416 DISEASES OF THE GREAT VESSELS. 



and are sometimes washed loose by the blood, and then form projec- 

 tions, upon which the fibrin of the blood is very apt to precipitate itself. 



At the outset of endarteriitis, the tunica media does not become 

 perceptibly altered. In advanced atheroma it grows yellow, relaxed, 

 and fissured. Large deposits of fat form between its lamellae. The 

 media is generally atrophied, and thinned by ossification of the intima. 

 In the beginning of the process the adventitia is also normal, but after- 

 ward becomes swollen, thickened, and indurated. 



In many cases we find all the various phases of the disease along- 

 side of one another in the aorta : in one place gelatinous or semi-carti- 

 laginous induration; in another, atheromatous pustules; here again 

 ulceration ; there calcification, in a slight depression, covered by the 

 tunica intima ; and at some other point we find 'plates of bone pro- 

 jecting free into the aorta. 



SYMPTOMS AND COURSE. No clinical description of acute inflam- 

 mation and ulceration of the adventitia can be given, as, in the few in- 

 stances in which the process has been watched, the disease has always 

 been complicated by other grave disorders. This is also the case in 

 chronic inflammation of the adventitia, and in the instances of abscesses 

 observed now and then in the tunica media. 



Chronic inflammation of the tunica intima and its results, generally 

 comprehended under the term atheroma, in its wider sense, furnish but 

 few symptoms as long as they do not cause aneurism, rupture, or stop- 

 page of one of the smaller arteries by detachment of a clot. We 

 shall consider the subjects of aneurism and rupture in the second and 

 third chapters. The results of embolism, as far as they affect internal 

 uigans, are treated of in various chapters of this work. 



If, in consequence of degeneration of its coats, the aorta have lost 

 its elasticity, and if, too, its branches take part in the disease, the de- 

 mands upon the heart are increased, and hypertrophy arises (see hyper- 

 trophy of heart). If the chronic inflammation spread from the arterial 

 wall to the valves, insufficience and stenosis may be the result. Hyper- 

 trophy often fails to take place, owing to depression of the general 

 nutritive condition, or it is not sufficiently pronounced to compensate 

 for the impediment which degeneration of the aorta and its ramifica- 

 tions presents to the circulation, or else the hypertrophy is soon con- 

 verted from a genuine to a false hypertrophy, from degeneration of the 

 substance of the heart. Symptoms of retarded circulation and over- 

 loading of the venous system then arise, cyanosis, dropsy, and sup 

 pression of urine, as described in a previous chapter. 



The most important token in the diagnosis of chronic inflammation 

 of the inner coat of the aorta is the evidence of the existence of 

 similar disease in the peripheral arteries, as the inference is thus war- 



