Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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?
|
1,25-diOH-D3
|
|
|
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 (24-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?
|
Calcitriol
|
|
|
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) |
