Hypocalcemia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]
Overview
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), Gs 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).
Pathophysiology
Physiology
The normal physiology of Hypocalcemia can be understood as follows:
- The normal concentrations of calcium in the body is maintained within the narrow range and that is required for the minimal activity of the many extra- and intracellular processes calcium regulates.
- Calcium transport within the blood is mainly bound to plasma proteins like albumin (45%), phosphate and citrate(15%) and ionized state(40%).
- Only the ionized form of calcium is active but most laboratories show report of total serum calcium concentrations.
- The normal concentration of calcium ranges between 8.5 and 10.5 mg/dL.
- The normal range of ionized calcium in the plasma is 4.65 to 5.25 mg/dL.
Pathogenesis
- It is understood that Hypocalcemia is the result caused by the following
Hypoalbuminemia
- When there is a fluctuation in the protein concentrations especially the one protein which is albumin,total calcium levels in the blood may change.
- Whereas the levels of ionized calcium(free form) remains mostly constant, because it is hormonally regulated.
- So that the total serum calcium levels may not accurately reflect the physiologically important ionized calcium concentration.
Hormone regulation
- Parathyroid hormone (PTH) and vitamin D play a important role in regulating serum calcium.[1]
- Calcium by itself controls to regulate its own serum levels via a calcium-sensing receptor (CaSR) in the parathyroid gland to inhibit parathyroid hormone (PTH) secretion and on a CaSR in the loop of Henle of the kidney to stimulate renal calcium excretion.[2][3]
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.[4]
References
- ↑ Riccardi D, Brown EM (March 2010). "Physiology and pathophysiology of the calcium-sensing receptor in the kidney". Am. J. Physiol. Renal Physiol. 298 (3): F485–99. doi:10.1152/ajprenal.00608.2009. PMC 2838589. PMID 19923405.
- ↑ Goodman WG (January 2004). "Calcium-sensing receptors". Semin. Nephrol. 24 (1): 17–24. PMID 14730506.
- ↑ Quarles LD (July 2003). "Extracellular calcium-sensing receptors in the parathyroid gland, kidney, and other tissues". Curr. Opin. Nephrol. Hypertens. 12 (4): 349–55. doi:10.1097/01.mnh.0000079682.89474.80. PMID 12815330.
- ↑ Taal, Maarten (2012). Brenner & Rector's the kidney. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1416061939.