anemia by dr betelehem tefera


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anemia by dr betelehem tefera

  1. 1. AnemiaOutlineIntroductionClassificationApproach to anemic patientInvestigationsFe deficincy anemiaAnemia of chronic illnessMegaloblastic anemias (folate,Vb12)Aplastic anemia
  2. 2. Introduction• Definition - A reduction of the Hemoglobin concentration,or Hematocrite, to below normal levels.• The likelihood and severity of anemia are defined based on deviation of patients hgb or hct from values expected for age & sex matched normal.Sex normal (hct) anemia (hct/hgb)male 47 (± 7) % < 39 (13g/dl)
  3. 3. Pathophysiology• Erythropoiesis is the process of RBC production in the erythroid bone marrow under the influence of stromal network,cytokins ,EPO (erythroid specific growth factor or hormone)• Erythropietin (EPO) is a glycoprotein produced in the kidney in response to a sense of hypoxia.• Normal BM which is repleted by Fe, Folate and cobalamine will increase
  4. 4. Epidemology• Research done in gondar indicates prevalence of anemia in rural population of gondar to be 40.5% and was 4th leading cause of hospitalization & death in 1982.• 1987, in black lion it was the 3rd cause of hematolgic admissions.• Iron deficiency anemia is the commonest type globally and especially in developing country like ours,Ethiopia.
  5. 5. Çlassifiçation1. Pathophysiologiç  Hypoproliferative anemia  Maturation disorder  Anemia due to inçreased destruçtion/blood loss2. Morphologiç  Noromoçytiç normoçhromiç  Maçroçytiç  Miçroçytiç hypoçhromiç
  6. 6. Approaçh to a patient• Thorough history and P/E gives a çruçial information to the cause and severity of anemia.• Sxs depend on the rapidity of anemia devt,severity,age,presence of underlying ds....• Usually the body tries to çomensate mild anemias and chronic anemias by different mechanisms:
  7. 7. Çont’d – Increased cardiac output when tissue demand for oxygen increases, and decrease in PVR to increase perfusion of tissues. – Redistribusion of blood flow from less vital organs to vital organs. – Increased bone marrow in response to decrease in red cell mass.** But this compensatory mechanisms fail if
  8. 8. Symptoms of anemia• Non specific• Fatigue ,dizziness,palpitation,sweating,angina, exercise and cold intolerance,tinnitus,verigo, nausea,anorexia,bowel habit change .....• Sxs of underlying disease; wt loss,fever,gi bleeding bone pain etc• Neurologic –irritability,difficulity concentrating, tingling and
  9. 9. SignsHEENT- pale conjuctiva,atrophied and beefy tongue angular stomatitisLGS –lymphadenopathyCVS –tachycardia,wide pulse pressure,ejeçtion sys. murmur,signs of CHF
  10. 10. Signs çont’dGUS – bleeding..Skin and muçous membrane – pallor,peteçhea,içterus,spooning of finger nailsMSS –bone tendernessNeurologiç exam –sensory or motor abnormalitiesFundusçopy- retinal hemmorage
  11. 11. Investigations1 Complete blood count A RBC count • Hemoglobin • Hct • Reticulocyte count B Red cell indicis • Mcv (mean corpuscular volume) 80-100 fl normal < 80fl microcytic > 100fl macrocytic
  12. 12. Invgn cont’d • MCH( mean corpuscular hgb) 27 -36 pg • MCHC (mean corpuscular hgb concentration) 32- 36%The above two measures indicate defect in hgbsynthesis. C -WBC count D -Paletlate count E –morphology • size (anisocytosis) • shape (poikilocytosis) • hgb content
  13. 13. 2 Iron supply studies – Serum iron level – Total iron binding capacity – Serrum ferritin3 bone marrow exam ( aspiration,biopsy) – M:E ratio – Morphology – Iron stain (prussian stain) – Cellularity4 work up for underlying causes Eg tuberculosis,leishmaniasis,cancer, CRF,HIV .......
  14. 14. Iron deficiency anemia• Commonest cause of anemia.• Causes both hypoproliferative disorder (mild to moderate ) and ineffective erythropoiesis or maturation disorder ( severe deficiency).• Marrow only synthesizes hgb when there is adequate Fe available.• The only natural source of Fe is diet (1-1.4mg/d) absorbed in the duodenum and jejnum circulation bound to transferrin ( transport protein) enters to BM & in mitocondria,Fe is realeased and transf.returns back some part is used for heme synthesis and the rest is stored as ferritin (storage form)When the RBC dies the Fe recycles back.
  15. 15. Causes of Fe def. anemia1- Increased demand – Pregnancy – Infancy – Blood loss2- Increased loss Blood loss ( mensus,hookworm ,gi loss)3- Decreased intake and malabsorption iron in vegetables ( w/ch contain phytates,phosphate decrease abs.) but Fe in liver, meat is absorbed well.
  16. 16. stages of iron deficiency anemia1st negative iron balance **Demands exceed absorption,early phase – Ferritin starts to fall – BM stainability decreases – Serum iron (SI) normal – TIBC – normal – Transferrin saturation –normal2nd Fe deficient erythropoiesis - iron store is depleted
  17. 17. Stages cont’d – Serum iron level begin to fall – TIBC increases – Transferrin saturation falls (<20%) – Morphology may remain normal3rd Fe deficiency anemia – Microcytic hypochromic – Fall in hgb and hct – TS falls (<10-15%) – Poikiloanisocytosis – Ineffective erythropoisis
  18. 18. • Sxs of Fe deficiency are similar to the general sign & symptoms of anemia but :pica Cheilosis , Koilonychia may be specific for Fe def. A• Treatment- Severe anemia with heart failure (uncompensated ) should be rxed with blood transfusion.- Compensated anemia- Fe replacment- Oral or parentral preparations- Hgb will normalize by 6-8 wks- But to replace store, Rx should continue for 4- 6month.
  19. 19. Anemia of chronic illness• Includes – infection ( TB,HIV) – Inflammation (RA,Crhon’s ds) – Maliganancy – Cronic renal failure, liver disease• Impotant DDx of fe def anemia b/se effects are due to inadequate delivery of Fe to BM despite nl or increases iron stores.• Mzm of damage  Hepsidine – decrease Fe absorption and release from storage forms  IL-1 directly decreases EPO production  TNF & IFN gamma –suppress the response of Bm to EPO
  20. 20. Diagnosis• Usually anemia is mild to moderate• Serum iron- low• TS – low 15-20%• Ferritin –normal or increased• Marrow –hypocellular• Other comorbid conditions evidenced from HX,P/E and lab findings.
  21. 21. Treatment• Treatment of underlying factors• EPO supplementation for CRF• Transfusion.• Avoid iron supplementation.
  22. 22. Megaloblastic anemias• This are disorders caused by imapaired DNA synthesis which helps for cells to mature• Only cell division is affected so cytoplasmic maturation will not be affected so eventhough the marrow production is normal or increased but the cells get dystroyed easily (ineffective erythropoisis).
  23. 23. Causes of MBA.1. Vit. B12 deficiency2. Folic acid deficiency 26
  24. 24. Folate and Cobalamin Daily Requirements Diet Vitamin B12 (Cobalamin) FolateSource Animal products WidespreadBody stores 5 mg( liver) 5 mg(liver)Daily requirement 2-5 µg 50-200 µgAbsorption site ileum duodenum and proxymal jejinum
  25. 25. Causes of Folic acid deficiency1. Inadequate intake - diet ; chronic alcoholism, total parenteral nutrition2. Malabsorption - small bowel disease (sprue, celiac disease,) - alcoholism3. Increased requirements: - pregnancy and lactation - infancy - chronic hemolysis - malignancy - hemodialysis4. Defective utilisation Drugs:folate antagonists(methotrexate, trimethoprim, triamteren), purine analogs (azathioprine), primidine analogs (zidovudine), RNA reductase inhibitor (hydroxyurea), miscellaneous (phenytoin, N2) 28
  26. 26. Cobalamin (Vitamin B12) deficiencyFunction –cofactor for 2 enzymes Methionine Synthase and methylmalonyl coA mutase which are involved in many reactions,esp DNA metablism.Causes 1 nutritional- vegeterians 2 malabsorption (commonest) A -gastic causes – Achlorhydria – Pernicious anemia (commonest) – Congenital lack or abnormality of IF – Total or partial gasrectomy
  27. 27. Enteric Processing and absorption of Cobalamin Stomach Food-Cbl H+ Peptic digestion Cbl + R-binder R-Cbl Duodenum Pancreatic enzymes Cbl-TC complex IF + Cb R-Cbl OH - Cbl-IFDistal ileum IF receptor Cbl + TC Cbl-IF
  28. 28. Causes cont’dB intestinal causes – Ileal disease (crhon’s ds,tropical sprue) – Bacterial overgrowth ,diphlobotrium latum-- competes for VB12. – Past ileal resectionC Rare causes – Transcobalamin deficency – drugs
  29. 29. Pernicious Anemia• Most common cause of vitamin B12 deficiency• Occurs in all ages and ethnic backgrounds• Results from immunologic destruction of parietal cells in stomach( antrum) which produces IF,like in atrophic gastritis.• ~90 % patients show parietal cell antibody.• Schilling test helps to identify underlying cause of Vb12 deficincy.• 24 hr urine cobalamine excreted is measured,normally > 8% should be excreted,but if not,it may indicate Vb12 malabsorption.
  30. 30. Radiolabled cobalamin (orally) +unlabled cobalamin IM to saturatebody needs.(1)
  31. 31. C/f of VB12 & folateHematologic, Gi, neurologic ( only for VB 12 deficiency)Hematologic Anemia (macrocytic) May –leucopenia and thrombocytopenia Pts have symptoms of anemia, stms bleeding.GI b/se GI epithelial cells are rapidly proliferating cells. Pts may experiance symptoms of malabsorption like diarrihea. Sore ,beefy tongueNeurologic ( demylination and axonal degeneration) Sxs – Spinal cord or PNS arestesia or numbness,weakness,sphincter disturbance,reflexes depressed or increased ,position and vibration sense loss.
  32. 32. MEGALOBLASTIC ANEMIAS Diagnosis(1)1. Blood cell count:• macrocytic anemia ( MCV>100fl )• thrombocytopenia• leucopenia (granulocytopenia)• low reticulocyte count2. Blood smear:• macroovalocytosis , anisocytosis, poikilocytosis• hypersegmentation of granulocytes 35
  33. 33. MEGALOBLASTIC ANEMIAS Diagnosis(2)3. Laboratory features• indirect hyperbilirubinemia• elevation of lactate dehrogenase (LDH)• serum iron concentration- normal or increased4. Bone marrow smear• hypercellular• increased erythroid /myeloid ratio• erythroid cell changes (megaloblasts, RBC precursor a abnormally large with nuclear- cytoplasmic asynchrony)• myeloid cell changes (giant bands and metamyelocytes , hypertsegmentation)• megakariocytes are decreased and show abnormal morphology5 serum levels of folate and cobalamine should be measured. 37
  34. 34. Treatment of VB12 def. Anemia• Almost always malabsorption,so Rx should be parentral.• 1000µg IM weekly for 8wks followed by 1000µg once every month for life.• emperical treatment with folate may correct the anemia but if pt has neurologic manifestations,may even worse the condition.• Neurologic complications may fail to respond to Rx
  35. 35. RX of FOLIC ACID DEFICIENCY ANEMIA1. Oral administration of folic acid 1 to 5 mg per day, for 3 months, and maintance therapy if it’s necessary.2. Reticulocytosis after 5-7 days3. Correction of anemia is over after 1-2 months therapy 39
  36. 36. Aplastic Anemia• Inherited, but can be acquired from chemical exposure or radiation• Other causes- viral ( EBV,HIV,Heptitis,parvovirus B19 ), pregnancy• Failure of bone marrow to produce adequate amounts of RBCs, leukocytes, & platelets• Pancytopenia• Usually seen in young individual, median age 25 years
  37. 37. Aplastic Anemia, cont.• BM suppression, destruction or aplasia resulting in failure of BM to produce adequate no of stem cells• Biopsy – BM cellularity < 25%• If severe (ANC < 500/ul) & platelet < 20,000/ul and retic count < 60000/ul
  38. 38. Clinical manifestations• Fatigue • Epistaxis• Dyspnea • Purpura • Petechiae• Multipel infections (late) • Ecchymosis•  temperature (late) • Pallor• Headache • Palpitations• Weakness • Tachycardia• Anorexia • Tachypnea• Gingivitis • Melena
  39. 39. Diagnostic Tests• degeneration with Prepheral blood smear - pancytopenia• BM biopsy- fatty few or no stem cells. Treatment• Stem cell transplantation• Bm transplant• Blood transfusion• Without treatment – rapid deterioration & death.
  40. 40. • There are also other many causes of anemia including hemolytic anemias (intravascular &extra-avascular),blood loss,mylofibrosis, myelophythias (infiltrative ds by tumor,infection), MDS.• Presentation of almost all forms of anemia are similar.• Transfusion is indicated for patients with decompensated anemia.
  41. 41. thankyou!
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