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Anaemias By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir
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Anaemias By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir

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anaemias and classification made easy for medical students.

anaemias and classification made easy for medical students.

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  • 1. ANEMIA By Dr Bashir Ahmed Dar Chinki pora sopore kashmir Associate professor of Medicine
  • 2. Classification of Anemia I. Etiologic Classification 1. Impaired RBC production 2. Excessive destruction 3. Blood loss II. Morphologic Classification 1. Macrocytic anemia 2. Microcytic hypochromic anemia 3. Normochromic normocytic anemia
  • 3. Impaired RBC Production 1. Abnormal bone marrow 1.1 Aplastic anemia 1.2 Myelophthisis : Myelofibrosis, Leukemia, Cancer metastasis 2. Essential factors deficiency 2.1 Deficiency anemia : Fe, Vit. B12, Folic acid, etc 2.2 Anemia in renal disease : Erythropoietin 3. Stimulation factor deficiency 3.1 Anemia in chronic disease 3.2 Anemia in hypopituitarism 3.3 Anemia in hypothyroidism
  • 4. Excessive Destruction of RBC (cont.) Hemolytic anemia 1. Intracorpuscular defect 1.1 Membrane : Hereditary spherocytosis Hereditary ovalocytosis, etc. 1.2 Enzyme : G-6PD deficiency, PK def., etc. 1.3 Hemoglobin : Thalassemia, Hemoglobino- pathies
  • 5. Excessive Destruction of RBC 2. Extracorpuscular defect 2.1 Mechanical : March hemolytic anemia MAHA (Microangiopathic HA) 2.2 Chemical/Physical 2.3 Infection : Clostridium tetani 2.4 Antibodies : HTR, SLE 2.5 Hypersplenism
  • 6. Blood Loss 1. Acute blood loss : Accident, GI bleeding 2. Chronic blood loss : Hypermenorrhea Parasitic infestation
  • 7. Macrocytic Anemia MCV > 94 MCHC > 31 1. Megaloblastic dyspoiesis 1.1 Vit. B12 deficiency : Pernicious anemia 1.2 Folic acid deficiency : Nutritional megaloblas- tic anemia, Sprue, Other malabsorption 1.3 Inborn errors of metabolism : Orotic aciduria, etc. 1.4 Abnormal DNA synthesis : Chemotherapy, Anticonvulsant, Oral contraceptives
  • 8. Microcytic Hypochromic Anemia MCV < 80 MCHC < 31 1. Fe deficiency anemia : Chronic blood loss, Inadequate diet, Malabsorption, Increased demand, etc. 2. Abnormal globin synthesis : Thalassemia with or without Hemoglobinopathies 3. Abnormal porphyrin and heme synthesis : Pyridoxine responsive anemia, etc. 4. Other abnormal Fe metabolism :
  • 9. Normocytic Normochromic Anemia MCV 82 - 92 MCHC > 30 1. Blood loss 2. Increased plasma volume : Pregnancy, Overhydration 3. Hemolytic anemia : depend on each cause 4. Hypoplastic marrow : Aplastic anemia, RBC aplasia 5. Infiltrate BM : Leukemia, Multiple myeloma, Myelofibrosis, etc. 6. Abnormal endocrine : Hypothyroidism, Adrenal insufficiency, etc. 7. Kidney disease / Liver disease / Cirrhosis
  • 10. Hemolytic Anemia
  • 11. What is Hemolysis
    • - Premature destruction of dead cells.
    • - Causes hereditary and acquired disorders.
    • Hemolysis occurs at two sites:
  • 12. Intravascular
    • Hemolysis occurs within systemic circulation.
    • Hemoglobin is released into plasma.
    • Hemoglobin is lost through kidneys or catabolized in the liver.
  • 13. Extravascular
    • Trapping of red cells in spleen or liver sinuses.
    • Lyses of trapped red cells.
    • Release of lysed hemoglobin and catabolism within the sequestering organ.
  • 14. Classification of Hereditary Hemolytic Anemia
    • Based on side effect:
    • - Metabolic defect
    • - Membrane defect
    • - Hemoglobin defect
  • 15. A) Metabolic defect:
    • Defect in hexose monophosphate shunt: G-6-PD deficiency.
    • Defects of glycolysis; pyrovate kinase def., glucose phosphate isomerase def.
    • Defects in red cell nucleotide metabolism: pyramidine-5-nucleotidase def.
  • 16. B) Membrane defect:
    • Heriditary spherocytosis
    • Heriditary elliptocytosis
    • Hereditary pyropoikilocytosis
  • 17. C) Hemoglobin defect:
      • Thalassemias
      • Sickle cell anemia
      • Hemoglobin C disease
      • Hemoglobin E disease
      • Unstable hemoglobin
  • 18. Laboratory Findings
    • Chemistry
      • Hyperbilirubinemia, predominantly unconjugated bilirubin due to breakdown of heme ring by reticuloendothelial cells in the liver.
      • elevated LDH: released from destroyed cells.
      • Hemoglobinemia: free hemoglobin level increases in hemolysis esp. intravascular hemolysis: levels of 10-20 mg/dl gives plasma amber color and 50-100 gm/dl reddish color.
  • 19.
      • Hemoglobinuria: red-brown color of urine due to free hemoglobin and methamoglobin.
      • Decreased Heptaglobin level: it is a alpha-2-globin produced in the liver. It binds free hemoglobin thus level is reduced in hemolysis.
      • Hemosidrinuria: it reflects extensive hemolysis for a prolonged period of time. When hemoglobin is filtered by nephron, proximal tubular cells metabolize hemoglobin and iron accumulate in the cells. Cells then exfoliate in the urine and iron can be detected by Prussian blue reaction.
  • 20. Drug-Induced Acute Hemolysis
    • Drugs that have been linked to G6PD:
    • Primaquine (an antimalarial )
    • Sulphonamide antibiotics
    • Sulphones (e.g. dapsone , used against leprosy )
    • Other sulphur-containing drugs: glibenclamide (an anti-diabetic drug )
    • Nitrofurantoin (an antibiotic often used for urinary tract infections )
    • Vitamin K analogues
    • Several others
    • Henna can cause a hemolytic crisis in G6PD deficient infants
  • 21. Acquired hemolytic anaemia
  • 22. Immune haemolytic anaemias
    • Are caused by AB production by the body
    • against its own red cells.
    • Divided into  1) warm  37c
    • 2) cold  4 c
  • 23. Warm AIHA
    • IgG alone ,Bind at 37c
  • 24. Cold AIHA
    • Usually IgM
    • Bind to red cell at 4c
  • 25. Coombs Test Antiglobulin Test RBC Red cell with bound antibody to membrane antigen + Anti-immunoglobulin
  • 26. Coombs Test Antiglobulin Test RBC RBC Agglutination
  • 27. Non-Immune Hemolytic Anemias
    • Hemolytic anaemias due to mechanisms or agents
    • other than antibodies +/or complement e.g.:
    • Mechanical (traumatic)
    • Toxins
    • Infections
    • Splenomegaly (hypersplenism)
    • Burn (physical)
    • Renal failure and liver failure
    • Chemical
  • 28. Mechanical (Traumatic) (Fragmentation)
    • This is due to direct trauma (stress) to the RBCs causing fragmentation of the RBCs & intra-vascular hemolysis. The fragmented cells can be seen on peripheral blood smears & are called (schistocytes).
      • Due to:
          • Prosthetic valves
          • Patches
          • Valvular diseasse e.g., stenosis
    Cont…
  • 29. Mechanical (Traumatic) (Fragmentation) (cont…)
    • Microangiopathic: mechanical hemolysis due to contact between the RBCs & the abnormal intema of thrombosed, narrowed, necrotic small vessels or fibrin strand formation.
    • Caused by many diseases e.g., DIC (disseminated intravascular coagulation), malignant hypertension, disseminated malignancies especially mucin secreting adenocarcinomas, TTP (thrombocytopenic purpura), hemolytic uremic syndrome (HUS).
  • 30. THE END
    • THANK YOU