THE PATHOLOGICAL ANATOMY 285 



generate. The available evidence at present suggests that they are true work 

 exhaustions, as can be readily demonstrated in cretinism of the lower ani- 

 mals where it is possible with very young cretin pups or lambs to cause 

 the highly atypical columnar thyroid* cells to return to a cuboidal form 

 with the accumulation of colloid by the administration of small amounts 

 of iodin or desiccated thyroid and later, by partial removal of such recov- 

 ered glands, to obtain a perfectly regular and uniform active hyperplasia. 

 Exhaustion atrophy is most commonly seen in children in endemic goiter 

 districts and in adults in the end stage of exophthalmic goiter. The essen- 

 tial anatomical changes in the thyroid are similar in both cretinism and 

 myxedema. In the typical case, the thyroid clinically is enlarged, or 

 there is a clear history of its having been enlarged. The gland is usually 

 very vascular. The colloid is practically absent; the epithelial cells have 

 lost their regular and uniform type characteristic of the early stage of 

 active hyperplasia. There is often piling up of the epithelial cells and 

 desquamation of the partially degenerated cells. The nuclei are usually 

 large, irregular in size, staining intensity and outline. Mitotic figures may 

 still be observed. The alveolar spaces^become smaller though still preserv- 

 ing the infoldings present in the well developed hyperplasia. The surround- 

 ing stroma is relatively, perhaps absolutely, increased and in animals 

 often edematous and myxomatous. As the alveoli become smaller from 

 the death of their secreting cells, the interlobular stroma increases and 

 finally gives the appearance of a generalized sclerosis in which the alveolar 

 elements appear as nests of compressed cells. In man, lymphoid foci are 

 scattered throughout the stroma much as it is in the actively hyperplastic 

 state of exophthalmic goiter. Most of the examples of this form of atrophy 

 in man do not appear as simple as the above description might indicate, be- 

 cause they are nearly always complicated by other changes such as ade- 

 nomata, cyst formation, hemorrhage, calcification, all of which may be 

 present in the same gland. Summing up then, the type of atrophy super- 

 vening in active hyperplasias and clinically associated with myxedema or 

 cretinism is a cell death due to exhaustion. The process is simple but the 

 interpretation of the anatomical changes in such glands, especially in long 

 standing cases, may be difficult. This type of atrophy is the usual end stage 

 of all active hyperplasias unless terminated by death or recovery of the in- 

 dividual, and considering the total number of active hyperplasias from 

 all causes and in all animals, it is a rare sequel. Pasteur, Roussy and 

 Clunet (a), Schultze, Sollier, West (&). 



Degeneration 



In thyroid histo-pathology, the term "degeneration" has often been 

 misused. The commonly accepted types of degeneration as hyaline, 

 calcareous, amyloid, parenchymatous, fatty, etc., are observed to an exag- 



