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I now have rich content across all major types of anemia. Let me compile the comprehensive viva answer.
Anemia - Complete Viva Practical Guide
1. DEFINITION
WHO Definition of Anemia (Hemoglobin thresholds):
| Group | Hb < (g/dL) |
|---|---|
| Adult males | 13 |
| Adult females (non-pregnant) | 12 |
| Pregnant women | 11 |
| Children 6 months - 6 years | 11 |
| Children 6 - 14 years | 12 |
Physiologic anemia of pregnancy: Hb < 11 g/dL or Hct < 33%, due to a 47% rise in plasma volume vs. only 17% rise in RBC mass (hemodilution effect after 28 weeks).
2. CLASSIFICATION (Etiologic - Robbins)
A. Blood Loss
- Acute (trauma)
- Chronic (GI tract lesions, gynecologic disturbances)
B. Increased Destruction - Hemolytic Anemias
Intrinsic (Intracorpuscular) Abnormalities
- Hereditary:
- Membrane abnormalities: spherocytosis, elliptocytosis
- Enzyme deficiencies: G6PD deficiency (HMP shunt), Pyruvate kinase deficiency (glycolytic)
- Hemoglobinopathies: Sickle cell anemia, Thalassemia
- Acquired:
- Paroxysmal Nocturnal Hemoglobinuria (PNH) - membrane defect
Extrinsic (Extracorpuscular) Abnormalities
- Antibody-mediated: Transfusion reactions, autoimmune (SLE), drug-induced
- Mechanical trauma: TTP, DIC (microangiopathic hemolytic anemia - MAHA), dysfunctional cardiac valves
- Infections: Malaria
C. Impaired Red Cell Production (Underproduction Anemias)
- Stem cell defects: Aplastic anemia, pure red cell aplasia
- Defective DNA synthesis: Megaloblastic anemias (B12 and Folate deficiency)
- Defective Hb synthesis: Iron deficiency, sideroblastic anemia, thalassemia
- Marrow replacement: Leukemia, MDS, myelophthisic (metastatic tumors, granulomas)
- Erythropoietin deficiency: Anemia of renal failure
- Anemia of chronic disease / chronic inflammation
3. MORPHOLOGIC CLASSIFICATION (MCV-based)
| Type | MCV | Causes | Blood Smear Finding |
|---|---|---|---|
| Microcytic | < 80 fL | Iron deficiency, Thalassemia, Sideroblastic, ACD | Hypochromic microcytic RBCs, target cells (thalassemia) |
| Normocytic | 80-100 fL | ACD, hemolytic, aplastic, acute blood loss, renal failure | Normal or polychromasia |
| Macrocytic | > 100 fL | Megaloblastic (B12/folate), liver disease, alcohol, hypothyroidism, reticulocytosis | Macro-ovalocytes, hypersegmented neutrophils |
Key point: MCV < 75 fL essentially rules out anemia of inflammation (ACD). A normal RDW in microcytic anemia favors thalassemia/hemoglobinopathy over iron deficiency.
4. IRON DEFICIENCY ANEMIA (IDA)
Lab Investigations (Most commonly asked)
| Test | IDA | Anemia of Chronic Disease (ACD) | Thalassemia |
|---|---|---|---|
| Serum iron | Low | Low | Normal/High |
| TIBC | High | Low | Normal |
| Serum Ferritin | Low (earliest marker) | Normal/High | Normal/High |
| % Saturation | Low | Low | Normal |
| RDW | High | Normal | Normal or High |
- Most sensitive early test = serum ferritin (drops first)
- Smear shows: hypochromic, microcytic RBCs with anisopoikilocytosis (pencil cells, target cells)
- Symptoms of IDA: fatigue, pallor, koilonychia (spoon nails), angular cheilosis, atrophic glossitis, PICA (ice hunger = pagophagia)
Treatment
- Ferrous sulfate/gluconate/fumarate 60-120 mg elemental iron, 2-3 divided doses/day
- Response: Reticulocytosis at 7-10 days, Hb rises ~1 g/dL per week
- Failure to respond: wrong diagnosis, malabsorption, ongoing blood loss, non-compliance
5. MEGALOBLASTIC ANEMIA
Key Distinction B12 vs Folate
| Feature | Vitamin B12 Deficiency | Folate Deficiency |
|---|---|---|
| Cause | Malabsorption (pernicious anemia, gastrectomy, ileal resection, Crohn's) | Poor dietary intake, alcohol, pregnancy, drugs (methotrexate, phenytoin) |
| Liver stores | 5-20 years | 3-4 months |
| Neurologic features | YES (subacute combined degeneration - dorsal + lateral columns) | NO |
| Blood smear | Macro-ovalocytes, hypersegmented neutrophils (>5 lobes) | Identical to B12 |
| Diagnosis | Serum B12, methylmalonic acid, homocysteine elevated | Serum folate, RBC folate (more accurate) |
Critical viva point: If folate alone is given in B12 deficiency, it corrects the hematologic picture but the neurologic damage continues and becomes irreversible. Always give both empirically while awaiting results.
Pathogenesis of Pernicious Anemia
- Autoimmune attack on gastric mucosa (chronic atrophic gastritis)
- Loss of parietal cells → loss of Intrinsic Factor (IF)
- Antibodies block B12-IF binding or block cubilin receptor binding in ileum
- B12 absorbed via: IF → binds B12-IF complex to cubilin receptor in terminal ileum → transcobalamin II carries it to tissues
Blood Smear in Megaloblastic Anemia
- Macro-ovalocytes (large oval red cells)
- Hypersegmented neutrophils (>5 lobes = pathognomonic; a single neutrophil with 6 lobes is diagnostic)
- Pancytopenia in severe cases
6. HEMOLYTIC ANEMIA
Lab Findings (Know these cold)
Suggestive of Hemolysis:
- Peripheral blood smear: polychromasia, abnormal RBC morphology
- Elevated reticulocyte count (corrected for anemia)
- Elevated serum bilirubin (indirect/unconjugated)
- Elevated LDH
- Slightly elevated AST
Confirmatory of Hemolysis:
- Decreased serum haptoglobin (lower in intravascular than extravascular)
- Increased plasma hemoglobin
- Increased urobilinogen
- Hemoglobinuria (intravascular only)
- Hemosiderinuria (intravascular; chronic/recurrent)
Smear Findings by Type
| RBC Shape | Condition |
|---|---|
| Spherocytes | Hereditary spherocytosis, AIHA |
| Schistocytes / Helmet cells | MAHA (TTP, DIC, HUS) |
| Sickle cells (drepanocytes) | Sickle cell anemia |
| Target cells (codocytes) | Thalassemia, HbC disease, liver disease, IDA |
| Elliptocytes | Hereditary elliptocytosis |
| Bite cells / Blister cells | G6PD deficiency |
| Teardrop cells (dacrocytes) | Myelofibrosis, myelophthisic anemia |
| Acanthocytes (spur cells) | Liver disease, abetalipoproteinemia |
| Polychromatophilic cells | Reticulocytes (increased production) |
Approach to Hemolytic Anemia (Diagnostic Flow)
- Examine peripheral smear first
- Microangiopathic changes (schistocytes) → TTP workup (life-saving urgency)
- Specific morphologic abnormalities → hereditary RBC defects (spherocytosis, elliptocytosis)
- If smear is normal or only few spherocytes → check Direct Antiglobulin (Coombs') Test
- Positive → Autoimmune hemolytic anemia (AIHA)
- Previous transfusion or pregnancy → check indirect Coombs' (antibody screen)
- If negative → consider metabolic/toxic causes (G6PD deficiency, pyruvate kinase, drugs)
Goldman-Cecil Medicine: Approach always begins with peripheral smear examination.
7. APLASTIC ANEMIA
- Definition: Pancytopenia + hypocellular bone marrow with replacement by fat cells
- Smear: leukopenia + thrombocytopenia + anemia with reticulocytopenia (no polychromasia - hypoproliferative)
- Causes: Idiopathic (most common), drugs (chloramphenicol, NSAIDs), radiation, viruses (EBV, hepatitis), PNH
- Key: Normal cellular morphology on bone marrow aspirate (vs. MDS which shows dysplasia)
- Treatment: Bone marrow transplant (young patients) or immunosuppression (anti-thymocyte globulin + cyclosporine)
8. SICKLE CELL ANEMIA
- Mutation: Glu→Val substitution at position 6 of β-globin chain
- HbS polymerizes when deoxygenated → rigid sickled cells → vascular occlusion + hemolysis
- Smear: elongated, spindled or boat-shaped irreversibly sickled cells
- RBC lifespan: ~20 days (vs. normal 120 days)
- Sickling promoted by: hypoxia, dehydration, acidosis, infection, fever
- Complications: vaso-occlusive crises, stroke, autosplenectomy, acute chest syndrome, priapism, avascular necrosis, renal papillary necrosis
9. THALASSEMIA
- Deficient globin chain synthesis (α or β chains)
- Smear: hypochromic microcytic cells, target cells, basophilic stippling, nucleated RBCs (severe forms)
- α-Thalassemia trait: MCV low, Hb electrophoresis normal
- β-Thalassemia minor: raised HbA2 (>3.5%) - diagnostic
- β-Thalassemia major: no HbA, requires transfusions, "crew-cut" skull X-ray appearance
10. ANEMIA OF CHRONIC DISEASE (ACD)
- Mechanism: IL-6 → ↑ hepcidin → blocks ferroportin → iron trapped in macrophages
- Serum iron LOW, TIBC LOW, ferritin NORMAL or HIGH
- Normocytic (most common), occasionally mildly microcytic (MCV rarely < 75 fL)
- Treatment: Treat underlying disease; erythropoiesis-stimulating agents if needed (e.g., renal failure)
11. COMMONLY ASKED VIVA PEARLS
| Question | Answer |
|---|---|
| Most sensitive test for IDA | Serum ferritin |
| What differentiates IDA from ACD? | TIBC (high in IDA, low in ACD); ferritin (low in IDA, normal/high in ACD) |
| Peripheral smear finding in megaloblastic anemia | Macro-ovalocytes + hypersegmented neutrophils (hallmark) |
| Why not give folate alone in suspected B12 deficiency? | Masks hematologic abnormality but neurologic damage (SCD) progresses irreversibly |
| Gold standard for iron stores | Bone marrow iron stain (Perl's Prussian blue) |
| Earliest RBC change in IDA | Decreased MCV → then hypochromia on smear |
| Coombs' test detects? | Antibodies or complement on RBC surface (direct) |
| Intravascular vs extravascular hemolysis | Intravascular: hemoglobinuria, hemosiderinuria, very low haptoglobin. Extravascular: splenomegaly |
| Autosplenectomy seen in | Sickle cell anemia (chronic infarction of spleen) |
| Chronic folate supplementation recommended in | All patients with chronic hemolytic anemia (1 mg/day) |
Sources: Robbins & Kumar Basic Pathology; Goldman-Cecil Medicine; Textbook of Family Medicine 9e; Tietz Textbook of Laboratory Medicine 7e; Harrison's Principles of Internal Medicine 22E (2025)
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