thickened, the channel is narrowed, and on section the vessels remain patent, while they assume a compact, translucent, shining appearance, so that they come to resemble silvery cords or threads. After a time the material extends to the cells and intercellular tissues, enlarging the former and making them more spherical, at the same time displacing- their normal contents, the nucleus being ultimately destroyed. The cells then coalesce; and the whole structure presents finally the peculiar glistening appear, ance mentioned above. It is supposed by some that the substance makes its way directly through the walls of the vessels, and afterwards extends into the tissues around.
2. Organs and tissues involved.—Albuminoid disease is particularly liable to affect small arteries and capillaries, cells, and involuntary muscular fibres. Any organ or tissue in the body may be implicated, and usually several organs are involved at the same time. The liver, spleen, kidneys, and absorbent glands are most frequently affected, but other structures are also attacked sometimes, namely, the stomach and intestines, supra-renal capsules, bones, voluntary muscles, brain and spinal cord and their membranes, tonsils, serous membranes, heart, lungs, pancreas, uterus, and bladder; morbid deposits, such as inflammatory exudations, tubercle, or cancer, may also present the albuminoid change. In some cases, when it follows disease of bones, it begins in the neighbouring lymphatic glands. In many of the organs above-mentioned the disease seems to be limited to the minute vessels.
Pathology.—Various theories have been held as to the nature and origin of the morbid material characteristic of albuminoid degeneration. Virchow, on account of its chemical reactions, formerly considered the substance to be allied to starch or cellulose—hence the term amyloid; others believed it to be a form of cholesterin. These views have, however, been entirely disproved, and that commonly adopted at present is, that the material is of an albuminoid nature, being allied to albumen and other protein elements. The results of chemical analysis show that at any rate it is a nitrogenous compound. Dr. Dickinson affirms that organs in which it exists are deficient in alkaline salts, and this observer has advanced the view that the substance consists of de-alkalized fibrin. Marcet found that the affected structures were deficient in potash and phosphoric acid, but contained excess of soda and chlorine. With regard to the origin of the albuminoid material, two distinct theories are held, viz., that it is the product of some local degeneration or metamorphosis of albuminous tissues; or that there is a direct deposit from the blood, in consequence of some alteration in this fluid, which deposit infiltrates the tissues. Nothing of the nature of this albuminoid substance has, however, been detected in the blood, and therefore the presumption is that it is modified after it escapes from the vessels. Dickinson thinks that the blood is deprived of its alkali, as the result of prolonged suppuration, and that the material is then deposited. Dr. Grainger Stewart strongly advocates the degeneration theory, and calls
