Can you explain the pathophysiology underlying SIADH and DI?

Article Advances in Understanding and Management of Antidiuretic Hor...

Certainly! The pathophysiology underlying Syndrome of Inappropriate Antidiuretic Hormone (SIADH) and Diabetes Insipidus (DI) involves dysregulation of antidiuretic hormone (ADH) or vasopressin, which plays a central role in regulating water balance in the body.

Pathophysiology of SIADH:Excessive ADH Release: In SIADH, there is inappropriate and excessive release of ADH from the posterior pituitary gland or ectopic sources (e.g., tumors, pulmonary disorders, central nervous system disorders). Increased Water Reabsorption: Excess ADH leads to increased water reabsorption in the renal collecting ducts, promoting the retention of free water and dilutional hyponatremia. Consequences: The retained water dilutes the plasma sodium concentration, resulting in hyponatremia and hypo-osmolality. Despite hyponatremia, serum osmolality remains low due to the dilutional effect of excess water. This can lead to neurological symptoms such as confusion, lethargy, seizures, and potentially life-threatening cerebral edema.

Pathophysiology of Diabetes Insipidus (DI): Central DI (Neurogenic DI):ADH Deficiency: In central DI, there is a deficiency or inadequate secretion of ADH from the hypothalamus or posterior pituitary gland due to damage or dysfunction of these structures (e.g., tumors, trauma, surgery, infections). Decreased Water Reabsorption: Without sufficient ADH, the renal collecting ducts are unable to reabsorb water effectively, resulting in excessive urine output (polyuria) and dilute urine. Polyuria and Thirst: The excessive loss of free water leads to polyuria and compensatory polydipsia (excessive thirst) as the body attempts to maintain fluid balance. Despite polyuria, serum osmolality may rise due to dehydration and hypernatremia. Nephrogenic DI:Renal Insensitivity to ADH: Nephrogenic DI occurs when the kidneys fail to respond to circulating ADH properly due to impaired ADH receptor function or downstream signaling pathways in the renal tubules. Decreased Water Reabsorption: Even though ADH levels may be normal or elevated, the kidneys are unable to concentrate urine, resulting in polyuria and dilute urine. Causes: Nephrogenic DI may be inherited (e.g., X-linked recessive) or acquired due to medications (e.g., lithium, demeclocycline), electrolyte abnormalities, renal diseases, or other factors.

In summary, the pathophysiology of SIADH involves excessive ADH release leading to increased water reabsorption and dilutional hyponatremia, while the pathophysiology of DI involves either ADH deficiency (central DI) or renal insensitivity to ADH (nephrogenic DI), resulting in polyuria and dehydration. Understanding these underlying mechanisms is essential for diagnosing and managing these disorders effectively.

Jeyatheepan Jeyaretnam

Also known as arginine vasopressin, ADH is produced in the hypothalamus and stored in the posterior pituitary gland via a pituitary stalk. The primary function of ADH is osmoregulation. When effective blood volume is greatly reduced, however, the function of ADH shifts to volume regulation, even at the expense of effective plasma osmolality or tonicity. ""Plasma osmolality" should be distinguished from "effective plasma osmolality" or ""plasma tonicity"", as the latter is determined by the effective osmoles in the extracellular fluid (ECF), such as sodium (which is not freely permeable through cell membranes), the major component of ECF. While glucose and urea also increase plasma osmolality, they are ineffective osmoles as they are freely permeable through cell membranes and do not contribute to the maintenance of plasma tone.

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