Page 311 - Textbook of Pathology, 6th Edition

ACUTE BLOOD LOSS. When the loss of blood occurs ABSORPTION. The average Western diet contains 10-15 mg 295
suddenly, the following events take place: of iron, out of which only 5-10% is normally absorbed. In
i) Immediate threat to life due to hypovolaemia which may pregnancy and in iron deficiency, the proportion of
result in shock and death. absorption is raised to 20-30%. Iron is absorbed mainly in
ii) If the patient survives, shifting of interstitial fluid to the duodenum and proximal jejunum. Iron from diet containing
intravascular compartment with consequent haemodilution haem is better absorbed than non-haem iron. Absorption of non-
with low haematocrit. haem iron is enhanced by factors such as ascorbic acid
iii) Hypoxia stimulates production of erythropoietin resul- (vitamin C), citric acid, amino acids, sugars, gastric secretions
and hydrochloric acid. Iron absorption is impaired by factors
ting in increased marrow erythropoiesis.
like medicinal antacids, milk, pancreatic secretions, phytates,
LABORATORY FINDINGS phosphates, ethylene diamine tetra-acetic acid (EDTA) and
i) Normocytic and normochromic anaemia tannates contained in tea.
Non-haem iron is released as ferrous or ferric form but
ii) Low haematocrit is absorbed almost exclusively as ferrous form; reduction of
iii) Increased reticulocyte count in peripheral blood ferric to ferrous form when required takes place at the
(10-15% after one week) reflecting accelerated marrow intestinal brush border by ferric reductase. Transport across
erythropoiesis. the membrane is accomplished by divalent metal trans- CHAPTER 12
porter 1 (DMT 1). Once inside the gut cells, ferric iron may
CHRONIC BLOOD LOSS. When the loss of blood is slow be either stored as ferritin or further transported to transferrin
and insidious, the effects of anaemia will become apparent by two vehicle proteins—ferroportin and hephaestin. The
only when the rate of loss is more than rate of production mechanism of dietary haem iron absorption is not clearly
and the iron stores are depleted. This results in iron deficiency understood yet but it is through a different transport than
anaemia as seen in other clinical conditions discussed below. DMT 1. After absorption of both non-haem and haem forms
of iron, it comes into mucosal pool.
HYPOCHROMIC ANAEMIA Major mechanism of maintaining iron balance in the body
Hypochromic anaemia due to iron deficiency is the is by intestinal absorption of dietary iron. When the demand
commonest cause of anaemia the world over. It is estimated for iron is increased (e.g. during pregnancy, menstruation,
that about 20% of women in child-bearing age group are iron periods of growth and various diseases), there is increased
deficient, while the overall prevalence in adult males is about iron absorption, while excessive body stores of iron cause
2%. It is the most important, though not the sole, cause of reduced intestinal iron absorption (Fig. 12.12,A page 297).
microcytic hypochromic anaemia in which all the three red TRANSPORT. Iron is transported in plasma bound to a
cell indices (MCV, MCH and MCHC) are reduced and occurs β-globulin, transferrin, synthesised in the liver. Transferrin-
due to defective haemoglobin synthesis. Hypochromic bound iron is made available to the marrow where the
anaemias, therefore, are classified into 2 groups: developing erythroid cells having transferring receptors utilise
I. Hypochromic anaemia due to iron deficiency. iron for haemoglobin synthesis. It may be mentioned here
II. Hypochromic anaemias other than iron deficiency. that tranferrin receptors are present on cells of many tissues
The latter category includes 3 groups of disorders— of the body but their number is greatest in the developing
sideroblastic anaemia, thalassaemia and anaemia of chronic erythroblasts. Transferrin is reutilised after iron is released Introduction to Haematopoietic System and Disorders of Erythroid Series
disorders. from it. A small amount of transferrin iron is delivered to
other sites such as parenchymal cells of the liver. Normally,
IRON DEFICIENCY ANAEMIA transferrin is about one-third saturated. But in conditions
where transferrin-iron saturation is increased, parenchymal
The commonest nutritional deficiency disorder present iron uptake is increased. Virtually, no iron is deposited in
throughout the world is iron deficiency but its prevalence is the mononuclear-phagocyte cells (RE cells) from the plasma
higher in the developing countries. The factors responsible transferrin-iron but instead these cells derive most of their
for iron deficiency in different populations are variable and iron from phagocytosis of senescent red cells. Storage form
are best understood in the context of normal iron metabolism. of iron (ferritin and haemosiderin) in RE cells is normally
not functional but can be readily mobilised in response to
Iron Metabolism increased demands for erythropoiesis. However, conditions
such as malignancy, infection and inflammation interfere
The amount of iron obtained from the diet should replace with the release of iron from iron stores causing ineffective
the losses from the skin, bowel and genitourinary tract. These erythropoiesis.
losses together are about 1 mg daily in an adult male or in a
non-menstruating female, while in a menstruating woman EXCRETION. The body is unable to regulate its iron content
there is an additional iron loss of 0.5-1 mg daily. The iron by excretion alone. The amount of iron lost per day is
required for haemoglobin synthesis is derived from 2 primary 0.5-1 mg which is independent of iron intake. This loss is
sources—ingestion of foods containing iron (e.g. leafy nearly twice more (i.e. 1-2 mg/day) in menstruating women.
vegetables, beans, meats, liver etc) and recycling of iron from Iron is lost from the body in both sexes as a result of
senescent red cells (Fig. 12.11). desquamation of epithelial cells from the gastrointestinal