• Sketchy
• Osmosis

Diabetes Insipidus.

• First Aid.

Vasopressin, also known as the antidiuretic hormone (ADH), is synthesized in the hypothalamus, particularly in the paraventricular and supraoptic nuclei. After synthesis, ADH is transported to the posterior pituitary for storage and subsequent release into the circulation.

• ADH maintains water balance by regulating water absorption from the kidney's collecting tubule.
• Loss of body water leads to increased serum osmolality and reduced vascular volume. These physiological changes stimulate the production and release of ADH, triggered by osmoreceptors in the hypothalamic nuclei and baroreceptors in the carotids and atria.
• Diabetes insipidus (DI) is a disease marked by polyuria (excessive urination) and polydipsia (excessive thirst), despite normal blood glucose levels. This stands in contrast to diabetes mellitus. These symptoms arise due to the lack of normal ADH activity and the consequent production of large volumes of very dilute urine.
• DI is caused by either deficient ADH production (central DI) or resistance to the action of ADH in the kidneys (nephrogenic DI).
• ADH level decreases in central diabetes insipidus (DI) and is normal or increased in nephrogenic DI.
• Nephrogenic DI can be caused by a mutation in the V2 receptor.
• Central DI can either be permanent or temporary.
• Damage to the posterior pituitary gland only results in transient central DI. The remaining magnocellular neurons in the hypothalamus hypertrophy and undergo axonal regeneration, enabling them to produce and release functional quantities of ADH into the circulation.
• Permanent central DI typically results from damage to the hypothalamic nuclei or the pituitary stalk. It is rare for permanent DI to occur from isolated damage to the posterior pituitary as the vasopressinergic neurons are located higher up in the hypothalamus and pituitary stalk. Permanent DI occurs after damage to the hypothalamus or supraoptic-hypophysial tract leads to the destruction of a significant number of these vasopressinergic neurons.
• In patients with suspected DI, a water deprivation test is performed.
• Minimal change in urine osmolarity after the water deprivation test indicates diabetes insipidus.
• A significant increase in urine osmolality after the water deprivation test points to primary polydipsia.