Wilson Flashcards
Respiratory acidosis
- caused by HYPOventilation
- increases pCO2
- point on normal buffer slope BELOW ph 7.4
respiratory alkalosis
- caused by HYPERventilation
- decreases pCO2
- Point on normal buffer slope above pH 7.4
Metabolic acidosis
- loss of HCO3-
- point on 40 torr isobar BELOW pH 7.4
Metabolic alkalosis
- Increases in HCO3- conc
- point on 40 torr isobar ABOVE pH 7.4
Compensation of the acid-base balance
goal is to maintain balance of HCO3-/pCO2
- Respiratory compensation
- hypo or hyperventilation regulates pCO2
- RAPID (HOURS)
- hypo or hyperventilation regulates pCO2
- Renal compensation
- regulation of HCO3- conc
- regulation of H+ EXCRETION
- SLOW (days)
role of kidney in regulation of pH
- kidneys regulate H+ excretion and HCO3- reabsorption
- H+ ions are removed by binding to filtered buffers or binding to NH3
-
ELIMINATION of HCO3- in urine is equivalent to ADDING H+ to the body
- cannot eliminate the H+ load unless virtually all filtered HCO3- is reabsorbed
describe the secretion of H+ by renal tubule cells
- Proximal acidification
- Na+/K+ ATPase generates a sodium potassium electrochemical gradient on the basolateral membrane
- on the luminal membrane there is an Na+/H+ exchanger that uses electrochemical gradient to move H+ outside of the tubule cell
- Distal acidification in the collecting duct
-
insertion of ATPase into luminal membrane stimualted by LOW pH (more protons are pumped out)
- high pH stimulates recycling of ATPase back to the cytoplasm
-
insertion of ATPase into luminal membrane stimualted by LOW pH (more protons are pumped out)
describe the reabsorption of bicarbonate in the PROXIMAL TUBULE
- H+ secreted into tubule lumen
- reacts with HCO3- in filtrate –> forms CARBONIC ACID
- Carbonic anhydrase converts carbonic acid to H2O and CO2
- H2O and CO2 diffuse into renal tubular cell
- carbonic anhydrase converts H2O and CO2 to carbonic acid
- Carbonic acid dissociates, H+ exported to tubule lumen and HCO3- exported to blood
NET = movment of NaHCO3 FROM filtrate to BLOOD
role of H2PO4- (filtered buffer)
- secreted H+ is buffered in filtrate and the buffer is excreted
- phosphate typically major non-bicarbonate urinary buffer
-
H+ secretion increases conc of H+ in tubule lumen
-
SHIFTS EQUILIBRIUM LEFTWARD
- drives fromation of H2PO4-, ELMINATED IN URINE
-
SHIFTS EQUILIBRIUM LEFTWARD
- Ability to excrete H+ as H2PO4 limited by
- amount of HPO4- in filtrate
- requirement of body to retain phosphate
Net result of formation of H2PO4- excretio in urine
One H+ eliminated
one NEW HCO3- formed and added to the blood
what is titratable acid
- it is a measure of H+ excreted in urine as UNDISSOCIATED WEAK ACID
- generally H2PO4- (most abundant)
- NORMAL = 0 to 20mmol/day
- acidosis = 40mmol/day
WILL SEE OTHER ACIDS DURING DIFFERENT PATHOLOGIC STATES:
- beta-hydroxybutyric acid - during ketoacidosis
- lactic acid - during lactic acidosis
Excretion of H+ as NH4+
- First step is generation NH4+ within renal tubules cells
- kidney expresses GLUTAMINASE
- converts glutamine to glutamate
- glutamate then CONVERTED to ALPHA-KETOGLUTARATE by GLUTAMATE DEHYDROGENASE
- glutamate metabolism ultimately yeilds 2 HCO3-
- NH4+ exported to tubular lumen
- HCO3- released to the blood
NET = excretion of protrons into lumen and addition of new molecules of HCO3- to the blood
describe the regulation of H+ excretion
- Rate of H+ secretion is pH DEPENDENT
- reduce pH ACTIVATES Na+/H+ antiporter and H+-ATPase
- increases the amount of proton is pushed into lumen
- reduce pH ACTIVATES Na+/H+ antiporter and H+-ATPase
describe the effects of H+ excretion during ACIDOSIS STATE
- DURING ACIDOSIS
- H+ secretion INCREASED
- all HCO3- Reabsorbed
- substantial titratable acid excreted
- NH4+ production INCREASED
- increased glutamine uptake/glutaminase activity
- increased NH4+ excretion in urine
describe the effects of H+ excretion DURING ALKALOSIS
- DURING ALKALOSIS
- H+ secretion insufficient to allow HCO3- reabsorption
- HCO3- SECRETED IN URINE
- B-Type intercalated cells of collecting duct ACTIVELY SECRETE BICARBONATE into tubular lumen
- no titratable acid or ammounium ions excreted in urine
- H+ secretion insufficient to allow HCO3- reabsorption