Metabolic Acidosis (10 Page Handout from Simon)

Causes
o Loss of HCO3

Diarrhea causes loss from the GI tract

Proximal Tubular Acidosis or treatment with Carbonic Anhydrase inhibitor
o Decreased H+ Excretion
Occurs during early renal failure (proximal tubule and collecting ducts)
Renal tubular acidosis creates a electrochemical barrier resistant to excretion
Aldosterone inhibition
o Acid Loading exceeding renal handling capacity
Requires a large amount of acid consumption (toxicity from Salicylates, methanol,
ethylene glycol) or endogenous production (lactic acidosis, diabetic Ketoacidosis)
Anion Gap
o Useful for differentiating Metabolic Acidosis into two forms, defined by the following formula
o High Anion Gap = addition of organic acids (not H+) such as lactic acid or ketoacids that
consume the bicarb without affecting the chloride concentration
Severe Renal Failure
Lactic Acidosis from hypoxia produces lactate
Ketoacidosis seen in diabetics and malnourished alcoholics
Poisonings such as Salicylates, methanol, and ethylene glycol
Remembered by the mnemonic MUDPILES (Methanol, Uremia, DKA, Paraldehyde,
Isoniazid, Lactic, Ethanol, Salicylates)
o Normal Anion Gap = addition of volatile acids (HCl) that combine with HCO3 decreasing HCO3
levels but reciprocally increasing the chloride levels, effectively leaving the anion gap
unchanged
Diarrhea causes a loss of HCO3
in the stool
Renal Tubule Acidosis
Type I = Distal Defect. There is no loss of HCO3 but instead there is an inability to
acidify the urine (intercalated cells of distal tubule cannot secrete H+ and make
HCO3). The urine is therefore never less than 6. Urine pH > 6
Type II = Proximal Defect. The proximal tubule normally reabsorbs all the filtered
bicarbonate. In fanconis syndrome the proximal tubule is bunk, and cannot resorb
bicarbonate. The distal tubule has limited capacity to resorb, so bicarb is lost in the
urine until a serum level low enough to be reabsorbed by the proximal tubule is
reached, Urine pH < 5.5. Also associated with Multiple Myeloma.
Type IV = Aldosterone Defect. It is the most common RTA associated with
hyperkalemia. It is common in diabetic nephropathy, ACEI administration, and
urinary obstruction. Things that reduce ReninAngiotensin Axis, block the effects of
ANG II, decrease renal sensitivity to ANG II or reduce aldosterone activity.