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DI and SIADH Cheat Sheet by

Diabetes Insipidus and Syndrome of Inappropriate Anti-Diuretic Hormone

DI

DECREASED ADH
Causes: Neurogenic - hypoth­alamus or pituitary lesion causes decreased synthesis, transport and release of ADH. Nephro­genic - inadequate response at the kidney tubules to ADH. Results in dilute urine.
Signs and Symptoms: polydi­psis, polyuria, hypern­atr­emia, change in mental status, fatigue, weakness, hemody­namic instab­ility.
Diagnosis: DDAVP test. A pt with neurogenic DI will respond by having an increase in urine osmolality concen­tra­tion.
Treatment: Neurogenic - 100-200 mU/h DDAVP with isotonic crysta­lloid. Nephro­genic - Chlorp­rop­amide, clofibrate and thiazide diuretics.
 

SIADH

INCREASED ADH RELEASE
Cause: small cell lung carcinoma - (50% of these pt's develop SIADH). Medica­tions that stimulate the release of ADH: chlorp­rop­amide (sulfo­nyl­urea), clofibrate (fibrate), thiazide diuretics, antine­opl­astic agents.
Signs and symptoms: Nausea, weakness, lethargy, confusion, depressed mental status, seizures
Lab values: hypona­tremia, decreased serum osmola­lity, normal­/in­creased Na+ excretion, normal­/in­creased urine osmolality
Treatment: Surgery to treat primary malign­ancy. Free water restri­ction (500-1­000­mL/­day). Demecl­ocy­cline: inhibits ADH at distal tubule. Convaptan: V2R antagonist (vasop­ressin 2 receptor). Severe hypona­tremia (<1­15mEq): 3% NS or 0.9% NS with furose­mide.
Anesthetic consid­era­tions: Replac­ement Na+ slowly to prevent pontine myelin­olysis
       
 

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