Acidosis/Alkalosis Flashcards
4 Causes of Hyperchlroemic Acidosis
- Impaired renal acid excretion (renal failure, distal renal tubule acidosis)
- Renal bicarb loss (CA inhibitors, proximal renal tubule acidosis)
- GI bicarb loss (diarrhea, pancreatic drainage, ureteral diversion)
- Acid gain (tpa, ammonium Cl ingestion)
8 Causes of High Anion Gap Acidosis
- M - methanol ingestion (formate and lactate)
- U -uremia (renal failure –> phosphate, sulfate, organic acids)
- D diabetic ketoacidosis (beta- hydroxybutyrate or acetoacetate)
- P - propylene glycol, paraldehyde
- I - infection, iron, isonazid, inborn errors
- L - lactic acidosis
- E - ethylene glycol ingestion (ocylate, glycolate)
- S - salicylates (aspirin –> ketoacids, lactate, salicylate)
Anion Gap Equation
AG = [Na] - [Cl-] - [bicarb]
normal is 10 +/- 2
Urinary Anion Gap Equation (+ what does it tell us?)
UAG = [Na] + [K] - [Cl] (no bicarb in urine normally)
- UAG <0 - non-renal cause of acidosis b/c make up for acidosis by ammonium production in kidney (+ charge so negative anion gap)
- UAG > 0 - renal cause of acidosis b/c no ammonium present
What kind of acidosis is present in chronic kidney disease?
BOTH
it can start as hypercholermic acidosis and later become high anion gap
Winter’s Formula
- Predicts the respiratory comp for metabolic acidosis
PCO2 = 1.5 x [bicarb] + 8 +/-2
- If actual meas PCO2 is > prediction by formula… compensatory
- If actual meas PCO2 is < prediction by formula … primary respiratory acidosis
What is the risk of chronic metabolic acidosis?
- Bone disease/rickets/growth fail in kids
- Osteoporosis in adults
Type I RTA
Classic distal RTA
- Defective distal nephron H+ pumps or back leak of H+ into tubular lumen
- Can be… impaired H-ATPase, bicarb/Cl exchanger, carbonic anhydrase
Type II RTA
Proximal RTA
- If congenital defect or proximal tube damage –> impaired H+ secretion –> lower threshold for bicarb reclamation (start spilling bicarb into urine at much lower threshold)
- Can be part of Fanconi Syndrome (mult prox tube defects - glycosuria, phosphate wasting, aminoaciduria and hypouricemia)
Type IV RTA
Hyperkalemic distal RTA
- Either aldosterone def/resistance
- OR voltage-dep defect in H+ excretion; if dec Na+ reabsorption then this dec gradient for H+ secretion
What 2 things must occur for metabolic alkalosis to take place?
- Generation (acid loss of alkali gain)
- Maintenance (why is alkalosis not being corrected by body?)
Generation of Metabolic Alkalosis
- Acid Loss
- In kidney - diuretics, mineralocorticoid excess, Cushing’s (steroid), severe K+ depletion, Bartter’s, Gitelman’s, Liddle’s
- In GI - vomiting, nasogastric drainage, chloride diarrhea - Alkali Gain
- Bicarb admin
- Milk-alkali syndrome
- Infusion of organic anions that are metabolized to bicarb (ex- citrate in blood transfusion; lactate; acetate)
Maintenance of Metabolic Alkalosis
- Dec GFR –> less bicarb filtered load; from either dec EABV or renal insufficiency
- Inc proximal tube bicarb reclamation; from dec EABV or chloride depletion
- Inc H+ excretion; from mineralocorticoid excess or hypokalemia
2 Classes of Metabolic Alkalosis Tx
1- Responds to saline (vol or Cl- depletion)
- This will enhance EABV and Cl- delivery to dec proximal bicarb reclamation - Can also give KCl in saline if hypokalemia is severe and contributing - Also give if GI losses or diuretic use
2- Resistant to saline (PT NOT VOL OR CL- DEPLETED)
- So due to mineralocorticoid excess; give aldosterone antagonist instead - Also due to severe hypokalemia (Barrters, Gitelmans, Liddles); give K-sparing diuretic instead