Info
🌱 來自: Huppert’s Notes
Posterior Pituitary🚧 施工中
Posterior Pituitary
↓Antidiuretic hormone (ADH): Diabetes insipidus (DI)
• Etiology: ADH channels do not function to reabsorb water, either due to inadequate ADH (central) or lack of response to ADH at the kidneys (nephrogenic)
- Central DI:
• Low posterior pituitary production of ADH
• Etiologies: Idiopathic (~50% of cases in adults), acquired (trauma/surgery, neoplasms, infiltrative/infectious [Langerhans, sarcoidosis, tuberculosis], vascular), congenital malformations, genetic
- Nephrogenic DI:
• Normal ADH production but the renal tubules do not respond to ADH appropriately
• Etiologies: Medications (lithium, cisplatin), metabolic (hypercalcemia, hypokalemia), ureteral obstruction
• Clinical features: Polyuria (>3 liters urine output in 24 hours), polydipsia. High serum osms, low urine osms
• Diagnosis:
- Confirm polyuria with 24-hr urine volume (typically >3 L/day); urine is typically hypotonic (<300 mosm/kg); exclude glucosuria as cause
- Differentiate between primary polydipsia (excessive fluid intake) and DI: history, serum sodium, and plasma osms can be helpful. Further testing that can be considered:
• Water deprivation test: Withhold fluids and measure urine osmolality (should follow strict protocol with weights, urine osm, and endocrine input): Increase in UOsm = primary polydipsia. Stable = DI.
• Hypertonic saline infusion test
• Plasma copeptin proAVP (CPAVP) measurement
- Differentiate between central and nephrogenic DI:
• ADH (desmopressin) challenge: Increase UOsm >50% = Central DI. Stable = Nephrogenic DI.
• Treatment:
- Central DI: Desmopressin (DDAVP), chlorpropamide increase ADH secretion and enhances effect
- Nephrogenic DI: No good treatments. Sodium restriction and thiazide diuretics can be useful.
- Pearl: Patients with central DI who don’t have access to water and are hospitalized can develop severe hypernatremia. While hospitalized, monitor strict intake/output.
↑ADH: Syndrome of inappropriate ADH (SIADH)/syndrome of inappropriate antidiuresis (SIAD)
• Etiology: Ectopic production of ADH by a tumor (e.g., small cell lung cancer), CNS trauma, pulmonary infection, medications (e.g., SSRIs, chlorpropamide, oxytocin, morphine, vincristine, desmopressin), postoperatively
• Clinical features:
- Low serum Na+ and osms because retain free water; normal or high urine sodium and osms
- Acute symptoms: Lethargy, somnolence, seizures, coma, death
• Diagnosis: Check serum/urine sodium and osms. Rule out other causes of hyponatremia – SIADH is a diagnosis of exclusion.
• Treatment:
- Fluid restriction is the mainstay of treatment in most cases
- Central: Consider desmopressin
- Peripheral: Consider thiazide diuretic
- Lithium-induced: Stop lithium if possible