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Anemia
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- 3. Specific Learning Objectives Atthe end of the class, the student should be able to Define anemia Discuss the classification of anemia Enumerate the blood cell indices Discuss the cause, morphological features and treatment of various forms of anemia Explain the effects of anemia Explain the basis of physiological anemia of pregnancy
- 4. Definition Qualitative or quantitativereduction in RBC count or Hemoglobin levels or both resulting in decrease in oxygen carrying capacity of blood Normal – Males 14 to 16 g/dL Females 12 to 14 g/dL
- 5. Clinical features Fatigue,Tiredeness Breathlessness Lethargy,headache Pallor of skin and mucous membranes Palpitations Menstrual disturbances Reduction in BMR
- 6. Investigations Hb RBCcount Blood indices Peripheral Blood smear Serum Iron, Ferritin, Vitamin B12 and folate levels Plasma Electrophoresis
- 7. Classification of anemia Morphological - according to the shape and amount of Hb Etiological – according to the cause of anemia
- 8. Morphological: 1. Normocyticnormochromic •Hemolytic anemias •After blood loss •Aplastic anemia 2. Microcytic hypochromic •Iron deficiency anemia •Thalassemia 3. Macrocytic normochromic •Megaloblastic anemia •Folic acid deficiency
- 9. Etiological: 1. DecreasedRBC production •Iron deficiency anemia •Pernicious anemia •Folic acid deficiency •Aplastic anemia •Chronic Renal failure •Myelofibrosis 2. Increased RBC destruction •Intracorpuscular --Hemolytic anemias •Extracorpuscular – Splenomegaly, snake venoms, Rh incompatibility 3. Excessive blood loss •Acute – sudden heavy loss •Chronic – menstrual loss, GI bleeding
- 10. Blood indices Indices FormulaNormal vaule Mean Corpuscular Volume – average volume of a single RBC 80 to 100 fL Mean Corpuscular Hemoglobin- amount of Hb in a single RBC 26 to 32 pg Mean Corpuscular Hemoglobin Concentration – concentration of Hb in a packed volume of RBCs 32 to 36 %
- 11. IRON deficiency anemia •Inadequate iron intake • Hookworm infestation (children) • Heavy menstrual loss • Bleeding Hemorrhoids (piles) • Peptic ulcer bleed
- 12. IRON deficiency anemia– microcytic hypochromic, central pallor MCV, MCH reduced MCHC reduced
- 15. Treatment Oral FeSO4tablets Parenteral iron therapy Blood transfusion
- 16. Response to treatment Reticulocytes – 0.5 to 1.5 %
- 17. Megaloblastic anemia • Defof B12, FA, IF • nutritional • Gastric atrophy, gastrectomy • tropical sprue malsbsortption • Sources of B12 –milk, meat, liver of animals • Sources of FA – leafy veg, pulses, liver
- 19. Methylene Tetrahydrofolateis essential for formation of DNA Formation of this requires vitamin B12 as a cofactor Hence deficiency of B12 or Folic acid both causes defect in formation and maturation of DNA • Slow reproduction of RBCs • Red cells too large with odd shapes with friable membranes Formation of megaloblasts
- 20. MCV, MCH increased MCHCnormal
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- 22. Pernicious anemia Intrinsicfactor from the parietal cells of stomach is essential for absorption of vitamin B12 from the ileum Hence IF deficiency causes Vit B12 malabsorption and megaloblastic anemia
- 23. Megaloblastic anemia Clinicalfeatures: Fatigue, breathlessness Soreness of tongue Glossitis, angular stomatitis Tingling of hands and feet due to peripheral neuropathy Severe Subacute Combined Degeneration of Spinal cord (SACD) • Treatment – • FA tabs • Vit B12 injections
- 24. Please note… Folatedeficiency during pregnancy is associated with Neural tube defects in babies Hence Folate supplementation before and during pregnancy is mandatory along with iron tablets
- 25. Aplastic anemia • X-rays •drugs • Gamma radiations from nuclear bombs • chemicals from industries Treatment: •Antithymocyte globulin • BM transplant Microcytic hypochromic
- 26. Sickle cell anemia Valine is present instead of glutamic acid in the 6th position of beta chain – HbS • HbS – heterozygous – only half of Hb is abnormal -- homozygous – all are abnormal hbs • In deoxygenated state, HbS tends to polymerize, forms sickle shaped cells, hemolyze and blocks blood vessels • Treatment • HbF – decreases polymerization • Hydroxyurea – increases HbF synthesis • Severe – bone marrow transplantation
- 29. Thalassemia Defect inthe regulatory portion of globin chain • α Thalassemia – rare β Thalassemia Major – complete absence of β chain - minor – reduced synthesis of β chain Compensatory increase in HbA2 and HbF Microcytic hypochromic anemia Failure to thrive • Treatment: • blood transfusion • Splenectomy • BM transplantation
- 30. Hereditary spherocytosis •Mutation inspectrin, the transmembrane protein which maintains the shape of the RBC cell membrane •And the linker protein, ankyrin •Spherocytes, trapped and hemolyze in spleen •Treatment : splenectomy
- 31. G6PDH deficiency • G6PDHis required for generation of NADPH which maintains RBC fragility • NADPH maintains Glutathione in reduced state • Def of G6PD leads to def of NADPH • RBC becomes more friable • Hemolysis • Especially when exposed to drugs and toxins, infections like malaria
- 32. Anemia of chronicdisease Chronic renal failure Normocytic normochromic anemia Treat the cause Erythropoeitin therapy
- 33. Severe anemia leadsto cardiac failure • Normal viscosity of blood -- 3 times that of waterr • In anemia - falls to 1.5 times that of water • Decrease in peripheral resistance increase in cardiac output • And also ,hypoxia induced peripheral vasodilation increases cardiac output • Increase in cardiac output maintains enough oxygenation of tissues • However it also increases cardiac workload • During exercise, the compensation cannot be done , hence leads to heart failure
Editor's Notes
- #12 Treatment: oral iron FeSO4 300 mg tid
- #17 The rate of erythropoiesis is measured by a reticulocyte count. Normally, a little less than 1% of the oldest RBCs are replaced by newcomer reticulocytes on any given day. It then takes 1 to 2 days for the reticulocytes to lose the last vestiges of endoplasmic reticulum and become mature RBCs. Thus, reticulocytes account for about 0.5–1.5% of all RBCs in a normal blood sample. A low “retic” count in a person who is anemic might indicate a shortage of erythropoietin or an inability of the red bone marrow to respond to EPO, perhaps because of a nutritional deficiency or leukemia. A high “retic” count might indicate a good red bone marrow response to previous blood loss or to iron therapy in someone who had been iron-deficient. It could also point to illegal use of epoetin alfa by an athlete. •
- #18 Def of B12, FA, IF Slow reproduction of RBCs Red cells too large with odd shapes with friable membranes Gastric atrophy, gastrectomy tropical sprue malsbsortption
- #23 Treatment – FA tabs 1 mg qd Vit B12 inj – 100 micro g im qd for 7 days
- #26 X-rays, drugs,nuclear bombs with gamma rad, chemicals from industries, HARRISON: Treatment: Antithymocyte globulin, BM transplant
- #27 Valine is present instead of glutamic acid in the 6th position of beta chain – HbS HbC—lysine HbE – lysine but in 26th position HbS – heterozygous – only half of Hb is abnormal -- homozygous – all are abnormal hbs In deoxygenated state, HbS tends to polymerize, forms sickle shaped cells, hemolyze and blocks blood vessels Treatment HbF – decreases polymerization Hydroxyurea – increases HbF synthesis Severe – bone marrow transplantation
- #30 Defect in the regulatory portion of globin chain Alpha and beta Major and minor respectively TreATMENT: blood transfusion Splenectomy BM transplantation
- #31 GANONG: Or congenital hemolytic icterus Mutation in spectrin, the transmembrane protein which maintains the shape of the RBC cell membrane And the linker protein, ankyrin Spherocytes, trapped and hemolyze in spleen Treatment : splenectomy
- #32 GANONG: G6pd required for oxdn of glu via HMP pathway This generates NADPH which maintains RBC fragility Def of G6PD leads to def of NADPH RBC becomes more friable Hemolysis Esp when exposed to drugs and toxins
- #33 Treatment Treat cause Erythropoeitin
- #34 Normal viscosity of blood -- 3 times that of waterr In anemia - falls to 1.5 times that of water Decrease in peripheral resistance increase in cardiac output And also due to hypoxia induced peripheral vasodilation increases cardiac output Increase in cardiac output maintains enough oxygenation of tissues However it also increases cardiac workload During exercise, the compensation cannot be done , hence leads to heart failure