goodies
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goljan RR pg. 505
I dont understand the lab findings of primary hyperparathyroidism. There is normal anion gap metabolic acidosis due to decreased proximal tubule reclamation of bicarbonate and type II renal tubular acidosis.
Why does primary hyperparathyroidism (increased PTH, increased calcium, decreased phosphorus) result in decreased reclamation of bicarb?
i don't get it. PLEASE explain!
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| Luckyall
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1) PTH INHIBITS Ph reabs. in PT--> Ph is Normally reabsorbed in PT thru a pump(luminal tub. mb) that countertransports Ph inside cell for a base(-) outside cell, in the tubular lumen.
2) Also there is bicarb reclamation going on the basal mb---> bicarb( base ) is transp. in the interstitium blood( bicarb comming from intracellulat CO2)
If inhibits 1)---> slowed down 2) ---> keeping base(-) inside cell by inhibiting 1)----> dont deliver HCO3 outside cell for the equilibr purpose---> decr HCO3 reclam---> renal tub acidosis by not having HCO3 delivered in the blood
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| new_n_lost
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In essence, the filtered HCO3- is converted to CO2 in the lumen, which diffuses into the proximal tubular cell and is then converted back to HCO3- to be returned to the systemic circulation, thus reclaiming the filtered HCO3-.
Na is the Major cation in the Body while HCO and CL r the Major Anions.
PTH dec the reabsorbtion of Phosphate. the most of the phosphate receptors r in the Proximal tubules and in Distal tubules ones r under PTH. THere has been no positive theory as y the Reclamation of Bicarb in RTA is decreased.
The Phosphate ion is actively transported across the Tubular Membrane it is not co-transported or counter transported. The current hypothesis is that there is a possiblity that the Phosphate ion accumulation in the Tubular Lumen binds the H ion thus decresing the H ion concerntration. AS the H ion conc. dec the Kidney dec its threshold for Bicarb reabsorbtion. This hypothesis hasnt been proven yet.
the Hyperchloremia we see in HyperPTH is due to th efact that there is a tranposter on the basolateral membrane which counter Transports the Cl/HCO3 ( CL is pushed towards the lumen so that it can trap Na+ and K+ ions for reabsorbtion and the HCO3 is pushed back into the blood) this normal mechanisms gets inhibited somehow due to the INC SEC of Phosphate and the Total Concerntration of the Cl- ion rises therefore leading to Hyperchloremic Acidosis. Due to the Presence of Cl ion the Anion Gap remains Normal.
The Abv conclusion is wht i made from reading different articles From
JAMA . NEJM and Emedicine and the Phosphate Reabsorbtion mechanism is given in Ganong.
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| new_n_lost
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Now Y & how Inc PTH Effects the Renal threshold for Bicarb is still yet unknown so just learn it thats all i can say.
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| new_n_lost
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but the imp thing to remember is that whenever there is a loss of Bicarb from the Kidney the Cl ion will absorbed more and thus u will have hyperchloremic Acidosis and ur Anion Gap will remain the same.
Furthermore u can look into Goljan RR New Edition pg. 73
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| ssrpk
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great explanation
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