Metabolic Alkalosis Flashcards
Why does vomiting produce alkalosis?
Parietal cells split H2O + CO2 into a HCO3- and H+.
The H+ enters the lumen, and the HCO3- enters the blood.
If the H+ is lost by vomiting, there’s a net gain of HCO3-.
When encountering a patient with sustained high serum bicarb, what 2 questions should you ask?
How did the bicarb increase?
How did the increased bicarb persist?
Why isn’t the bicarb produced from vomiting excreted by the kidney?
Vomiting also causes volume depletion.
Volume depletion -> renin, angiotensin-II.
A-II stimulates Na+/H+ exchanger in the proximal tubule.
Increased H+ secretion in the proximal tubule drives bicarb reabsorption (the H+ is recycled).
Where in the nephron is H+ secreted / HCO3- generated?
How?
alpha-intercalated cells in the collecting duct.
Carbonic anhydrase intracellular converts CO2 + H2O -> HCO3- + H+.
K+/H+ exchangers moves H+ into lumen, where it is buffered by NH3.
This leaves behind HCO3-, which is reabsorbed via Cl- exchange.
Why is Cl- necessary to secrete bicarb?
In the collecting duct intercalated cells, bicarb is secreted into urine via HCO3-/Cl- exchangers.
If there isn’t Cl- in the filtrate, this exchange won’t happen.
(Cl- is a treatment for alkalemia)
What are urine electrolyte levels like during vomiting?
How at post-vomiting?
During vomiting: bicarb-uria, higher pH.
Post-vomiting: acidic, high K+, low Na+ (A-II / aldosterone effects)
2 ways (thiazide and loop) diuretics contribute to akalosis?
Increased Na+ delivery to distal tubule -> more Na+ absorbed -> negative lumen -> more H+ and K+ secretion.
Relative volume depletion -> aldosterone (which promotes the above mechanism, but also directly stimulates H+ and K+ secretion).
Why do people with edematous disorders (e.g. CHF) often have alkalosis from increased HCO3- generation?
Mainly from the diuretics used to treat the disorder.
Diuretics and salt-wasting nephropathies cause a low (effective) volume alkalosis. What would cause a volume-replete alkalosis?
Primary mineralocorticoid excess.
How does hypokalemia drive continued alkalosis?
Low K+ drives H+ to enter cells.
When more H+ is in the cells of the distal nephron, it’s easier for H+ to be secreted / bicarb to be generated.
Treatment of volume-depletion metabolic alkalosis?
NaCl-containing fluids + KCl.
Treatment of volume-expanded metabolic alkalosis?
As this is probably primary hyperaldosteronism,
antagonize aldosterone, give K+.
