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==Introduction==
== <span></span> [[Category:OpenPages]] Introduction ==
Calcium is essential for many intracellular and extracellular functions. These include:
Calcium is essential for many intracellular and extracellular functions. These include:
==Serum Calcium Abnormalities==
==Serum Calcium Abnormalities==
'''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.
==Calcium Homeostasis==
==Calcium Homeostasis==
===Parathyroid Hormone (PTH)===
===Parathyroid Hormone (PTH)===
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.
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;
'''Calcitriol''', or '''1,25-dihydroxycholecalciferol''' is the biologically active metabolite of vitamin D. It is classified as a steroid hormone and acts to raise blood calcium levels.
'''Calcitriol''', or '''1,25-dihydroxycholecalciferol''' is the biologically active metabolite of vitamin D. It is classified as a steroid hormone and acts to raise blood calcium levels.
There are two dietary sources of Vitamin D3 -
There are two dietary sources of Vitamin D3
1. '''Vitamin D2''' is produced in plants (ergocalciferol).
1. '''Vitamin D2''' is produced in plants (ergocalciferol).
===Calcitonin===
===Calcitonin===
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:
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.
There are also slight (insignificant) effects on the kidney and [[Alimentary System Overview - Anatomy & Physiology|gastrointestinal tract]].
There are also slight (insignificant) effects on the kidney and [[Alimentary System Overview - Anatomy & Physiology|gastrointestinal tract]].
==Links==
==Calcium Homeostasis in the Rabbit==
The blood calcium concentration is not as closely regulated in the rabbit as in other species. Absorption of calcium from the gut is '''independent of metabolic need or vitamin D levels'''. Serum calcium increases in direct proportion to dietary calcium content. High concentrations of 3-4mmol/L are commonly found in rabbits fed calcium-rich diets, such as alfalfa-based diets.
The primary route of calcium excretion in rabbits is renal, unlike in other species where bile is the primary route of removal. Thus, the '''high urinary excretion''' of calcium may simply reflect the high blood concentrations.
High calcium levels along with other physiologic or pathologic processes may result in '''urolithiasis''', urine sludge, or metastatic calcification and chronic renal disease, especially if excessive vitamin D is provided.
Dilution or replacement of alfalfa-based diets might be advisable if problems occur.
[http://www.cabdirect.org/search.html?q=title:(calcium)+AND+od:(horses)&fq=sc:%22ve%22 Calcium in horses publications]
{{Learning
|flashcards = [[Calcium_Homeostasis_Flash_Cards_- Anatomy & Physiology|calcium homeostasis]]
[[Small Mammals Q&A 06]]
|literature search = [http://www.cabdirect.org/search.html?q=title:(calcitriol)&fq=sc:%22ve%22 Calcitriol publications]<br>[http://www.cabdirect.org/search.html?q=title:(%22Vitamin+D%22)&fq=sc:%22ve%22 Vitamin D publications]<br>[http://www.cabdirect.org/search.html?q=title:(%22calcitonin%22)&fq=sc:%22ve%22 Calcitonin publications]<br>[http://www.cabdirect.org/search.html?q=title:(calcium)+AND+od:(dogs)&fq=sc:%22ve%22 Calcium in dogs publications]<br>[http://www.cabdirect.org/search.html?q=title:(calcium)+AND+od:(cats)&fq=sc:%22ve%22 Calcium in cats publications]<br>[http://www.cabdirect.org/search.html?q=title:(calcium)+AND+od:(horses)&fq=sc:%22ve%22 Calcium in horses publications]<br>[http://www.cabdirect.org/search.html?start=0&q=title:(calcium)+AND+od:(cattle)+&fq=sc:%22ve%22 Calcium in cattle publications]<br>[http://www.cabdirect.org/search.html?q=title:(calcium)+AND+od:(sheep)+&fq=sc:%22ve%22 Calcium in sheep publications]<br>[http://www.cabdirect.org/search.html?q=title:(calcium)+AND+od:(goats)+&fq=sc:%22ve%22 Calcium in goats publications]<br>[http://www.cabdirect.org/search.html?it=any&q2=homeostasis&q1=calcium&calendarInput=yyyy-mm-dd&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&options1=AND&options2=AND&options3=AND&occuring3=freetext&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:%22ve%22&y=8&x=47 Calcium Homeostasis publications]<br>[http://www.cabdirect.org/search.html?it=any&q2=serum&q1=calcium&calendarInput=yyyy-mm-dd&occuring1=title&rowId=1&rowId=2&rowId=3&show=all&options1=AND&options2=AND&options3=AND&occuring3=freetext&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:%22ve%22&y=7&x=56 Serum Calcium publications]<br>[http://www.cabdirect.org/search.html?it=any&q1=Parathyroid+Hormone&calendarInput=yyyy-mm-dd&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&options1=AND&options2=AND&options3=AND&occuring3=freetext&occuring2=freetext&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc:%22ve%22&y=9&x=63 Parathyroid Hormone publications]
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2008/20083206581.pdf '''Disorders of calcium regulation in the dog and cat.''' Taboada, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Volume 22, Orlando, Florida, USA, 2008, 2008, pp 477-479]
}}
==References==
Harkness, J. (2010) '''Harkness and Wagner Biology and Medicine of Rabbits and Rodents''' ''John Wiley and Sons''
Cheeke, R. (2010) '''Comparative Animal Nutrition and Metabolism''' ''CABI''
{{OpenPages}}
[[Category:Electrolytes]]
[[Category:Electrolytes]]
[[Category:Endocrine System - Anatomy & Physiology]]
[[Category:Endocrine System - Anatomy & Physiology]]
[[Category:A&P Done]]
[[Category:A&P Done]][[Category:Minerals]]