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Phys3 RenalAcid/Base

What is the most important buffer system? CO2 HCO3- system.
Maintiaining H+ balance is the same as maintaining HCO3- balance.
sources of fixed acids & bases 1.Metabolism of dietary protein. 2.Metabolism of dietary weak acids, citrus fruits, veggies. 3.Anaerobic metabolism of carbs and fat.
Influence of GI parietal cell and pancreatic ductal cells on lumen & interstitium acid base balance Parietal cells: 1.GI lumen: H+. 2.Interstitium: HCO3-. Pancreatic ductal cell: 1.GI Lumen: HCO3-. 2.Interstitium: H+. **slight net HCO3- in lumen
Acid/Base balance: PT For every HCO3- filtered, there is 1 reabsorbed. NO H+ are excreted, instead they combine w/ filtered HCO3- to form H20+CO2 in lumen (these are then catalyzed by CA, HCO3- reformed & reabsorbed).
HCO3- recovery involves tubular secretions of ____ ions. H
% reabsorbances of filtered HCO3- 1.PT: 80%. 2.Thick Ascending loop: 10-15%. 3.DCT & CD: ALL REMAINING (5%)+ secreted HCO3-.
How does HCO3- cross the basolateral membrane to be reabsorbed? Na-HCO3- symporter.
Type A Intercalated cells Found in the CD: uses a Cl-HCO3 antiporter to return HCO3- across basolateral membrane to interstitium. **H+ is ACTIVELY secreted across apical membrane into lumen.
Type B Intercalated cells found in the CD: secretes HCO3- into lumen across apical membrane via Cl-HCO3 antiporter. **H+ is ACTIVELY reabsorbed across basolateral membrane into interstitium.
Is it completely true to say the filtered HCO3- has been "reabsorbed"? NO, the filtered HCO3 combines with H+ to form H2O and CO2 which diffuse back into the cells and are broken down by CA. A new HCO3- is then reabsorbed.
2 Results of H+ secretion 1.Excretion + generation of a new HCO3-. 2.Recovery of a base (HCO3-).
Determining the net urinary acid (H+) excretion. =Excreted H+ as (H2PO4) + Excreted H+ as (NH4) - excretion of filtered HCO3-.
Where will there be considerable H+ secretion onto phosphate? 1.End of PT. 2.DCT. (HPO4 2-) + (H+) = (H2PO4-). **Allows creation of absorption of 3 Bicarbs
What will lead to reabsorption of NEW HCO3- 1.Titration with phosphate. 2.Filtered glutamine. Once absorbed into the cell from the lumen, it is broken down into: 1.HCO3- (reabsorbed via Na symporter). 2.NH4+ (Ammonium, secreted back into lumen via Na exchanger).
Where does the formation of NEW HCO3- from glutamine occur? Mostly in the PT
When is glutamine production by the liver enhanced? during periods of low extracellular pH. **this makes sense b/c it leades the creation & reabsorption of a NEW HCO3-
3 fates of H+ in the kidney 1.Titrate filtered HCO3- in order to recover an HCO3-. 2.Titrate with phosphate, H+ is excreted & new HCO3- formed. 3.Titrate with NH3, H+ excreted as NH4 & new HCO3- formed.
Main acid base regulation on the kidneys 1.PaCO2 (b/c of its effects on renal intracellular pH). 2.Arterial pH (b/c extracellular pH acts directly on tubular cells). 3.Enhanced Na reabsorbed (Inc H+ secretion via Na/H exchanger). 4.Plasma [K+]
effect of Decreased pH 1.Inc Na/H exchanger activity on apical membrane. 2.Inc H+ secretion. 3.Inc renal ammonia synthesis. 4.Recruitment of H ATPases
effect of increased pH Decreased H+ secretion.
Why would an Inc in PCO2 change the intracellular pH? Inc in PCO2 increases the formation of H+ from the CA reaction. This leads to increased renal H+ secretion.
Is excess base ever excreted? YES. 1.Some filtered HCO3- passes through to urine. 2.Type B intercalated cells also secrete HCO3- in the CD (via apical HCO3-/Cl exchanger).
Compensatory response of Kidneys: respiratory acidosis INC H+ excretion. **due to Inc PCO2.
Compensatory response of Kidneys: respiratory alkalosis Inc HCO3- excretion. **due to Dec PCO2.
Compensatory response of Kidneys: metabolic acidosis Inc H+ excretion. **coupled with alveolar hyperventilation.
Compensatory response of Kidneys: metabolic alkalosis Inc HCO3- excretion. **coupled with alveolar hypoventilation.
Effect of Hypokalemia on kidneys? 1.K+ leaves renal cells to enter plasma. 2.H+ moves from plasma into renal cell. 3.Dec Intracellular pH. 4.Inc H+ secretion. 5.Inc HCO3- reabsorption. **Metabolic ALKALOSIS.
Effect of Hyperkalemia on kidneys? 1.K+ leaves plasma to enter renal cells. 2.H+ moves from renal cells into plasma. 3.Inc intracellular pH. 4.Dec H+ secretion. 5.Dec reabsorption of HCO3-. **Metabolic ACIDOSIS.
Effects of Aldosterone on acid/base reg. 1.Inc apical H-ATPase in type A intercalated cells (Inc H+ secretion). 2.Inc CD Na reahsorption, leaving CD lumen negative (Inc H-ATPase H+ secretion). 3.Inc K secretion causing hypokalemia (Inc H+ secretion & alkalosis).
Hyperaldosteronism leads to ALKALOSIS.
Hypoaldosteronism leads to ACIDOSIS.
Created by: WeeG



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