1 IRON DEFICIENCY ANAEMIA.pptx134467788

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1. IRON DEFICIENCY ANAEMIA

2. IRON DEFICIENCY ANAEMIA The commonest nutritional deficiency disorder present throughout the world is iron deficiency but its prevalence is higher in the developing countries.

3. IRON METABOLISM The amount of iron obtained from the diet should replace the losses from the skin, bowel an 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. The iron required for haemoglobin synthesis is derived from 2 primary sources ingestion of foods containing iron (e.g. leafy vegetables, beans, meats , liver etc) and recycling of iron from senescent red cells

4. Daily iron cycle. Iron on absorption from upper small intestine circulates in plasma bound to transferrin and is transported to the bone marrow for utilisation in haemoglobin synthesis. The mature red cells are released into circulation, which on completion of their lifespan of 120 days, die . They are then phagocytosed by RE cells and iron stored as ferritin andhaemosiderin . Stored iron is mobilised in response to increased demand and used for haemoglobin synthesis, thus completing the cycle

5. ABSORPTION Iron is absorbed mainly in the duodenum and proximal jejunum. The absorption is regulated by mucosa

6. TRANSPORT Iron is transported 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 transferrin receptors utilise iron for haemoglobin synthesis. Transferrin is reutilised after iron is released from it . A small amount of transferrin iron is delivered to other sites such as parenchymal cells of the liver

7. EXCRETION The body is unable to regulate its iron content by excretion alone. The amount of iron lost per day is 0.5-1 mg which is independent of iron intake. This loss is nearly twice more (i.e. 1-2 mg/day) in menstruating women . Iron is lost from the body in both sexes as a result of desquamation of epithelial cells from the gastrointestinal tract , from excretion in the urine and sweat, and loss via hair and nails . Iron excreted in the faeces mainly consists of unabsorbed iron and desquamated mucosal cells

8. Etiology of iron deficiency anaemia. I. INCREASED BLOOD LOSS 1. Uterine e.g. excessive menstruation in reproductive years, repeated miscarriages, at onset of menarche, post-menopausal uterine bleeding 2. Gastrointestinal e.g. peptic ulcer, haemorrhoids hookworm infestation, cancer of stomach and large bowel, oesophageal varices , hiatus hernia, chronic aspirin ingestion, ulcerative colitis, diverticulosis

9. 3. Renal tract e.g. haematuria , haemoglobinuria 4. Nose e.g. repeated epistaxis 5. Lungs e.g. haemoptysis

10. II. INCREASED REQUIREMENTS 1. Spurts of growth in infancy, childhood and adolescence 2. Prematurity 3. Pregnancy and lactation

11. INADEQUATE DIETARY INTAKE 1. Poor economic status 2. Anorexia e.g. in pregnancy 3. Elderly individuals due to poor dentition, apathy and

12. DECREASED ABSORPTION 1. Partial or total gastrectomy 2. Achlorhydria 3. Intestinal malabsorption such as in coeliac disease

13. Clinical features 1. Onset: Onset is insidious and most of the patients complain of fatigue, palpitations, headache, dizziness, Breathlesness,Tierd and irritability. These symptoms worsen as the severity of anemia increases. Patients become symptomatic as Hb falls below 7 gm/' dL Patients alsocomplain of paleness of skin.

14. 2. Growth and development'. Growth in infancy is impaired Iron, deficient children are irritable and demonstrate lack of interest in surroundings. When iron deficiency occurs in the critical period of neurorievelopmcnt (6-24 months), changes are irreversible and development, of child is affected. 3. Pica: This may be the cause rather than the effect of iron deficiency and is observed in 40% of the cases.

15. 4. Epithelial changes: Fingernails become thin, flattened , brittle and finally spoonshaped ( koilonychia ). There is atrophy of papillae of tongue making the surface smooth (bald tongue). There are fissures and ulcerations at the angles of mouth— angular stomatitis

16. Pharyngeal webs: Plummer Vinson syndrome is characterized by IDA with dysphagia in middle aged women

17. Diagnosis 1. Peripheral blood findings 2 Bone marrow morphology and iron stores 3. Iron status and 4 Clinical evaluation

18. Peripheral blood findings Absolute values • MCV is < 80 fl. MCV is reduced first and also anisocytosis is an important early sign. RDW is increased • MCH < 25 pg

19. Microcytic hypochromic red cells in peripheral smear There is mild to moderate degree of anisopoikilocytosts Red cells are microcytic hypochromic with poikilocytosis showing few pencil/cigar shaped red cells. The red cell membrane is stiff in iron deficent cells and that results in development of red cells with abnormal shapes like pencil cells. Hypochromia is recognized by central pallor being more than l/3rd the diameter of the cell

20. In severe anemia , central pallor becomes 2/3rd to 3/4th of the cell and only peripheral rim of hemoglobin is seen (ring/ pessary cells), Microcytosis in red cells in the peripheral smear is recognized by their size being smaller than the nucleus ofsmall lymphocytes

21. Reticulocyte , count : Reticulocyte count of 1-2% in untreated patients is observed and is low for the degree of anemia . • Platelets: Platelets are increased, more so in cases associated with hemorrhage

22. Severe iron deficiency anemia : A. Red cells are smaller than the nucleus ' small lymphocyte and only ring of hemoglobin . B. Iron deficiency anemia : B film from a case of severe Iron deficiency demonstrates elongated pencll /cigar shaped red cells (4). C. Iron deficiency anemia : Thrombocytosis is present in seme cases of iron deficiency anemia (4), Red cells are microcytic hypochromic winh only ring of hemoglobin -ring/ pessary cells