This section is from the book "A Manual Of Pathology", by Joseph Coats, Lewis K. Sutherland. Also available from Amazon: A Manual Of Pathology.
From what has gone before it will be apparent that in the different forms of anaemia the state of the blood will vary considerably, and it will be proper to refer to each individually. The condition of the red corpuscles is the most important point. Their numbers may be estimated by one of the forms of Haemocytometer founded on the method of Malassez, and the amount of their haemoglobin may be determined by the Haemoglobino-meter, in which the depth of colour is compared with a standard solution.
In anaemias due to haemorrhage, in-which a direct destruction of the red corpuscles has occurred, the number of the corpuscles is reduced, and the plasma is watery.
Immediately after a severe haemorrhage we have an actual Oligemia, but this simple reduction in the bulk of the blood does not long remain, as various processes ensue which modify the condition of the blood. In the first place the bulk of the blood is rapidly made up by absorption from the tissues and alimentary canal, and by diminution of the excretion of water by the kidneys. The result is that, while the bulk of the blood is made up, the plasma is watery and the red corpuscles deficient, a condition of Oligocythsemia and Hydremia. In the blood, soon after a haemorrhage, there is a certain proportional excess of white corpuscles, a Leuco cytosis. This arises partly from the fact that the leucocytes, being more adhesive than the red corpuscles, do not escape so readily as these, and also because the leucocytes are more rapidly renewed than the red corpuscles.
If there has been a single haemorrhage the blood is gradually, although slowly, restored. The plasma comparatively soon recovers its due concentration, but the red corpuscles are very slowly replenished, and it may be weeks or months before their number is made up. The condition of the blood itself will interfere with the activity of the blood-forming organs amongst the others. Where there are repeated, although small, haemorrhages, a more or less permanent hydraemia and oligocythaemia result.
In malarial fevers and in conditions characterized by haemoglobin-uria, the conditions are similar to those resulting from haemorrhage; there is a defect in the number of the red corpuscles.
Pernicious anaemia, or essential anaemia, is a condition in which, without apparent cause, the blood becomes progressively deteriorated. In some cases which were supposed during life to present the features of this disease, post-mortem examination has revealed organic disease of the intestinal canal, such as a deep-seated cancerous tumour, or (according to Nothnagel and Fenwick) an induration of the stomach with atrophy of the gastric glands, but these cases ought to be removed from the present category, and to be assigned to the group of secondary anaemias of which they form severe examples.
The observations of Quincke, Peters, Russell, and others, which have been confirmed and elaborated by Hunter, show that in pernicious anaemia there is a great excess of pigment, containing iron (hemosiderin) in the liver. The iron is demonstrable by micro-chemical tests, sulphide of ammonium giving a dark colour, and ferrocyanide of potassium with dilute hydrochloric acid, the usual Prussian blue. The pigment is present chiefly in the outer two thirds of the hepatic lobules, and is contained in the hepatic cells (Fig. 19). The cells in the central parts of the lobules usually show fatty degeneration. A similar pigment is sometimes present in the kidney, where it is mostly in the epithelium of the convoluted tubules. The bone-marrow also contains an excess of pigment in which iron is present. On the other hand, the spleen does not contain an excess of iron, although usually enlarged.
From these observations it may be inferred that in pernicious ansamia there is a great destruction of red corpuscles in the blood, the haemoglobin not passing unchanged into the urine as in haemoglobinuria, but being caught and stored, in an altered form, in the liver. Toluylendiamin, when injected into the blood of animals, induces a similar destruction of red corpuscles in the portal circulation and a similar accumulation of iron in the liver. In these experiments also there was no hsemoglobinuria. On the analogy of this poison, it is inferred by Hunter that pernicious anaemia is due to a poison absorbed from the intestine. It is not, however, necessary to infer that the destruction of the red corpuscles occurs in the portal vessels, as granular pigment in the general circulation is known to be deposited by preference in the liver.
In this disease there is a marked deficiency in number in the red corpuscles; they have been found to number as few as 500,000 instead of 5,000,000 in the cubic millimetre. Although deficient in number, they are not usually defective in haemoglobin. Besides this the red corpuscles present marked varieties in size and shape. In most cases there are to be detected in the blood during life, small, globular, deeply-coloured red corpuscles, which are evidently altered red corpuscles. These have been named Microcytes. There have also been observed red corpuscles of various forms (Poikilocytes). Nucleated red corpuscles are also occasionally present. These are young red corpuscles or erythrocytes and represent probably an attempt to replenish the blood for those which have been destroyed.

Fig. 19. - Liver in pernicious anaemia. The dark granules are blue in the specimen. They are in the cells in the peripheral parts of the lobules.
The condition of the spleen varies considerably; sometimes it is enlarged, it may be greatly so, sometimes it is scarcely at all altered. There may be also in it variously altered red corpuscles, as in the bone-marrow. In some cases the lymphatic glands are enlarged.
Chlorosis is a form of anaemia which occurs in females, usually about the time of puberty. The condition here is rather that of deficiency of haemoglobin than of corpuscles, as the latter, although usually deficient in number, may not be so. The achromatosis may be such as to indicate that the haemoglobin is reduced to a half or a fourth of the normal. The rapid recovery of cases of chlorosis under treatment with iron is consistent with the fact that it is not so much replenishment of red corpuscles as of haemoglobin that is needed.
The occurrence of chlorosis at puberty has suggested as its cause some defect in the sexual organs, and there are cases in which the uterus or ovaries have been imperfect (Rokitansky). But in the majority of cases this is not so, and it is more probable that the changes at puberty develop the condition by throwing an extra strain on the blood-forming organs. Virchow has observed in cases of chlorosis certain congenital defects in the vascular apparatus, the chief of which are narrowness and thinness of the aorta, irregularity in the origin of the branches from the aorta, and smallness of the heart. The narrowness of the aorta may lead to compensatory hypertrophy of the heart in the same way as a narrowness of the aortic orifice. These lesions do not explain the chlorosis, but they suggest the existence of a congenital defect in the vascular system which may extend to the blood-forming organs, and may cause them to give way to the strain of puberty.
Secondary anaemias are generally due to grave exhausting diseases, such as phthisis pulmonalis, ulcerating cancers, Hodgkin's disease (which is also called anaemia lymphatica), leukaemia, fevers, albuminuria, etc. The condition of the blood in secondary anaemia is usually that of hydraemia or hypalbuminosis with oligocythaemia; the blood is watery and deficient in red corpuscles, but the remaining corpuscles are generally of normal colour.
 
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