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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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