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  • 1. INTRODUCTION Name : Rabia Manzoor Roll No: 04 Topic: ANEMIADepartment Of Eastern Medicine & Surgery Faculty of Medical & Health Sciences University of Poonch Rawalakot Aj&K
  • 2. What is ANEMIA?Anemia is present when there is decreased LevelofHb in blood below the reference levelFor age ,sex and individuals
  • 3. Classification of ANEMIA Types of classification. 1. According to cause 2. According to morpholology Cause: 1. Blood loss 2. Increase of red cell destruction 3. Decrease of red cell production
  • 4. Morphological classification According to shape and size1. Hypo chromic microcytic with low MCV2. Norm chromic normacytie with normal MCV3. Macrocytic with high MCV
  • 5. S/S of Anemia1. Pallor2. Tachycardia3. Breathlessness4. Head ache5. Fatigue6. faintness
  • 6. Microcytic anemiaRBCS become smallMCV<80Causes of microcytic anemia•Iron low to iron deficiency Anemia•Iron normal to sedroblastic and Thalasemia
  • 7. Iron deficiency anemiaIron deficiency is the most common cause of anemiain world.iron deficiency anemia is defined as when there isInadequateAmount of iron for HB synthesis.
  • 8. Daily Requirement. 2 to 4 gmSource of iron.Meat, Egg, Vegetables, Milk , Spinach.Storage of iron•Liver 50 to 60 percent•Muscles 20 percent•Bone marrow•Plasma
  • 9. Etiology of iron deficiency1. Dietary deficiency2. .Increase in iron demand3. Malobsorption of iron4. Acute and chronic blood loss
  • 10. Pathology•Iron absorbed in intestine iron intake through diet to stomach towhere gastric secretion made complex with vitamin c and enter inintestine where it combine with apotransferin and foam transferringand then enter in circulation. In normal person this transferring inabout 33 percent saturated with iron.•When iron in excessive amount :•Lost in feces because transferring is already saturated.•When there is iron deficiency this saturation decreases andtransferring accept more iron to iron balance. Excessive iron storedin liver , spleen, bone marrow, skeletal muscles here it combine withprotein called apoferitin and foam ferretin storage iron.•In iron deficiency initially depletion of stored iron. There follows adecreased in circulating iron with low level of serum iron and rise inserum transferring iron binding capacity.
  • 11. •S/S OF IRON DEFICIENCYANEMIA•Pallor•Lethargy•Fatigue•Kolinchyia•Dysnea•Numbness•Joint pain•Vomiting•Body ache
  • 12. InvestigationBlood pictureBone marrow study
  • 13. Sedroblastic AnemiaIt is an inherited or acquired disorder characterized bydyserthropoesis inability of iron utilization and thereforeiron overload . There is a disordered accumulation ofiron in erythroblast because it can not be utilized due todefect in enzymes involve in heam synthesis.
  • 14. Diagnosis: Microcytic cellsBone marrow show erythroblast with ring ofiron granules around. The nucleus ringsidreoblasts.
  • 15. ThalasemiaIt is genetic disorder of hb synthesis characterized bydecreased synthesis of goblin chain .Two alpha and 2 b chain of globins polypeptidecombine with heam to foam HB therefore if synthesisof globins is reduced it will lead to decreased HB toanemia.
  • 16. Types1.Alpha2.Beta
  • 17. AlphaIt occurs due to reduction or absence of alpha chainsynthesis .There are four alpha gene1.If one is deleted there is no clinical effect.2.If two are deleted there is mild Hypochromic anemia.3.If three are deleted pt has hb (hbh). It has functionallyunless →moderate anemia and spleenomegaly.4.If four r deleted the baby is still born.
  • 18. BetaThis occur due to reduction or absencesof alpha chain synthesis.In normal (homozygote) both polypeptidegenes are normal and produce normal Bpolypeptide chain in normal quantity.In abnormal both B chain are abnormaland do not produce B polypeptide chain→B Thalasemia major
  • 19. B Thalasemia intermediateElectrophoresis which shows reduced HBA while HBA2and F elevated (asymptomatic + moderate anemia)
  • 20. Minors.In heterozygote to one gene is normal and other isabnormal which does not produced B polypeptidechain . In this person normal gene produce enoughB chain to maintain HB level about to maintain.This Thalasemia is asymptomatic and oftendetected when iron therapy for mild microcyticHypo chromic anemia fails,.
  • 21. Macrocytic Anemia]1.Megloblastic anemia√.vita B12 deficiency√folic acid deficiency
  • 22. Megloblastic anemiaIn this type of anemia RBC became enlarged and odd shape.CausesVit B12 deficiencyFolic acid deficiency
  • 23. Vit b12 deficiencyThis is type of anemia in which there is atrophy of gastric mucosa so failure of intrinsic factor production so Vit b12 not absorbed.Causes
  • 24. PathogenesisTissue perforation need DNA.DNA need VIT 12 and folic acid--- deficiency of both—DNA not formed— cell division stop.While cytoplasm progressive continuously — RNAincrease in amount — erthroyid tend to destroy marrow—RBC—↓↓
  • 25. s/s•Pallor•Dysnea•Vibration sense loss•Neurological disorder•Tachycardia
  • 26. InvestigationBlood c/pBone marrowLow serum Vit. B12
  • 27. Folic acidCauses:Decrease diet inakeIncrease demandMal absorptionInvestigationLow serum folic acidMacrocytic Blood cpResultFolic and supplement 5mg readyMaintence dose 5mg/wk.
  • 28. NORMOCYTIC ANEMIACAUSES•Chronic disease•Acute blood loss•Blood disorder
  • 29. CHRONIC DISEASE PathogenesisFailure of transport of storage ironfrom bone marrow to plasma developingErythrocytes→ decrease HB and cause anemia.
  • 30. Investigation Increase iron in bone marrow. Increase serum iron level. Increase ferretin level.
  • 31.  Anemia due to acute blood loss ? Blood disorder A plastic Anemia. Hemolytic Anemia.
  • 32. A plastic Anemia ?C/FAnemiaInfectionBleedingInvestigationsBlood PictureBone marrow biopsy
  • 33. Hemolytic Anemia ?MechanismCell Membrane abnormalityAbnormal HBAbnormality of nasal wallsInherited Hemolytic AnemiaHereditary spherocytosisSickle cell AnemiaThalassaemia
  • 34. Hereditary spherotosis? Pathogenesis? C/F Anemia Jaundice Spleenomegely A plastic crises Gallstone Leg cancer
  • 35. Sickle cell disease There is presence of abnormal HBS which upon low oxygen tension become crystal giving shape Rbcs as sickle and not passes through capillaries and destruct
  • 36. Pathogenesis? C/F AnemiaTissue infraction
  • 37. Investigations Hb descreasedsickles erythrocytes