Xll 



INTRODUCTION 



ment from reaching the cells; or from intrinsic causes, affecting protoplasmic 

 metabolism. The intrinsic causes may interfere with the proper assimilation 

 (anabolism) of the food, even though it may reach the cells in adequate quantity 

 and quality; or they may occasion an abnormally rapid consumption (katabo- 

 lism) of the food, thereby creating a condition of relative inanition. 



Thus among the extrinsic causes of inanition in the higher organisms, in 

 addition to (a) lack of adequate food, there may exist (b) faulty ingestion or 

 mastication of the food, due to oral defects, stenosis of the alimentary canal, etc.; 

 (c) faulty digestion, due to glandular deficiency; (d) faulty absorption through the 

 alimentary mucosa; or (e) faulty transportation, through defects in the blood or 

 vascular system. 



Similarly, various intrinsic conditions may prevent the normal metabolism 

 of the food, even though it is brought to the cells in normal quantity and quality. 

 Thus the faulty cell metabolism may arise from (a) hereditary, inherent defects 

 in cell structure or composition; (b) toxic influences which prevent normal metab- 

 olism; or (c) lack or excess of the hormones normally concerned with cell 

 metabolism. For example, a condition of inanition may arise either from lack 

 of the pancreatic hormone (insulin) in diabetes mellitus, or from excess of the 

 thyroid hormone (thyroxin) in hyperthyroidism (cf. Lubarsch '03; Watson '99; 

 Barker '16). 



The various types of inanition are summarized in the following table: 



I 1. Complete (no food whatever) 

 2. Incomplete (insufficient nutriment; general under- 



A. Total 



(quantitative) 



Inanition \ 



B. Partial (qualitative) 



