Classification of Acquired Anemias

Acquired anemias classify pathophysiologically into decreased production, increased destruction, and blood loss.

Pathophysiologic Categorization

Mechanism	Primary Acquired Etiologies
Decreased production	Nutritional deficiency, bone marrow failure, anemia of chronic disease, marrow infiltration,,,
Increased destruction	Immune hemolysis, microangiopathy, infections, toxins, hypersplenism, paroxysmal nocturnal hemoglobinuria,,
Blood loss	Gastrointestinal hemorrhage, trauma, fetomaternal hemorrhage,

Results from complete failure of erythropoiesis or ineffective erythropoiesis.

Iron deficiency: Causes microcytic hypochromic anemia; secondary to inadequate diet, poor absorption, or occult blood loss,.
Folate deficiency: Causes macrocytic megaloblastic anemia; secondary to inadequate intake, malabsorption, or specific drugs like methotrexate,,.
Vitamin B12 deficiency: Causes macrocytic megaloblastic anemia; secondary to pernicious anemia, strict vegan diet, or ileal resection,,.
Protein deficiency: Kwashiorkor causes mild normocytic anemia.
Vitamin C deficiency: Causes scurvy-associated anemia.

Idiopathic aplastic anemia: Immune-mediated destruction of hematopoietic stem cells; represents majority of acquired cases,.
Drug-induced aplasia: Predictable (chemotherapy) or idiosyncratic (chloramphenicol, antiepileptics, nonsteroidal anti-inflammatory drugs),.
Toxin-induced aplasia: Benzene, insecticides, heavy metals,.
Infection-induced aplasia: Viral hepatitis, human immunodeficiency virus, Epstein-Barr virus, cytomegalovirus,.
Radiation exposure: Direct stem cell cytotoxicity,.
Transient erythroblastopenia of childhood: Post-viral, temporary red cell aplasia occurring primarily between 6 months and 3 years of age.
Parvovirus B19 infection: Selective transient erythrocytopenia; causes aplastic crisis in chronic hemolytic conditions,,.

Anemia of chronic disease: Normocytic hypoproliferative anemia secondary to inflammation, malignancy, or autoimmune disease; mediated by hepcidin excess,.
Chronic kidney disease: Decreased erythropoietin production causes normocytic anemia,.
Marrow infiltration: Leukemia, lymphoma, neuroblastoma replace normal marrow space,,.

Accelerated destruction exceeds compensatory marrow production capacity.

Isoimmune: Hemolytic disease of newborn (maternal-fetal incompatibility), mismatched blood transfusion,.
Warm autoimmune hemolytic anemia: Immunoglobulin G autoantibodies mediate splenic extravascular destruction; idiopathic or secondary to systemic lupus erythematosus, immunodeficiency, malignancy,,.
Cold agglutinin disease: Immunoglobulin M autoantibodies mediate intravascular complement destruction; often post-Mycoplasma pneumoniae or Epstein-Barr virus infection,.
Paroxysmal cold hemoglobinuria: Donath-Landsteiner immunoglobulin G autoantibody; associated with viral infections or syphilis.
Drug-induced immune hemolysis: Hapten mechanism (penicillins), ternary complex (quinine), or autoantibody induction (methyldopa),.

Microangiopathic hemolytic anemia: Mechanical fragmentation causing schistocytes; includes hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation,,.
Mechanical trauma: Artificial heart valves, severe burns causing spherocytic hemolysis,.
Infections: Direct parasitic invasion (malaria, babesiosis), bacterial toxins (clostridium perfringens),,,.
Chemical injury and toxins: Snake bites, lead toxicity, copper toxicity (Wilson disease),,.
Hypersplenism: Excessive splenic sequestration and destruction secondary to portal hypertension or infection.
Paroxysmal nocturnal hemoglobinuria: Acquired intrinsic membrane defect; somatic mutation causes deficiency of complement regulatory proteins,.

Acute or chronic loss depletes red cell mass and iron stores.

Gastrointestinal bleeding: Peptic ulcer, Meckel diverticulum, inflammatory bowel disease, cow milk protein allergy.
Menorrhagia: Heavy menstrual losses causing chronic iron deficiency.
Recurrent epistaxis: Chronic loss depletes iron stores,.