CALCIUM HOMEOSTASIS
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| Calcium Regulation: Parathyroid hormone vs Calcitonin |
Calcium is one of the most pronounced mineral in human body which not only forms your bones and teeth, but perform several other essential functions. However, these normal calcium levels can go haywire due to pathological cause, thereby causing either increased calcium levels or Hypercalcemia or Decreased Calcium levels, called Hypocalcemia.
Not just the bones and teeth, Plasma calcium or Calcium levels in blood is going to be important too. Nevertheless, it is necessary to understand the medical physiology behind the regulation of calcium levels before one can proceed to its abnormal values.
Today, we are going to cover up Normal physiology of the calcium as an medical entity, how the Parathyroid hormone (PTH) from parathyroid gland clashes with Calcitonin from the thyroid gland.
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| Calcium Regulation Physiology |
CALCIUM IN BODY: VALUES AND FUNCTIONS
Approximately 99% of the body calcium is used up in maintaining skeletal structure of your body, rest of the 1% calcium goes to extra-cellular fluid for physiological actions like blood coagulation, cellular communication, exocytosis, endocytosis, muscle contraction and neuromuscular transmission. Calcium in its intra-cellular state, uses calcium-binding regulatory protein, Calmodulin.
Apart from being in bones and teeth, Plasma calcium or Calcium in blood, is another significant factor. The normal value of Plasma calcium is 9-11 mg/dL. It exists in 3 forms:
- Biologically active Ionized form- 50%: 4.5-5.5 mg/dL
- Bound to plasma proteins- 45%
- Complexed to phosphate and citrate- 5%
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| Calcium Distribution in Body |
Effects of Acidosis and Alkalosis on Plasma Calcium Levels
Metabolic acidosis decreases the protein binding of calcium, thereby increasing the ionized form of calcium. RTA or Renal tubular acidosis is the primary cause of hypocalcaemia apart from protein available for binding being reduced, as in hypoproteinemia.
Metabolic Alkalosis increases the protein binding of calcium, thereby decreasing the ionized form of calcium. Excessive supplementation of calcium or Increased phosphates (Hyperphosphatemia) can be the cause.
PARATHYROID PTH REGULATION
Parathormone or Parathyroid hormone is secreted by the chief cells of Parathyroid glands in response to decreased levels of calcium in the blood. Hypocalcemia is indeed the most targeted trigger for release of Parathormone and thereby asking it to come into play.
Calcium-sensing Receptors or CaSR detect any changes in calcium in serum, thereby allowing parathyroid hormone and ascending loop of henle in kidneys to function and bring back the normal levels of calcium in blood.
Once decreased concentration of calcium in blood is detected by CaSR in parathyroid glands, chief cells start secreting Parathormone. Once released, parathormone grabs everything it can! PTH initiates two steps: Production of 1,25 (OH)2D , or simply, Vitamin D from kidneys and Osteoclastic activity on bones for resorption of calcium. It's like STOP WASTING CALCIUM AND BRING ME MORE CALCIUM! Distal renal tubular resorption is produced within minutes, whereas, release of calcium from skeleton takes 1-2 hours.
Kidneys
PTH stimulates 1 alpha-hydroxylase activity, which leads to production of Vitamin D [1,25 (OH)2D] from calcitriol [25-(OH) D3], inactive calcium. This Vitamin D causes increased calcium and phosphate absorption (remember calcium and phosphate are against each other).
Bones
Poor bones have to pay the prices. The osteoclastic activity causes calcium from bones to move out and move to serum in blood.
Here's an image that might help understand the things easy way:
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| Summary of Calcium Regurgitation Diagram |
CALCITONIN REGULATION
Calcitonin is more like alone worker. It doesn't require CaSR to detect calcium levels, but it has receptors for calcium which tell calcitonin when to gear up. Calcitonin is secreted by parafollicular cells of thyroid. Increased or high calcium levels in blood force Calcitonin to come into play. Upon arrival, Calcitonin causes following to send back the calcium:
Inhibits renal tubular resorption of calcium, thereby, forcing the kidney to excrete calcium.
Inhibits osteoclastic activity on bones, hence preventing re-absorption of calcium from bones.
Promotes osteoblastic activity on bones, let calcium feed the bones.
It also inhibits phosphate re-absorption by kidneys, thereby decreasing phosphate levels too.
Therefore, Calcitonin from thyroid gland actually antagonizes the functions of PTH, and stopping anything PTH is capable of. But, this Calcitonin is still not important hormone is calcium homeostasis, POOR GUY!
Therefore, PTH and Calcitonin act together as follows:
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| Calcium Homeostasis Parathyroid Calcitonin |
Labels: Fluid-Electrolyte imbalance, Medicine, Paediatrics