white_o
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So I get that when serum calcium is low, PTH causes it to rise, and one of the ways is by making calcium available from bone. Is this demineralisation, and therefore causes rickets?
If not what exactly causes it as I'm very confused.

Thanks!
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macpatgh-Sheldon
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Hi white_o sorry you are confused.com!

High PTH level leads to increased calcium levels in the blood, partly by demineralization of bone, yes.

However, the term rickets is used to refer to the disease caused by deficiency of Vitamin D (cholecalciferol = D3 and/or ergocalciferol = D2) IN EARLY CHILDHOOD - the result is a "rickety rosary" (bulging costochondral (junction of bone to cartilage) junctions [of ribs] on the anterior [front] chest, hypocalcaemia, which can cause tetany (not tetanus, which is an infection caused by a bacterium called Clostridium tetani), etc.

Lack of Vitamin D in adults causes osteomalacia [this differs from osteoporosis, in simple terms, in that it affects the mineral component of bone, whereas osteoporosis involves thinning of both mineral and protein parts].

Hyperparathyroidism (you might know the parathyroid glands [usually 2-5 of them] are embedded within the sunstance of the thyroid gland in the neck) has different manifestations (google it).

Hope this helps you to eradicate this website (confused.com) from your browser!!

M
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Jpw1097
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(Original post by white_o)
So I get that when serum calcium is low, PTH causes it to rise, and one of the ways is by making calcium available from bone. Is this demineralisation, and therefore causes rickets?
If not what exactly causes it as I'm very confused.

Thanks!
Yes, you're right, when serum calcium is low, PTH is released from the parathyroid glands which raises serum calcium by increasing osteoclast activity (causing release of calcium and phosphate from bone) as well as increasing calcium reabsorption in the kidneys. PTH also increases the synthesis of vitamin D, which increases calcium and phosphate absorption from the GI tract.

Rickets is caused by vitamin D deficiency in children. You're exactly right, low vitamin D leads to low serum calcium which leads to increased PTH release which, as I've already mentioned, mobilises calcium from the bone by increasing bone resorption (via increased osteoclast activity) - this is known as secondary hyperparathyroidism.
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white_o
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(Original post by macpatgh-Sheldon)
Hi white_o sorry you are confused.com!

High PTH level leads to increased calcium levels in the blood, partly by demineralization of bone, yes.

However, the term rickets is used to refer to the disease caused by deficiency of Vitamin D (cholecalciferol = D3 and/or ergocalciferol = D2) IN EARLY CHILDHOOD - the result is a "rickety rosary" (bulging costochondral (junction of bone to cartilage) junctions [of ribs] on the anterior [front] chest, hypocalcaemia, which can cause tetany (not tetanus, which is an infection caused by a bacterium called Clostridium tetani), etc.

Lack of Vitamin D in adults causes osteomalacia [this differs from osteoporosis, in simple terms, in that it affects the mineral component of bone, whereas osteoporosis involves thinning of both mineral and protein parts].

Hyperparathyroidism (you might know the parathyroid glands [usually 2-5 of them] are embedded within the sunstance of the thyroid gland in the neck) has different manifestations (google it).

Hope this helps you to eradicate this website (confused.com) from your browser!!

M
Thank you, it certainly has!!😁
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white_o
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(Original post by Jpw1097)
Yes, you're right, when serum calcium is low, PTH is released from the parathyroid glands which raises serum calcium by increasing osteoclast activity (causing release of calcium and phosphate from bone) as well as increasing calcium reabsorption in the kidneys. PTH also increases the synthesis of vitamin D, which increases calcium and phosphate absorption from the GI tract.

Rickets is caused by vitamin D deficiency in children. You're exactly right, low vitamin D leads to low serum calcium which leads to increased PTH release which, as I've already mentioned, mobilises calcium from the bone by increasing bone resorption (via increased osteoclast activity) - this is known as secondary hyperparathyroidism.
Thank you, very helpful 😁
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