Control of Plasma pH Flashcards
State the normal plasma pH range
7.35-7.45
Compare Acidaemia and Acidosis
Is Acidaemia or Alkalaemia more dangerous?
Acidaemia is low blood pH due to acidosis
Alkalaemia is more dangerous
How does Alkalaemia affect Ca and nerves?
- Reduces solubility of Ca salts, so free Ca2+ leaves ECF and binds to bone and proteins-> Hypocalcaemia
- This makes nerves more excitable-> Parasthesia and Tetany (Uncontrolled muscle contractions)
What is the mortality rate if pH is above;
- 7.55
- 7.65
- pH>7.55 mortality: 45%
- pH>7.65 mortality: 80%
How does Acidaemia affect K+ movement?
When are effects of Acidaemia seen? When is it life threatening?
- Affects enzyme function, leading to K+ movement out of cells-> Hyperkalaemia
- Effects seen below pH 7.1
- Life threatening below pH 7.0
The ECF [H+] is very low so small amounts of acid would change pH dramatically. This is buffered by H+ binding to various sites
What is the most important ECF buffer for H+?
The CO2/ HCO3 system
Compare Respiratory Acidaemia and Alkalaemia
How are they compensated really?
- Acidaemia: Rises in pCO2
- Renal compensation: Increased HCO3
- Alkalmaemia: Falls in pCO2
- Renal compensation: Decreased HCO3
Compare Metabolic Acidosis and Alkalosis
How are they compensated by the respiratory system?
- Acidosis: Decreased HCO3
- Respiratory compensation: Reduced pCO2 (hyperventilation)
- Alkalosis: Increased HCO3
- Respiratory compensation: Increased pCO2 (hypoventilation)
Why is Respiratory compensation of metabolic alkalosis limited?
Hypoventialtion is limited as it can cause hypoxaemia
If acid is produced metabolically, recovery of l filtered HCO3 will be insufficient to restore plasma [HCO3].
How does the kidney compensate?
- Kidney makes HCO3 (normally only made in RBCs)
- The byproduct of this, H+, must be excreted into urine
- To prevent a damaging urinary acidity, the H+ must be buffered by other filtered substances or by buffers made in the kidney
How much HCO3 is reabsorbed in;
- PCT
- TAL
- DCT, via Intercalated cells
PCT: 80-90%
TAL: Up to 15%
DCT, Intercalated cells: Remaining
(Overall, 100% of HCO3 is reabsorbed)
Describe HCO3 reabsorption in CD Intercalated cells
- H-ATPase on AM pumps H+ out (Na gradient too low to use NHE)
- CO2 enters cell and reacts with water-> H2CO3 which dissociates into H+ and HCO3-
- New HCO3- ions enter blood via HCO3-Cl Antiport on BM
Compare H+ buffering systems in PCT and DCT
PCT;
- NH3 from Glutamine diffuses into lumen and combines with H+-> NH4+
DCT;
- H+ pumped out via H-ATPase into lumen and combines with Monobasic phosphate (HPO4 2-)-> H2PO4-
Describe how HCO3 is created in PCT (and also some in DCT)
- Glutamine broken down into NH4+ and Alpha-ketoglutarate
- NH4+ dissociates into NH3 and H+, NH3 diffuses into lumen and binds to H+ to reform NH4+ (in lumen)
- Alpha-ketoglutate breaks down into 2 HCO3 ions, which enter blood via Na-HCO3 symport on BM
How does ECF pH affect secretion of acid by kidney?
Why is this done?
Fall in pH-> Increased acid secretion into lumen
To prevent HCO3 depletion (Used to neutralise pH)