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17 Cards in this Set

  • Front
  • Back
Why is Vitamin D considered a vitamin and not a hormone?
Though we produce it, sometimes we don't produce enough.
What is the active form of Vitamin D?
What form of D is consumed in diet / how activated?
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)
What are the enzymes that regulate D3 activation?
Liver: 25-hydroxylase
Kidney: 1-hydroxylase
What increases/decreases the activity of 1-hydroxylase?
Activity increases: PTH (parathyroid hormone)
Decreases: Ca++, PO4, and 1,25-itself
What is the name of 1,25-diOH-D3?
How is the activity of 1-hydroxylase mediated?
PTH attached to receptor on renal cell/ causes ATP to lose PO4 which gets transfered to enzyme; increases the rate.
How is Calcium absorbed? Where is it absorbed?
Passively at high levels; actively at phsiological doses.

Active absorption occurs in the duodenum and upper jejunum
How does Vitamin D impact Calcium absorption?
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.
How does Calbindin D enhance absorption of Ca? (entry across brush border)
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
How does Calbindin D facilitate diffusion across the cell?
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.
How does Ca leave the cell?
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 (?)
How is Calcium homeostatis regulated?
By regulation of osteoclasts and osteoblasts. The relative activity of these cell-groups determines the amount of bone resportion occuring.
Describe the response if hypocalcemia.
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.
Describe the response if hypercalcemia.
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
How does to body know the status of Ca?
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.
What are the effects of Vit D deficiency?
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)