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Pituitary & Water Balance Disorders — SIADH & Diabetes Insipidus

💧 Water Balance Disorders

SIADH and Diabetes Insipidus — ADH excess vs ADH absence. Opposite physiology, opposite biochemistry, and a diagnostic test that distinguishes them all.

ADH: The Master of Water

ADH (antidiuretic hormone, also called vasopressin) is produced in the hypothalamus and released from the posterior pituitary. Its job is simple: signal the collecting ducts of the kidney to reabsorb water. Too much ADH → too much water retained → dilution. Too little (or resistance to) ADH → too much water lost → concentration and dehydration.

The Central Axis

The entire topic rests on one principle: ADH controls free water reabsorption in the collecting duct via aquaporin-2 channels. When ADH acts → water stays → urine concentrates. When ADH is absent or ineffective → water goes → urine is dilute.

SIADH = ADH stuck ON → concentrated urine, dilute blood (hyponatraemia)
DI = ADH OFF (or ignored) → dilute urine, concentrated blood (hypernatraemia)

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SIADH
Syndrome of Inappropriate ADH Secretion
ADH EXCESS
Core defectADH secreted regardless of plasma osmolality — water inappropriately retained
Blood📉 Hyponatraemia (dilutional) | Normal/low plasma osmolality | Euvolaemic
Urine📈 Concentrated — urine osmolality > plasma osmolality; urine Na⁺ > 20 mmol/L
CausesSurgical stress, head injury, small cell lung Ca, drugs (carbamazepine, SSRIs)
ManagementFluid restriction ± demeclocycline ± hypertonic saline (severe)
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Diabetes Insipidus
Central (↓ ADH) or Nephrogenic (ADH resistance)
ADH ABSENT / INEFFECTIVE
Core defectADH absent (central) or collecting duct is unresponsive (nephrogenic)
Blood📈 Hypernatraemia | High plasma osmolality | Dehydration
Urine📉 Massive dilute urine — urine osmolality < plasma osmolality; polyuria (3–20 L/day)
CausesCentral: post-pituitary surgery, head trauma, craniopharyngioma | Nephrogenic: lithium, hypercalcaemia
ManagementCentral: desmopressin | Nephrogenic: treat cause, thiazides, low-salt diet
ADH Axis — Normal, SIADH and DI NORMAL SIADH DIABETES INSIPIDUS Hypothalamus Senses osmolality → makes ADH Post. Pituitary Releases ADH proportionally Collecting Duct AQP-2 opens → water reabsorbed RESULT: NORMAL Na⁺: 135–145 mmol/L Plasma Osm: 285–295 Urine: appropriate concentration ADH released Inappropriately — regardless of osm SCLC / Surgery drugs / head injury Collecting duct AQP-2 constantly open ↑↑ Water retained Blood diluted, urine concentrated RESULT: SIADH 📉 Na⁺ LOW (hyponatraemia) 📉 Plasma Osm LOW 📈 Urine Osm > Plasma Osm ADH absent (central) OR ignored (nephrogenic) Pituitary surgery / lithium / hypercalcaemia Collecting duct AQP-2 closed → water cannot be reabsorbed Massive free water loss in urine Polyuria 3–20 L/day · dehydration RESULT: DI 📈 Na⁺ HIGH (hypernatraemia) 📈 Plasma Osm HIGH 📉 Urine Osm LOW (dilute)
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