Serum calcium is normally maintained in a narrow range that’s required for optimal activity of extra and intracellular processes.
Where is it in our body?
Calcium is typically transported partly bound to plasma proteins (i.e. albumin), to small anions (phosphate and citrate) and partly in the ‘free’ or ionised state. Of note, only the ionised state is metabolically active.
What controls it?
Directly by hormonal control
Parathyroid hormone causes increase in serum Ca by:
Increasing reabsorption of calcium in kidneys and GIT
Releasing Ca and Phosphate from bones
Vitamin D (calcitriol) causes increase in serum Ca by:
Increasing calcium and phosphate absorption in the GIT
Increasing calcium and phosphate reabsorption in the kidneys
Calcitonin causes decrease in serum Ca by:
Opposing PTH and inhibits bone resorption
Magnesium: Hypomagnesemia reduces PTH secretion or causes PTH resistance and therefore indirectly leads to hypocalcaemia.
Phosphate: Hyperphosphataemia leads to hypocalcaemia as phosphate binds to serum calcium
Directly impacting ratio of protein bound calcium to ionised calcium
Serum protein levels (e.g. albumin)
Acid base status (e.g. low pH
Confirm true hypocalcaemia
Screen for symptoms and monitor for haemodynamic instability
If low and symptomatic or severely low, start management immediately
Hypocalcaemia with low PTH
Surgical removal of the PTH glands intentionally or non-intentionally
Autoimmune destruction of the PTH glands
Loss of PTH glands from surgical/autoimmune/development)
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