tinabg
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A 23 y.o. woman drinks lots of diet coke containing high amounts of phosphate, but no calcium. What changes are expected?
a) Decreased 1,25 DHCC and decreased PTH
b) Decreased 1,25 DHCC and increased PTH
c) Incareased 1,25 DHCC alone
d) Increased 1,25 DHCC and decreased PTH
e) Increased 1,25 DHCC and increased PTH
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| sprint123
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Hi..I am thinkig of this sequence..
Increased Po4--Increased precipitation with calcium-->Decreased calcium--->Increased PTH,VIT-D AND 1,225-DHCC
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| tinabg
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This is what I was thinking too. However, the answer was b - increased PTH and decreased Vit.D. I can't figure out how this is possible, since PTH is the main regulator of Vit. D. I just read that lack of phosphate activates 1 alfa hydroxylase, but I didn;t see anything saying that excess PO4 inhibits 1 alfa hydroxilase. May be the answer they are giving is wrong? Any thoughts?
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| mytime
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It is said that 1alfa hydroxylase stimulated by
1 low S. Ca2+
2 high PTH
3 low S. po4
So the high PO4 maybe inhibiting the process.
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| new_n_lost
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My 2 Cents.
The excess ingested phosphate is excreted by the kidneys to maintain phosphate balance. Major sites of regulation of phosphate excretion are the early proximal renal tubule and the distal convoluted tubule. In the proximal tubule, phosphate reabsorption by type 2 sodium phosphate cotransporters is regulated by dietary phosphate, PTH, and vitamin D. High dietary phosphate intake and elevated PTH levels decrease proximal renal tubule phosphate absorption, thus enhancing renal excretion.
Conversely, low dietary phosphate intake, low PTH levels, and high vitamin D levels enhance renal proximal tubule phosphate absorption. To some extent, phosphate regulates its own regulators. High phosphate concentrations in the blood down-regulate the expression of some phosphate transporters, decrease vitamin D production, and increase PTH secretion by the parathyroid gland. Distal tubule phosphate handling is less well understood. PTH increases phosphate absorption in the distal tubule, but the mechanisms by which this occurs are unknown. Renal phosphate excretion can also be increased by the administration of loop diuretics.
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| mytime
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that's better more on the line of my thought process but so much better! 
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| epica
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Oh, I was late. Good explanation, nnl.
Did u see IM forum Q about Digoxin toxicity, somebodr wrote --- hearing. Strange...
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| new_n_lost
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yeah its strange but his definition of Symptom n Sign is right just based on that reason Bradycardia is nullified.
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| paganini
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TOXICOLOGY / OVERDOSE COMPREHENSIVE — Symptoms of acute overdose include vomiting, hyperkalemia, sinus bradycardia, S-A arrest and AV block are common, ventricular tachycardia, and fibrillation. Symptoms of chronic intoxication include visual disturbances, weakness, sinus bradycardia, atrial fibrillation with slowed ventricular response, and ventricular arrhythmias. After GI decontamination, treat hyperkalemia if >5.5 mEq/L with sodium bicarbonate and glucose with insulin or Kayexalate®. Treat bradycardia or heart block with atropine or pacemaker and other arrhythmias with conventional antiarrhythmics. Use Digibind® for severe hyperkalemia, symptomatic arrhythmias unresponsive to other drugs, and for prophylactic treatment in massive overdose.
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| mytime
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Ya u right coz we were meant to talk of toxic doses not normal so tinnitus is out coz it happens at low doses..........good work! 
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| paganini
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None of us will forget Digoxin toxicity after this long discusion
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| me007
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means that sodas make such a changes in human body like
hyperparatyroidism (secondary to this hypercalcemia and bone loss) and hypovitaminosis D.
if another peson eats a lots of yogurts
how and by what mechanisms his 1'25 DHCC and PTH will change?
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| Luckyall
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i guess if a person gets lots of yogurt... Ca-emia would be at the high side of N interval----> low PTH and low 1,25 DHCC
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| mytime
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