Hyperchloremic Non-Anion Gap Metabolic Acidosis Flashcards
2.3 Causes of Non-AG Acidosis
Loss of bicarb (diarrhea or proximal renal tubular acidosis)
Retention of HCl (distal renal tubular acidosis)
If bicarb decreases, have to increase Cl or else would increase AG
Type II Renal Tubular Acidosis (RTA)
Proximal tubule can’t reabsorb HCO3- (can get rid of HCL).
Damage to microvilli/inhibits CA will cause loss bc can’t convert into CO2/H2O to diffuse into cell and be excreted. Patients frequently very hypokalemic bc K+ trapped by bicarb and can’t be reabsorbed
2 Drugs that Cause T2RTA
Inhibitors of CA: Acetozolamide (Diamox) for glaucoma, and Topiramate (Topamax) for migraines
Fanconi’s Syndrome (what it is and 6 findings)
Acid/base and electrolyte abnormalities as a result of proximal tubule damage
Type II RTA (hyperchloremic NAG metabolic acidosis)
Tubular proteinuria (500-200 mg)
Hypophosphatemia secondary to hyperphosphaturia (PT reabs)
Hypouricemia secondary to hyperuricosuria (PT reabs)
Hypokalemia bc HCO3 sequesters cats
Glycosuria w/ normal serum glucose (or low)
T2RTA Tx (2)
Oral HCO3 doesn’t work that well bc just leaks out anyway
K+ supplementation necessary
Type I RTA
Anything that damages/inhibits principal (aldosterone responsive) or intercalated cell (secrete H+) in CCT will lead to H+ retention
2 Drugs and 2 Diseases that Cause T1RTA
Amphotericin B
Lithium
Autoimmune: SLE/Sjogren’s
Sickle cell
Nephrolithiasis
Kidney stones almost exclusively seen w/ T1RTA, not T2. Composed of calcum phosphate bc urine pH alkaline bc can’t secrete H+. Require bone dissolution, carbonate secretion to buffer, so Ca and phosphorous released and filtered in urine
Nephrocalcinosis
Precipitations of Ca/PO4 in interstitium of kidney in T1RTA, clearly seen on X ray
Labs for Hyperchloremic NAG Metabolic Acidosis
Low pH, CO2, and HCO3
Slightly low Na, low K, high Cl
Tx and Severity of RTAs
Distal more severe (bone loss, stones, nephrocalcinosis), but definitely easiest to treat. Just give enough oral HCO3- to match daily production of H+ and it’s safely absorbed in PT
Proximal it always leaks out, can just give a shitload and keep it at like 15-17
Type IV RTA
Inhibition of aldosterone production or action leads to impaired Na reab and subsequently impaired H+ secretion (causes hyperkalemia too, which causes more acidosis)
T4RTA Tx
Main focus treating hyperkalemia bc acidosis won’t get better until. So add diuretic/HCO3 supplement/Fludrocortisone (synth mineralocorticoid to act like ald, best)
Short Bowel Syndrome
In NAG, bc huge chunk including colon resected so now can’t absorb HCO3 rich stuff from pancreas, lose a lot of V
Urinary Diversion
Make a fake bladder from colonic tissue, when urine sits there Cl gets reabsorbed and HCO3- excreted into “pseudobladder”
