On the pathology of pernicious anaemia / by Walter K. Hunter, M.D., B.Sc.

  • Hunter, Walter King.
Date:
[1897?]
Catalogue details

Licence: Public Domain Mark

Credit: On the pathology of pernicious anaemia / by Walter K. Hunter, M.D., B.Sc. Source: Wellcome Collection.

Provider: This material has been provided by The University of Glasgow Library. The original may be consulted at The University of Glasgow Library.

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    corpuscles is not a very convincing explanation of the small spleen so often found in this disease. Is it not more probable that while the poison of pernicious anaemia stimulates the white blood corpuscles to increase, it itself destroys the red corpuscles ? It must surely at least affect their vitality, for otherwise no moderate leucocytosis would destroy them. In some of our cases enlarged lymphatic glands were found, but this has little bearing on the pathology of pernicious anaemia. I have been endeavouring, then, in the foregoing pages, to point out that there is a certain relationship between all pro- found anaemias. They would seem to differ less in their physical signs than in their etiology, and it is the etiology which largely determines their pathological anatomy. Most of them are due in some measure to an excessive destruction of red blood corpuscles, and this in turn depends for its production and maintenance on a poison in some part of the circulation. The origin and nature of this poison have not yet been clearly defined, but we have seen that it differs in several respects in the different groups of cases. One of these groups is associated with, and probably the result of, certain wasting diseases, and its poison, which is in the general circulation, is slow and constant in its action. None of the iron liberated from the red blood corpuscles destroyed is deposited in the liver cells. In another group the poison seems to be absorbed from the alimentary tract and to be confined in its action to the portal circulation. In destroying the red corpuscles it liberates an iron pigment which is taken up by the hepatic cells, any small amount reaching the general circulation being deposited in the renal epithelium. There is yet a third group, in which, in physical aspect, the cases resemble very closely those last mentioned. They differ, however, in seeming to depend for their production on single or repeated haemorrhages and also in having little iron in the liver cells. The anaemia in some of these is doubtless due to the amount of blood lost; but in others, where a rapidly progressive anaemia follows one single haemorrhage, this explanation seems inadequate. It may be that certain cases have the capacity of recovery from an haemorrhage, while in others the efforts of the organism