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ANAEMIA- INTRODUCTION

ANAEMIA- INTRODUCTION. RBC main function is oxygen transport So can be defined as a reduction in O 2 carry capacity of blood Due to Reduction below normal limit of total circulating red cell mass

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ANAEMIA- INTRODUCTION

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  1. ANAEMIA- INTRODUCTION • RBC main function is oxygen transport • So can be defined as a reduction in O2 carry capacity of blood • Due to Reduction below normal limit of total circulating red cell mass • This is not usually measured, so better defined as reduction in the volume of packed cells as measured by the hematocrit, or reduction in the Hbconc of blood • Thus fluid retention/loss can give false values

  2. ERYTHROCYTES (RBCS) • Flexible biconcave shape • Mature cells lack nucleus and organelles • Contains hemoglobin – aids in gas transport • O2 binds to heme group; CO2 to globin portion • Erythropoietin stimulate RBC production & maturation • Carbohydrates, lipids, proteins, iron, vitamin B12 and folic acid are needed for RBC synthesis • Limited life span about 120 days – because cells are anucleate, Components broken down and recycled or excreted from the body

  3. Mainly defined as a decline of the RBC parameters namely Hb and the RBC count or PCV. ‘Normal’ Hb in a given population depends largely on the mix of sex, age and ethnicity. The WHO defines anaemia as: • MenHb < 13 g/dL or PCV < 41 L/L • WomenHb < 12 g/dLor PCV < 36 L/L Variations wide and require redefinition for specific populations-eg athletes & people living at high altitude Can be classified based on underlying mechanisms oronmorphology

  4. Based on underlying mechanism 1. BLOOD LOSS - acute -Chronic- GI lesions, gynaecology 2. INCREASED RATE OF DESTRUCTION (HEMOLYTIC) • Hereditary -mb disorders like spherocytosis, Enzyme deficiencies like G6PD; disorders of Hb synthesis like SS & Thalassemia

  5. INCREASED RATE OF DESTRUCTION contd b) Acquired causes Antibody mediated- transfusion reactions, erythroblastosisfetalis Mechanical trauma- microangiopathichemolytic anaemia, DIC Infections- malaria Chemical injury- lead poisoning Sequestration in mononuclear phagocytic system- hyperslenism

  6. 3. IMPAIRED RED CELL PRODUCTION • Disturbance of proliferation & differentiation of stem cells- aplastic, renal failure • Maturation disturbance- B12 & Folic acid, \iron deficiency • Unknown/multiple mechanisms- seen in chronic infections, HIV/AIDS

  7. MORPHOLOGICAL CLASSIFICATION • classified by cell size (microcytic, normocytic, macrocytic) & • Staining intensity (Hb concentration -hypochromic and normochromic).

  8. RED CELL INDICES- MCHC • measure of the mean concentration of Hb in a red cell • MCHC (g/dl) = Hb (g/dl) x 100 / PCV (%) • Normal range is 31- 35 g/dl • RBCs cannot contain more than 35g/dl of Hb so cells are either hypochromic or normochromic

  9. RED CELL INDICES- MCV • Mean cell volume • PCV x 10 / RBC • Measured in femtolitres • Normal range is 77-91 fL • IfMCV is < 80 fL- microcytic; if >100 fL macrocytic; • for values between these two = normocytic

  10. MICROCYTIC • most often accompanied by hypochromasia (MCH of less than 27pg) • Pathway leading to microcytosiscomprises: • reduced iron availability • reduced globin productionin thalassaemias or otherhaemoglobinopathies • reduced haem synthesis such as in lead poisoning

  11. MACROCYTIC ANAEMIAS • When the MCV is greater than 115fL the anaemia is called megaloblastic. • Causes include:vitamin B12/folate defciency,– inadequate intake/insufficientabsorption e.g. pernicious anaemia, liver disease, alcohol abuse • Characteristic of juvenile RBC. Thus, often seen in haemolytic anaemias, which are associated with increased production and release of red cells (reticulocytosis)

  12. BLOOD LOSS ANEMIA • After rapid hemorrhage, body replaces fluid portion of plasma in 1 to 3 days, but this leaves a low conc. of RBCs. If a second hemorrhage does not occur, red cell conc. usually returns to normal within 3 to 6 weeks • In chronic, person cannot absorb enough iron from intestines to form hbas rapidly as it is lost. RBCs produced are much smaller and have too little hb inside them, giving rise to microcytic, hypochromicanemia

  13. APLASTIC ANEMIA • Destruction or inhibition of red bone marrow • Bone marrow aplasia means lack of functioning bone marrow • Causes include exposure to gamma ray radiation & excessive x-ray treatment, certain industrial chemicals, and even drugs to which the person might be sensitive

  14. MEGALOBLASTIC ANEMIA • Deficiency of vit B12, folic acid to slow reproduction of erythroblasts in BM. RBCs grow too large, have odd shapes, & called megaloblasts. • Cells thus rupture easily • Also atrophy of the stomach mucosa (loss of intrinsic factor from the stomach mucosa) - pernicious anemia • intestinal sprue, in which folic acid, vitamin B12, and other vitamin B compounds are poorly absorbed

  15. HEMOLYTIC – PREMATURE RUPTURE OF RBCS • Many hereditarily acquired, make cells fragile, so rupture easily as they go through the capillaries, especially through the spleen. • Number formed may be normal, or greater in some hemolytic diseases, the life span of fragile red cell is so short that the cells are destroyed faster than they can be formed • In hereditary spherocytosis, the red cells are very small and spherical rather than being biconcave discs. So cannot withstand compression forces because they do not have the normal loose, baglike cell membrane structure of the biconcave discs

  16. HEMOLYTIC- SICKLE CELL ANEMIA • seen W. Africans and American blacks, cells have an abnormal type of HB- hemoglobin S (faulty beta) • When exposed to low O2 concs of oxygen, HB precipitates into long crystals which elongate the cell and give it the appearance of a sickle • Precipitated hb also damages membrane, so that the cells become highly fragile, leading to serious anaemia • Frequently a vicious circle of events - sickle cell "crisis," : low O2 tension in tissues causes sickling, which leads to ruptured red cells, thus further decrease in oxygen tension and still more sickling and red cell destruction

  17. HEMOLYTIC- ERYTHROBLASTOSIS FETALIS • Rh-positive red blood cells in the fetus are attacked by antibodies from an Rh-negative iso-sentisized mother. • These antibodies make the Rh-positive cells fragile, leading to rapid rupture

  18. EFFECTS OF ANEMIA • Palor, weakness, malaise and dyspnea on mild exertion • In acute blood loss and shock, oliguria and anuria may lead to shock kidney • CNS hypoxia –headache, dimness of vision and faintness • In severe anemia, the blood viscosity may falls. This decreases the resistance to blood flow in the peripheral blood vessels, greater than normal quantities flow through tissues & return to the heart, thereby greatly increasing cardiac output. • Thus, one major effect is greatly increased cardiac output, as well as increased pumping workload on the heart which can cause acute cardiac failure

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