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14 Cards in this Set

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  • Back

calcium plasma concentration and distribution

-8.5-10.2 mg/dL

-50% ionized, 40-45% protein bound, 5-10% complexed with other ions

-ONLY ionized is sensed and regulated

phosphate plasma concentration and distribution

-3-4.5 mg/dL

-52% ionized, 13% protein bound, 35% complexed with other ion

renal handling of calcium

-99% of FL is reabsorbed; 70% in the PT, 20% in the TALH, 9% in the DT

-paracellular is through solvent drag in the PT and through electrochemical gradient in TALH, doesn't occur in the DT

-transcellular is through apical TRPV5 Ca++ channel, intracellular calbindin, and basolateral NCX and Ca++ ATPase

-regulation: PTH stimulates reabsorption(DT);1,25-(OH)2D3 promotes calbindin; activation of CaSR (TALH) inhibits reabsoprtion

renal handling of phosphate

-~80% of the FL is reabsorbed in the PT, another 10% in the DT, with 10% being excreted

-PT is transcellular, mediated by apical Na+/Pi symporters and basolateral Pa-anion exchangers

-PTH causes internalization of NPT2, FGF-23 reduced NPT2 levels and inhibits 1alpha hydroxylase

intestinal absorption of calcium

-only 20-60% is absorbed, primarily in the duodenum and jejunum

-transcellularabsorption is stimulated via 1,25-(OH)2D3 binding the VDR, which heterodimerizes with the retinoid X receptor and stimulates expression of brush border Ca++ channel and calbindin, which buffers intracellular calcium to deliver it to basolateral membrane

intestinal absorption of phosphate

-70% is absorbed

-occurs mainly in the jejunum

-mediated by the Na+-Pi co-transporter NPT2, which is upregulated by 1,25-(OH)2D3

mechanisms regulating osteoclast differentiation and bone resorption

-PTH and 1,25(OH)2D3 promote osteoclast differentiation by activating their receptors in osteoblasts and upregulating RANKL and downregulating OPG

-this increases the availability of RANKL for RANK binding and activation


parathyroid hormone

-regulator of serum calcium; 84 AAs

-serum Ca++ levels monitored by calcium sensing receptor (CaSR), which suppresses PTH

-at setpoint secretes 50% of max, so can be adjusted up or down

-increases renal reabsorption of calcium, bone resorption, and production of 1,25-dihydroxyvitaminD3; decreases renal Pi reab

1,25-dihydroxyvitamin D3 synthesis

-vitamin D3 is produced in the skin from 7-dehydrocholesterol and obtained in the diet

-in the liver, vitamin D is hydroxylated at 25 by a constitutive enzyme

-in the PT of the nephron 25-hydroxyvitamin D3 is hydroxylated by 1alpha-hydroxylase to yield the active hormone


-theorized because diseases are associated with excessive phosphate excretion

-e.g. FGF-23

-produced in osteocytes then is either cleaved by PHEX or enters circulation

-inhibits tubular reabsorption of Pi, causing phosphate wasting and osteomalacia; also inhibits 1alpha-hydroxylase, preventing compensatory increase in 1,25-dihydroxyvitamin D3

-role in normal physio poorly understood

1,25-dihydroxyvitamin D3 regulation

-1alpha-hydroxylase is stimulated by PTH and low Pi and inhibited by Ca++ and FGF-23

1,25-dihydroxyvitamin D3 action

-acts via steroid hormone like nuclear receptor

-increases osteoclast formation and bone resportion

-timulates calcium and phosphate absorption in the intestine, which promotes bone mineralization

-stimulated Ca++ resorption and calbindin expression in kidney

-might play a role in muscle strength, immune function, ant-cancer


-stimulated by rise in Ca++

-inhibits osteoclastic bone resorption

-not required for maintenance

-overexpression does not cause hypocalcemia and underexpression does not cause hypercalcemia

impact of diuretics on renal Ca++ handling

-loop diuretics (e.g. furosemide) inhibit Ca++ resorption by dissapating the positive lumen potential

-thiazide diuretics promote Ca++ resorption through unclear mechanism