erythrocyte

Erythrocytes are the most abundant blood cells, lacking a nucleus and organelles (extruded during maturation), which maximizes space for hemoglobin (Hb) and allows flexibility to pass through narrow capillaries. Their biconcave shape increases surface area-to-volume ratio for efficient gas exchange. Each RBC contains ~270 million hemoglobin molecules, each binding up to 4 oxygen molecules. RBCs rely on anaerobic glycolysis (no mitochondria) for ATP production, and the pentose phosphate pathway (via G6PD) to generate NADPH, protecting against oxidative stress—deficiency in G6PD leads to hemolytic anemia under oxidative stress.

Erythropoiesis occurs in the bone marrow, stimulated by erythropoietin released from renal peritubular cells in response to hypoxia. Maturation stages: proerythroblast → basophilic erythroblast → polychromatophilic erythroblast → orthochromatic erythroblast → reticulocyte → mature erythrocyte. Reticulocyte count reflects marrow erythropoietic activity and is clinically used to assess anemia response.

After ~120 days, senescent RBCs are removed by macrophages in the spleen (extravascular hemolysis) via recognition of membrane changes; hemoglobin is broken down into heme and globin—heme further degraded to biliverdin, then bilirubin (unconjugated), transported to liver for conjugation and excretion.

Clinical relevance: RBC indices (MCV, MCH, MCHC) help classify anemias (microcytic, normocytic, macrocytic). Morphological abnormalities (e.g., spherocytes, schistocytes, target cells, sickle cells) provide diagnostic clues to underlying hematologic or systemic diseases. Membrane defects (hereditary spherocytosis), enzyme deficiencies (G6PD deficiency, pyruvate kinase deficiency), and hemoglobinopathies (sickle cell disease, thalassemias) are classic board topics involving erythrocyte pathology.