Anaemia This is defined as reduction in the haemoglobin concentration of the blood.

Clinical features of anaemia: Symptoms: –Shortness of breath particularly on exercise. –Weakness. –Lethargy. –Palpitation. –Headache. –Cardiac failure. –Visual disturbance.

Signs: Pallor of mucous membranes (conjunctiva, tongue, palm of the hands). Pallor of mucous membranes (conjunctiva, tongue, palm of the hands). Nails are delicate and break easily. Nails are delicate and break easily. Heir is thin. Heir is thin. Angular stomatitis. Angular stomatitis. Rough skin. Rough skin.

Signs: Retinal haemorrhage. Retinal haemorrhage. Spoon nails (iron deficiency anaemia). Spoon nails (iron deficiency anaemia). Jaundice (haemolytic anaemia, megaloblastic anaemia). Jaundice (haemolytic anaemia, megaloblastic anaemia). Leg ulcer (sickle cell anaemia). Leg ulcer (sickle cell anaemia). Bone deformations (thalassaemia major). Bone deformations (thalassaemia major).

Classification of Anaemia: Depends on the morphology of RBC under the microscope: –Normocytic normochromic anaemia: due to acute blood loss, like traffic accident, surgery, delivery, renal failure and liver diseases. –Microcytic hypochromic anaemia: due to iron deficiency, thalassemia, and sideroblastic anaemia. –Macrmocytic normochromic anaemia: due to deficiency of Folic acid and Vitamin B12.

Pathophysiology (causes of anaemia): Nutritional: Iron Deficiency Anaemia. Iron Deficiency Anaemia. Vitamin B12 deficiency. Vitamin B12 deficiency. Folic Acid. Folic Acid.

Haemolytic Anaemia: a- Membrane defect: - Hereditary spherocytosis. - Hereditary spherocytosis. - Hereditary elleptocytosis. - Hereditary elleptocytosis. b- Haemoglobinopathies: b- Haemoglobinopathies: - Sickle cell anaemia. - Sickle cell anaemia. - Thalassaemia. - Thalassaemia. - Haemoglobin E disease. - Haemoglobin E disease. c- Enzyme deficiency: c- Enzyme deficiency: - G6PD deficiency. - G6PD deficiency. - Pyruvate deficiency. - Pyruvate deficiency. d- Immunohaemolytic anaemia: - Allo antibodies. - Allo antibodies. - Auto antibodies. - Auto antibodies.

e- Aplastic anaemia: - Primary causes (idiopathic). - Secondary causes (radiation, infections, and drugs). g- Infections: - Malaria. - Worms. - Salmonella. h- Hormonal abnormalities: - Decrease of erythropoietin.

IRON DEFICIENCY ANAEMIA. Iron deficiency is the most common cause of anaemia in every common country of the world, and it is the most important cause of microcytic hypochromic anaemia.

Nutritional and metabolic aspects of the iron: Iron in the body is about g. Iron in the body is about g. Iron in the Haemoglobin of the RBC represents a greatest percent of body constitutes (60-70%). Iron in the Haemoglobin of the RBC represents a greatest percent of body constitutes (60-70%). Iron presents in the body in two forms: Iron presents in the body in two forms: - Ferrittin. - Ferrittin. - Haemosiderin. - Haemosiderin.

Ferrittin: Ferrittin: –It is a soluble iron form. –Found in the liver, plasma, and placenta. –It is protein and iron compound. –It is soluble, non-stainable and can be measured by Radio Immuno Assay (RIA). –Males have higher values than females (100 ng/ml for male and 30 ng/ml for female).

Haemosiderin: –Is the plasma protein responsible for carrying the iron. –It is produced in the liver. –1 molecule of transferrin binds two atoms of iron. –Total iron binding capacity of transferrin is 300µg.

Dietary iron:  Iron presents in meat and liver…  The daily consumption is mg.  Body absorbed only 5-10 % of taken iron, but the proportion can be increased to % in iron deficiency and pregnancy.  Absorption as ferrous chloride in duodenum and upper part of the jejunum.  HCl in the stomach converts ferric to ferrous to facilitate absorption. HCl HCl Fe+3 Fe+2 Fe+3 Fe+2

Iron deficiency: It is a type of anaemia which caused due to deficiency of iron. Clinical features:  Patients develop all general symptoms and signs of the anaemia.  Angular stomalitis.  Spoon nails.  Dysphagia.

Causes of iron deficiency anaemia: –Chronic blood loss, especially uterine of gastrointestinal tract. –Increased demands, during pregnancy, infancy, growth, lactation and menstruated women. –Malabsorption especially in the cases of gastroectomy. –Poor diet, like in developing countries.

Laboratory findings: Stained peripheral blood film: shows microcytic hypochromic RBS, with occasional target cell and pencil-shaped cell. Pale view. Stained peripheral blood film: shows microcytic hypochromic RBS, with occasional target cell and pencil-shaped cell. Pale view. PCV, MCV, MCH, MCHC, Hb, RBC count, serum iron, serum ferritin are low. PCV, MCV, MCH, MCHC, Hb, RBC count, serum iron, serum ferritin are low. TIBC, serum transferrin saturation are raised. TIBC, serum transferrin saturation are raised. Reticulocyte count is low. Reticulocyte count is low.

MEGALOPLASTIC ANAEMIA. It is a macrocytic anaemia in which RBC are abnormally large (MCV>95fl).

There are two reasons of this type of anaemia: Folic acid deficiency (Folate). Folic acid deficiency (Folate). Vitamin B12 deficiency (Cobalamine). Vitamin B12 deficiency (Cobalamine).

Vitamin B12: This vitamin is synthesized in nature by micro- organism in the intestine of man and animals, but we can not obtain it from the bacteria in our bodies, because it is synthesizing in the large colon after the site of absorption and it is wasted in the faeces in about 5µg/day. So we obtain it from animal food such as liver, kidney, meat and dairy products as milk and cheese.

Diary requirements: The human body needs about 1-2 µg daily. The human body needs about 1-2 µg daily.Absorption: B12 is combined with glycoprotein called the intrinsic factor (IF), which is synthesized in the gastric cells. The absorption occurs in the distal ileum. B12 is combined with glycoprotein called the intrinsic factor (IF), which is synthesized in the gastric cells. The absorption occurs in the distal ileum.Transportation: Transport by a protein synthesized in the liver called Transcobalamine II, which carry vitamin B12 to liver, nerves and bone marrow. Transport by a protein synthesized in the liver called Transcobalamine II, which carry vitamin B12 to liver, nerves and bone marrow.

Causes of vitamin B 12 deficiency: 1. Nutrition as in vegetarian food. 2. Lack of IF due to chronic gastritis or antibodies against stomach cells. 3. Some diseases which causing malabsorption. 4. Increased needs to the vitamin as in pregnancy and in childhood. 5. Some parasites.

Folic Acid: –It a vitamin which yellow in colour, water soluble, necessary for the production of the RBC, WBC and platelets. –It is not synthesized in the body. –It is found in large number of green vegetables.

Daily requirement: The human body needs about µg daily. The human body needs about µg daily.Absorption: Duodenum and Jejunum. Duodenum and Jejunum.Transportation: Weakly bound to albumin. Weakly bound to albumin.

Causes of vitamin folic acid deficiency: 1. Nutritional deficiency. 2. Increased utilization as pregnancy, old people, liver diseases and haemolytic conditions. 3. Renal failure.

Clinical features: 1. Patients develop all general symptoms and signs of the anaemia. 2. Mild jaundice. 3. Glossitis (a red sore tongue) 4. Angular stomalitis. 5. Sever deficiency of the folic acid causes neuropathies diseases. 6. Deficiency during pregnancy causes neural tube defect.

Laboratory findings: Stained peripheral blood film: shows macrocytic normochromic RBS, Oval cells, and hypersegmented neutrophil (six or more lobs). Stained peripheral blood film: shows macrocytic normochromic RBS, Oval cells, and hypersegmented neutrophil (six or more lobs). PCV, Hb, and RBC count PCV, Hb, and RBC count MCV and MCH are high, MCHC is normal. MCV and MCH are high, MCHC is normal. Reticulocyte count is low. Reticulocyte count is low.

How to differentiate between Folic acid deficiency and B12 deficiency in the laboratory?

Normal red cell morphology

Hypochromic Hyperchromic Macrocytic Microcytic

IDA Target cells Sickle cells Poikiolocytosis Stomatocytes Acanthocytes Ovalocyte Spherocytes Nucleated RBC