Syndrome of inappropriate antidiuretic hormone secretion
| Syndrome of inappropriate antidiuretic hormone secretion | |
|---|---|
| Synonym | Schwartz-Bartter syndrome, syndrome of inappropriate antidiuresis(SIAD) |
| Explanation of SIADH | |
| Classification and external resources | |
| Specialty | Endocrinology |
| ICD-10 | E22.2 |
| ICD-9-CM | 253.6 |
| DiseasesDB | 12050 |
| MedlinePlus | 003702 |
| eMedicine | emerg/784 med/3541 ped/2190 |
| MeSH | D007177 |
Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source. The increase in blood volume (hypervolemia) often results in dilutional hyponatremia in which the plasma sodium levels are lowered and total body fluid is increased. Although the sodium level is low, SIADH is brought about by an excess of water rather than a deficit of sodium.
It was originally described in people with small-cell carcinoma of the lung, but it can be caused by a number of underlying medical conditions. The treatment may consist of fluid intake restriction, various medicines, and management of the underlying cause. Salt administration may help prevent brain swelling by increasing attractive force to keep water in the bloodstream, preventing fluid buildup in tissue. SIADH was first described in 1957.
Certain prominent physical findings may be seen only in severe or rapid-onset hyponatremia.
Causes of SIADH include conditions that dysregulate ADH secretion in the central nervous system, tumors that secrete ADH, drugs that increase ADH secretion, and many others. A list of common causes is below:
The normal function of ADH on the kidneys is to control the amount of water reabsorbed by kidney nephrons. ADH acts in the distal portion of the renal tubule (Distal Convoluted Tubule) as well as on the collecting duct and causes the retention of water, but not solute. Hence, ADH activity effectively dilutes the blood (decreasing the concentrations of solutes such as sodium), causing hyponatremia; this is compounded by the fact that the body responds to water retention by decreasing aldosterone, thus allowing even more sodium wasting. For this reason, a high urinary sodium excretion will be seen.
ADH is secreted to prevent water loss in the kidneys. When water is ingested, it is taken up into the circulation and results in a dilution of the plasma. This dilution, otherwise described as a reduction in plasma osmolality, is detected by osmoreceptors in the hypothalamus of the brain and these then switch off the release of ADH. The decreasing concentration of ADH effectively inhibits the aquaporins in the collecting ducts and distal convoluted tubules in the nephrons of the kidney. Hence, less water is reabsorbed, thereby increasing urine output, decreasing urine osmolality, and normalizing blood osmolality.
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