Anemia definition and classification from robbins

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Based on Robbins & Kumar Basic Pathology, here's the definition and classification of anemia:

Definition and Causes

Anemia is defined as a reduction in hemoglobin concentration, resulting in decreased oxygen-carrying capacity of blood. The causes of anemia include:

Blood loss (hemorrhage)
Increased red cell destruction (hemolysis)
Decreased red cell production (marrow failure)

Classification by Morphology (RBC Size)

Robbins classifies anemias based on red blood cell morphology:

Microcytic Anemias

Most often caused by:

Iron deficiency
Thalassemia

Macrocytic Anemias

May be caused by:

Folate deficiency
Vitamin B12 deficiency
Elevated reticulocyte count (as seen during recovery from bleeding)

Normocytic Anemias

Often associated with characteristic red cell shape changes, such as:

Hereditary spherocytosis
Sickle cell disease

Clinical Manifestations

The presentation of anemia depends on:

Tempo of development (acute vs. chronic)
Mechanism (production failure vs. increased destruction)

Acute onset anemia (e.g., large hemorrhage) presents with:

Shortness of breath
Organ failure
Shock

Chronic onset anemia presents insidiously with:

Pallor
Fatigue
Lassitude

Special Features by Pathophysiology

Extravascular hemolysis: Associated with jaundice and gallstones
Ineffective erythropoiesis: May lead to iron overload causing cardiac and endocrine failure
Severe congenital anemias: Associated with growth retardation and bone deformities from reactive marrow hyperplasia

---Robbins & Kumar Basic Pathology, p. 433

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Detailed Classification of Anemia from Robbins

Based on Robbins, Cotran & Kumar Pathologic Basis of Disease, here are the two main classification systems for anemia:

I. CLASSIFICATION BY UNDERLYING MECHANISM (Table 14.1)

A. BLOOD LOSS

Acute blood loss: Trauma
Chronic blood loss: Gastrointestinal tract lesions, gynecologic disturbances

B. INCREASED RED CELL DESTRUCTION (HEMOLYSIS)

Inherited Genetic Defects

Red cell membrane disorders: Hereditary spherocytosis, hereditary elliptocytosis
Enzyme deficiencies:
- Hexose monophosphate shunt deficiencies: G6PD deficiency, glutathione synthetase deficiency
- Glycolytic enzyme deficiencies: Pyruvate kinase deficiency, hexokinase deficiency
Hemoglobin abnormalities:
- Deficient globin synthesis: Thalassemia syndromes
- Structurally abnormal globins: Sickle cell disease, unstable hemoglobins

Acquired Genetic Defects

Deficiency of phosphatidylinositol-linked glycoproteins: Paroxysmal nocturnal hemoglobinuria
Antibody-mediated destruction: Hemolytic disease of the newborn (Rh disease), transfusion reactions, drug-induced, autoimmune disorders

Mechanical Trauma

Microangiopathic hemolytic anemias: Hemolytic uremic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura
Cardiac traumatic hemolysis: Defective cardiac valves
Repetitive physical trauma: Bongo drumming, marathon running, karate chopping

Other Causes

Infections of red cells: Malaria, babesiosis
Toxic or chemical injury
Membrane lipid abnormalities: Abetalipoproteinemia, severe hepatocellular liver disease
Sequestration: Splenomegaly from various causes

C. DECREASED RED CELL PRODUCTION

Inherited Genetic Defects

Defects leading to stem cell depletion: Fanconi anemia, telomerase defects
Defects affecting erythroblast maturation: Thalassemia syndromes

Nutritional Deficiencies

Deficiencies affecting DNA synthesis: Vitamin B₁₂ and folate deficiencies
Deficiencies affecting hemoglobin synthesis: Iron deficiency

Other Causes

Erythropoietin deficiency
Immune-mediated injury of progenitors
Inflammation-mediated iron sequestration
Primary hematopoietic neoplasms
Space-occupying marrow lesions: Leukemias, lymphomas, carcinomas
Drug-induced suppression: Chemotherapy, certain antibiotics

II. CLASSIFICATION BY MORPHOLOGY (Morphologic Approach)

This clinically useful classification is based on red cell indices and morphologic characteristics that provide etiologic clues.

Key Red Cell Indices (Adult Reference Ranges):

Measurement	Males	Females
Mean cell volume (fL)	82-96	-
Mean cell hemoglobin (pg)	27-33	-
Mean cell hemoglobin concentration (g/dL)	33-37	-
Red cell distribution width	11.5-14.5	-

A. MICROCYTIC HYPOCHROMIC ANEMIAS

Cause: Disorders of hemoglobin synthesis (low mean cell volume <82 fL, low hemoglobin content)

Common conditions:

Iron deficiency
Thalassemia syndromes
Sideroblastic anemia
Lead poisoning
Anemia of chronic disease (some cases)

B. MACROCYTIC ANEMIAS

Cause: Abnormalities that impair erythroid precursor maturation in bone marrow (high mean cell volume >96 fL)

Common conditions:

Vitamin B₁₂ deficiency (megaloblastic)
Folate deficiency (megaloblastic)
Reticulocytosis (in recovery from bleeding or hemolysis)
Hypothyroidism
Liver disease
Myelodysplastic syndromes

C. NORMOCYTIC NORMOCHROMIC ANEMIAS

Characteristics: Normal red cell size and hemoglobin content (MCV 82-96 fL)

Diverse etiologies; classified by reticulocyte response:

High reticulocyte count (appropriate response):

Acute blood loss
Hemolytic anemias (hereditary spherocytosis, sickle cell disease, G6PD deficiency, autoimmune hemolytic anemia)
Red cell shape often provides etiologic clues

Low/normal reticulocyte count (inadequate response):

Chronic kidney disease (erythropoietin deficiency)
Hypothyroidism
Bone marrow disorders (aplastic anemia, myelodysplasia, malignancy infiltration)
Mixed defects (combined iron and B₁₂ deficiency)

III. MORPHOLOGIC CHARACTERISTICS ASSESSED ON PERIPHERAL SMEAR

Red cell size: Normocytic, microcytic, macrocytic

Hemoglobinization: Normochromic (normal color), hypochromic (pale—low hemoglobin content)

Red cell shape (provides diagnostic clues in normocytic anemias):

Spherocytes: Hereditary spherocytosis, autoimmune hemolytic anemia
Schistocytes: Microangiopathic hemolytic anemia (MAHA)
Sickle cells: Sickle cell disease
Polychromasia: Reticulocytosis/hemolysis
Howell-Jolly bodies: Post-splenectomy, asplenia
Target cells: Liver disease, thalassemia

Robbins, Cotran & Kumar Pathologic Basis of Disease, Table 14.1 & pp. 594-646

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