Which of the following is true of body iron stores?

Correct Answer: Absorption is increased in iron deficiency and reduced in iron overload
Description: IRON DEFICIENCY ANAEMIA Iron Metabolism The amount of iron obtained from the diet should replace the losses from the skin, bowel and genitourinary tract. These losses together are about 1 mg daily in an adult male or in a non-menstruating female, while in a menstruating woman there is an additional iron loss of 0.5-1 mg daily. ABSORPTION. Iron is absorbed mainly in the duodenum and proximal jejunum. Iron from a diet containing haem is better absorbed than non-haem iron. Absorption of non-haem iron is enhanced by factors such as ascorbic acid (vitamin C), citric acid, amino acids, sugars, gastric secretions and hydrochloric acid. Iron absorption is impaired by factors like medicinal antacids, milk, pancreatic secretions, phytates, phosphates, ethylene diamine tetra-acetic acid (EDTA) and tannates contained in tea. Transpo across the membrane is accomplished by divalent metal transpoer 1 (DMT 1). Once inside the gut cells, ferric iron may be either stored as ferritin or fuher transpoed to transferrin by two vehicle proteins--ferropoin and hephaestin. The major mechanism of maintaining iron balance in the body is by intestinal absorption of dietary iron. When the demand for iron is increased (e.g. during pregnancy, menstruation, periods of growth and various diseases), there is increased iron absorption, while excessive body stores of iron cause reduced intestinal iron absorption. TRANSPO. Iron is transpoed in plasma bound to a b-globulin, transferrin, synthesised in the liver. Transferrin-bound iron is made available to the marrow where the developing erythroid cells having transferring receptors utilise iron for haemoglobin synthesis. Transferrin is reutilised after iron is released from it. But in conditions where transferrin-iron saturation is increased, parenchymal iron uptake is increased. The storage form of iron (ferritin and haemosiderin) in RE cells is normally not functional but can be readily mobilised in response to increased demands for erythropoiesis. Ref: TEXTBOOK OF PATHOLOGY 6th EDITION - HARSH MOHAN PAGE NO: 295-296
Category: Pathology
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