CATEGORY
MECHANISM
KEY CAUSES
FIRST CLUE
Anemia — basics
↓ Hb / Hct
Less O₂-carrying capacity → tissue hypoxia, compensatory ↑ cardiac output.
Fatigue, pallor, dyspnea on exertion, tachycardia, flow murmur; high-output heart failure if severe
Pale conjunctivae and palmar creases
Too little hemoglobin made → extra cell division → small, pale cells.
Iron deficiency, anemia of chronic disease (late), thalassemia, sideroblastic anemia (lead, B6, alcohol), copper deficiency
Iron studies decide — page 5.02
Normocytic, low retic
underproduction
Marrow can't respond.
Early iron deficiency or ACD, CKD (↓ EPO), aplastic anemia, marrow infiltration, pure red cell aplasia, hypothyroidism
Reticulocyte production index < 2
Normocytic, high retic
destruction or loss
Marrow responds to RBC loss.
Hemolysis (intrinsic or extrinsic), acute blood loss (after several days)
RPI > 3; polychromasia on smear
Macrocytic — megaloblastic
MCV > 100
Impaired DNA synthesis → nucleus lags behind cytoplasm.
B12 or folate deficiency; methotrexate, hydroxyurea, zidovudine, 5-FU; orotic aciduria
Hypersegmented neutrophils
Macrocytic — nonmegaloblastic
MCV > 100
Membrane lipid changes or immature cells — DNA synthesis is normal.
Alcohol, liver disease, hypothyroidism, reticulocytosis, MDS, Diamond-Blackfan anemia
No hypersegmented neutrophils
Reticulocyte count
marrow report card
Corrected retic = retic % × (Hct ÷ 45). RPI also divides by a maturation factor.
RPI > 3 = good response · < 2 = inadequate
Large bluish RBCs = polychromasia
Hemolysis panel
destruction signs
RBC contents spill or are processed by macrophages.
↑ LDH, ↑ indirect bilirubin, ↓ haptoglobin, ↑ retic · intravascular adds hemoglobinuria, hemosiderinuria
Extravascular → splenomegaly, jaundice, gallstones
Acute: whole blood lost, so Hct is normal at first. Chronic: iron is lost.
Acute: normocytic, retic ↑ after ~5–7 days · chronic: iron-deficiency microcytosis
GI bleed, menorrhagia