Hypocalcemia pathophysiology: Difference between revisions
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{{Hypocalcemia}} | {{Hypocalcemia}} | ||
{{CMG}} | {{CMG}}; {{AE}} | ||
==Overview== | |||
==Pathophysiology== | ==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<sub>s</sub> 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]]). | 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<sub>s</sub> 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=== | ===Alkalosis=== | ||
In [[alkalosis]], [[hydrogen ion]]s dissociate from the negatively charged [[albumin]], which allows for increased calcium binding and leads to a decreased concentration of free calcium. | In [[alkalosis]], [[hydrogen ion]]s dissociate from the negatively charged [[albumin]], which allows for increased calcium binding and leads to a decreased concentration of free calcium. | ||
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[[Category: | [[Category:Needs content]] | ||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
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Revision as of 12:08, 22 July 2016
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Hypocalcemia Microchapters |
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Hypocalcemia pathophysiology On the Web |
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American Roentgen Ray Society Images of Hypocalcemia pathophysiology |
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Risk calculators and risk factors for Hypocalcemia pathophysiology |
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), 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).
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.[1]
References
- ↑ Taal, Maarten (2012). Brenner & Rector's the kidney. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1416061939.