Acid-Base Buffering Flashcards
Henderson-Hasselbach solved for pH?
pH = pKa + log ( [buffer-] / [buffer-H] )
Review: Normal plasma pH?
Normal intracellular pH?
Normal plasma pH: 7.4
Normal intracellular pH: 7.1
Nit-picking difference between “acidemia” and “acidosis”?
Acidemia = low pH. Acidosis = pathophysiological process that leads to low pH.
3 ECF buffers?
Bicarb
Proteins
Inorganic phosphate
3 ICF buffers?
Hemoglobin (in RBCs, obviously)
Proteins
Inorganic phosphate
What organ has a reservoir of buffers that can be released?
Bone - lots of phosphate can be released in response to acid load.
What is the Henderson-Hasselbach equation applied to bicarb/carbonic acid system?
pH = pKa + log ( [HCO3-] / (s * PCO2) )
Where pKa = 6.1, s = solubility coefficient = 0.03, and PCO2 is partial-pressure of CO2.
Which organs regulate the 2 parts of the bicarb buffer system?
Lungs: regulate CO2.
Kidneys: regulate HCO3-
Is having lungs good for acid-base balance?
Yep… PCO2 can be lowered even below that of environment’s.
4 responses to increased H+ load?
Suppressed rate of endogenous acid production.
Buffering.
Compensatory hyperventilation.
Increased renal H+ excretion.
Is extracellular or intracellular buffering quicker?
Extracellular buffering is quicker.
4 jobs of the kidney in acid/base balance?
H+ excretion.
Inorganic acid anion excretion.
Reabsorb HCO3-.
Create new HCO3-.
Where in the kidney does most bicarb synthesis happen?
In the DCT (but some happens in the proximal tubule).
What’s the formula for urinary net acid excretion? (there are 4 components)
NAE = H+ + Titratable Acid + NH4+ - HCO3-.
but it’s mostly titratable acid - phosphate - and ammonium salts
Review: Is bicarb reabsorbed as bicarb?
Nope. It’s converted to CO2 + H2O by carbonic anhydrase at the cell surface, then back to bicarb within the cell.
8 factors affecting HCO3- reabsorption?
Delivery of HCO3- (GFR, tubular flow rate). Blood pH and HCO3-. Blood pCO2. Carbonic anhydrase activity. ECF volume status. Endothelin, catecholamines. Parathyroid hormone. Serum K+.
How does ECF volume affect HCO3- reabsorption?
Increases bicarb resorption via increased Na+/H+ exchange.
via A-II and catecholamines
How do endothelins and catecholamines affect HCO3- reabsorption?
Increase HCO3- reabsorption via increased Na+/H+ exchange.
How does parathyroid hormone affect HCO3- reabsorption?
Decreases HCO3- reabsorption by inhibiting Na+/H+ exchange.
How does hyperkalemia affect intracellular pH?
What’s the most important result of this?
Extra K+ moves into cells, driving H+ to move out.
ICF pH is increased.
The important result is decreased intracellular ammoniagenesis… in renal tubules.
How does hypokalemia affect intracellular pH?
Important result of this?
Hypokalemia -> decreased intracellular pH (H+ moves into cells).
This stimulates increased renal ammoniagenesis.
When bicarb is synthesized in the proximal tubule?
CO2 + OH- -> HCO3-
the OH-‘s proton has been buffered by something else
H+ secretion in the PCT is done via Na+/H+ exchangers.
How is H+ secretion done in the collecting tubules?
What cells does this happen in?
H+/K+ exchanger.
H+ ATPase.
(this results in bicarb reabsorption)
This happens in alpha-intercalated cells.
4 factors affecting distal H+ secretion?
Aldosterone. Transepithelial voltage. Buffer availability (Pi, NH3). Endothelin.
How does aldosterone increase H+ secretion?
Increased ENaC activity -> more Na+ reabsorption.
This creates an EC gradient that drives increased H+ and Na+ excretion.
Biochemical pathway of ammonia generation?
Where, intracellularly, does this happen?
Glutamine -> glutamate -> alpha-ketoglutarate.
Each step produces NH3.
This happens in the mitochondria (mostly in the proximal tubule).
What happens to NH4+ if it’s reabsorbed?
It’s made into urea in the liver, consuming bicarb.
Through what channels does NH3/NH4+ move from blood to lumen in the collecting duct?
Rhbg and Rhcg
Lower urinary pH corresponds with increased NH4+ / NH3 excretion.
That makes sense..
