April 29, 2016 - Metabolic Alkalosis

Question 1

Mechanisms of Metabolic Alkalosis

Answer 1

1. ECF volume depletion
2. Hypokalemia

Question 2

Reduced EABV and Metabolic Alkalosis

Answer 2

In states of low EABV due to vomiting, we are losing HCl in the vomit. As we are losing chloride, we need to bring more chloride across through the parietal cell, and the only way to do this is with a bicarbonate/chloride anti-transporter which brings a bicarbonate ion into the blood in exchange for a chloride ion.

After the RAAS system is activated, we uptake more Na+ through NHE3 which, unfortunately, also pumps more hydrogen out of the cell and brings more bicarbonate back into the cell. The price for reabsoring more sodium is reabsorbing more bicarbonate.

Question 3

Hypokalemia and Intracellular Fluid

Answer 3

As potassium ions are leaving, the cell becomes more and more negative inside the cell. To compensate, the cell retains hydrogen ions which creates a more acidic environment inside the cell. Hypokalemia causes ICF acidosis.

Unfortunately, glutaminase activity is pH and dependent and glutaminase only sees the inside of the cell. As a result, it ramps up production of ammonium to get rid of excess acid but it also ramps up bicarbonate production (even though we have more than enough outside the cell).

Question 4

Urine Chloride and Low EABV

Answer 4

The kidney is fantastic at holding onto chloride when it has to. In the state of low EABV, we can look at the urine chloride to assess kidney function. If the chloride is low (<10 mmol/L), the kidney is working. If the chloride is high, the kidney is not working.

Question 5

Acetazolamide

Answer 5

Inhibits carbonic anhydrase.