Acid-Base Regulation and Metabolic Acidosis

Question 1

1. Describe the pathogenesis of metabolic acidosis.

Answer 1

decrease in bicarbonate:
loss of bicarbonate: proximal RTA II, diarrhea
bicarb consumption: excessive exogenous or endogenous acid
failure to regenerate bicarbonate: renal failure, distal RTA (I,IV)

Question 2

2. Explain the notion of the anion gap.

Answer 2

anion gap is the difference between Na+ and chloride and bicarbonate, K+ and unmeasured anions are normally thought to held constant

normal anion gap is 12 mEq/L 2+/-

Question 3

3. Differentiate anion gap and normal anion gap in metabolic acidosis.

Answer 3

normal gap-bicarbonate loss: RTA or diarrhea leads to a non-gapped acidosis bicarbonate, usually with addition of a chloride containing acid (so as bicarb decreases, Cl- increases)

increased gap: bicarb consumption or failure to regenerate will lead to a gap: bicarb decrease because of unmeasured anions (sulfate, organic acids, albumin, phosphate)

Question 4

4. Utilize a stepwise approach to acid base disorders.

Answer 4

1. access pH
2. access bicarb level
3. access anion gap
4. access pCO2
5. determine primary disorder
6. use compensation formula to determine appropriate physiological response for single disorder
   Met. Ac PCO2= 1.2 change in bicarb
   Met Al PCO2= 0.7 change in bicarb
   Rep acid/alkalosis
   acute: bicarb= 0.2 change in pCO2
   chronic bicarb= 0.4 change in pCO2
7. decide whiter it is simple or mixed

Question 5

Describe the pathogenesis of renal failure M.A. and how it is treated

Answer 5

essentially patients cannot generate enough bicarbonate, to handle phosphoric acid from bone or sulfuric acid from cells, in the later stages GFR also decreases (decreasing NH4+ excretion)

treat with oral sodium bicarbonate to replace bicarbonate

Question 6

Describe the pathogenesis of lactic acidosis/ DKA M.A. and how it is treated.

Answer 6

LA accumulates in severe illnesses (hypo perfusion or liver disease), produced bicarbonate cannot keep up

treatment: sometimes with IV bicarb if pH<7.2 and treatment of underlying cause

similar course for DKA- acids due to production of ketoacids by liver for energy; treat with insulin and IV fluids

Question 7

What is the treatment of salicylate intoxication?

Answer 7

accumulation of salicylic acid leads to intoxication as well as direct neurotoxicity caused by primary r. alkalosis

tx. includes gastric lavage and charcoal, grin alkalization, dialysis if severe and psychiatric consult if necessary

Question 8

Contrast the different types of RTA.

Answer 8

Type I- distal hypokalemic: decreased secretion of H in collecting duct, urine pH always>5.5: prototype Amphotericine B (anti fungal) treatment

Type II- proximal: decreased bicarb reabsorption (still able to acidify urine, prototype Fanconi Syndrome) essentially the set point is reset for reabsorption so if you give acid, urine will acidify

Type IV- distal hyperkalemic: most common, due to defects in NH4+ metabolism, obstruction, drugs or aldosterone deficiency (retain ability to acidify urine): prototype diabetes