Diseases of metabolism and of the blood : animal parasites, toxicology / ed. by Richard C. Cabot ... An authorized translation from "Die deutsche klinik" under the general editorial supervision of Julius L. Salinger, M. D. With one colored plate and fifty-eight illustrations in the text.

  • Richard Clarke Cabot
Date:
1906
Catalogue details

Licence: Public Domain Mark

Credit: Diseases of metabolism and of the blood : animal parasites, toxicology / ed. by Richard C. Cabot ... An authorized translation from "Die deutsche klinik" under the general editorial supervision of Julius L. Salinger, M. D. With one colored plate and fifty-eight illustrations in the text. Source: Wellcome Collection.

Provider: This material has been provided by the Augustus C. Long Health Sciences Library at Columbia University and Columbia University Libraries/Information Services, through the Medical Heritage Library. The original may be consulted at the the Augustus C. Long Health Sciences Library at Columbia University and Columbia University.

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    followed by similar periods of increased X-excretion. This phenomenon is particularly frequent and familiar when the subject is on a regime rich in albumin (more than 20 grams of X in the daily food). In contrast with these irregularities of the excretion of nitrogen in the urine which occasionally occur in the healthy, and more frequently in renal disease and in gout, we have the NT-retention which is observed in cachectic patients during the formation of transudates and edemas. Concerning tin'- quite a number of investigations have been made, par- ticularly in patients with hepatic cirrhosis. Several times during the reac- cumulation of an ascites (after paracentesis) the nitrogen balance has been estimated (Schubert,1 Marischler and Ozarkiewicz2). That the ^-retention which is noted in these cases does not indicate an actual albumin accumulation is clear. The retained nitrogen is not utilized as albumin to build up tissue but goes to form edema or ascites. Authors have therefore often spoken of a pathological N-retention, and explained it by the hypothesis thai while the organism normally possesses the faculty of destroying albumin and digest- ing it, this function is now lost. Must probably, however, purely mechanical disturbances of absorption here play a role in causing the retention of X. These disturbances depend upon changes in the amount of mineral salt> in the fluids of the body, the osmotic changes being dependent upon variations in the concentration of these salts which cooperate with the active properties of the endothelia to govern absorption. There is no considerable interest in the often-discussed question whether the albumin in these re-accumulating transudates (ascites) comes from the albumin of the food, or whether the body albumin is utilized. The question becomes meaningless if we discard Vbit's differentiation of two varieties of albumin in the body (organic albumin and circulating albumin). This deci- sion cannot he arrived at by analysis of the mineral metabolism in such cases, for the albumin of the food has been absorbed, taken up into the fluids of the body, and thence also into the cell protoplasm; thence together with the organic albumin it issues in the fluids <>)' pathological transudates. DISTURBANCES IN THE ABSORPTION OF FOOD In determining the food requirement of a patient, we must consider () changes in the amount of oxidation due to the disease, (b) consumption of albumin due to toxic influences, and (c) other factors, important among which are the losses of energy which the body suffers by giving off food sub- stances which it should retain. These losses are 30 manifold and so various that it is impossible to place them side by side as equivalents. Some of these losses are ao\ susceptible to quantitative estimation; on the other hand, in so far as they are due t,. 1 Schubert, üeber den V and CI Umsatz während der Bildung und Dach <1<t Punk tion des Ascites bei Lebercirrhose. Dissert., Breslau, 1895. - Marischler und Ozarkiewicz, Stoffwechsel ii abnehmenden] und Eunehmendera Ascites. Arch. /'. Veraauungskrankh., rol. v, p. 222,