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Anaemia is defined as a haemoglobin concentration in blood below the lower limit of the normal range for the age and sex of the individual. :

Normal hb value: MALES:13.0 gm/dl FEMALES:11.5 gm/dl Newborn infants :15 g/dl at 3 months :9.5 g/dl the red cell counts, haematocrit (PCV) and absolute values (MCV, MCH and MCHC) provide alternate means of assessing anaemia. Anaemia is defined as a haemoglobin concentration in blood below the lower limit of the normal range for the age and sex of the individual.

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PATHOPHYSIOLOGY OF ANAEMIA Subnormal level of haemoglobin causes lowered oxygen carrying capacity of the blood ,this in turn have compensatory physiologic adaptation. Increases release of oxygen from haemoglobin Increases blood flow to tissues maintenance of the blood volume redistribution of blood flow to maintain cerebral blood supply

Clinical features:

5 Clinical features Development of anaemia in patient depends upon 3 main factors: The speed of onset of anaemia The severity of anaemia The age of the patient


6 SYMPTOMS Tiredness Easy fatiguability Generalised muscular weakness Lethargy Headache In older patients Cardiac failure Angina pectoris Intermittent claudication Confusion and visual disturbances


7 SIGNS Pallor 2. Cardiovascular system. A hyperdynamic circulation may be present with tachycardia, collapsing pulse, and in the case of elderly, congestive heart failure. 3. Central nervous system. faintness, headache, drowsiness, numbness and tingling sensations of the hands and feet.

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8 4. Reproductive system. Menstrual disturbances 5. Renal system. Mild proteinuria and impaired concentrating capacity of the kidney 6. Gastrointestinal system. Anorexia, nausea, constipation and weight loss

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10 cells larger than normal (macrocytosis) megaloblastic anaemia; aplastic anaemia, or cells smaller than normal (microcytosis) :iron deficiency anaemia, thalassaemia both microcytosis and macrocytosis are present (dimorphic). 2. Variation in shape e.g. in megaloblastic anaemia, iron deficiency anaemia 3. Inadequate haemoglobin formation Increased central pallor either from Unusually deep pink staining of the red cells due to increased haemoglobin concentration is termed hyperchromasia and may be found in megaloblastic anaemia lowered haemoglobin content (e.g. in iron deficiency anaemia, chronic infections), due to thinness of the red cells

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11 Miscellaneous changes

Classification of Anaemias :

12 Classification of Anaemias PATHOPHYSIOLOGIC I. Anaemia due to increased blood loss a) Acute post-haemorrhagic anaemia b) Chronic blood loss II. Anaemias due to impaired red cell production a) Cytoplasmic maturation defects 1. Deficient haem synthesis: Iron deficiency anaemia 2. Deficient globin synthesis: Thalassaemic syndromes b) Nuclear maturation defects Vitamin and/or folic acid deficiency: Megaloblastic anaemia

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13 c) Defect in stem cell proliferation and differentiation 1. Aplastic anaemia 2. Pure red cell aplasia d) Anaemia of chronic disorders e) Bone marrow infiltration (f)Congenital anaemia III. Anaemias due to increased red cell destruction (Haemolytic anaemias) A. Extrinsic (extracorpuscular) red cell abnormalities B. Intrinsic (intracorpuscular) red cell abnormalities B.MORPHOLOGIC I. Microcytic, hypochromic II. Normocytic, normockromic III. Macrocytic, normochromic


14 Pathophysiology of IRON DEFICIENCY ANAEMIA Iron balance is achieved largely by regulation of iron absorption in the proximal small intestine. Either diminished absorbable (Achlorhydria) dietary iron or excessive loss (excessive menstruation, haematuria) of body iron can cause iron deficiency. mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filters chronic blood loss is the most common cause of iron deficiency


15 CLINICAL FEATURES Unusual dietary cravings such as pica Atrophy of mucous membrane of alimentary tract : It is due to depletion of iron dependent oxidative enzymes Koilonychia (spoon-shaped finger nails) nails that are brittle and breaks easily


16 TREATMENT ORAL THERAPY : Oral iron salt of ferrous sulfate or 60mg of elemental iron administered thrice daily PARENTERAL THERAPY : It may be given as single intramuscular injection of iron dextran or repeated injections of iron sorbitol citrate


17 PATHOPHYSIOLOGY OF MEGALOBLASTIC ANAEMIA Vitamin B12 and folic acid are coenzymes in the DNA synthetic pathway If deficient, defective nuclear maturation due to deranged or inadequate synthesis of DNA The synthesis of RNA and protein are unaffected, so cytoplasmic enlargement is not matched by DNA synthesis and there is block in mitotic division.


18 CLINICAL FEATURES GLOSSITIS: Typically , patient has smooth, beefy, red tongue Jaundice, weight loss, degeneration of spinal cord


19 TREATMENT MEGALOBLASTIC ANAEMIA need therapy with appropriate vitamin i.e. hydroxycobalamin as intramuscular injection 1000ug for 3 weeks and oral folic acid 5mg tablet daily for 4 months


20 PATHOPHYSIOLOGY OF PERNICIOUS ANAEMIA There is evidence to suggest that the atrophy mucosa in PA is caused by an autoimmune reaction against gastric parietal cells as under: Its incidence high in patients with other autoimmune disease such as Grave’s disease Patients with PA have abnormal circulating antibodies such as anti-parietal cell antibody


21 Anaemia, Glossitis, Neuroabnormalities Gastrointestinal manifestations (diarrhoea,anorexia, weight loss, dyspepsia), Congestive heart failure Haemorrhagic manifestations. Symptoms


22 TREATMENT BLOOD TRANSFUSION MARROW STIMULATING AGENTS such as androgen may be administered orally IMMUNOSUPPRESSIVE THEARPY with agents such as anti-thymocyte globulin & anti-lymphocyte serum or high dose of glucocorticoids may yield similar response BONE MARROW TRANSPLANTATION it is considered in severe cases under age of 40 years Replacement therapy with vitamin B12


23 PATHOPHYSIOLOGY OF HAEMOLYTIC ANAEMIA It is characterised by following features * Shortening of the normal red cell life span, i.e. premature destruction of red cells. * Accumulation of the products of haemoglobin catabolism. * Increase in erythropoiesis, in bone marrow to compensate loss of red cells.

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25 CLINICAL FEATURES Anaemia and lowered tissue oxygen tension stimulate increased production of erythropoietin, leading to marked increase in the number of normoblasts in the marrow. Elevated levels of bilirubin promote the formation of pigment gallstones. Phagocytosed of RBCs or haemoglobin lead to haemosiderosis Urine turns dark upon standing due to excess of urobilinogen in urine

Sickle cell anemia :

26 Sickle cell anemia


27 CLINICAL FEATURES The symptoms begin to appear after 6th month of life when most of the HbF is replaced by HbS. These features are as under: Anaemia. 2. Vaso-occlusive phenomena. VasoObstruction affecting different organs and tissues results in infarcts which may be of 2 types: i) Microinfarcts affecting particularly the abdomen, chest, back and joints ii) macroinfarcts involving most commonly the spleen, bone marrow 3. Constitutional symptoms..


APLASTIC ANAEMIA CAUSES A. PRIMARY APLASTIC ANEMIA 1 Fanconi anemia (congenital) 2. Immunologically-mediated (acquired) B. SECONDARY APLASTIC ANAEMIA i. Drugs Dose-related aplasia e. . with antimetaboiites (methotrexate) ii) Idiosyncratic aplasia e.g. with chloramphenicol 2. Toxic chemicals e.g. benzene derivatives 3. Infections e.g. infectious hepatitis 4. Miscellaneous e.g. association with SLE


29 PATHOGENESIS Stem cell Injury occur Genetically altered stem cell Express New antigens Reduced proliferative Bone marrow aplasia T-cell response


30 CLINICAL FEATURES Anaemia and its symtoms Infections of mouth & throat Thrombocytopenia Lymph nodes , livers and spleen are not enlarged

Treatment Review:

31 Treatment Review IRON DEFICIENCY ANAEMIA * ORAL THERAPY : Oral iron salt of ferrous sulfate or 60mg of elemental iron administered thrice daily * PARENTERAL THERAPY : It may be given as single intramuscular injection of iron dextran or repeated injections of iron sorbitol citrate MEGALOBLASTIC ANAEMIA * hydroxycobalamin as intramuscular injection for 3 weeks * oral folic acid tablet daily for 4 months PERNICIOUS ANAEMIA * BLOOD TRANSFUSION * MARROW STIMULATING AGENTS * IMMUNOSUPPRESSIVE THEARPY * BONE MARROW TRANSPLANTATION * Replacement therapy with vitamin B12

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