The following are some of the most common anemias. They are arbitrarily grouped according to RBC color and size; other sources may group them in different ways.
1. Anemia Due to Bleeding: Hypochromic-Microcytic Anemia
A temporary anemia can occur after a rapid hemorrhage due to trauma such as a car accident, surgery, or childbirth. The body quickly replaces plasma, but it usually needs several weeks to replace RBCs. With chronicblood loss, as in undiagnosed internal hemorrhaging, anemia develops due to lack of sufficient functional iron and RBCs contain too little hemoglobin.
2. Anemia Due To Deficient RBC Formation: Hypochromic-Microcytic Anemia
Iron-deficient anemia is very common. It is often due to defective production of heme or globin. The iron deficiency may, in turn, be due to:
• Lack of dietary iron (strict vegetarianism or poor diet)
• Defects in iron utilization. Called sideroblastic anemia, the condition is characterized by ineffective RBC formation and the presence of ferritin in developing RBCs
• Defects in iron reutilization. This is the second most common form of anemia and is related to a variety of chronic diseases, infections, and cancers
• Defects in iron transport; a very rare condition called atransferrinemia
3. Anemias Due to Deficient RBC Formation: Normochromic-Normocytic Anemias
Anemia Due to Renal Failure. Chronic kidney failure shortens the life span of RBCs, probably due to an interaction with uremia (excess nitrogen waste in the blood). Replacing RBCs is hindered because failing kidneys release erythropoietin inefficiently.
Aplastic or Hypoplastic Anemia. Both aplastic and hypoplastic indicate incomplete or defective
development. They describe an anemia that arises from partial failure of the bone marrow. Some physicians prefer the term pancytopenia, which means reduced numbers of all types of blood cells. Causes include x-rays, toxic chemicals (benzene, DDT), therapeutic drugs (chloramphenicol, phenylbutazone), or infections such as viral hepatitis.
4. Anemias Due to Excessive RBC Destruction
Hemolytic Anemias. Hemolysis (lysis = break down) is a process in which red cells fall apart and spill out their hemoglobin. Some hemoglobin normally leaks out of cells and dissolves in plasma. Anemia arises when hemolysis occurs in response to a number of factors: spleen dysfunction, immunologic abnormalities, trauma,blood transfusion reactions, malaria, use of some therapeutic drugs, exposure to toxic chemicals, or infections.
Genetic hemolytic conditions include a deficiency in the enzyme G6PD (glucose 6-phosphate dehydrogenase). In some inherited conditions, RBC abnormalities cause the cells to rupture easily, especially in the spleen. In the resulting anemias, sufficient or even excessive RBCs are formed, but their life span is very short. Types of hemolytic anemias due to RBC defects include:
• Hereditary spherocytosis. Microcytic spherical RBCs rupture easily.
• Sickle cell anemia. Hemoglobin S, an abnormal hemoglobin, precipitates into crystals when exposed to oxygen, damaging the cell membrane and causing it to assume a sickle shape. Anisocytosis and poikilocytosis are present. This serious condition is present in about 1% of West African and American Blacks.
• Thalassemia. Faulty or incomplete formation of hemoglobin causes production of tremendous numbers of hypochromic, microcytic, fragile RBCs that often rupture before leaving the bone marrow. Anisocytosis and poikilocytosis are present.
• Erythroblastosis fetalis. RBCs in the fetus are attacked by antibodies from the mother, causing the child to be born with serious anemia.
5. Megaloblastic Anemia (Pernicious Anemia)
These patients remain in constant need of RBCs due to production of oversized, strangely shaped,
normochromic RBCs that rupture easily. Causes are inadequate vitamin B12 or folic acid, or both (Table Below).
Pregnancy increases folic acid requirements and can lead to “megaloblastic anemia of pregnancy” in the last trimester and in pregnancies involving multiple fetuses.