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The 4 parathyroid glands derive from the third and fourth pharyngeal pouches and descend caudally to the anterior neck. They are embedded in the posterior thymus, with ectopic locations occurring as well. Through the secretion of PTH, the parathyroid glands are primarily responsible for maintaining extracellular calcium and phosphate concentrations. PTH is secreted in 3 distinct ways: tonic secretion, circadian dynamics (with the highest amount secreted in the morning and lowest in the evening), and a pulsatility that appears to be stochastic (occurring unpredictably, 10 or more times a day). Most PTH is secreted continuously [6, 13, 14]. It has well-described effects on bone, kidney, and intestine, which play a role in controlling serum calcium and phosphate levels [1]. PTH is a central regulator of bone homeostasis, through its action on bone-forming osteoblasts, osteocytes, and bone-resorbing osteoclasts [4]. The final effect of PTH on bone mass is either anabolic or catabolic, and will depend on the dose and periodicity of PTH signaling [6]. In the kidney, the effects of PTH are targeted to enhance synthesis of active vitamin D, 1,25(OH)₂D₃, enhance tubular calcium reabsorption, a calcium-conserving property, and enhance phosphate excretion, a phosphaturic property [6].

PHPT is a common disorder of mineral metabolism that is due to excessive secretion of PTH from 1 or more of the 4 parathyroid glands. The clinical consequences of abnormally active parathyroid tissue are typically hypercalcemia and concentrations of PTH that are either clearly elevated above the normal range or inappropriately normal in the context of hypercalcemia.