22 August 2010

Acid-base: My Achilles' Heel

ACID-BASE BALANCE IS THE BANE OF MY EXISTENCE!!!

There are not very many things in this life that I naturally suck at.  Basically the list just includes team sports and acid-base balance. 























My strategy for overcoming this obstacle has thus far been identical to my strategy for dealing with team sports: complete and utter avoidance.  Unfortunately, acid-base keeps poking its' ugly snout back into my USMLE business, and I realize I must meet this enemy head-on (or risk having my ass handed to me on a platter on test day).

To date, physiology textbooks like Sherwood and Guyton (both my usual favorites) have failed me dismally.  So it is with a heavy heart that I turn to USMLE Step 1 Secrets in the vain hope that somehow this high-yield review source will explain the mysteries of protons and bicarbonate in such a way as my currently feeble mind can unravel.

God's teeth!  What witchery be this?  It is starting to make sense! (Just a little bit.)

Stuff I didn't know until now:
- The kidney is 'better' at excreting bicarbonate than it is at retaining it.  This explains why renal compensation in respiratory alkalosis (compensatory mechanism = excrete bicarb) is faster and more complete than the renal compensation for respiratory acidosis (compensatory mechanism = retain/synthesize bicarb).

- There are a gajillion things that can cause metabolic alkalosis, but they all revolve around a couple of major mechanisms:
  1. Hypokalaemia: three main effects ...
    (1) ↓ K+ secretion at distal tubule --> ↑ H+ loss at distal tubule (serum pH ↑s)
    (2) Cells exchange K+ for H+ --> ↓H+ in serum and ↑H+ in cells (serum pH ↑s)
    (3) Proximal tubule cells excrete excess intracellular proton in the form of ammonium ion (serum pH ↑s)
  2. Excessive activation of aldosterone receptor - promotes K+ & H+ excretion in exchange for Na+ retention (serum pH ↑s through direct effect of excreting protons and indirect effect of hypokalaemia)
  3. Volume depletion - causes ↑ Na+ retention (attempt to maintain plasma volume) --> ↑H+ loss and ↑bicarb retention at proximal tubule; also indirect effects of RAAS --> ↑ aldosterone activity
  4. Proton loss to the outside world - loss of acid to outside world --> ↑ serum pH
So, things that cause metabolic alkalosis include:
  • Loop & thiazide diuretics - vol depletion & hypokalaemia
  • Bartter syndrome - loss of Na+/K+/2Cl- transporter - mimics loop diuretic
  • Gitelman's syndrome - loss of Na+/Cl- transporter - mimics thiazide diuretic
  • Vomiting & antacid overuse - loss of acid
  • Conn's syndrome - primary hyperaldosteronism
  • Cushing syndrome - excess glucocorticoid exerts effect on aldosterone receptor
  • Liddle's syndrome - mimics hyperaldosteronism
  • 11β-hydroxycortisol dehydrogenase deficiency (essential or secondary to licorice) - decreased breakdown of steroids - mimics hyperaldosteronism
I think it's better to learn the mechanisms than to memorize the list.

Metabolic acidosis coming up soon!  Stay tuned ...

Xo --KM <3