Ca2+,Pi,Mg2+ Regulation Flashcards
1
Q
- What is normal plasma Ca2+ level
A
- 5.0 mEq/L
2
Q
- Where is Ca2+ stored in the body?
A
- 99% Bone
- 1% ICF
- 0.1% ECF
3
Q
- Normal level of biologically active plasma?
A
- 2.4 mEq/L
4
Q
- How much of Ca2+ is filterable at the glomerulus?
- Which Ca2+ is NOT freely filterable at the glomerulus?
A
- 60% (the filtered Ca2+ is the calcium that is ionized or diffusible complexes)
- Protein bound Ca2+
5
Q
- H+ and Ca2+ compete for binding on which plasma protein?
- Which is the stronger of the two?
A
- Albumin
- H+
6
Q
- Hypoalbuminemia _ plasma Ca2+
- Hyperalbuminemia _ plasma Ca2+
A
- Increases
- Decreases
7
Q
- Acidosis _ plasma Ca2+ levels
- Alkalosis _ plasma Ca2+ levels
A
- Increases (More acid, more H+ binding to albumin, less binding sites for Ca2+)
- Decreases (predisposes to hypocalcemic tetany-also why acute alkalosis can mimic hypocalcemia)
8
Q
- What is the name of the biologically active form of Vitamin D?
A
Calcitriol
(Has other names, but she said to focus on this one)
9
Q
- What is the overall goal of calcitriol?
- Through which receptor does calcitriol work?
- Where are these receptors located?
A
- Increase serum Ca2+ and Pi
- VDR (Vitamin D receptors)
- Throughout the body (we will talk about bone, intestines, and kidney)
10
Q
- How does calcitriol act on bone?
A
- Promotes osteoid mineralization
- Osteoclastic mediated bone resorption (taking Ca2+ out of bone and putting it back into the blood stream-remember goal is to increase overall serum Ca2+ and Pi levels)
11
Q
- How does calcitriol act on the intestine?
A
- Increases Ca2+ absorption (30% dietary intake)
- Increases phosporus absorption
12
Q
- How does calcitriol act on the kidney?
A
- Stimulates phosphate reabsorption
- Stimulates Ca2+ reabsorption (by acting on NKCC?*)
13
Q
- What is the overall goal of calcitonin?
- What is it stimulated by?
A
- Increased excretion of Ca2+ and Pi
- Decreases activity and number of osteoclasts
- Stimulated by hypercalcemia (makes sense since the overall goal is to increase excretion of Ca2+)
- ALSO OPPOSES PTH
14
Q
- How does calcitonin act on bone?
A
- Inhibits osteoclast mediated bone resorption (so keeps the Ca2+ in the bones and prevents it from coming back out into the blood stream)
- Also decreases the activity and number of osteoclasts
15
Q
- How does calcitonin act on the kidney?
A
- Promotes phosphate and Ca2+ excretion
16
Q
- Pharmacological doses of Calcitonin can be used to treat:
A
- Hypercalcemia
- Paget’s disease
- Osteoporosis (leaves Ca2+ in bone)
17
Q
- What is the overall goal of PTH?
A
- Increase Serum Ca2+ and Decrease Serum Pi
18
Q
- How does PTH work on bone?
A
- Increased osteoclastic resorption (which increases Ca2+ going from bone back into the bloodstream)
33
Q
- How much Pi is reabsorbed in the proximal tubule?
- How is Pi reabsorbed in the proximal tubule?
A
- 80%
- Reabsorption is primarily driven by the Na+/K+ ATPase on the basolateral membrane
- This creates a gradient for Na+ to move into the cell
- Na+-Pi transporter on the APICAL membrane
- Pi crosses the BASOLATERAL membrane via its own unknown transporter
40
Q
_ is the most important hormone that regulates Pi excretion
A
- PTH
- PTH inhibits Na+-Pi symporter on the APICAL membrane of the proximal tubule and inhibits the Na+/H+ antiporter on the APICAL membrane
- PTH also works on the distal tubule to increase Ca2+ reabsorption
43
Q
- How is Mg2+ reabsorbed in the thick ascending limb of the LOH?
A
- Paracellularly
- Mg2+ reabsorption in TAL dependent on uptake of Na+ and K+ via NKCC2 (which depends on lumen positive voltage of TAL)
44
Q
- How is Mg2+ reabsorbed in the distal tubule?
A
- Crosses APICAL membrane via TRPM 6
- Crosses BASOLATERAL membrane via unknown mechanism
- Electrical potential is primary driver of Mg2+ influx into the cell (since Mg2+ concentration is similar intracellularly and extracellularly)
