Flashcards in Metabolic Acidosis Deck (31)
4 types of cause of metabolic acidosis?
Loss of bicarb.
Insufficient bicarb production.
Increased endogenous organic acid generation.
Ingestion of exogenous acid (or substance that becomes acid).
What's the anion gap?
Anion gap = Na - (Cl + HCO3)
It's the mEq of anions that aren't Cl- and HCO3-, which are often the anions of acids.
What's a normal anion gap?
2 organs from which bicarb can be lost, causing a metabolic acidosis?
GI loss (diarrhea, usually).
If an added or retained organic acid is causing metabolic acidosis, what will the ion gap be?
The anion gap will be >10, because the acid's anion is present.
What kind of anion gap does diabetic ketoacidosis produce?
How about acidosis caused by alcohol ingestion?
Both produce high anion gap metabolic acidosis.
What kind of anion gap will acidosis from reduced GFR produce? Why?
The anion gap will be high.
There is failure of bicarb absorption/production, but there is also retention of phosphoric and sulfuric acid.
3 types of renal tubular acidosis (RTA)?
Proximal (Type II) - failure or bicarb reabsorption.
Distal (Type I) - defect in acid excretion (bicarb generation).
Distal hyperkalemic (Type IV) - defect in acid excretion (ammoniagenesis).
How does proximal RTA affect the amount of bicarb that appears in the urine?
As bicarb isn't being absorbed as well in proximal RTA, bicarb will start to appear in the urine at lower serum bicarb concentrations.
Review: How is bicarb absorbed in the proximal tubule? Name 4-5 required proteins.
Na/K ATPase generates Na+ gradient.
Na+/H+ exchanger moves H+ into lumen. (and H+ pump)
HCO3- + H+ --> H2O + CO2 via carbonic anhydrase.
CO2 + H2O diffuse into cell, carbonic anhydrase converts to HCO3- + H+.
Na/HCO3 cotransporter moves HCO3 to blood.
(note that an H+ keeps cycling from lumen to cytosol, but bicarb is reabsorbed)
Is HCO3 reabsorption normal in distal RTA?
What can't be done to the urine in distal RTA?
The urine can't be acidified.
There are 5 listed mechanism for distal RTA. 3 involved impaired proton secretion. What are those 3 precise mechanisms?
H+ ATPase defect. (primary or autoimmune)
H+/K+ defect. (rare, toxins)
H+ backleak. (amphotericin toxicity)
2 mechanisms for distal RTA that don't directly involve H+ secretion?
Defect in Carbonic Anhydrase II (usually also causes proximal RTA).
Defect in HCO3/Cl exchanger (brings HCO3 to blood).
These are rare.
How is serum K+ in both proximal and distal RTA?
Typically a little low.
(several reasons... including increased aldosterone, increased distal Na+ delivery,
What broader syndrome can proximal RTA be a part of?
Fanconi Syndrome: Impaired glucose, amino acid, bicarb, etc. reabsorption.
What underlies hyperkalemic RTA?
Aldosterone insufficiency / lack of response to aldosterone.
2 main endogenous acids that cause metabolic acidosis?
5 common toxins that cause an exogenous acidosis?
Difference between Type A and Type B lactic acidemia?
Type A: Caused by relative hypoxia (shock, severe anemia, etc.)
Type B: Caused by impaired metabolism of lactate.
What's the osmolar gap?
The difference between observed and calculated osmolality.
What's a common osmolyte implicated in high osmotic-gap acidosis?
Ethanol is the most common osmolyte found in high osmotic gap acidosis.
What's the old treatment for methanol poisoning? Why?
Ethanol, as it would compete for alcohol dehydrogenase, decreasing conversion of methanol to formic acid.
What's the significance of delta anion gap / delta HCO3?
If there is just one process happening, the magnitude of change of the anion gap and the HCO3 gap should be about the same.
If there's mismatch, another acid-base disorder may be co-occurring.
4 clinical features of acidosis?
Musculoskeletal problems (when chronic).
How do the lungs compensate in acidemia?
Increased ventilation -> reduced pCO2
How can you judge if the respiratory compensation to acidemia is appropriate?
What is Winter's formula?
Expected pCO2 = 1.5*bicarb + 8 +/- 2.
(in metabolic acidosis)
Affect of metabolic acidosis on NH4+ synthesis / excretion?
Increased synthesis and excretion.