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Anaemia Pathology - A Complete Teaching Guide

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1. Definition & Overview

• Haematocrit (packed red cell volume/total blood volume)
• Haemoglobin concentration (below the normal range for age and sex)

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2. Classification

A. By Mechanism (Pathophysiologic)

B. By Red Cell Size (Morphologic - MCV based)

• MCV - mean cell volume (fL)
• MCH - mean cell haemoglobin (pg)
• MCHC - mean cell Hb concentration (g/dL)
• RDW - red cell distribution width (coefficient of variation of red cell volume; elevated in mixed deficiencies)

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3. Haemolytic Anaemias

1. Shortened RBC lifespan (normal = 120 days)
2. Elevated erythropoietin → compensatory erythroid hyperplasia → reticulocytosis
3. Accumulation of Hb degradation products (bilirubin, haemosiderin)

Extravascular vs. Intravascular Haemolysis

In both types, bilirubin is unconjugated, and excess excretion into bile can lead to pigment gallstones.

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3a. Hereditary Spherocytosis

• Genetics: Autosomal dominant (usually); mutations in RBC membrane skeleton proteins (ankyrin, band 4.2, alpha/beta spectrin)
• Pathogenesis: Loss of membrane surface area without corresponding volume loss → spherocyte formation → trapped and destroyed in splenic cords
• Blood smear: Spherocytes (small, dense, no central pallor), reticulocytosis
• Lab: Positive osmotic fragility test; negative DAT (Coombs)
• Features: Anaemia, splenomegaly, jaundice
• Treatment: Splenectomy (removes site of destruction)

3b. G6PD Deficiency

• Genetics: X-linked; mutations destabilize G6PD enzyme
• Pathogenesis: G6PD is essential for the hexose monophosphate shunt, which generates NADPH. NADPH maintains glutathione in reduced form, protecting RBCs from oxidant damage. Without G6PD, oxidant stress (from infections, certain drugs - primaquine, dapsone, fava beans) → oxidation of Hb → Heinz bodies (precipitated Hb) → membrane damage → haemolysis
• Blood smear: Bite cells (where macrophages have "bitten out" Heinz bodies), blister cells
• Key point: Episodic, triggered haemolysis - not chronic

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3c. Sickle Cell Disease

• Genetics: Autosomal recessive; point mutation in beta-globin gene (GAG→GTG; Glu→Val at position 6) producing HbS

• On deoxygenation, HbS polymerizes → stacks into long rigid tactoids → distorts RBC into sickle shape
• Early sickling is reversible on reoxygenation; repeated cycles cause irreversibly sickled cells
• Sickled cells: (a) less deformable → extravascular haemolysis, (b) express increased adhesion molecules → stick to endothelium → microvascular occlusion
• Free Hb from lysed cells binds and inactivates nitric oxide → increased vascular tone + platelet aggregation → worsens vascular occlusion

• Peripheral smear: Irreversibly sickled cells, target cells, Howell-Jolly bodies (due to asplenia), reticulocytosis
• Bone marrow: Erythroid hyperplasia → bone resorption → "crew-cut" appearance on skull X-ray
• Spleen: Initially enlarged (red pulp congestion); progressive autosplenectomy by adolescence (fibrosis after repeated infarcts)
• Other infarcts: Bones, brain, kidney, liver, retina, pulmonary vessels (cor pulmonale)

• Moderate-severe haemolytic anaemia (Hct 18-30%)
• Vaso-occlusive crises - severe bone pain
• Dactylitis in children (hand-foot syndrome)
• Increased susceptibility to encapsulated organisms (due to functional asplenia) - Streptococcus pneumoniae
• HbF protects - disease is milder in early infancy

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3d. Thalassaemias

• Alpha-thalassaemia: Deletion of alpha-globin genes (chromosome 16). Severity depends on number of deleted genes: 1 deletion (silent) → 4 deletions (Hb Bart's - incompatible with life)
• Beta-thalassaemia: Point mutations reducing (beta+) or eliminating (beta0) beta-globin synthesis. Excess alpha chains precipitate in RBCs → premature RBC destruction (ineffective haemopoiesis) and haemolysis
• Morphology: Microcytic hypochromic RBCs, target cells, tear-drop cells; markedly expanded marrow (maxilla prominences, "chipmunk facies", osteoporosis); extramedullary haemopoiesis (hepatosplenomegaly)
• HbA2 elevated in beta-thal trait (diagnostic)
• Treatment: Transfusion + iron chelation; stem cell transplant for severe disease

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3e. Autoimmune Haemolytic Anaemia (AIHA)

• IgG autoantibodies bind RBC surface antigens
• Opsonized RBCs phagocytosed in spleen → extravascular haemolysis
• Positive direct antiglobulin test (DAT/Coombs)
• Causes: Idiopathic, SLE, CLL, drugs (methyldopa, penicillin)

• IgM antibodies bind RBCs in cold peripheral vessels → agglutination + C3b deposition → extravascular haemolysis in warmer core
• Causes: Mycoplasma pneumonia (anti-I), infectious mononucleosis (anti-i), lymphoma

• IgG Donath-Landsteiner antibodies; bind RBC P antigen in cold → complement-mediated intravascular lysis when blood warms
• Often post-viral in children

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3f. Microangiopathic Haemolytic Anaemia (MAHA)

• Mechanical destruction of RBCs by narrowed microvascular lumens (thrombi in DIC, TTP, HUS, malignant hypertension)
• Blood smear: Schistocytes (helmet cells, triangle cells, burr cells)

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4. Iron Deficiency Anaemia

Iron Metabolism

• Total body iron: ~2.5 g (women), ~3.5 g (men)
• 80% in functional pool (Hb, myoglobin, enzymes); 15-20% in storage pool (ferritin, haemosiderin - in macrophages of liver, spleen, BM)
• Transport: Bound to transferrin (normally ~33% saturated; serum iron ~120 µg/dL men, ~100 µg/dL women)
• Hepcidin (liver peptide): Negatively regulates ferroportin → controls iron absorption and release
• Inflammation → IL-6 → hepcidin upregulation → ferroportin degradation → iron sequestration (basis of anaemia of chronic disease)

Causes

1. Inadequate intake - poverty, restricted diet, infants on cow's milk
2. Malabsorption - coeliac disease, post-gastrectomy (duodenum bypassed)
3. Increased requirements - pregnancy, infancy, adolescence
4. Chronic blood loss (most common cause in developed countries) - GI tract (peptic ulcer, colorectal cancer, angiodysplasia), gynaecologic (menorrhagia)
   • In adult males and postmenopausal females: GI blood loss must be excluded before attributing iron deficiency to any other cause - an occult GI cancer must be ruled out.

Stages of Iron Deficiency

1. Depletion of iron stores - serum ferritin falls; no anaemia yet; BM iron absent (Prussian blue stain)
2. Iron-deficient erythropoiesis - serum iron falls, TIBC rises, transferrin saturation <15%; no overt anaemia yet
3. Iron deficiency anaemia - Hb/Hct fall; full picture of microcytic hypochromic anaemia

Morphology

Labs

Clinical Features

• Fatigue, pallor, exertional dyspnoea (general anaemia symptoms)
• Severe/chronic iron deficiency also causes:
  • Koilonychia (spoon nails)
  • Pica (craving for non-food items - clay, ice/pagophagia, flour)
  • Angular cheilitis, glossitis (atrophic tongue)
  • Alopecia, intestinal malabsorption
  • In children: cognitive impairment

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5. Megaloblastic Anaemia

• Vitamin B12 (cobalamin) deficiency
• Folate deficiency
• Drugs impairing DNA synthesis (methotrexate, hydroxyurea, certain anticonvulsants)
• Myelodysplasia

Pathogenesis

• B12 and folate are both required for synthesis of thymidylate (for DNA)
• B12 deficiency traps folate in an unusable form (methyltetrahydrofolate trap)
• Result: Impaired DNA synthesis → cells grow but cannot divide → large cells with immature-appearing nuclei

Morphology

• Macrocytic anaemia (oval macrocytes, MCV often >110 fL)
• Hypersegmented neutrophils (>5 lobes or any cell with ≥6 lobes) - classic hallmark
• Pancytopenia in severe cases

• Markedly hypercellular
• Megaloblasts - large erythroid precursors with finely dispersed ("open") nuclear chromatin despite cytoplasmic haemoglobinization
• Nuclear-cytoplasmic asynchrony (nucleus looks immature, cytoplasm is mature/haemoglobinized)
• Giant metamyelocytes and band forms
• Hypersegmented megakaryocytes
• Ineffective haemopoiesis - most precursors undergo apoptosis in marrow → pancytopenia despite hyperplastic marrow

Pernicious Anaemia (B12 deficiency)

• B12 absorption pathway: Dietary B12 freed by pepsin → binds haptocorrin in stomach → transferred to IF in duodenum → IF-B12 complex absorbed in terminal ileum via cubilin receptors
• Autoantibodies against: (1) parietal cells, (2) IF itself (blocking antibody), (3) IF-B12 complex (binding antibody)
• Associated with: Atrophic gastritis, achlorhydria, elevated gastrin
• Neurologic complication: Subacute combined degeneration of the spinal cord - demyelination of dorsal (posterior) and lateral columns → sensory ataxia, loss of vibration/proprioception, spastic paraparesis
  • This neurological complication does NOT occur in folate deficiency - an important distinguishing feature
• Treatment: Intramuscular B12 injections (bypasses GI absorption)

Folate Deficiency

• Dietary sources: Green leafy vegetables, liver, nuts (destroyed by cooking)
• Daily requirement: ~100 µg; body stores last ~3-4 months only (much less than B12)
• Causes: Dietary deficiency (alcoholism, poverty), malabsorption, increased demand (pregnancy), drugs (methotrexate, trimethoprim, phenytoin)
• No neurological features (unlike B12 deficiency)

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6. Aplastic Anaemia

Pathogenesis

• Idiopathic (50-70%)
• Chemical agents:
  • Dose-related (predictable): Alkylating agents, antimetabolites, benzene, chloramphenicol, inorganic arsenicals
  • Idiosyncratic (unpredictable): Chloramphenicol, phenylbutazone, gold salts, carbamazepine
• Viral infections: Hepatitis (~5%), EBV, CMV, HIV
• Whole-body radiation (dose-dependent)
• Inherited: Fanconi anaemia (autosomal recessive; DNA repair defects)

Morphology

• Bone marrow: Markedly hypocellular - fatty replacement of haemopoietic cells; scattered lymphocytes and plasma cells; virtual absence of erythroid, myeloid precursors and megakaryocytes
• Peripheral blood: Pancytopenia; normocytic normochromic anaemia; no reticulocytosis (production failure)

Clinical Features

• Anaemia: Fatigue, pallor, dyspnoea
• Neutropenia: Recurrent serious infections (opportunistic organisms)
• Thrombocytopenia: Mucosal bleeding, petechiae, ecchymoses
• Prognosis: Severe aplastic anaemia is fatal without treatment

Treatment

• Young patients (<40 yrs): Allogeneic BMT (curative)
• Older patients / no matched donor: Immunosuppression (anti-thymocyte globulin + cyclosporin + eltrombopag)
• Supportive: Transfusions, growth factors, antibiotics

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7. Anaemia of Chronic Disease (ACD)

• Chronic infections (TB, osteomyelitis, HIV)
• Chronic inflammatory conditions (rheumatoid arthritis, SLE, IBD)
• Malignancy

1. Inflammation → IL-6 → liver produces hepcidin
2. Hepcidin degrades ferroportin on macrophages and enterocytes
3. Iron is trapped in macrophage stores and cannot be released to developing erythrocytes
4. Erythroid precursors are starved of iron despite adequate (or increased) body iron stores
5. Additionally, cytokines suppress erythropoietin production and erythroid proliferation

• Serum ferritin: HIGH (stored iron is abundant)
• TIBC: LOW (unlike iron deficiency where TIBC is high)
• Serum iron: Low
• BM macrophage iron: Increased (Prussian blue +ve)

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8. Quick Summary Table - Distinguishing Features

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9. Clinical Approach to Anaemia

1. History: Diet, bleeding, drugs, chronic illness, family history, ethnicity
2. Exam: Pallor, jaundice, splenomegaly, koilonychia, glossitis, neurological signs
3. First investigations: CBC + differential, peripheral smear, reticulocyte count
4. Reticulocyte count - key decision point:
   • High reticulocytes → Haemopoiesis intact; problem is loss or destruction → haemolytic anaemia or blood loss
   • Low reticulocytes → Production failure → iron deficiency, megaloblastic, aplastic, ACD
5. MCV-directed workup:
   • Low MCV → iron studies, Hb electrophoresis
   • High MCV → B12, folate levels; assess for oval macrocytes + hyperseg. neutrophils
   • Normal MCV → broad differential; check RFTs, TFTs, LFTs, bone marrow

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• Robbins, Cotran & Kumar Pathologic Basis of Disease, 10th ed. (Chapter 14)
• Robbins & Kumar Basic Pathology (Chapter 10)
• Harrison's Principles of Internal Medicine, 22nd ed. (Chapter 66)
• Henry's Clinical Diagnosis and Management by Laboratory Methods

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Anaemia Classification by MCV

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The MCV Framework

The reticulocyte count works alongside MCV. A high reticulocyte count (>2% corrected, or RPI >2) points to blood loss or haemolysis, regardless of MCV. A low reticulocyte count points to underproduction.

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1. MICROCYTIC ANAEMIA (MCV < 80 fL)

Core Concept

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1A. Iron Deficiency Anaemia (IDA)

• Peripheral smear: Microcytic + hypochromic cells, pencil cells (elongated poikilocytes), anisocytosis, poikilocytosis
• MCV: Typically 60-79 fL
• RDW: Elevated (anisocytosis - red cells vary greatly in size)

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1B. Thalassaemia

• Peripheral smear: Microcytic + hypochromic, target cells (codocytes), basophilic stippling, tear-drop cells
• MCV: Often very low (can be <65 fL in beta-thal major), disproportionately low compared to the haemoglobin level
• RDW: Normal or mildly elevated (cells are uniformly small, unlike IDA)

Mentzer Index = MCV ÷ RBC count

• >13 → suggests Iron Deficiency (fewer, larger cells)
• <13 → suggests Thalassaemia (many small cells)

• Serum iron: Normal or high
• Ferritin: Normal or high
• HbA2 elevated (>3.5%) → diagnostic of beta-thalassaemia trait
• HbF elevated in beta-thal major
• Hb electrophoresis is essential

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1C. Anaemia of Chronic Disease (ACD)

• Usually normocytic; becomes microcytic only in long-standing disease
• Serum iron: Low
• TIBC: Low (unlike IDA - key distinguishing point)
• Ferritin: High (iron trapped in macrophages)
• Background: Chronic infection, malignancy, autoimmune disease, renal failure

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1D. Sideroblastic Anaemia

• Defect in haem synthesis despite iron being present and even accumulating
• Iron loads into mitochondria around the nucleus → ring sideroblasts on Prussian blue stain of BM (pathognomonic)
• Peripheral smear: Dimorphic - two populations of red cells: one hypochromic microcytic, one normal/macrocytic → MCV may be normal or even high

• Inherited (X-linked): Mutations in ALAS2 gene (first enzyme of haem synthesis); responds to pyridoxine (vitamin B6)
• Acquired:
  • Alcohol (most common acquired cause; reversible)
  • Isoniazid, chloramphenicol, lead (inhibit pyridoxal phosphate)
  • Myelodysplastic syndrome (MDS with ring sideroblasts - clonal, serious)
  • Copper deficiency, zinc toxicity

• Serum iron: High (iron cannot be used)
• Ferritin: High
• TIBC: Low/normal
• Transferrin saturation: High

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Distinguishing the Microcytic Anaemias

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2. NORMOCYTIC ANAEMIA (MCV 80-100 fL)

Core Concept

Normocytic Anaemia
       │
       ├── Reticulocyte count HIGH (RPI >2)
       │         → Haemolysis or Acute blood loss
       │
       └── Reticulocyte count LOW (RPI <2)
                 → Underproduction
                       ├── Anaemia of Chronic Disease
                       ├── Renal disease (↓ EPO)
                       ├── Aplastic anaemia
                       ├── Endocrine (hypothyroidism, Addison's, hypogonadism)
                       ├── BM infiltration (malignancy, granulomas)
                       └── Early iron deficiency

2A. Anaemia of Chronic Disease / Anaemia of Inflammation

• Most common normocytic anaemia
• Mild, insidious; dominated by symptoms of the underlying disease
• Normochromic normocytic (occasionally microcytic)
• Low reticulocyte count

2B. Anaemia of Chronic Kidney Disease (CKD)

• Deficient erythropoietin (EPO) production from the damaged kidney
• Normochromic normocytic; echinocytes (burr cells) occasionally seen
• Reticulocyte count low for degree of anaemia
• EPO levels inappropriately low relative to the degree of anaemia
• Treatment: Recombinant EPO (epoetin/darbepoetin) + iron supplementation

2C. Aplastic Anaemia

• Destruction of haemopoietic stem cells → pancytopenia
• Normocytic normochromic anaemia, very low reticulocytes
• BM: Markedly hypocellular (fatty marrow)
• WBC and platelet count also low

2D. Haemolytic Anaemias (Normocytic/Macrocytic)

• Spherocytes → Hereditary spherocytosis or warm AIHA
• Sickle cells → Sickle cell disease
• Schistocytes (helmet/triangle cells) → Microangiopathic haemolytic anaemia (DIC, TTP, HUS)
• Bite cells, blister cells → G6PD deficiency
• Target cells → Haemoglobinopathy, liver disease

2E. Endocrine Causes

• Hypothyroidism: Usually normocytic (can be macrocytic)
• Adrenal insufficiency (Addison's): Normocytic
• Hypogonadism (androgen deficiency): Androgens stimulate EPO; their deficiency causes mild normocytic anaemia

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3. MACROCYTIC ANAEMIA (MCV > 100 fL)

Core Concept

Macrocytic Anaemia
       │
       ├── MEGALOBLASTIC (hypersegmented neutrophils PRESENT)
       │         ├── Vitamin B12 deficiency
       │         ├── Folate deficiency
       │         └── Drugs (methotrexate, hydroxyurea, AZT, phenytoin)
       │
       └── NON-MEGALOBLASTIC (hypersegmented neutrophils ABSENT)
                 ├── Alcohol
                 ├── Liver disease
                 ├── Hypothyroidism
                 ├── Myelodysplastic syndrome (MDS)
                 └── Reticulocytosis (reticulocytes are larger than mature RBCs)

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3A. Megaloblastic Anaemia - B12 and Folate Deficiency

• Oval macrocytes (not round)
• Hypersegmented neutrophils (≥5 lobes, or any with ≥6 lobes) - the single most specific finding

• Hypercellular
• Megaloblasts with finely open (non-pyknotic) chromatin despite haemoglobinisation
• Giant metamyelocytes
• Ineffective haemopoiesis → pancytopenia despite hyperplastic marrow

Giving folate to a B12-deficient patient corrects the blood picture but NOT the neurological damage - always check B12 before treating with folate alone.

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3B. Non-Megaloblastic Macrocytic Anaemia

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4. Practical Diagnostic Algorithm

ANAEMIA CONFIRMED (low Hb/Hct)
           │
           ▼
 ┌─────────────────────┐
 │  PERIPHERAL SMEAR   │
 │  + MCV + Retics     │
 └─────────────────────┘
           │
     ┌─────┴──────────────────────┐
     │                            │
  MCV <80                      MCV ≥80
  (MICROCYTIC)               (Normal/Macro)
     │                            │
     ▼                       Reticulocytes?
  Iron studies                    │
  Ferritin, TIBC            ┌─────┴─────┐
  Hb electrophoresis        HIGH       LOW
  BM if needed              │           │
                        Haemolysis  Production failure
                        / Blood loss      │
                                   MCV 80-100:
                                   ACD, renal, aplastic, endocrine
                                   MCV >100:
                                   B12/folate vs non-megaloblastic
                                   (look for hyperseg. neutrophils)

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5. Summary - MCV-Based Differential at a Glance

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• Goldman-Cecil Medicine, International Edition (Table 144-9)
• Henry's Clinical Diagnosis and Management by Laboratory Methods
• Symptom to Diagnosis: An Evidence-Based Guide, 4th ed.
• Harrison's Principles of Internal Medicine, 22nd ed.

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Etiological Classification of Anaemia

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The Three Fundamental Mechanisms

                        ANAEMIA
                           │
           ┌───────────────┼───────────────┐
           │               │               │
     BLOOD LOSS      HAEMOLYSIS     DECREASED
                    (↑ Destruction)  PRODUCTION
                                   (↓ Output)

In some diseases both decreased production and increased destruction contribute simultaneously - for example, thalassaemia (ineffective erythropoiesis + haemolysis) and sickle cell disease (haemolysis + vaso-occlusion).

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CATEGORY 1: BLOOD LOSS

1A. Acute Blood Loss

• Plasma and RBCs lost in equal proportion → Hb/Hct do NOT fall immediately
• Over hours to days, interstitial fluid shifts into intravascular space → haemodilution → Hb/Hct fall, revealing true extent of loss
• Compensatory reticulocytosis peaks at 5-7 days
• Acutely: normocytic normochromic; after reticulocyte response: may show mild macrocytosis (reticulocytes are larger)

1B. Chronic Blood Loss

• Iron is continuously lost with each bleed (Hb contains ~0.5 mg iron/mL blood)
• Over time, iron stores are depleted → Iron Deficiency Anaemia develops (microcytic hypochromic)
• In adult males and postmenopausal women: chronic blood loss = GI malignancy until proven otherwise

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CATEGORY 2: INCREASED RED CELL DESTRUCTION (HAEMOLYTIC ANAEMIAS)

Broad Sub-classification

HAEMOLYTIC ANAEMIA
        │
        ├── INTRINSIC (Intracorpuscular) - defect within the RBC itself
        │         ├── Inherited
        │         └── Acquired
        │
        └── EXTRINSIC (Extracorpuscular) - normal RBC destroyed by outside forces
                  └── Always acquired

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2A. Intrinsic / Intracorpuscular Defects

i. Membrane Disorders (Inherited)

ii. Enzyme Deficiencies (Inherited)

G6PD deficiency is the most common enzyme defect. Triggers: primaquine, dapsone, nitrofurantoin, infections, fava beans. X-linked → primarily affects males.

iii. Haemoglobin Abnormalities (Inherited)

iv. Acquired Membrane Defect

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2B. Extrinsic / Extracorpuscular Causes

i. Antibody-Mediated (Immune Haemolysis)

ii. Mechanical Trauma

Schistocytes (helmet cells, triangle cells, burr cells) on peripheral smear = hallmark of mechanical haemolysis.

iii. Infections of Red Cells

iv. Toxic / Chemical Injury

v. Sequestration

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CATEGORY 3: DECREASED RED CELL PRODUCTION (AREGENERATIVE ANAEMIAS)

3A. Inherited / Genetic Defects

Stem Cell Depletion

Defects Affecting Erythroblast Maturation

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3B. Nutritional Deficiencies

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3C. Erythropoietin (EPO) Deficiency

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3D. Immune-Mediated Injury of Progenitors

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3E. Inflammation-Mediated Iron Sequestration (Anaemia of Chronic Disease / ACD)

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3F. Primary Haematopoietic Neoplasms

3G. Space-Occupying Marrow Lesions (Myelophthisic Anaemia)

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Complete Etiological Classification - Summary Tree

ANAEMIA (Etiological Classification)
│
├── 1. BLOOD LOSS
│       ├── Acute: Trauma, surgery, internal haemorrhage
│       └── Chronic: GI (carcinoma, ulcer), gynaecologic, hookworm
│
├── 2. INCREASED DESTRUCTION (HAEMOLYSIS)
│       │
│       ├── INTRINSIC (Intracorpuscular)
│       │       ├── Membrane: Hereditary spherocytosis, elliptocytosis
│       │       ├── Enzyme: G6PD deficiency, PK deficiency
│       │       ├── Hb: Sickle cell disease, thalassaemia, HbC
│       │       └── Acquired: PNH
│       │
│       └── EXTRINSIC (Extracorpuscular)
│               ├── Immune: AIHA (warm/cold), transfusion reaction, HDN, drug-induced
│               ├── Mechanical: MAHA (DIC/TTP/HUS), prosthetic valves, march
│               ├── Infections: Malaria, babesia, Clostridium
│               ├── Toxic: Venoms, arsenic, oxidant drugs
│               └── Sequestration: Hypersplenism
│
└── 3. DECREASED PRODUCTION
        ├── Inherited: Fanconi, Diamond-Blackfan, thalassaemia, CDA
        ├── Nutritional: Iron, B12, folate, B6, copper
        ├── EPO deficiency: CKD, hypothyroidism, hypopituitarism
        ├── Immune-mediated: Aplastic anaemia, PRCA (parvovirus B19)
        ├── Inflammation (ACD): Hepcidin ↑ → iron sequestration
        ├── Neoplastic: AML, MDS, myeloma, myelofibrosis, CLL
        └── Marrow infiltration: Metastases, TB, storage disorders

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Key Distinguishing Lab Clue: Reticulocyte Count

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