ACIDOSIS 219 



the cause of increased acid content of the blood and such causes are not absent in 

 many of the dietary treatments of diseases of adults, whether in the height of the 

 disease or during convalescence. 



From the laboratory standpoint acidosis is usually recognized by an increase in the 

 urinary acetone bodies or by noting an increase in the ammonia quotient due to 

 demands upon the alkali for neutralization of the increased acid production. Ace- 

 tone, diacetic acid and /3-oxybutyric acid (acetone bodies) come from abnormal met- 

 abolism of fats. When not formed in excessive amounts the two acids are con- 

 verted into acetone and appear in the urine as such. With more marked production 

 acetone formation falls behind and diacetic acid appears or, with still more marked 

 acid production, /3-oxybutyric acid. 



These acids, of themselves, seem harmless and their injurious 

 action is connected with abstraction of alkali from the blood. 



There are some who think lactic acid may be formed from abnormal metabolism 

 of carbohydrates and that certain cases of acidosis failing to show increase of acetone 

 bodies may be connected with lactic acid increase. Of course, retention of acids of 

 normal metabolism would also cause acidosis. To prevent this the organism 

 utilizes a sufficient amount of the ammonia from protein or rather amino-acid 

 metabolism instead of further changing it into urea. So that an increased am- 

 monia quotient may signify that nature has control of the abnormal acid production. 



In the acidosis connected with chronic nephritis the preformed 

 ammonia may be lower than normal indicating some defect in the 

 mechanism of ammonia neutralization of acids. 



Acetone bodies can come from proteins as well as fats. Whatever may be the 

 explanation of abnormal formation of acetone bodies it seems to be associated with 

 inability of the organism to obtain sugar for its tissues, hence the therapeutic value 

 of giving glucose in acidosis conditions where the trouble is carbohydrate deficiency. 

 Glucose administration is frequently combined with alkali treatment in acidosis. 

 Of course, where the trouble is an inability on the part of the cells to utilize the sugar, 

 which may be circulating in greatly increased amounts in the blood, from lack of 

 pancreatic internal secretion (as in diabetes), sugar injection would have no effect on 

 this abnormal acid production. 



Even in ordinary metabolism great amounts of acid are produced 

 but these are eliminated normally by way of lungs as well as urine. 

 In this connection a failure on the part of the kidneys to remove 

 acid would result in acid retention and, if sufficiently marked, acidosis. 



Besides the phosphoric and sulphuric acid produced in the metabolism of the 

 phosphorus and sulphur of proteids we have enormous amounts of carbonic acid 

 formed in the tissues. 



The alkalinity of the blood is maintained by the bicarbonate of soda, 

 by sodium and potassium phosphates and to some extent proteins can 



