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approach to anemia.pptx
- 1. APPROACH TO ANEMIA Guidedby Dr SHIDRAM K sir Presented by -Dr Gadeppa
- 2. Definition of Anemia Anemia– The World Health Organisation defines anemia as a hemoglobin level <13gm/dl in men and <12 gm/dlin women.
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- 4. Erythron • • Erythron is themachinery of RBC production EPO, IL, Growth factors, Cytokines – stimulate it • Hypoxia is strong stimulus for the Erythron • Its functioning is influenced by 1. Normal renal production of EPO 2. A functioning Erythroid marrow 3. An adequate supply of substrates for Hb production
- 6. ERYTHROPOIETIN • Glycoprotein hormone •Produced by peritubular capillary lining of cells in kidney • Small amount in liver • EPO gene regulation is by Hypoxia inducible factor 1α • Normal levels 10 – 25 U/l • T1/2 – 6-9 hrs
- 7. Normal Red Cells Nonucleus,Enzymepackets Biconcavediscs–Haem+Gl Center1/3pallor Pinkcytoplasm(Hbfilled) Cellsize7- 8µm
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- 10. EVALUATION- HISTORY • Age/Sex •Rate of onset - Rapid/Slow • Blood loss - Haematemesis/malena/bleeding piles/menorrhagia/ metorrhagia/epistaxis/hematuria /haemoptysis • Abdomen - Appetitie/weight loss/dysphagia/regurgitation/dyspepsia/ abd pain/diarrhoea/constipation/jaundice/soreness of tongue/previous abd surgeries • Reproductive - Menstrual history in detail/number & interval between pregnancies/miscarriages • Urinary system - Nocturnal polyuria • CNS-Parasthesiae / difficulty in walking
- 11. EVALUATION- HISTORY • Bleedingtendency - Easy bruising / prolonged bleeding after trivial injuries/bleeding from more than one site • Skeletal system - Bone pain / Arthritis / Arthralgia • Temperature - Fever / Night sweats • Drug ingestion - Previuos / current • Occupation - Metal dusts / solvent fumes / lead • Diet • Social history – Alcoholism • Past H/o-Previous anaemia: diag & Rx, response to Rx • Family H/o-Anaemia / recurrent jaundice / IUD & childhood deaths
- 12. EVALUATION - EXAMINATION: •Skin - Colour, texture, petechiae, ecchymoses, scratch marks. • Nails - Brittleness, longitudinal ridging, koilonychia • Conjunctiva/Sclera - Pallor, icterus, haemorrhages • Retina - Haemorrhages, s/o HTN/renal failure, other changes • Mouth - Mucous membrane: Pallor, petechiae • Gums: Bleeding, hypertrophy • Tongue: Redness, atrophy of papillae • Abdomen - HSM, either HM or SM, tenderness, mass, ascites • CVS-BP, valvular, vascular prosthesis • CNS- Peripheral neuritis, s/s/o SADSC
- 13. EVALUATION - EXAMINATION: •Supf LN- Enlargement of cervical, axillary, inguinal, epitrochlear nodes • Bones - Tenderness (esp. of sternum), tumour • Legs - Ulcers / scars of healed ulcers • P/R-Haemorrhoids / CA Rectum • Pelvic - Menorrhagia, metorrhagia, uterus, cervix
- 14. WORK UP FORANEMIA
- 15. The Three BasicMeasures Measurement Normal Range A. RBC count 5 million 4 to 6 B. Hemoglobin 15 g% 12 to 17 C. Hematocrit 45 38 to 50
- 16. The Three DerivedIndicies Measurement A. RBC count Normal 5 million Range 4 to 6 B. Hemoglobin 15 g% 12 to 17 C. Hematocrit 45 38 to 50 MCV C ÷ A x 10 = 90 fl MCH B ÷ A x 10 = 30 pg MCHC B ÷ C x 100 = 33%
- 17. RETICULOCYTE COUNT % •Reticulocytes are immature RBC • ‘RBC to be’ or Apprentice RBC • Fragments of nuclear material • RNA strands which stain blue • Normal Less than 2%
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- 19. Reticulocyte correction • Correction1 - in presence of anemia, reticulocyte count spuriously elevated when it is related to reduced number of RBCs in anemic patient. (relatively more in number due to reduced mature RBC) • Correction 2 - An additional correction needs to be made because reticulocytes released under intense EPO stimulation remain in the peripheral blood for more than usual 1 day (prematurely released Reticulocyte remains longer in circulation) Reticulocyte count %of reticulocytes in RBC population Corrected reticulocyte count %reticulocytes ×(patient Hct/45) Reticulocyte production index Corrected reticulocyte count ÷ maturation time in peripheral blood in days Absolute reticulocyte count %reticulocytes ×RBC count/L
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- 21. Red cell distributionwidth • RDW measures range of variation of red cell volume • Normal range is 11.5 to 14.5 % • It is measure of anisocytosis • Usually elevated in deficiency of Iron, Folate, B12 • Usually normal in Hemoglobinopathy
- 22. RBC Size –Anisocytosis Different sizes of RBC
- 23. MENTZERS INDEX • MCV/RBC •>13 - S/O IRON DEFICIENCY ANEMIA • 11-13 - INDETERMINATE • <11 - THALASSEMIA TRAIT
- 24. Peripheral Smear Study •Are all RBC of the same size ? • Are all RBC of the same normal discoid shape ? • How is the colour (Hb content) saturation ? • Are all the RBC of same colour/ multi coloured ? • Are there any RBC inclusions ? • Are intra RBC there any hemo-parasites ? • Are leucocytes normal in number and D.C ? • Is platelet distribution adequate ?
- 25. Cell size Hb content Anisocytosis Poikilocytosis Polychromasia Givesclues to specific disorders Normal peripheral smear
- 26. Severe Iron defeciency anemia Anisocytosis(size), Poikilocytosis (shape) Macrocytosis Macrocytes, Ovalocytes Myelofibrosis Tear drop shaped cells, nucleated cells Thallassemia Target cells
- 27. Howell-Jolly bodies Red cellfragmentation Uremia Spur cells
- 28. Target Cells 1. LiverDisease 2. Thalassemia 3. HbDDisease 4. Post splenectomy
- 29. Shistocytes Fragmented, Helmet ortriangle shaped RBC 1. MAHA 2. Prosthetic valves 3. Uremia 4. Malignant HT
- 30. Tear Drop Cells 1.Myelofibosis 2. Infiltration of BM 3. Tumours of BM 4. Thalassemia
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- 35. Mean Cell Volume(MCV) measured by M and RDW Microcytic < 80 fl MCV Normocytic CV Macrocytic 80 -100 fl > 100 fl < 6.5 µ 6.5 - 9 µ > 9 µ
- 36. Anaemia Workup -MCV Microcytic MCV Normocytic Macrocytic IronDeficiency IDA Chronic Infections Thalassemias Hemoglobinopathies SideroblasticAnemia Chronic disease Early IDA Hemoglobinopathies Combined deficiencies Increaseddestruction Megaloblastic anemias Liver disease/alcohol Hemoglobinopathies Marrowdisorders Increaseddestruction
- 37. Hypoproliferative Anaemias Failureofcell maturation Nuclear breakdown Cytoplasmi c breakdown MegaloblasticAnaemia DefectiveDNAsynthesis FolateorB12 deficiencyHaemdefect Globindefect Thalassemia SicklecellA Fe Phorph IDA, SA
- 38. IDA – SpecialTests Iron related tests Normal IDA Serum Ferritin (pmo/L) 33-270 < 33 TIBC (µg/dL) 300-340 > 400 Serum Iron (µg/dL) 50-150 < 30 Saturation % 30-50 < 10 Bone marrow Iron ++ Absent
- 39. Microcytic Anaemias MCV <80 fl Serum Iron TIBC BM Perls stain Iron Def. Anemia ↓↓ ↑↑ 0 Chronic Infection ↓↓ ↓↓ + + Thalassemia ↑↑ N + + + + Lead poisoning N N + + Sideroblastic ↑↑ N + + + +
- 40. IDA • Microcytic • RDW •Hypochromic • RPI • Serum ferritin • TIBC • Serum Iron • BM Fe Stain • Response to Fe Rx. MCV < 80 fl, RBC < 6 µ Widened and shift to left MCH < 27 pg, MCHC < 30% < 2 Very low < 30 (p mols/L) Increased > 400 (µg/dL) Very low < 30 (µg/dL) Absent Fe Excellent
- 41. IDA • Look foroccult blood loss – 2 days non veg. free • Pica and Pagophagia • Absorption of Haem Iron > Fe++ • Food, Phytates, Ca, Phosphate, antacids ↓absorption • Ascorbic acid ↑absorption • Oral iron Rx. always is the best
- 42. • Oral irontherapy. • Packed cell transfusion in emergency • Continue Fe Rx at least 2 months after normal Hb • 1 gram ↑in Hb every week can be expected • Always supplement protein for the Globin component
- 43.
- 44.
- 45. Ringed Sideroblasts inBM PrussianBlueStain
- 46. Macrocytic Anaemias • MegaloblasticMacrocytic –B12 and Folate↓ • Non Megaloblastic Macrocytic Anaemias 1. Liver disease/alcohol 2. Hemoglobinopathies 3. Metabolic disorders, Hypothyroidism 4. Myelodystrophy, BM infiltration 5. Accelerated Erythropoesis -↑destruction 6. Drugs (cytotoxics, immunosuppressants, AZT, anticonvulsants)
- 47. Anemia - Macrocytic(MCV > 100) – Macrocytic anemias may be asymptomatic until the Hb is as low as 6 grams – MCV 100-110 fl must look for other causes of macrocytosis – MCV > 110 fl almost always folate or B12 deficiency
- 48. Macrocytosis of Alcoholism •MCV elevation usually slight (100-110 fl) • Minimal or no anemia • Macrocytes round (not oval) • Neutrophil hyper segmentation absent • Folate stores normal
- 49. DRUGS CAUSING MEGALOBLASTICANEMIA Folate antagonists (e.g., methotrexate) Purine antagonists (e.g., 6-mercaptopurine) Pyrimidine antagonists (e.g., cytosine arabinoside) Alkylating agents (e.g., cyclophosphamide) Zidovudine (AZT , Retrovir) Trimethoprim Oral contraceptives Nitrous oxide Arsenic
- 50. Megaloblastic Hematopoiesis Marrow failuredue to • Disrupted DNA synth. & ineffective erythropoesis • Giant precursors (Megaloblasts) • Nuclear : Cytoplasmic dyssynchrony in marrow • Neutrophil hyper segmentation & macro ovalocytes • Anemia (and often leukopenia & thrombocytopenia) • Almost always due to B12 or folate deficiency
- 51. Pernicious Anaemia -Tongue Bald, smooth, lemon yellowish red tongue
- 52.
- 53. Anisocytosis - MacrocyticAnaemia
- 54. Normocytic Anaemias • Chronicdisease • Early IDA • Hemoglobinopathies • Primary marrow disorders • Combined deficiencies
- 55. Anaemia of ChronicDisease • Thyroid diseases • Malignancy • Collagen Vascular Disease – Rheumatoid Arthritis – SLE – Polymyositis – Polyarteritis Nodosa • IBD – Ulcerative Colitis – Crohn’s Disease • Chronic Infections – HIV, Osteomyelitis – Tuberculosis • Renal Failure
- 57. • Anaemia isusually mild and non-progressive, rarely less than 9 gm/dL. • Anaemia is never severe • Anaemia resolves when underlying cause is treated. • Anaemia of chronic inflammation is not responsive to haematinics like iron, folate, vitamin B12. • Transfusion is rarely indicated. • Higher doses of Epo is required to treat ACD than for the therapy of renal anaemia.
- 58. ‘Dimorphic’ Anaemia • Folate& Fe deficiency (pregnancy, alcoholism) • B12 & Fe deficiency (PA with atrophic gastritis) • Thalassemia minor & B12 or folate deficiency • Fe deficiency & hemolysis (prosthetic valve) • Folate deficiency & hemolysis (Hb SS disease) • Peripheral smear exam is critical to assess these • RDW is increased very much
- 59. Hemolytic Anaemia Anemia ofincreased RBC destruction – Normochromic, normocytic anemia – Shortened RBC survival – Reticulocytosis – due to ↑ RBC destruction Will not be symptomatic until the RBC life span is reduced to 20 days – BM compensates 6 times
- 60. Tests Used toDiagnose Hemolysis 1. Reticulocyte count 2. Combined with serial Hb 3. Serum LDH 4. Serum bilirubin 5. Haptoglobin 6. Urine hemosiderin 7. Hemoglobinuria
- 61. Findings in HemolyticAnaemia Reticulocyte count and RPI Increased Serum Unconjugated Bilirubin Increased Serum LDH 1: LDH 2 Increased Serum Haptoglobin Decreased Urine Hemoglobin Present Urine Hemosiderin Present Urine Urobilinogen Increased Cr 51 labeled RBC life span Decreased
- 62. Tests to define thecause of hemolysis 1. Hemoglobin electrophoresis 2. Hemoglobin A2 (βeta-Thalassemia trait) 3. RBC enzymes (G6PD, PK, etc) 4. Direct & indirect antiglobulin tests (immune) 5. Cold agglutinins 6. Osmotic fragility (spherocytosis) 7. Acid hemolysis test (PNH) 8. Clotting profile (DIC)
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- 66. Micro Angiopathic HemolyticAnaemia
- 68. ANEMIA DUE TOIMPAIRED BONE MARROW RESPONSE Red blood cell aplasia Aplastic anemia Myelodysplasia Leukemias Myelophthisic anemia Marrow infiltration Myeloma Congenital Dyserythropoietic Anemias
- 69. Aplastic Anaemia 1. Chloramphenicol 2.Carbimazole 3. Sulfonamides 4. Phenytoin 5. Anti Ca drugs
- 70. BM - AplasticAnaemia
- 71.
- 76. CONDITION SERUM IRON TIBC FERRITINCOMMENT Iron deficiency ↓ ↑ ↓ Responsive to iron Chronic inflammation ↓ ↓ Unresponsive to iron Thalassemia major ↑ N N Reticulocytosis and indirect bilirubinemia Lead poisoning N N N Basophilic stippling of RBCs Sideroblastic anemia ↑ N Ring sideroblasts in marrow
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- 78. RPI <2.5 RPI>2.5 • Anemia of chronic disease • CKD • Acute Bloodloss • Leukemia • Approach to Pancytopeni a • Approach to Hemolytic anemia
- 79.
- 83. REFERENCES • Harrison’s Principlesof Internal Medicine 20th edition • The Washington’s Manual of Medical Therapeutics 34th edition • Robbins & Cotran Pathologic Basis of Disease, 8th edition