lecture 7a: acid-base regulation Flashcards
amount of volatile acid excreted by lungs vs kidneys
lungs: 99%, kidneys: 1%
blood pH range
7.35-7.45 as this is regulatee
urine pH range
5-9 as this is regulator (so broad range)
where is HCO3- reabsorbed in nephron (fully reabsorbed)
80% PCT, 10% ascending limb, 6% DCT, 4% collecting duct
HCO3- buffer
IC and EC buffer that responds to changes in metabolic acid; can be produced from volatile respiratory acid
Henderson-Hasselbach equation for pH
pH = pK +log10 ([HCO3-]/[CO2]); pK is 6.1
Davenport diagram - definitely copy the diagram
pH at bottom (log transformation), [H+] at top (this axis is not linear); [HCO3-] on left y-axis; PCO2 on own axis within top right corner
Davenport diagram
green areas are normal ranges and where all cross is normal range for all
metabolic alkalosis
curves up top right as almost moves along PCO2 lines (gradient becomes steeper as hypoventilation); increase in pH and HCO3-
metabolic acidosis
curves down bottom left as decrease in HCO3-, pH and PCO2 (gradient becomes shallower as hyperventilation)
chronic respiratory acidosis
curves up top left as decrease in pH and increase in HCO3- and PCO2; large broad overlap with normal pH as physiology can change to bring pH back down
acute respiratory acidosis
linear very left and slightly up; narrow; big decrease in pH and small increase in HCO3-; larger increase in PCO2
chronic respiratory alkalosis
linear bottom right but more bottom than right); increase in pH with decrease in PCO2 but large decrease in HCO3- to compensate; significant overlap with normal pH as physiology can change to bring pH back down
acute respiratory alkalosis
linear bottom right but more right than bottom; increase in pH with bigger decrease in PCO2 and smaller decrease in HCO3-
HCO3- reabsorption after filtration into tubule lumen
HCO3- and H+ via carbonic anhydrase to H2O and CO2; CO2 moves into cell; reverse reaction IC so H+ and HCO3- in cell; H+-ATPase (primary) or Na+/H+ antiporter (2ndry active transport) pumps H+ out; HCO3- into capillary by chloride bicarbonate exchanger or sodium bicarbonate contransporter; restore Na+ balance exchanged in basal membrane by Na+/K+-ATPase; Cl- returns to interstitium by Cl- channels
acid-secreting cell intercalating cells of collecting duct
alpha cell
HCO3- secreting cell intercalating cells of collecting duct
beta cell (can both change into each other)
alpha cell
HCO3- in same way; H+ out of apical membrane (Na+/H+ symptorter, H+/K+-ATPase antiporter, H+-ATPase); save HCO3- also to do more buffering (mop up protons) so exchanged into capillary by Cl-/HCO3- exchanger
beta cell
same mechanisms but apical and basolateral flipped; H+ pumped into capillary, HCO3- exchanged out
if no HCO3- to save, must be generated
glutamine split into HCO3- (absorbed) and NH4+ (removed)
HPO42- in filtrate
HCO3- (exchanged into capillary) and H+ produced by carbonic anhydrase IC and pumped out and combines with HPO42- to form H2PO4- so allows information of what happens in kidneys
fully compensated respiratory acidosis
base excess and PCO2 are abnormal in same direction (higher)
fully compensated respiratory alkalosis
base excess and PCO2 are abnormal in same direction (lower)
fully compensated metabolic acidosis
base excess and PCO2 are abnormal in same direction (lower)
fully compensated metabolic alkalosis
base excess and PCO2 are abnormal in same direction (higher)
how can metabolic acidosis and alkalosis coexist
HCl excreted by vomiting but lactic acid accumulation
