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Iron role and metabolism with nutritional Anemia
- 1. Iron and NutritionalAnemia Faisal Al-shormany. MD.PhD.SCOPE Fellow Associate Professor,
- 3. Synthesis: Hemoglobin (Hb)is synthesized in a complex series of steps. The heme part is synthesized in a series of steps in the mitochondria and the cytosol of immature red blood cells, while the globin protein parts are synthesized by ribosomes in the cytosol.
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- 8. • Iron isone of the most essential trace element • Total body iron content is 3to 5g. • 75%present in blood, the rest is in liver, bone marrow & muscles. • Iron is present in almost all cells. • Heme is the most predominant iron-containing substance. • It is a constituent of proteins/enzymes (hemoproteins)-Hb, myoglobin, cytochromes, catalase, peroxidase.
- 9. • Non-heme iron-transferrin,ferritin, hemosiderin. • Sources: • The best sources of food iron include liver, meat, egg yolk, green leafy vegetables, dates, whole grains and cereals.
- 10. RDA 15to 20mg 30to 60mg •Adult man &postmenopausal women:10 mg • Premenopausal women: • Pregnant women: • Women require greater amount than men due to physiological loss during menstruation.
- 11. Biochemical functions • Ironis a component of several functionally important molecules. • Iron is required for the synthesis of hemoglobin, myoglobin, cytochromes, catalase and peroxidase. • Cytochromes &certain non-heme proteins are necessary for ETC&oxidative phosporylation. • Peroxidase, the lysosomal enzyme is required for phogocytosis &killing of bacteria.
- 12. • Iron isalso essential for the synthesis of non heme iron (NHI) compounds like, succinate dehydrogenase, iron-sulfur proteins of flavoproteins, NADH dehydrogenase. • Iron helps mainly in the transport, storage and utilization of oxygen. • Iron is associated with effective immuno- competence of body.
- 13. Metabolism of iron •Absorption: • Iron iscalled as one way substance,because it isabsorbed and excreted from small intestine. • Iron is absorbed from upper small intestine. • Iron is absorbed in three forms: (1)ferrous iron (2)ferric iron (3)heme iron. • Iron is absorbed mainly in the ferrous form.
- 14. • Ferric ionsare reduced with ascorbic acid & glutathione of food to more soluble ferrous (Fe2+) form which is more readily absorbed than Fe3+ • After taken up by the intestinal mucosa, iron is either stored in the form of ferritin in the mucosal cells or transported across the mucosal cells to the plasma in the form of transferrin.
- 15. Factors affecting ironabsorption • Factors increasing the iron absorption: • Iron is mainly absorbed in the ferrous form. • Ascorbic acid &cysteine favors the reduction of ferric form of iron to ferrous form. • HCLalso favors the reduction of ferric form of iron to ferrous form. • In iron deficiency state, the iron absorption is increased to 2-10times that of normal.
- 17. Factors decreasing ironabsorption • Phytates and phosphates in the food decreases iron absorption. • The deficiency of HCLresults in impaired conversion of ferric form of iron to ferrous form of iron. • Iron absorption is deceases in the presence of gastrointestinal diseases.
- 18. Transport • Iron inthe mucosal cells: • The iron (Fe2+) entering the mucosal cells by absorption is oxidized to ferric form (Fe3+) by the enzyme ferroxidase (ferroxidase activity of ceruloplasmin) • Major sourcesof iron in the plasma isfrom degraded erythrocytes. • Fe3+combines with apoferritin to form ferritin, which the temporary storage form of iron.
- 19. • From themucosal cells, iron may enter the blood stream. • Transport of iron in the plasma: • Iron enters plasma in ferrous state. • It is oxidized to ferric form by a copper containing protein, ceruloplasmin - ferroxidase activity. • Ferric iron binds with a specific iron binding protein-transferrin. • Transport form of iron is transferrin. • It is a glycoprotein, synthesized in liver.
- 20. • Normal plasmalevel of transferrin is 250mg/dl. • One molecule of transferrin can transport 2 ferric atoms and the half-life of transferrin is 7- 10days. • Serum iron and serum iron binding capacity: • Total iron binding capacity (TIBC) of transferrin is 250-450µg/dl; • In iron deficiency anemia, serum iron level is decreased and TIBCisincreased.
- 21. Storage • Iron isstored in liver, spleen &bone marrow in the form of ferritin. • In the mucosal cells, ferritin is the temporary storage form of iron. • Ferritin contains about 23%iron. • Ferritin in plasma level is elevated in iron over load.
- 22. • Ferritin levelin blood is an index of body iron stores. • Ferritin is an acute phase reactant protein, elevated in inflammatory diseases. • Hemosiderin: • It is another iron storage protein, which can hold about 35%of iron by weight. • Hemosiderin accumulates when iron levels are increased.
- 25. Summary – ironabsorption and transport
- 26. Excretion • The normalIron excretion is about 1mg/day. • The major excretory pathway is through intestine. • Iron is not excreted in urine, but in nephrotic syndrome loss of transferrin may lead to increased loss of iron in urine.
- 27. Disorders of ironmetabolism • Iron deficiency &iron overload are themajor disorders of iron metabolism. • Iron deficiency • Iron deficiency causes a reduction in the rate of haemoglobin synthesis & erythropoiesis. • It can result in iron deficiency anemia.
- 28. Causes: • Irondeficiency is caused by inadequate intake, impaired absorption, chronic blood loss &increased demand. • Iron deficiency anemia mostly occurs in growing children, adolescent girls, pregnant &lactating women.
- 30. 1- Haematological Investigations Hemoglobin level ( decrease ) RBCs count ( decrease ) MCV mean corpuscular volume and MCH mean corpuscular hemoglobin ( decrease ) Hypochromia Platelets (usually thrombocytosis) ( increase ) 2- Biochemical Laboratory findings Serum ferritin level ( decrease ) Transferrin saturation index ( decrease ) Total iron-binding capacity TIBC ( increase ) Serum iron concentration ( decrease )
- 31. The hand ofa person with severe anemia compared to one without
- 32. Human blood froma case of iron deficiency anemia
- 33. Clinical features • Microcytichypochromic anemia in which the size of the red blood cells are smaller than normal and have much reduced haemoglobin content. • Weakness, fatigue, dizziness and palpitation, • Nonspecific symptoms are nausea, anorexia, constipation, and menstrual irregularities.
- 34. Iron over load •Haemosiderosis and haemochromatosis and iron poisoning are conditions associated with iron over load. • Haemosiderosis: • It refers to accumulation of hemosiderin in liver &other reticulo-endothelial system. • There is no significant tissue destruction. • Haemosiderosis is an initial stage of iron over load.
- 35. Haemochromatosis • Haemochromatosis isa clinical condition in which iron is directly deposited in the tissues (liver, spleen, pancreas & skin). • Haemochromatosis may be genetic (primary) or acquired (secondary).
- 36. Genetic or primaryhaemochromatosis • It is a hereditary disorder, due to an unregulated increase in the intestinal absorption of iron from normal diet. • Iron is deposited as haemosiderin in liver, pancreas, heart and other organs. • After accumulation, excessive amounts of intracellular iron lead to tissue injury and organ failure.
- 37. Acquired or secondaryhaemochromatosis • It is caused by excess intake of iron, increased hemolysis and repeated blood transfusions.
- 38. Clinical features • Haemochromatosisare related to the involved organ systems as follows: • Liver: leading to cirrhosis • Pancreas: leading to fibrotic damage to pancreas with diabetes mellitus • Skin: skin pigmentation • Endocrine organs: leading to hypothyroidism, testicular atrophy
- 39. • Joints: leadingto arthritis • Heart: leading to arrhythmia &heart failure • Iron poisoning: • Acute overdose, mainly occurring in children may cause severe or even fatal symptoms due to toxic effect of free iron in plasma which may life threatening. • Symptoms: • Nausea, vomiting, abdominal pain, diarrhoea.
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