Never say No, never say, ‘I cannot’, for you are infinite. Even time and space are as nothing compared with your
nature. You can do anything and everything.
-- Swami Vivekananda
….. foundation of clinical medicine
Shashidhar Venkatesh MurthyA/Prof & Head of PathologyCollege of Medicine & Dentistry
Clinical Pathology: RBC 1.3: Hemolytic Anemia - Acquired
Pathogenetic Classification of Anemia: Decreased Production: Nutrient Deficiency.
Iron def (IDA) / Megaloblastic (MBA) Hemopoietic cell defect:
Anemia of chronic disorders (ACD) Aplastic anemia (AA). Dysplastic anemia. Myelodysplastic Syndromes
Increased loss / destruction: Blood loss anemia – Acute / Chronic - bleeding. Hemolytic anemia – Congenital / Acquired.
Acquired / External injury. Immune AIHA (Warm/Cold) Mechanical, Drugs & Parasites
Congenital / Internal RBC defect Defective Membrane (Spherocytic an) Defective Hemoglobin (Sickle cell an.) Deficient Enzyme (G6PD)
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Top 6 Anemias:1. Iron Def. A2. Megaloblastic3. Anem. Of Chronic Dis.4. Aplastic An.5. Immune Hemolytic – Warm6. Immune Hemolytic - Cold
Haemolytic Anemia: Introduction Anemia due to Increased RBC destruction life span (<120d) - Abnormal forms Bilirubin Jaundice (Unconjugated) RBC production – BM Hyperplasia &
Reticulocytes. Acute: Pallor, Jaundice (normal urine) Chronic: Splenomegaly, pigment gall stones. Intravascular & Extravascular Hemolysis*.
Jaundice
2. Jaundice
4. Splenomegaly
3. Pigment Gall stones
1. Pallor
ImmuneMech.Infection
Porphyrin Bil. Unconj
GlobinsIron
Bil. ConjConjugation
Normal
Intravascular Hemolysis.
Etiology: Immune, Mechanical, Enzyme def.
transfusion mismatch, drugs, infections.
Lab diagnosis: Absent Haptoglobins. Haemoglobinemia Haemoglobinuria Haemosiderinuria
Clinical features: Shock, Renal failure,
In Extravascular Hemolysis: Unconjugated hyperbilirubinemia only* 5
Breakdown of RBC within Blood Vessel
Renalfailure
Hemolytic anemia: Morphology
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Abnormal RBC shapesspherocytes in WIHA, target forms in thalasssemia etc.
Polychromatophils.(Immature RBC - large, bluish, no central palor - Reticulocytes)
Nucleated RBCsmall nucleus inside reticulocyte.
Thalassemia Warm Ab Hemolytic Anemia
Giems stain (routine blood film) Bluish, Large RBC ( MCV)
Hemolytic Anemia: Reticulocytes
Reticulocyte
RBC
Reticulocytosis Increased RBC production
Methylene blue stainfor cytoplasmic RNA
Giemsa stain (routine blood film) Bluish, Large RBC ( MCV)
Cell MemHb
Enzymes
Haemolytic Anemia: classification Acquired / External Injury:
Immune: IgG / Warm & IgM / Cold Physical: valve dis, March Hb.nuria, trauma, burns. Drugs: α-Methyldopa, cephalosporins, ibuprofen etc. Parasites / infections (malaria, septicemia (DIC)
Congenital / Internal defects: Defective Membrane: Spherocytic anemia. Defective Haemoglobin: Sickle cell anemia, Thalassemia Deficient Enzyme: G6PD deficiency anemia.
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Immune Hemolytic anemia IgG/IgM:
Causes: RBC Antibody (Commonest.)
Pathogenesis: Warm / IgG coated RBC lysis in spleen. Drugs,
Idiopathic. (predominantly extravascular) Cold / IgM - (Infections, Lymphoma) RBC
Clumping & complement fixation lysis in BV & Liver. (predominantly intravascular)
Morphology: Spherocytes (warm) / RBC clumps (cold).
Clinical Features: Anemia, Jaundice. Splenomegaly in chronic. Diagnosis: Comb’s test *.
IgG
WARM
IgM
COLD
WARM / IgG
COLD / IgM
IgG Antibody
AIHA: Lab diagnosis – Coombs test.
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Direct Coombs Test: (for antigen on patient RBC)
Indirect Coombs Test: (for antibodies in the serum.)Pos
Neg
Online Video Tutorial
Patient RBC Patient Serum
MAHA - Microangiopathic Hemolytic An.
Mechanical damage:Etiology: DIC, TTP, HUS Valve disease / Artificial valves. March Hemoglobinuria.
Morphology: Fragmented RBC: Schistocytes. Polychromasia – reticulocytes.
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- Theodore Roosevelt
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