Endocrine System 1 out of 251
Two days after undergoing an emergency laparotomy following a motor vehicle collision, a 37-year-old man has increased thirst. Examination shows dry mucous membranes and decreased skin turgor. A review of his chart shows his urine output to be in excess of his fluid intake. Laboratory studies show a serum sodium concentration of 151 mEq/L and urine osmolality of 110 mOsmol/kg H2O. One hour after the administration of desmopressin, the serum sodium concentration is 147 mEq/L and urine osmolality is 400 mOsmol/kg H2O. One week later, his laboratory values are within normal limits. This patient's condition was most likely caused by damage to which of the following structures?
Proximal renal tubuleDamage to the proximal renal tubule can manifest with polyuria, which is seen in this patient. However, the polyuric phase typically follows an acute anuric phase, which is not described here. Furthermore, damage to the proximal tubule is not associated with a reversal of the changes in serum and urine osmolality after desmopressin administration. Posterior pituitary
Antidiuretic hormone (ADH) is produced in the hypothalamus (supraoptic nucleus and paraventricular nucleus). This hormone is then stored in, and subsequently released by, the posterior pituitary gland. Ischemia or direct damage (e.g., major surgery or head trauma) to the pituitary gland can affect ADH secretion and cause transient central DI. Features of central DI include polyuria, polydipsia, and increased serum osmolality in the presence of low urine osmolality. In the majority of cases, patients recover the ability to maintain serum osmolality, and ADH secretion is restored. Supraoptic nucleusThe supraoptic nucleus produces ADH. Damage to this nucleus leads to central DI, which can manifest with thirst, polyuria, and hypernatremia as seen in this patient. However, because the majority of ADH is produced in the supraoptic nucleus, damage to this structure typically leads to permanent DI, not a quick recovery (transient DI) like the one seen here. Collecting ductDamage to the collecting duct can cause nephrogenic DI. This condition manifests with thirst, polyuria, and hypernatremia as seen in this patient. However, because nephrogenic DI is not responsive to desmopressin, its administration would not result in a reversal of the changes in serum and urine osmolality. Adrenal cortexThe adrenal cortex produces glucocorticoids and mineralocorticoids. Acute adrenal insufficiency can occur in the postoperative period (Addisonian crisis) because of ischemic adrenal damage. Furthermore, acute adrenal insufficiency can be transient, as seen here. However, adrenal insufficiency typically manifests with hypotension and hyponatremia, and this condition would be diagnosed with an ACTH stimulation test, not with desmopressin administration.
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