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

Pre-renal vs. Intra-renal Ischaemia

Holy crap - busiest month ever.  I srsly don't know where the last month went.  It just disappeared. :S

USMLE studying has basically gone out the window lately.  :( But I am trying to get back into it with renal!  Renal physiology is kind of meh but the pathology is amazingly cool.

Acute tubular necrosis is the commonest intra-renal cause of acute renal failure.  It can be caused by toxins or ischaemia.  At first this seemed straightforward to me, but then I realized that pre-renal acute renal failure is ischaemic.  This caused me to question, how in the &$%! do you tell the difference between intra-renal ischaemic acute renal failure and pre-renal ischaemic acute renal failure??

Apparently it goes like this:

Pre-renal: renal cells are hypoperfused, but tubular function remains intact!  Tubule cells increase reabsorption of sodium, and urea is retained in the medulla.  This is an attempt to create concentrated urine and maintain plasma volume (...and thereby maintain perfusion).
-BUN/Creatinine ratio (quick and dirty, but not specific): Elevated >20:1
-Fractional excretion of Na+ (more specific measure .. basically the clearance of sodium weighted by creatinine clearance): Reduced <1%

Intra-renal: renal tubule cell function is impaired!  Sodium and urea cannot be reabsorbed.
-BUN/Creatinine ratio: Reduced <10:1
-FENa+: Elevated >2%

Also, toxins which can cause ATN:
"Color, contrast, and chemo"
= Heme pigments (Hb and Mb) 
= Radiography contrast media 
= Chemotherapeutic agents: cisplatin, aminoglycoside A/Bs, & Amphotericin B