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14 Cards in this Set
- Front
- Back
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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 |
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phosphate plasma concentration and distribution |
-3-4.5 mg/dL -52% ionized, 13% protein bound, 35% complexed with other ion |
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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 |
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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 |
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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 |
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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 |
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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 |
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PTH |
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 |
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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 |
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phosphatonins |
-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 |
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1,25-dihydroxyvitamin D3 regulation |
-1alpha-hydroxylase is stimulated by PTH and low Pi and inhibited by Ca++ and FGF-23 |
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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 |
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calcitonin |
-stimulated by rise in Ca++ -inhibits osteoclastic bone resorption -not required for maintenance -overexpression does not cause hypocalcemia and underexpression does not cause hypercalcemia |
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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 |
