Caused by disorders of iron metabolism, disorders of porphyrin and heme synthesis or disorders of globin synthesis Iron deficiency is the most common cause Iron is the essential component of hemoglobin and is in constant demand during erythropoiesis IDA develops slowly in 3 stages: 1. first the body’s iron stores are depleted but erythropoiesis continues, with normal hbg content, 2. iron transport to bone marrow is diminished and iron deficient erythropoiesis takes place 3. small hbg-deficient cells enter the circulation in sufficient numbers and replace normal erythrocytes that have reached maturity and have been removed from the circulation. This stage is assoc with IDA and is characterized by depletion of iron stores and diminished hbg production.
Serum ferritin is the diagnostic test of choice to diagnose iron deficiency anemia Treatment is iron supplementation Normocytic Anemia the most common form of anemia Erythrocytes are normal in size and hemoglobin but insufficient in number 1. Caused by decreased production of normal-sized RBC’s Anemia of chronic disease (most common) such as chronic inflammatory conditions, infections, neoplasms-due to impaired ability to use stored iron.
Renal failure (acute and chronic)-uremic metabolites decrease the life span of circulating RBCs Endocrine deficiency-hypothyroidism, adrenal or pituitary insufficiency-secondary bone marrow failure because of reduced stimulation of erythropoietin secretion Aplastic anemia- iron is present, but unavailable for use, due to hypoplastic bone marrow, normal bone marrow infiltrated by fat, either idiopathic primary, or secondary caused by chemicals or ionizing radiation
Other uncommon causes-bone marrow infiltration, fibrosis, myeloproliferative diseases, and sideroblastic anemias 2. Increased destruction or loss of RBC’s Drug induced autoimmune hemolytic anemias-esp in pts with G6PD deficiency, drugs implicated include-methyldopa, penicillin, cephalosporins, erythromycin, acetaminophen, procainamide Acute blood loss/hemorrhage-symptoms depend on severity/amount of blood loss.
Hypersplenism-due to removal of RBC’s from the circulation (spleen 3-4 x normal size) Hemolytic disorders-due to decreased survival of RBC’s-may be inherited or acquired Uncompensated increase in plasma volume Pregnancy-physiologic hemodilution Fluid overload-diabetes insipidus Macrocytic Anemia Aka megaloblastic anemia Larger than normal RBC’s with smaller than normal nuclei
Caused by Vitamin B12 deficiency or Folate deficiency B12 Deficiency-Pernicious Anemia Vit B12 important for RBC formation and neural development Requires presence of Intrinsic Factor (produced by parietal cells in gastric pits) for absorption Usually assoc with chronic gastritis/GI dysfunction, stomach surgeries or extreme malnutrition (strict vegetarianism) Treated with Vit B12 injections Folate Deficiency Folate essential for RBC production and maturation Alcoholism, and chronically malnourished individuals Treated with oral folic acid preparations, improvement in anemia within 1-2 weeks.
McCance, H. & Huether, S. (2002). Pathophysiology: The Biological basis for disease in adults and children. St. Louis: Mosby.
Anemia Review Panel. (2004). Guidelines for the management of anemia (1st ed.) Toronto: MUMS Guideline Clearinghouse.