Anemia3 Hemolytic acquired

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

FBC Result: Hemolytic Anemia.

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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)

Only educated person is one who has learned how

to learn and change.

-- Carl Rogers

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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