect: hyponatremia
or chloropropamide
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nephrogenic
A low-salt, low-protein diet reduces urine outpu
thiazide diuretics lead to sodium depletion, which causes sodium and water reabsorption in the proximal tubules. As a result, less water reaches the ADH-sensitive distal collecting tubules
NSAIDs - indomethacin
Amiloride : Indicated in patients with lithium-induced NDI; amiloride blocks lithium entry through the sodium channel.