Changes In The Tissues

Amyloid degeneration, being due to a condition of the blood, is nearly always present in a number of organs simultaneously, although its degree varies greatly in different organs. It is particularly frequent in the spleen, liver, kidneys, intestine, and lymphatic glands, but may occur in almost every organ and tissue of the body.

In all these organs it begins in the walls of the blood-vessels, more especially the walls of the capillaries and smaller arteries, or in the connective tissue. In advanced cases the amyloid substance is in such quantity, and the proper tissue of the organs is in many cases so much atrophied, that it is often difficult to determine its precise seat. In early cases, however, it will be found that the arteries and capillaries are nearly always the primary seat. It is readily seen in the liver, for instance, that the capillaries are affected, the hepatic cells undergoing atrophy. Even in advanced cases the arrangement is often suggestive of radiating capillary tubes, as in Fig. 50. In the kidneys, again, it is always the* vessels which are first affected, although extension may occur to the basement membrane of the tubules. In the spleen the arteries are mostly affected, and in addition to these either the walls of the sinuses in the pulp or the reticulum of the Malpighian bodies. (See under Spleen).

The distribution of amyloid disease varies greatly in different cases, both in regard to the organs chiefly affected and the parts of the organs. Thus in phthisis pulmonalis it may be chiefly present in liver, spleen, or kidney, and it may be absent in one of these organs while present in the others. Of the two forms of amyloid disease of the spleen, one (the sago spleen) is characteristic of phthisis pulmonalis, while the other is probably the form mostly met with in syphilis.

Considerable discussion has occurred as to the existence of amyloid disease in epithelial structures. It is now generally admitted that these are rarely if ever involved, and if they are it is in advanced cases. In the liver it is admitted that the arteries and capillaries are chiefly affected, but Kyber and others have asserted that the hepatic cells are involved. The author has not been able to detect any amyloid change in the hepatic cells.

The amyloid substance is a very inert matter. It is insoluble in water and alcohol and even in gastric juice. During life it renders the structures involved passive, so that they are incapable of vital changes. This material is insoluble in the juices of the body, but consistently with its character as inert matter it gives ready passage to fluids, so that during life the prominent symptom of amyloid disease in the intestine is diarrhoea, and in the kidneys an excessive discharge of watery urine.

A frequent result of amyloid disease is diminution in the calibre of the blood-vessels, and this must lead to anaemia of the organs. To this may be partly ascribed the fatty degeneration and atrophy which so frequently accompany the process, although these are also due to the pressure of the swollen structures.

Structures which have undergone amyloid degeneration are greatly increased in bulk and weight, and this tells on the organ as a whole. The liver, spleen, and kidneys are often greatly enlarged, and they present a peculiar dense translucent appearance, which has given rise to the names waxy and lardaceous disease, often applied to amyloid degeneration.

Localized Amyloid Disease

This does not occur in tissues previously unaltered; there is alwayssomeprecedinglocallesion. It is met with chiefly in new-formed inflammatory tissue and cicatrices, especially when of syphilitic origin, and also in tumours. It has been seen in syphilitic cicatrices in the liver, tongue, and larynx, in degenerating cartilage, etc. In some cases the piece of amyloid tissue is of considerable size, and as it differs in its hard translucent character from the tissues around, it may itself look like a tumour.

Fig. 51. - Corpora amylacea: a, from the prostate; b, from a haemorrhagic infarction of the lung; c, from the spinal cord. X400. (Ziegler).

Amyloid Concretions. Corpora Amylacea

In old extravasations of blood in the lungs we sometimes meet with round or oval stratified bodies of small size (see Fig. 51 b), which somewhat resemble starch granules, and give with iodine the amyloid reaction. Sometimes they contain in their central parts a foreign body, such as a blood crystal. Again in the prostate gland (a) we meet with concretions of considerable size, it may be visible, as brown granules, to the naked eye, with all the characters of stratified amyloid concretions. They are also met with in the tissues of the central nervous system (c); they are present in the normal brain, especially in the ependyma of the ventricles, but in cases of sclerosis they may be present in enormous numbers.

The reaction of these bodies is not quite the same as that of ordinary amyloid matter. They give with iodine more of a blue tint, and that without adding sulphuric acid. They sometimes fail to give a red colour with methylviolet. Their significance is not usually very great from a practical point of view, but their presence under these various conditions seems to prove that various albuminous substances may undergo conversion into the so-called amyloid substance.

In the nervous system there are frequently developed artificially clear glancing bodies which somewhat resemble amyloid bodies. They occur as a result of the action of alcohol in hardening the tissue, and this agent should therefore, as a general rule, be avoided in preparing the brain and spinal cord for histological investigation. The bodies give with iodine a pale yellow, and with methylviolet a reddish colour. They are devoid of pathological significance, although some writers have referred to them as true morbid lesions. (See a review of the subject by Middleton, who regards them as formed by the action of alcohol on the myeline of the medullated nerve-fibres).

Literature

Vikchow, Virch. Arch., vi.; Wilks, Guy's Hosp. Rep., 1856; Kekule, Heidelberg Jahrb., 1858; Kuhne und Rudneff, Virch. Arch., vol. xxxiii.; Cobnil, Arch. d. phys., 1875; Kybek, Virch. Arch., vol. lxxxi.; Budd, Lancet, 1880; Report, on lardaceous disease, Path. Soc. trans., vol. xxii.; Fagge, Path. Soc. trans., vol. xxvii.; Dickinson, Discussion on lardaceous disease, Path. Soc. trans., vol. xxx.: see also Greenfield, Goodhart, and others in this discussion; Coats (Amyloid dis. in Phthisis), in Gairdner and Coats' Lect. to practitioners, 1888; Zahn (Local amyloid dis.), Virch. Arch., vols, lxxii. and lxxiii.; Middleton, Glas. Med. Jour., xxii., 1884; Wichmann (Bibliography), Ziegler's Beitriige, xiii., 1893.