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Flashcards in Metabolic Alkalosis Deck (12)
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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 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-.


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?

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+.