PhysiologyTier 2Medical Sciences concept

Mechanism of hypokalaemia in vomiting-induced metabolic alkalosis (distal K+ secretion)

Core concept

The potassium is lost in the URINE, not the vomitus - gastric fluid contains only ~5-10 mmol/L K+
Three sequential drivers
- 1. Loss of HCl -> metabolic alkalosis
  - Each H+ secreted generates an HCO3- into blood ("alkaline tide") that is normally neutralised by pancreatic HCO3- secretion
  - Vomiting removes the H+ -> the HCO3- is retained unopposed
- 2. Volume depletion -> secondary hyperaldosteronism
  - inc aldosterone -> inc ENaC Na reabsorption -> lumen-negative potential -> inc K+ secretion via ROMK/BK
  - -> the principal route of potassium loss
- 3. inc distal HCO3- delivery
  - Filtered HCO3- exceeds proximal reabsorptive capacity -> a poorly reabsorbed anion arrives distally -> obligates cation loss -> further inc K+ secretion, and inc H+ secretion
The alkalosis and the hypokalaemia perpetuate each other
- Alkalosis -> K+ shifts intracellularly and inc K+ secretion
- Hypokalaemia -> inc H+/K+-ATPase activity and inc proximal ammoniagenesis -> maintains the alkalosis
- Paradoxical aciduria - despite systemic alkalosis, urine is acid because Na/volume avidity and hypokalaemia force H+ secretion

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