Do you know the three causes of metabolic acidosis?

Studies have found that there are three main causes of metabolic acidosis: lactic acidosis, ketoacidosis, and renal failure. In the face of these symptoms, acid reduction is imperative, otherwise the symptoms will become more and more serious and may even cause complications.

(1) Lactic acidosis : Lactic acidosis can be seen in hypoxia caused by various reasons. Its pathogenesis is that the glycolysis process is enhanced during hypoxia, and the production of lactic acid increases. Due to insufficient oxidation, lactic acid accumulates, leading to an increase in blood lactate levels. This type of acidosis is common.

(2) Ketoacidosis : Ketoacidosis occurs when a large amount of body fat is mobilized, such as in patients with diabetes, hunger, prolonged vomiting due to pregnancy reaction, or vomiting due to alcohol poisoning and little food intake for several days. The oxidation of fatty acids in the liver is enhanced, the production of ketone bodies increases and exceeds the amount of ketone body utilization outside the liver, resulting in ketonemia. Ketone bodies include acetone, β-hydroxybutyrate, and acetoacetate, the latter two of which are organic acids that cause metabolic acidosis. This acidosis is also a normal blood chloride metabolic acidosis with increased AG.

(3) Renal failure : If renal failure is mainly caused by tubular dysfunction, the metabolic acidosis at this time is mainly caused by the reduced production of NH3 and H+ excretion by tubular epithelial cells. Glutamine and amino acids in normal renal tubular epithelial cells are supplied by the blood, and NH3 is continuously generated under the catalysis of glutaminase and amino acid dehydrogenase. NH3 diffuses into the tubular lumen and combines with H+ secreted by the tubular epithelial cells to form NH4+, which increases the pH value of urine. This enables H+ to be continuously secreted into the tubular lumen, completing the acid excretion process. The Na+ in the original urine is continuously exchanged for NH4+, and re-enters the blood together with HCO3- to become NaHCO3. This is the main function of the renal tubules to excrete acid and retain alkali. Acidosis can occur when the renal tubules become diseased and this function is severely impaired. This type of acidosis does not cause significant changes in the glomerular filtration function, and no acid anions are retained in the body due to filtration disorders. It is characterized by normal AG-type hyperchloremic metabolic acidosis. That is to say, anions such as HPO4= and SO4= are not retained, so AG does not increase, and HCO3- is not reabsorbed enough, so it is replaced by another easily regulated anion Cl-, resulting in an increase in blood chloride.