Hypocalcemia pathophysiology

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Hypocalcemia Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Pathophysiology

Hypocalcemia may develop in disorders associated with insufficient parathyroid hormone or vitamin D production or resistance to hormonal activities. Perturbations of calcium homeostasis can be caused by environmental factors or occur as a result of genetic mutations in the calcium-sensing receptor (as in type 1 autosomal dominant hypocalcemia), G_s α subunit (as in type 1A and 1B pseudohypoparathyroidism), vitamin D hydroxylase (as in type 1 vitamin D-dependent rickets , and calcitriol receptor (as in type 2 vitamin D-dependent rickets).

Alkalosis

In alkalosis, hydrogen ions dissociate from the negatively charged albumin, which allows for increased calcium binding and leads to a decreased concentration of free calcium.

For an increase in pH of 0.1 unit, there is an approximately 0.05 mmol/L (0.1 mEq/L) fall in the serum level of ionized calcium.

Respiratory Alkalosis

Reduced ionized calcium concentration and hypocapnia associated with hyperventilation may contribute to symptoms of vasoconstriction including lightheadedness, fainting, and parasthesia.

Globulin Binding

Calcium binding to globulin is relatively small (1.0 g of globulin binds 0.2–0.3 mg of calcium) and generally does not influence the total serum calcium concentration.

References