Acid Base Balance In The Kidney Flashcards
Normal plasma pH range
7.35 - 7.45
What is alkalemia?
Buildup of alkaline substances in body
High pH
What is acidemia?
Increase in [H+] in blood
Decreases in pH
Impact of alkalemia on Ca2+
- lowers free calcium by causing Ca2+ to come out of solution + bind to albumin
- Ca2+ swaps with H+
- increases neuronal excitability > fire action potentials at small signals
- numbness or tingling + muscle twitching
- paralysis of respiratory muscles if severe
Impact of acidemia on Ca2+
- increases free calcium by causing Ca2+ to go into solution (breaks off from albumin)
- affects AP excitability > arrhythmia
What are the 3 mechanisms to control pH of blood
Buffers
Ventilation
Renal regulation of H+ and HCO3-
Sources of acids in diet
Lipids as fatty acids
Proteins as amino acids
How do the kidneys alter pH?
- directly by excreting or reabsorbing H+
- indirectly by changing rates at which HCO3- is reabsorbed or excreted
What is the % of H+ output of the lungs and kidneys?
Lungs 75% | rapidly
Kidneys 25% | over a couple days
How much HCO3- is aimed to be reabsorbed in the kidney?
100%
What are the buffer systems in the PCT?
- Ammonia: NH3 + H+ > NH4+
- Hydrogen phosphate: HPO42- + H+ > H2PO4-
- Glutamine in cell: glutamine > alpha ketoglutarate > 2HCO3- reabsorbed | glutamine > 2NH4+ > 2NH3 + H+ > H+ back into lumen + NH3 diffuses back
Primary cause of respiratory alkalosis
Excessive artificial ventilation - hyperventilation
Compensation of respiratory alkalosis
From renal mechanisms:
- HCO3- not reabsorbed in PCT
- late DCT/CD HCO3- secreted + H+ reabsorbed in intercalating cells
Cause of respiratory acidosis
Hypoventilation > CO2 retention
Compensation of respiratory acidosis
From renal mechanisms that secrete H+ + reabsorb HCO3-
- glutamine
- alpha intercalated cells
When does metabolic acidosis occur?
- When dietary and metabolic input of H+ exceeds excretion
lactic acidosis | ketoacidosis - or when body loses HCO3- e..g diarrhoea
Causes of metabolic alkalosis
- excessive vomiting of acidic stomach contents
- excessive ingestion of bicarbonate containing antacid
Compensation of metabolic alkalosis
Respiratory compensation
- hypoventilation to retain CO2
- this creates more H+ + HCO3-
- restores pH but also makes more bicarbonate
Renal compensation
- HCO3- not reabsorbed in PCT
- late DCT/CD HCO3- secreted + H+ reabsorbed in intercalating cells
Compensation of metabolic acidosis
Respiratory compensation
- increases ventilation > CO2 decreases
Renal compensation
- late DCT/CD secretion of H+ + reabsorption of HCO3-
Compare respiratory and metabolic acidosis in regards to pH, pCO2 and HCO3-
- both pH low
- respiratory acidosis: pCO2 + HCO3- high
- metabolic acidosis: pCO2 normal/low + HCO3- low
Metabolic follows pH change
Compare respiratory + metabolic alkalosis in regards to pH, pCO2 and HCO3-
- both pH high
- respiratory acidosis: pCO2 + HCO3- low
- metaboIic acidosis: pCO2 normal/high + HCO3- high
Metabolic follows pH change
Outline the action of glutamine in the PCT
- becomes aKG (alpha ketoglutamate) > 2HCO3- > reabsorbed into blood with Na+
- becomes 2NH4+ > NH3 + H+ > H+ back into lumen swapped with Na2+ | NH3 diffuses back
What is the anion gap?
Difference between the concentrations of cations and anions in the body due to anions that are not measured
Equation for the anion gap
([Na+] + [K+]) - ([Cl-] +[HCO3-])
When does the anion gap increased?
If HCO3- is replaced by other anions e.g. lactic acid
??