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17 Cards in this Set
- Front
- Back
Why is Vitamin D considered a vitamin and not a hormone?
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Though we produce it, sometimes we don't produce enough.
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What is the active form of Vitamin D?
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1,25-diOH-D3
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What form of D is consumed in diet / how activated?
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D3 absorbed.
Two hydroxylations to activate: 1 in liver --> to 25-OH-D3 1 in Kidney --> to 1,25-diOH-D3 it also can --> 24,25-diOH-D3 (inactive) |
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What are the enzymes that regulate D3 activation?
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Liver: 25-hydroxylase
Kidney: 1-hydroxylase (24-hydroxylase) |
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What increases/decreases the activity of 1-hydroxylase?
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Activity increases: PTH (parathyroid hormone)
Decreases: Ca++, PO4, and 1,25-itself |
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What is the name of 1,25-diOH-D3?
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Calcitriol
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How is the activity of 1-hydroxylase mediated?
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PTH attached to receptor on renal cell/ causes ATP to lose PO4 which gets transfered to enzyme; increases the rate.
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How is Calcium absorbed? Where is it absorbed?
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Passively at high levels; actively at phsiological doses.
Active absorption occurs in the duodenum and upper jejunum |
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How does Vitamin D impact Calcium absorption?
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High levels of Vitamin D stimulate the production of Calbindin-D; Calbindin D is the carrier of Calcium that facilitates diffusion across the intestinal cell from brush border to basolateral side.
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How does Calbindin D enhance absorption of Ca? (entry across brush border)
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The concentration gradient of free Ca outside vs free Ca inside is magnified: when Ca enters cell, it's bound to calbindin-D; the bound form does not "count" as free Ca
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How does Calbindin D facilitate diffusion across the cell?
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Bucket brigade. The concentation gradient of Calbindin-D across the cell is much steeper than if it were just Ca alone: this is why we see an increase by 100x of the rate of diffusion. Another conc. gradient is Calbindin-D w/out Ca.
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How does Ca leave the cell?
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Binding w/Calbindin-D is transitory. At basolateral side, free Ca is extruded out via Ca/Mg-ATPase; the concentration gradient here too is enhanced by Calbindin-d (?)
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How is Calcium homeostatis regulated?
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By regulation of osteoclasts and osteoblasts. The relative activity of these cell-groups determines the amount of bone resportion occuring.
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Describe the response if hypocalcemia.
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Low calcium. Need to stimulate osteoclasts:
PT stimulated; produces more PTH which increases the rate of 1-hydroxylase (more active vit D & thus more Calcibindin-D too!) PTH & Active D also stimulate the activation of osteoclast precursur cells. Lastly, PTH lowers kidney secretion of Ca. |
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Describe the response if hypercalcemia.
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Signal removed for PT stimulation. Drop in PTH (more Ca released through kidney).
*Calcitonin released by thyroid "C" cells: - direct action on osteoclast to reduce activity - increases osterblast activity |
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How does to body know the status of Ca?
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In all cells that regulate Ca, they are CaR: Cacium receptors. These are proteins that bind to Ca. If unbound - response of hypocalcemia; if bound, response is of hypercalcemia.
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What are the effects of Vit D deficiency?
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Young: Rickets (Rachitic Rosary early sign; appears 6-24 mo of age - short stature?)
Old: Osteomalacia (weak bones; esp. seen in women after bearing several children) |