Hemolytic Anemias Overview

Hemolytic Anemias

• Characterized by premature destruction of red blood cells (RBCs)
• Share features such as shortened RBC life span (less than 120 days), elevated erythropoietin levels, and compensatory increase in erythropoiesis.
• Extravascular hemolysis: RBC destruction occurs within macrophages (in spleen, liver, and bone marrow)
• Triggered by age-dependent changes in RBC surface proteins recognized and removed by phagocytes.
• Can cause splenomegaly (enlarged spleen) in cases of persistent extravascular hemolysis.
• Altered RBC shape or reduced deformability causes difficulty navigating splenic sinusoids, leading to sequestration and eventual phagocytosis.
• Reduced plasma haptoglobin levels (a protein that binds free hemoglobin) due to hemoglobin leakage from phagocytes.
• Intravascular hemolysis: RBC destruction occurs within blood vessels.
• Less common than extravascular hemolysis.
• Can be caused by mechanical injury, complement fixation, intracellular parasites (e.g., malaria), or exogenous toxic factors.
• Results in hemoglobinemia (free hemoglobin in plasma), hemoglobinuria (free hemoglobin in urine), and hemosiderinuria (iron deposits in urine).
• Free hemoglobin can oxidize to methemoglobin which is brown in color, resulting in red-brown urine.
• Unconjugated hyperbilirubinemia may occur due to liver's inability to promptly process the increased bilirubin.

Chronic Blood Loss Anemia

• Anemia occurs when blood loss rate surpasses the body's ability to replenish red blood cells.
• Anemia occurs when loss exceeds marrow's regenerative capacity or when iron reserves are depleted, leading to iron deficiency anemia.
• Symptoms include shortened red blood cell life span.
• Elevated erythropoietin levels and compensatory erythropoiesis.