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| ==Serum Calcium Abnormalities== | | ==Serum Calcium Abnormalities== |
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− | '''Elevated''' blood calcium levels (hypercalcaemia) can be attributed to increased parathyroid hormone (PTH) concentration and increased active vitamin D3. '''Reduced''' blood calcium levels (hypocalcaemia) can occur with decreased PTH, reduced Vitamin D activation and calcitonin inhibition of calcium mobilisation from bone. | + | '''Elevated''' blood calcium levels ([[Hypercalcaemia|hypercalcaemia]]) can be attributed to increased parathyroid hormone (PTH) concentration and increased active vitamin D3. '''Reduced''' blood calcium levels ([[Hypocalcaemia|hypocalcaemia]]) can occur with decreased PTH, reduced Vitamin D activation and calcitonin inhibition of calcium mobilisation from bone. |
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| ==Calcium Homeostasis== | | ==Calcium Homeostasis== |
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| ===Parathyroid Hormone (PTH)=== | | ===Parathyroid Hormone (PTH)=== |
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− | Synthesis of PTH is from a preprohormone of 115 amino acids into a [[Prohormones - Anatomy & Physiology|prohormone]] of 90 amino acids. This prohormone is then packaged into vesicles, as the 84 amino acid PTH molecule. It is secreted by the chief cells of the parathyroid gland continuously with a basal secretory rate of around 25% of the maximum possible rate. Secretion rate increases with a '''decrease in serum ionised calcium''' (hypocalcemia). Regulation of PTH is highly sensitive due to membrane receptors on chief cells coupled to G-proteins. Receptor stimulation decreases secretion; this is therefore a direct [[Negative Feedback - Anatomy & Physiology|negative feedback]] mechanism. The half-life of PTH in circulation is short - less than 10 minutes which also allows tight regulation of calcium levels. PTH is metabolised in the liver and kidneys. | + | Synthesis of PTH is from a preprohormone of 115 amino acids into a [[Prohormones - Anatomy & Physiology|prohormone]] of 90 amino acids. This prohormone is then packaged into vesicles, as the 84 amino acid PTH molecule. It is secreted by the chief cells of the parathyroid gland continuously with a basal secretory rate of around 25% of the maximum possible rate. Secretion rate increases with a '''decrease in serum ionised calcium''' ([[Hypocalcaemia|hypocalcemia]]). Regulation of PTH is highly sensitive due to membrane receptors on chief cells coupled to G-proteins. Receptor stimulation decreases secretion; this is therefore a direct [[Negative Feedback - Anatomy & Physiology|negative feedback]] mechanism. The half-life of PTH in circulation is short - less than 10 minutes which also allows tight regulation of calcium levels. PTH is metabolised in the liver and kidneys. |
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| PTH leads to increased calcium levels in the blood by actions on bone. There are two phases; | | PTH leads to increased calcium levels in the blood by actions on bone. There are two phases; |
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| ===Calcitonin=== | | ===Calcitonin=== |
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− | Calcitonin acts to decrease calcium levels in the plasma. It is overall a weaker regulatory mechanism than PTH. Secreted by the parafollicular cells of the thyroid gland, calcitonin is stimulated by hypercalcemia, and has the opposite effects of PTH on the bone: | + | Calcitonin acts to decrease calcium levels in the plasma. It is overall a weaker regulatory mechanism than PTH. Secreted by the parafollicular cells of the thyroid gland, calcitonin is stimulated by [[Hypercalcaemia|hypercalcemia]], and has the opposite effects of PTH on the bone: |
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| 1. Fast Phase - puts calcium into bone fluid by inhibiting osteoclasts' absorptive abilities. | | 1. Fast Phase - puts calcium into bone fluid by inhibiting osteoclasts' absorptive abilities. |