On the pathology of arterio-sclerosis / by F. Parkes Weber.

  • Weber, Frederick Parkes, 1863-1962.
Date:
1894
Catalogue details

Licence: Public Domain Mark

Credit: On the pathology of arterio-sclerosis / by F. Parkes Weber. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    syphilis, arthritism, and the uric acid diathesis (if the latter be not in- cluded under arthritism) ; probably only through the diathesis is there any relation with actual uricsemia; furthermore, it must be allowed that an hereditary tendency to arterio-sclerosis, allied to inherited arthritism, may exist. How uncertain are the alleged causes of arterio-sclerosis may be gathered from the fact that of two well-known French writers, Hu- chard1 includes alcohol, tobacco, saturnism, inheritance, acute and chronic diseases, such as typhoid, smallpox, syphilis, malaria, etc.; whereas Lancereau maintains that arterio-sclerosis always owes its origin to nervous causes. It will be here impossible to do more than allude briefly to the most important of the alleged causes, but in examining them one is struck by the uncertain nature of their claims. Sir George Johnson2 considered that the kidney disease is primary, that in conse- quence of this the blood contains uriuary excreta, and is otherwise altered, that the minute arteries throughout the body resist the passage of this abnormal blood, and in consequence of this the muscular walls of the arteries and lefc ventricle become hypertrophied, as seen at autopsies. Johnson's theory was combated by Gull and Sutton; they pointed out that the vascular changes could precede the kidney disease, or, as Bamberger has stated, appear in its earlier stages ; moreover, they stated that extreme degeneration of the kidneys (either large white or contracted3) may be accompanied by oedema and ursemic-symptoms, which indicate doubtless a noxious state of the blood, and yet the char- acteristic cardio-vascular changes may be absent. Neither does it appear proved that the high-pressure pulse of arterio-sclerosis is due usually to an abnormal contraction of the arterioles, though doubtless this may occasionally occur. If it were so, one would expect to find the muscular coat of the arterioles hypertrophied, as Sir George Johnson described them to be; but, according to most observers, when this thickening exists it is due to increase of fibrous tissue. Certainly in some cases of chronic Bright's disease the arterial tension can be lowered by nitrite of amy],4 but this does not affect the point, because arterio-sclerosis, although a generalized disease, by no means affects all parts of the body equally. The mechanical arterio-capillary fibrosis may be the cause of increased arterial pressure, and yet the arterioles over lai'ge I Maladies du Coeur, 2d ed., Paris, 1893, pp. 119 et seq. = See Brit. Med. Journal, April 16.1870. 3 Med.-Ctair. Trans., vol. lv. p. 294. So also it has been stated that chronic interstitial nephritis can be caused through obstruction to the ureters by uterine cancer, without any hypertrophy of the heart resulting. On the other hand, it is stated that high arterial pressure and hypertrophy of the heart may follow hydro-nephrosis, say from impacted calculus, in a few weeks. (See Brit. Med. Journal, November 4,1893, p. 998.) Gull and Sutton referred to cases of contracted kidneys in young subjects, not over twenty years of age, and believed that such cases were of cpuite a different nature to ordinary cases of contracted kidney. 4 Vide Fagge, op. cit., 3d ed., vol. il. p. 467.