metabolic acidosis Flashcards
causes of metabolic acidosis (4)
- addition of acid
- reduction/ loss of bicarbonate
- inability to properly excrete H ions
- inability to appropriately restore bicarbonate buffer
some affects of chronic metabolic acidosis
- bone disease
- reduced albumin synthesis
- increased muscle wasting
- acceleration of kidney disease
- impaired glucose tolerance
adverse effects of acute metabolic acidosis
- impaired leukocyte function
- changes in mental status
- stimulation of apoptosis
4 homeostatic response to an acid load
- immediate- extracellular buffering by HCO3
- minutes to hours: respiratory buffering by lowering pCO2
- two to four hr- intracellular and bone buffering
- hours to days- increased renal H+ excretion
how is the respiratory compensation for metabolic acidosis
important and rapid
anion gap
- what is it?
- nl range
- measured sodium and cl- and HCO3-
- nl: 8-12
- mostly made up albumin
addition of an organic acid; what happens to the anion gap
rises H+ and thus there is a drop in HCO3
- increase in anion gap
addition of mineral acid
rise in H+ and there is a decrease in bicarb but there is no drop in anion gap
examples of an organic acid
lactic acid, ketoacids
examples of a mneral acid
hydrochloric acid
exaplain the difference in hydrogen load btwn organic and mineral
- organic: there is increase in unmeasured acid but cl- stays constant
- there is an increase in cl- and a decrease in unmeasured acid
example of a process that leads to a nl anion gap
- loss of bicarb due to diarrhea
impaired acid excretion examples
- renal failure
- distal (type 1) RTA
increased anion gap in mechanism of acidosis
- lactic acidosis
- ketoacidosis: diabetes mellitus, starvation, alcohol associated
- ingestions: aspirin, methanol
- chronic kidney disease stages 4-5
normal anion gap in metabolic acidosis
- diarrhea
- early chronic kidney disease
- proximal/distal RTA
- intestinal, pancreatic or billiary fistula
bicarb is reclaimed in
proximal tubular cell by CO2 intermediate
excrete H+ ions in the form of
tritratable acid
secrete H+ ions in the distal nephron to make the
NH3 into NH4+
chronic kidney disease is where we have a decreased in
acid excretion
what is wrong in chronic kidney disease
loss of functioning nephrons leads to a disruption in acid base balance where intially it is mantained by increased ammonium ecretion but eventually you see a decrease in bicarb and increase in unmeasured anion concetration
stage 2-3 CKD we see an anion gap that is
normal
stage 4-5 CKD we see an anion gap that is
high
distal (type 1) renal tubular acidosis
inability to decrease urine pH < 5.5-6.0 due to decrease hydrogen ion secretion
common mechanism of distal (type 1) renal tubular acidosis
impaired apical H+-ATPase pump
proximal (type 2) renal tubular acidosis
impaired bicarb reabsorption by the proximal tubule which leads to urinary bicarb loss until the lower resportive capcity is reached and once all of the filtered bicarb is reabsorbed
lactic acid mechanism (2)
- increased lactate production: alterd redox state/pyruvate
- decreased lactate utilization
primary goal for lactic acidosis treatment
- restore perfusion which leads to decrease lactate production and enable hepatic metabolism of lactate to HC)3
diabetic ketoacidosis is both a
insulin deficiency and glucagon excess
consequences of Diabetic ketoacidosis
hyperglycemia and hyperosmolarity
- wee see a loss of hypotonic fluids and loss of ketoacid anions
treatment of diabetic ketoacidosis
- insulin therapy
- volume resucitation
- potassium replacement
- careful bicarb replacement
metabolic acidosis from diarrhea leads to
non-anion gap
diarrhea treatment
- bicarb replacement
- volume resuscitation
- correction of hypokalemia and other electrolyte disturbances
