Specific Considerations with Endocrine Disease - Calcium Metabolism and Parathyroid Disease

Specific Considerations with Endocrine Disease - Calcium Metabolism and Parathyroid Disease is a topic covered in the Clinical Anesthesia Procedures.

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Calcium is essential for neuromuscular excitability, cardiac automaticity, mitotic division, coagulation, muscle contraction, neurotransmitter and hormone secretion and action, and the activity of many enzymes. Parathyroid hormone (PTH) and vitamin D maintain the extracellular calcium concentration within a narrow range. PTH increases intestinal calcium absorption, increases osteoclastic release of calcium and phosphorus from bone, decreases renal clearance of calcium, and enhances formation of 1,25-dihydroxyvitamin D by the kidney. Levels of ionized calcium and magnesium determine the secretion of PTH. Vitamin D augments the effects of PTH and is necessary for calcium absorption from the GI tract. Calcitonin from thyroid “C” cells lowers calcium and phosphorous concentrations by inhibiting renal calcium reabsorption and osteoclast activity but has a limited physiologic role in humans.

Serum calcium is divided into bound (primarily to albumin) and unbound (free, ionized) forms. Phosphate, citrate, and other anions complex about 6% of the total serum calcium. Hypoalbuminemia produces a decrease in total calcium of approximately 0.8 mg/dL for each gram per deciliter of albumin below normal (4.0 g/dL). Acidosis increases, and alkalosis decreases, ionized calcium due to alterations in albumin binding. Ionized calcium, the physiologically important form, can be measured directly in whole blood.

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