Figure 519

Physiologic response to hypercalcemia. Hypercalcemia directly inhibits both parathyroid hormone (PTH) release and synthesis. The decrease in PTH and hypercalcemia decrease the activity of the 1-a-hydroxylase enzyme located in the proximal tubular (PT) cells of the nephron, which in turn, decreases the synthesis of 1,25-dihydroxy-vitamin D3 (1,25(OH)2D3). Hypercalcemia stimulates the C cells in the thyroid gland to increase synthesis of calci-tonin (CT). Bone resorption by osteoclasts is blocked by the increased CT and decreased PTH. Decreased levels of PTH and 1,25(OH)2D3 inhibit Ca reabsorption in the distal convoluted tubules (DCT) of the nephrons and overwhelm the effects of CT, which augment Ca reabsorption in the medullary thick ascending limb leading to an increase in renal Ca excretion. The decrease in 1,25(OH^D3 decreases gastrointestinal (GI) tract absorption of dietary Ca. All of these effects tend to return serum Ca to normal levels [1].

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