Acid Base
Acidosis from HCO and CO2
Drop in HCO3- or increase in pCO2 cause acidosis
H+ rise is limited by
HCO3-, proteins, phosphate, carbonate
pH buffering
Bicarb
HPO4 2-
Proteins
Respiratory
Renal
Kidneys in acid base
Regulate bicarb concentration
Can reabsorb all filtered HCO3-
Produce new bicarb
Excrete acids
H+ excretion
99.9% H+ that is excreted is bound to acid
most as NH4+ and HPO4-
Minimum pH is 4.5
Titratable acids
Measure the amount of NaOH needed to bring the urine pH back to pH of blood
Amount of H+ that are excreted combined with urinary buffers
usually H2PO4-
Bowman's Capsule pH
7.4
Mostly H2PO4-
Ammonia
NH4+ is the preferred from because pKa is 9, so it will almost always be in NH4+
PCT pH
H+ secretion by NHE3 (2/3) and H+ ATPase (1/3)
pH is around 6.7
NH3 diffuses and binds secreted H+
TDL pH
pH increases to 7.4 since water is reabsorbed but nothing else
NH4+ can leak out
TAL pH
back to 6.7
H+ secreted by NHE3, NBC1n
Reabsorbs NH4+, paracellulary
NHE4 at basolateral allows recycling of NH4+
Distal nephron pH
HCO3- reabsorbed, titratable acid is formed
, Ammonia diffuses and NH3 by Rhcg and Rhbg rushed out to capture H+ that is
secreted
Intercalated cells pH
Type A secretes acid
Facilitates H+ secretion by IC-A
Increase in systemic acidity leads to increase H+ secretion
If alkalosis -> secrete more bicarb
Regulation of HCO3- PCT
Acidemia -> inc NHE3 and basolateral transport HCO3- and ammoniagenesis
Ag II -> Inc NHE3 and NBC
Hypokalemia -> inc H+ secretion -> inc HCO3- reabsorption
Parathyroid -> inhibit NHE3
Catecholamines-> inc NHE3 -> H+ secretuin and HCO3- reabsorption
Regulation of HCO3- TAL
10% filtered out
increased by acidosis
Volume contraction and metabolic alkalosis
When volume is down solution gets concentrated more Bicarb increases pH
Aldosterone -> secrete K and phosphate, more alkalosis
Cl- rneal handling of HCO3-
Hypochloremia accompanied with hypokalemia -> more HCO3- reabsorb and H+
secretion
Hypochloremia alone limits Pendrin secretion of HCO3- and limits NCC -> distal
nephron secretion of H+ (ENaC used more and create more of a negative charge
that pulls out H+)
Thiazide
Increase absorption of Na+ by ENaC
DCC is inhibited
Leads to Cl- depletion from vomiting, incomplete secretion of bicarb
Volume decrease -> increase HCO3- reabsorption -> alkalosis
Decrease in pH
Increases
NHE3
NBC
AE1
H+ ATPase
Ammonia synthesis
Glutamine transporters, glutamate dehydrogenase, PEPCK, NKCC2, Rhcg
Acidosis from HCO and CO2
Drop in HCO3- or increase in pCO2 cause acidosis
H+ rise is limited by
HCO3-, proteins, phosphate, carbonate
pH buffering
Bicarb
HPO4 2-
Proteins
Respiratory
Renal
Kidneys in acid base
Regulate bicarb concentration
Can reabsorb all filtered HCO3-
Produce new bicarb
Excrete acids
H+ excretion
99.9% H+ that is excreted is bound to acid
most as NH4+ and HPO4-
Minimum pH is 4.5
Titratable acids
Measure the amount of NaOH needed to bring the urine pH back to pH of blood
Amount of H+ that are excreted combined with urinary buffers
usually H2PO4-
Bowman's Capsule pH
7.4
Mostly H2PO4-
Ammonia
NH4+ is the preferred from because pKa is 9, so it will almost always be in NH4+
PCT pH
H+ secretion by NHE3 (2/3) and H+ ATPase (1/3)
pH is around 6.7
NH3 diffuses and binds secreted H+
TDL pH
pH increases to 7.4 since water is reabsorbed but nothing else
NH4+ can leak out
TAL pH
back to 6.7
H+ secreted by NHE3, NBC1n
Reabsorbs NH4+, paracellulary
NHE4 at basolateral allows recycling of NH4+
Distal nephron pH
HCO3- reabsorbed, titratable acid is formed
, Ammonia diffuses and NH3 by Rhcg and Rhbg rushed out to capture H+ that is
secreted
Intercalated cells pH
Type A secretes acid
Facilitates H+ secretion by IC-A
Increase in systemic acidity leads to increase H+ secretion
If alkalosis -> secrete more bicarb
Regulation of HCO3- PCT
Acidemia -> inc NHE3 and basolateral transport HCO3- and ammoniagenesis
Ag II -> Inc NHE3 and NBC
Hypokalemia -> inc H+ secretion -> inc HCO3- reabsorption
Parathyroid -> inhibit NHE3
Catecholamines-> inc NHE3 -> H+ secretuin and HCO3- reabsorption
Regulation of HCO3- TAL
10% filtered out
increased by acidosis
Volume contraction and metabolic alkalosis
When volume is down solution gets concentrated more Bicarb increases pH
Aldosterone -> secrete K and phosphate, more alkalosis
Cl- rneal handling of HCO3-
Hypochloremia accompanied with hypokalemia -> more HCO3- reabsorb and H+
secretion
Hypochloremia alone limits Pendrin secretion of HCO3- and limits NCC -> distal
nephron secretion of H+ (ENaC used more and create more of a negative charge
that pulls out H+)
Thiazide
Increase absorption of Na+ by ENaC
DCC is inhibited
Leads to Cl- depletion from vomiting, incomplete secretion of bicarb
Volume decrease -> increase HCO3- reabsorption -> alkalosis
Decrease in pH
Increases
NHE3
NBC
AE1
H+ ATPase
Ammonia synthesis
Glutamine transporters, glutamate dehydrogenase, PEPCK, NKCC2, Rhcg
