* This is the Professional Version. *
Etiology of Anemia
Patient Education
- Approach to the Patient With Anemia
- Red Blood Cell Production
- Etiology of Anemia
- Evaluation of Anemia
- Treatment of Anemia
(See also Red Blood Cell Production.)
Anemia is a decrease in the number of RBCs, hematocrit (Hct), or hemoglobin (Hb) content.
The RBC mass represents the balance between production and destruction or loss of RBCs. Thus, anemia can result from one or more of 3 basic mechanisms (see Table: Classification of Anemia by Cause):
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Blood loss
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Excessive hemolysis (RBC destruction)
Classification of Anemia by Cause
Mechanism |
Examples |
Blood loss |
|
|
Acute |
Childbirth Injuries Surgery |
|
Chronic |
Cancer or polyps in GI tract Kidney tumors Ulcers in the stomach or small intestine |
Deficient erythropoiesis* |
|
|
Microcytic |
Iron reutilization defect (anemia of chronic inflammation, infection, cancer) Iron-transport deficiency (iron refractory iron deficiency anemia [IRIDA]) Iron utilization defect (inherited sideroblastic anemia) Thalassemias (also classified under excessive hemolysis due to intrinsic RBC defects) |
|
Normochromic-normocytic |
Anemia of chronic inflammation, infection, or cancer Kidney disease Endocrine failure (thyroid, pituitary) Malnutrition |
|
Macrocytic |
Liver disease Malabsorption (eg, tropical sprue) Myelodysplasia |
Excessive hemolysis due to extrinsic RBC defects |
|
|
Reticuloendothelial hyperactivity with splenomegaly |
|
|
Immunologic abnormalities |
Drug-induced Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) |
|
Infection |
Ebstein Barr virus (EBV) infection |
|
Mechanical injury |
Cardiac valvular disease Foot strike hemolysis |
|
Drugs/toxins |
Phenazopyridine Ribavirin Spider bites |
Excessive hemolysis due to intrinsic RBC defects |
|
|
Membrane alterations, acquired |
|
|
Membrane alterations, congenital |
|
|
Metabolic disorders (inherited enzyme deficiencies) |
|
|
Hemoglobinopathies |
Sickle cell disease (Hb S) Thalassemias (beta, beta-delta, and alpha) |
|
*Classified according to RBC indices. |
|
Blood losscan be acute or chronic. Anemia does not develop until several hours after acute blood loss, when interstitial fluid diffuses into the intravascular space and dilutes the remaining RBC mass. During the first few hours, however, levels of polymorphonuclear granulocytes, platelets, and, in severe hemorrhage, immature WBCs and normoblasts may rise. Chronic blood loss results in anemia if loss is more rapid than can be replaced or, more commonly, if accelerated erythropoiesis depletes body iron stores (see Iron Deficiency Anemia).
Deficient erythropoiesis has myriad causes. Complete cessation of erythropoiesis results in a decline in RBCs of about 7 to 10%/wk (1%/day). Impaired erythropoiesis, even if not sufficient to decrease the numbers of RBCs, often causes abnormal RBC size and shape.
Excessive hemolysis can be caused by intrinsic abnormalities of RBCs or by extrinsic factors, such as the presence of antibodies or complement on their surface, that lead to their early destruction. An enlarged spleen sequesters and destroys RBCs more rapidly than normal. Some causes of hemolysis deform as well as destroy RBCs. Hemolysis normally causes increased reticulocyte production unless iron or other essential nutrients are depleted.
Resources In This Article
Drugs Mentioned In This Article
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Drug NameSelect Trade
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RibavirinVIRAZOLE
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PhenazopyridineNo US brand name
- Approach to the Patient With Anemia
- Red Blood Cell Production
- Etiology of Anemia
- Evaluation of Anemia
- Treatment of Anemia
* This is the Professional Version. *





Kimia
Meghan