RT Book, Section A1 Rabaglia, Jennifer L. A1 Moore, Francis D. A2 Morita, Shane Y. A2 Dackiw, Alan P. B. A2 Zeiger, Martha A. SR Print(0) ID 6162914 T1 Chapter 10. Secondary and Tertiary Hyperparathyroidism T2 McGraw-Hill Manual: Endocrine Surgery YR 2010 FD 2010 PB The McGraw-Hill Companies PP New York, NY SN 978-0-07-160645-5 LK accesssurgery.mhmedical.com/content.aspx?aid=6162914 RD 2023/03/29 AB The precise regulation of the serum ionized calcium concentration is necessary to sustain human life. The calcium cation is central to a myriad of reactions, from enzymatic function to the coagulation cascade to muscle fiber contraction and neurotransmission to the dynamic buildup and breakdown of the scaffolding that houses it all. The majority of calcium in the human body is found in the skeleton and comprises approximately 2% of the average individual's body weight. Serum calcium levels are precisely maintained through an intricate interplay of checks and balances that begin and end with the parathyroid glands. The regulatory axis of calcium consists of the parathyroid glands, parathyroid hormone (PTH), membrane calcium receptors, the kidneys, the gut, and bone. Membrane calcium receptors on the cells of the parathyroid glands sense minute decreases in serum ionized calcium levels, triggering a cascade beginning with the secretion of PTH. This stimulates mobilization of calcium from bone, a reduction in renal calcium excretion, and an increase in renal hydroxylation of vitamin D, indirectly affecting calcium absorption in the duodenum and proximal jejunum. When calcium increases to within an acceptable range, calcium receptor-based stimulation of the parathyroids ceases, and secretion of PTH is inhibited. Thus, under normal conditions, the defining relationship between serum calcium and serum PTH is inverse: that is, high serum calcium begets low serum PTH and vice versa.