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anemia final ppt .pptx
- 1. Dr Dujana KadeejaAshraf APPROACH TO ANEMIA
- 2. Definition • Defined asa decrease in circulating red blood cell mass- Hb less than 12g/dl or Hct <36% for non pregnant women and Hb< 13g/dl or Hct <39% in men • Anemia is basically an objective sign of disease and needs further evaluation to determine the underlying cause and appropriate treatment.
- 3.
- 4. ERYTHROPOIETIN • Glycoprotein hormone •Produced by peri tubular capillary lining of cells in kidney • Small amount by liver • EPO gene regulation is done by HIF 1alpha
- 5. RETICULOCYTES • They areprematurely released RBCs from the bone marrow • Appear in circulation due to EPO stimulation or bone marrow damage(fibrosis, infiltration by malignant cells) • Appear greyish blue due to residual ribosomal RNA • Reticulocyte count - 1-2 %
- 6. CORRECTION • RC% =(No. of reticulocytes/RBC) X 100 • First correction - CRC • CRC = (Hb/15) x RC OR (Hct/45)x RC • This is done to correct reticulocyte count based on the reduced number of RBCs
- 7. Second correction • Thisis done if there are polychromatophilic macrocytes • They are known as shift cells - prematurely released reticulocytes • CRC/2 (correction factor can be 1-3) • This is known as reticulocyte production index (RPI)
- 8. CLASSIFICATION • ETIOLOGICAL- • Bloodloss - acute and chronic • Decreased RBC production • Increased RBC destruction (Hemolysis) • MORPHOLOGICAL • Microcytic when MCV is less than 80fl • Normocytic-MCV IS 80-96 fl • Macrocytic - MCV more than 96fl 8
- 9. EVALUATION • HISTORY • PHYSICALEXAMINATION • LABORATORY INVESTIGATIONS
- 10. HISTORY • Acute -Patientwith abrupt onset of anemia tolerate diminished RBC mass poorly.Experience symptoms of fatigue, malaise, dyspnea, syncope angina • Chronic anemia are usually less symptomatic.Experience symptoms with increased activity or exertion. • CVS AND PULMONARY FEATURES- • Exertional fatigue, • dizziness, palpitations • Angina • Symptoms of cardiac failure
- 11. • GI FEATURES •occult bleeding (Malena) • PICA (consumption of substances of no nutritional value like ice, clay) • Dysphagia in pernicious anemia
- 12. • CNS FEATURES •Peripheral neuropathy,paresthesia,seizures (Vit B12 def ) • confusion • dementia • Restless leg syndrome (IDA)
- 13. • OBSTETRIC ANDMENSTRUAL HISTORY- symptoms of menorrhagia • PAST HISTORY- GI surgery ,gastric atrophy, renal disease,rheumatologic disease, history of blood transfusion • Hookworm infection • FAMILY HISTORY - hemoglobinopathies • DRUG INTAKE - • DIETARY INTAKE- vegetarian/non vegetarian,PICA • Symptoms suggestive of other cytopenias like bruising,recurrent infections
- 14. PHYSICAL EXAMINATION • Vitals- PR and BP • HEAD TO FOOT EXAMINATION • Pallor- Is examined at lower palpebral conjunctiva, palms, tongue, mucous membrane of mouth, Nail bed skin • scleral icterus- haemolytic anemia • Glossitis - pernicious anemia • lymphadenopathy • Sternal tenderness
- 15. • Koilonychia -iron defieciency anemia • Petechia in skin- suggests of bone marrow failure or anemia due to bleeding disorde • Chronic leg ulcers- sickle cell anaemia, hereditary spherocytosis • THALASSEMIA FEATURES
- 17. • knuckle hyperpigmentation- •CVS • signs of congestive cardiac failure • flow murmur • RESPIRATORY SYSTEM • Wheeze in acute chest syndrome • PAH due to vascular occlusion in sickle cell anaemia
- 18. • CNS • Ataxia •decreased vibratory and position sense • GIT • Splenomegaly- extra medullary hematopoiesis
- 21. MICROCYTIC ANEMIA CLASSIFICATION • IRONDEFICIENCY ANEMIA • DISORDERS OF GLOBIN SYNTHESIS- THALASSEMIAS • SIDEROBLASTIC ANEMIAS • ANEMIA OF CHRONIC DISEASE
- 22. IRON DEFICIENCY ANEMIA •Mcc of anemia • usually chronic with a low reticulocyte count • causes-1.Increased iron loss -GI loss, menses, hookworm infection, • 2. decreased iron intake or absorption - bariatric surgery, gastrectomy, crohn’s disease, celiac disease • 3. increased iron requirement - pregnancy, rapid growth in infancy or adolescence • 4.Drugs - glucocorticoids,NSAIDs,proton pump inhibitors
- 23. STAGES 1. NEGATIVE IRONBALANCE 2. IRON DEFICIENT ERYTHROPOIESIS 3. IRON DEFICIENCY ANEMIA
- 24. LAB • S Feand TIBC • S Ferritin low • Bone marrow iron stores • Red cell protoporphyrin levels • S levels of transferrin receptor protein
- 26. • DIAGNOSTIC TESTS •Bone marrow biopsy shows absent staining to iron is the definitive test to diagnose • ID IS NOT THE FINAL DIAGNOSIS, IT IS INDICATIVE OF AN UNDERLYING ETIOLOGY
- 27. TREATMENT • Oral irontherapy - • ferrous sulphate is the most common prescribed formulation • Dosage - 100-200mg of elemental iron per day (50mg/day) • with normal bone marrow and normal EPO stimulus this results in RBC production of • 2-3 times of normal • Goal of treatment is to correct anemia +0.5-1g for stores • Duration is 6-12 months
- 28. • Reticulocyte responsebegins in 4-7 days • Reticulocyte response peeks in 1-1.5 weeks • Increase in Hb 14-21 days • Normal iron stores 4-5 months • Absence of response – rule out compliance , absorption issues
- 29. • Parenteral irontherapy - • Indications- • Inadequate response to oral iron • poor absorption • intolerance to oral preparation • Need for rapid response • Persistant bleeding • GI causes- bariatric surgery,celiac sprue • Organ dysfunction - CKD,
- 30. • Total ironrequirement- • MODIFIED GANZONI FORMULA- weight x (15-hb) x 2.4+ 500 • IV PREPARATIONS • First generation- iron dextran • Second generation - iron sucrose, ferric gluconate • Third - ferumoxytol,ferric carboy maltose, iron isomaltoside
- 31. • RED CELLTRANSFUSION • Indications • severe anemia with hemodynamic instability • excessive blood loss which needs an immediate intervention • ADVANTAGES • can correct anemia acutely • transfused RBC provide a source of iron for reutilisation
- 32.
- 33. THALASSEMIA • Inherited disorderscharacterised by reduced Hgb synthesis associated with mutations in either alpha or beta gene of molecule • BETA THALASSEMIA - decreased production of beta globin chain that results in excess alpha globin chain synthesis forming insoluble alpha tetramers which leads to ineffective erythropoiesis • ALPHA THALASSEMIA - Due to deletion of one or more alpha globin chains leading to beta globin excess
- 34. • DIAGNOSIS • Peripheralsmear - microcytic hypochromic RBCs with target cells, tear drop cells (s/o extra medullary heamtopoiesis) • DIAGNOSTIC -Hgb electrophoresis ( increased percentage of Hgb A2 and HgbF ) • For alpha thalassemia - alpha globin gene analysis
- 35. • TREATMENT • Insevere forms of the disease- RBC transfusions done to maintain an Hb level o • coupled with oral iron chelation to prevent accumulation of iron • Repeated transfusions can lead to iron overload • Iron chelation therapy is indicated when ferritin is consistently >1000 ng/ml oral - deferasirox,deferiprone IV- deferoxamine • Hydroxyurea - to increase HgbF
- 36. • To improveineffective erythropoiesis - Luspatercept (enhances late stage erythropoiesis) given s/c 1mg/kg every 3 weeks
- 37. MENTZER INDEX • MCV/RBC<13 is seen in thalassemia
- 38. SIDEROBLASTIC ANEMIA • Characterisedby abnormal iron metabolism associated with the presence of ring sideroblasts in the developing RBCs • ETIOLOGY • ACQUIRED • Primary sideroblastic anemia (MDS) • Secondary sideroblastic anemia is caused by • drugs like chloramphenicol,cycloserine,ethanol,isoniazid, • lead and zinc toxicity • HEREDITARY • X linked-ALA synthetase deficiency
- 39. • Fe profile- all increases except TIBC • Peripheral smear - Papenheimer bodies- siderocyte stained with ramonowsky stain due to non heme iron deposition • Marrow iron stores increase Investigations
- 41. Treatment • No definitivetreatment • Pyridoxine - INH induced
- 42. ANEMIA OF CHRONICDISEASE
- 43. • CHRONIC INFECTIONSMALIGNANT DISEASES • Pulmonary infections-abscesses,TB,pneumonia carcinomas • SABE hodgkin disease , NHL • Pelvic inflammatory diseases Leukemia • osteomyelitis • chronic urinary tract infections • meningitis • INFLAMMATIONS • Rheumatoid arthritis • SLE • Severe trauma
- 44. MACROCYTIC ANEMIA • Groupof disorders characterised by presence of distinctive morphological appearances of developing red cells in bone marrow. • Can be 1. Megaloblastic - nuclear maturation defect 2. Non megaloblastic - nuclear maturation normal
- 45. • MEGALOBLASTIC NONMEGALOBLASTIC • Nuclear maturation defect Normal • CAUSES • VIT B12 deficiency- chronic liver disease • Pernicious anemia, thyroid diseases • nutritional deficiency drugs • Folate deficiency - dietary,antifolates • Folate deficiency- mcc is dietary deficiency,
- 47. Thiamine responsive megaloblasticanemia • Triad of megaloblastic anemia with ringed sideroblast+DM+SNHL
- 48. DIAGNOSIS • MCV high •Earliest PS finding is macro ovalocyte • PS- anisocytosis,poikilocytosis • hypersegmented neutrophil (>5 lobes) • leucopenia due to decrease in granulocyte and lymphocyte • BONE MARROW - hypercellular with accumulation of primitive cells • megaloblasts • giant band forms • enlarged hyperploid megakaryocyte are characteristic
- 50. TESTS FOR COBALAMINAND FOLATE
- 51. COBALAMIN DEFICIENCY 1. S.cobalamin- normal range -148-738pmol/l 2. S MMA - used for early diagnosis of cobalamin deficiency 3. S Homocysteine -high in both early cobalamin and folate deficiency
- 52. FOLATE DEFICIENCY • Sfolate - 11-82 nmol/l • Rises in severe cobalamin deficiency
- 53. TREATMENT OF B12AND FOLATE DEFICIENCY • B12 for replenishing stores - 1000mcg IM inj at 3-7 day interval for 8 weeks. • Maintenance dose - 1000mcg IM monthly • oral doses 50mcg daily • Folate - 5 to 15 mg FA daily at least 4 months till all folate deficient cells are replaced • Folinic acid - mtx/DHF reductase inhibitors
- 54. In megaloblastic anemia,when only FA is corrected, • Anemia is corrected due to tetrahydrofolate formation from FA . • Neurological manifestations worsen as methionine is not formed ( methyl B12 absent)
- 55. HEMOLYTIC ANEMIA • Thereis premature destruction of RBC so to compensate there is increase in production capacity of RBCs by bone marrow • When the rate of production exceeds the bone marrow capacity of producing more will manifest as haemolytic anemia
- 56. CLASSIFICATION • Inherited/Acquired • Acute/Chronic •Intravascular/Extravascular • Intracorpuscular/Extracorpuscular
- 57.
- 60. LABORATORY SIGNS OFHEMOLYSIS • Increased indirect bilirubin • increased serum LDH • Decreased serum haptoglobin • hemoglobinemia • hemoglobinuria • Metheamoglobinemia • reticulocytosis
- 61. • PERIPHERAL SMEAR •Polychromatophilia,nuceated RBCs • basophilic stippling • B.M aspirate - erythroid hyperplasia
- 62.
- 63. REFERANCES • Harrisons principles •Washington manual of medical therapeutics