Symptoms These depend upon whether the anaemia is sudden in onset, as in severe haemorrhage, or gradual. In all cases, however, the striking sign is pallor, the depth of which depends upon the severity of the anaemia. The colour of the skin may be misleading, except in cases due to severe haemorrhage, as the skin of many Caucasian people is normally pale. The best guide is the colour of the internal lining of the eyelid. When the onset of the anaemia is sudden, the patient complains of weakness and giddiness, and loses consciousness if he or she tries to stand or sit up. The breathing is rapid and distressed, the pulse is rapid and the blood pressure is low. In chronic cases the tongue is often sore (GLOSSITIS), and the nails of the ?ngers may be brittle and concave instead of convex (koilonychia). In some cases, particularly in women, the Plummer-Vinson syndrome is present: this consists of di?culty in swallowing and may be accompanied by huskiness; in these cases glossitis is also present. There may be slight enlargement of the SPLEEN, and there is usually some diminution in gastric acidity.
CHANGES IN THE BLOOD The characteristic change is a diminution in both the haemoglobin and the red cell content of the blood. There is a relatively greater fall in the haemoglobin than in the red cell count. If the blood is examined under a microscope, the red cells are seen to be paler and smaller than normal. These small red cells are known as microcytes.
Treatment consists primarily of giving suf?cient iron by mouth to restore, and then maintain, a normal blood picture. The main iron preparation now used is ferrous sulphate, 200 mg, thrice daily after meals. When the blood picture has become normal, the dosage is gradually reduced. A preparation of iron is available which can be given intravenously, but this is only used in cases which do not respond to iron given by mouth, or in cases in which it is essential to obtain a quick response.
If, of course, there is haemorrhage, this must be arrested, and if the loss of blood has been severe it may be necessary to give a blood transfusion (see TRANSFUSION – Transfusion of blood). Care must be taken to ensure that the patient is having an adequate diet. If there is any underlying metabolic, oncological, toxic or infective condition, this, of course, must be adequately treated after appropriate investigations.
Megaloblastic hyperchromic anaemia There are various forms of anaemia of this type, such as those due to nutritional de?ciencies, but the most important is that known as pernicious anaemia.
PERNICIOUS ANAEMIA An autoimmune disease in which sensitised lymphocytes (see LYMPHOCYTE) destroy the PARIETAL cells of the stomach. These cells normally produce INTRINSIC FACTOR, the carrier protein for vitamin B12 (see APPENDIX 5: VITAMINS) that permits its absorption in the terminal part of the ILEUM. Lack of the factor prevents vitamin B12 absorption and this causes macrocytic (or megaloblastic) anaemia. The disorder can affect men and women, usually those over the age of 40; onset is insidious so it may be well advanced before medical advice is sought. The skin and MUCOSA become pale, the tongue is smooth and atrophic and is accompanied by CHEILOSIS. Peripheral NEUROPATHY is often present, resulting in PARAESTHESIA and numbness and sometimes ATAXIA. A rare complication is subacute combined degeneration of the SPINAL CORD.
In 1926 two Americans, G R Minot and W P Murphy, discovered that pernicious anaemia, a previously fatal condition, responded to treatment with liver which provides the absent intrinsic factor. Normal development requires a substance known as extrinsic factor, and this depends on the presence of intrinsic factor for its absorption from the gut. The disease is characterised in the blood by abnormally large red cells (macrocytes) which vary in shape and size, while the number of white cells (LEUCOCYTES) diminishes. A key diagnostic ?nd is the presence of cells in the BONE MARROW.
Treatment consists of injections of vitamin B12 in the form of hydroxocobalamin which must be continued for life.
Aplastic anaemia is a disease in which the red blood corpuscles are very greatly reduced, and in which no attempt appears to be made in the bone marrow towards their regeneration. It is more accurately called hypoplastic anaemia as the degree of impairment of bone-marrow function is rarely complete. The cause in many cases is not known, but in rather less than half the cases the condition is due to some toxic substance, such as benzol or certain drugs, or ionising radiations. The patient becomes very pale, with a tendency to haemorrhages under the skin and mucous membranes, and the temperature may at times be raised. The red blood corpuscles diminish steadily in numbers. Treatment consists primarily of regular blood transfusions. Although the disease is often fatal, the outlook has improved in recent years: around 25 per cent of patients recover when adequately treated, and others survive for several years. In severe cases promising results are being reported from the use of bone-marrow transplantation.
Haemolytic anaemia results from the excessive destruction, or HAEMOLYSIS, of the red blood cells. This may be the result of undue fragility of the red blood cells, when the condition is known as congenital haemolytic anaemia, or of acholuric JAUNDICE.
Sickle-cell anaemia A form of anaemia characteristically found in people of African descent, so-called because of the sickle shape of the red blood cells. It is caused by the presence of the abnormal HAEMOGLOBIN, haemoglobin S, due to AMINO ACID substitutions in their polypeptide chains, re?ecting a genetic mutation. Deoxygenation of haemoglobin S leads to sickling, which increases the blood viscosity and tends to obstruct ?ow, thereby increasing the sickling of other cells. THROMBOSIS and areas of tissue INFARCTION may follow, causing severe pain, swelling and tenderness. The resulting sickle cells are more fragile than normal red blood cells, and have a shorter life span, hence the anaemia. Advice is obtainable from the Sickle Cell Society.
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