Ca2+ Flashcards
what is the effect of hypoalbuminemia on Ca+
increases plasma calcium
what is the effect of hyperalbuminemia on Ca+
decreases plasma calcium
what happens to calcium in acidosis
more H+ binds to albumin to increase the pH so less calcium binds, leading to more free calcium in circulation
what happens to calcium in alkalosis
less H+ binds to albumin so more Ca2+ binds, leading to less free Ca2+ in the plasma
why does acute alkalosis mimick hypocalcemia
in acute alkalosis, less H+ is bound to albumin to decrease the pH, so more calcium is bound instead leading to less free Ca2+ in the blood which mimicks hypocalcemia, even if there is actually enough Ca2+ in the body
effect of calcitriol (vitamin D) on bone
works with PTH to resorb bone and pull Ca2+ from the bone into the blood, increasing plasma Ca2+ levels
bone –> blood
effect of calcitriol in the intestines
increases Ca2+ absorption (increasing calcium plasma levels)
lumen of intestines –> blood
effect of calcitriol in the kidney
increases calcium reabsorption from the tubule into the blood
tubule –> blood
what receptor is used to resorb, absorb, and reabsorb Ca2+
VDR (vitamin D receptor)
effect of calcitonin on bone
inhibits osteoclastic mediated bone resorption by decreasing activity and # of osteoclasts
(decreases plasma Ca2+)
effect of calcitonin on kidney
promotes calcium excretion
decreases plasma Ca2+
what stimulates calcitonin
hypercalcemia
how is calcitonin used pharmacologically
osteoporosis
paget’s disease
hypercalcemia
what is the effect of calcitonin on the intestines
none
effect of PTH on bone
increases osteoclastic resorption
increases plasma Ca2+
effect of PTH on intestines
increases Ca2+ absorption indirectly via calcitriol production
effect of PTH on kidney
- on Ca2+
- on Na+/H+
- on bicarbonate reabsorption
increases Ca2+ reabsorption primarily in DCT
- also decreases Na+/H+ antiporter
- decreases bicarbonate reabsorption
excess PTH can cause
hypercalcemia
hypophosphatemia
hypercholermic metabolic acidosis
what senses calcium and how does it work
CaSR (calcium sensing receptor)
- on basolateral membrane
- inhibits reabsorption of Ca2+ when hypercalcemic by inhibiting the NKCC2 on the apical membrane
how to calculate filtered load for calcium
FL = GFR x plasma concentration x 0.6
where does most of calcium reabsorption take place
and how does it take place
proximal tubule 65-70%
- passively
- follows Na+ and H2O
- primarily paracellularly
how does Ca2+ get reabsorbed in the thick ascending limb
paracellularly from the lumen positive voltage gradient
- stimulated by ADH
how does Ca2+ get reabsorbed in the distal tubule
8%
- active transport from the lumen negative voltage gradient
- via TRPV5
what prevents adverse reactions (like apoptosis) from occurring during excessive intracellular Ca2+ concentration
calbindin
how does volume contraction affect Ca2+ reabsorption
increases it
it follows Na+
how do loop diuretics affect Ca2+ reabsorption in the TAL
loop diuretics like furosemide inhibit the NaK2Cl transporter which blocks calcium reabsorption and increases calcium excretion
- thus can treat hypercalcemia
in the DT, how does calcium cross the basolateral membrane and how does it cross the apical membrane
basolateral: Na+-Ca2+ exchanger (NCE)
apical: TRPV5
what stimulates TRPV5
PTH
calcitriol (vitamin D)
how do thiazide diuretics affect Ca2+ reabsorption and how do they treat kidney stones
they inhibit the Na+-Cl- transporter and increase Ca2+ reabsorption, reducing Ca2+ excretion in the urine
- used to treat kidney stones
how does acidemia affect Ca2+ reabsorption
decreases reabsorption and increases excretion by inhibiting TRPV5
how does alkalemia affect Ca2+ reabsorption
increases reabsorption and decreases excretion by stimulating TRPV5
how does low ECV affect Ca2+ reabsorption
increases it (follows Na+)
