Types of Anemias

Anemias can be classified using two basic approaches:

• etiology (pathophysiology): the causes of erythrocyte and hemoglobin depletion
• morphology: the characteristic changes in the erythrocytes red blood cells (RBCs), size, shape, and color

An etiologic classification is based on the various conditions that can result from any of the physiologic changes and helps determine direction for planning care. A morphologic classification provides an orderly method for ruling out certain diagnoses when establishing a cause for a particular anemia.

Such morphologic changes in the red blood cell are described in this manner:

• Cell size: (Terms that refer to cellular size end with "cytic".)

normocytes (normal)

microcytes (smaller than normal)

macrocytes (larger than normal)

anisocytes (various sizes)

• Cell shape:

poikilocytes (irregularly-shaped cells)

spherocytes (globular cells)

drepanocytes (sickle cells)

• Cell color: (generally refers to the staining characteristics which reflects the hemoglobin concentration. Terms that describe hemoglobin content end with "chromic".)

normochromic (sufficient or normal amounts of hemoglobin)

hyperchromic (containing an unusually high concentration of hemoglobin in its cytoplasm)

hypochromic (containing an abnormally low concentration of hemoglobin)

These changes produce the following categories of anemias:

• Macrocytic-normochromic anemias (pernicious and folate-deficiency)
• Microcytic-hypochromic anemias (iron-deficiency, sideroblastic, thalassemia)
• Normocytic-normochromic anemias (aplastic, posthemorrhagic, hemolytic, chronic disease, sickle cell)

Macrocytic-normochromic anemia, also known as megaloblastic anemia, produces large, abnormally shaped erythrocytes but normal hemoglobin concentrations. The unusually large stem cells (megaloblasts) in the bone marrow mature into abnormally large erythrocytes (macrocytes) in the circulation. Megaloblastic stem cells are larger at all maturational stages than normal stem cells (normoblasts). In addition, the nucleus of the megaloblast is unusually small in relation to the size of the cell. As the cell matures and begins to synthesize hemoglobin, chromatin in the nucleus fails to clump normally, although the hemoglobin content remains normal. Defective DNA synthesis, caused by deficiencies of vitamin B12 or folate, produces a pattern of ineffective erythropoiesis (cell formation), causing premature cell death with reduced numbers of mature erythrocytes. It is unknown why such a deficiency would cause this outcome, but suggested mechanisms include a delay in nuclear maturation and an imbalance in the normal distribution of RNA and DNA. Nuclear functions or DNA replication and cell division are blocked or delayed. However, RNA and protein synthesis, both cytoplasmic functions proceed normally. The imbalance in the RNA/DNA ratio causes derangement of cell growth.

Microcytic-hypochromic anemia produces small, abnormally small erythrocytes and reduced hemoglobin concentrations. However, hypochromia can occur even in cells of normal size. This type of anemia results from a variety of conditions that are caused by disorders of iron metabolism, porphyrin and heme synthesis, or globin synthesis.

Normocytic-normochromic anemia produces a destruction or depletion of normal or mature erythrocytes. Although the erythrocytes are relatively normal in size and in hemoglobin content, they are insufficient in number. This type does not share any common cause, pathologic mechanism, or morphologic characteristics and is less common than the others. The five distinct anemic conditions exemplify the diversity of this classification.

• Aplastic anemia (caused from depressed stem cell proliferation resulting in bone marrow aplasia)
• Posthemorrhagic anemia (caused from an abnormal amount of blood loss)
• Hemolytic anemia (premature destruction [lysis] of mature erythrocytes in the circulation)
• Anemia of chronic disease (chronic infection or inflammation or malignancy causes an abnormally increased demand for new erythrocytes)
• Sickle cell anemia (congenital dysfunction of hemoglobin synthesis causing abnormal cell shapes)

Data used to identify anemia types include the erythrocyte indicators:

• mean corpuscular volume (MCV), measures the average erythrocyte volume
• mean corpuscular hemoglobin (MCH), measures the average amount of hemoglobin per erythrocyte
• mean corpuscular hemoglobin concentration (MCHC), measures the average concentration of hemoglobin in erythrocytes.

Some types of anemia include the following:

• Achrestic anemia is a megaloblastic type, morphologically resembling pernicious anemia but with multiple other causes.
• Aplastic anemia is a form generally unresponsive to specific anti-anemia therapy and is often accompanied by granulocytopenia (a sudden drop in the production of leukocytes) and thrombocytopenia (a decrease in the number of platelets in circulating blood), in which the bone marrow may not necessarily be lacking cells or a normal cellular structure (acellular) but still fails to produce adequate numbers of blood elements. The term actually is all-inclusive, generally encompassing several clinical syndromes.
• Autoimmune hemolytic anemia (AIHA) is a general term used to cover a large group of anemias involving auto-antibodies against red cell antigens.
• Cooley's anemia is the homozygous form of beta-thalassemia.
• Deficiency anemia refers to a nutritional deficiency that causes anemia.
• Drug-induced immune hemolytic anemia is, as the name suggests, an immune hemolytic anemia caused by drugs, classified by such mechanisms as:

the penicillin type, in which the drug, acting as a hapten is bound to the red cell membrane which induces the formation of specific antibodies

the methyldopa type, in which the drug, possibly by inhibition of suppressor T cells, indicates the formation of anti-Rh antibodies, and

the stibophen or "innocent bystander" type, in which the circulating drug-antibody immune complexes binds nonspecifically to red cells.

• Erythroblastic anemia (see Cooley’s anemia).
• Hemolytic anemia is caused by a shortened survival of mature erythrocytes and the ability of bone marrow to compensate for their decreased life span. It may be hereditary or acquired and usually results from an infection or chemotherapy, or occurs as part of an autoimmune process. Hypochromic anemia occurs when there is a decrease in hemoglobin that is proportionately much greater than the decrease in the number of erythrocytes.
• Hypoplastic anemia is the result of the incapacity of blood-forming organs. Such anemias as Diamond-Blackfan, Pearson’s, transient,erythroblastopenia of childhood (TEC), and Fanconi’s are classified under hypoplastic anemia.
• Hypoplastic congenital anemia, also called erythrogenesis imperfecta and Fanconi's syndrome, is an idiopathic progressive form occurring in the first year of life and without leukopenia and thrombocytopenia. It is unresponsive to hematinics (an agent that improves the quality of the blood) and requires multiple blood transfusions to sustain life.
• Iron-deficiency anemia is characterized by low or absent iron stores, low serum iron concentration, low transferrin saturation, elevated transferrin (total iron-binding capacity), low hemoglobin concentration or hematocrit, and hypochromic and microcytic red blood cells. Its frequent occurrence in children is usually the result of prolonged milk feeding without the provision of a variety of foods or supplemental iron.
• Lederer's anemia is an acute hemolytic form of short duration and unknown etiology.
• Macrocytic anemia results when the erythrocytes become much larger than normal.
• Mediterranean anemia (see Cooley’s anemia)
• Megaloblastic anemia is characterized by the presence of megaloblasts in the bone marrow. Megaloblasts are large, nucleated, immature progenitors of an abnormal erythrocytes and form in certain types of anemia. These cells are irregular in shape and size but contain normal concentrations of hemoglobin and the numbers are below normal. This reaction involves the abnormal production of red cells, white cells, and platelets. There are two types of megoblastic anemias and both are the result of a deficiency (folic acid or B12).
• Microcytic anemia is characterized by a decrease in size of erythrocytes.
• Myelopathic, or myelophthisic, anemia is caused by the destruction or crowding out of hematopoietic tissues by space-occupying lesions. (Hematopoietic pertains to or affecting the formation of blood cells.)
• Normochromic anemia occurs despite the hemoglobin content of the red blood cells, as measured by the MCHC (mean corpuscular hemoglobin concentration), is still within the normal range.
• Normocytic anemia is characterized by proportionate decreases in hemoglobin, packed red cell volume, and the number of erythrocytes per cubic millimeter of blood.
• Nutritional anemia, also known as "deficiency anemia", is caused by a deficiency of an essential substance in the diet, and may be caused by poor dietary intake or by malabsorption.
• Pernicious anemia is a serious form that results from a lack of vitamin B12, generally because of a decreased secretion by the gastric mucosa of IF (intrinsic factor) essential to the formation of erythrocytes and the absorption of vitamin B12. This condition may be secondary to an illness or idiopathic (formed from unknown causes). Treatment consists of regular, lifetime administrations of the vitamin.
• Sickle cell anemia, sometimes called sickle cell disease, is a genetically determined defect of hemoglobin synthesis associated with poor physical development and skeletal anomalies.
• Spur-cell anemia occurs when the red cells have a bizarre spiculated shape and are destroyed prematurely, primarily in the spleen. It is an acquired form occuring in severe liver disease and represents an abnormality in the cholesterol content of the red cell membrane.
• Von Jaksch’s anemia, also known as pseudoleukemica infantum, is an anemic leukemia of infants and probably not a distinct disease. It is a syndrome caused by many factors: malnutrition, chronic infection, malabsorption, or other conditions. There seems to be some developmental basis for the inability of these babies to react to infectious processes in a normal manner. This disease follows, or is associated with, some severe nutritional or infectious disease and is characterized by anemia of increasing severity, splenomegaly and myeloid leucocytosis, together with the symptoms of the underlying disease. It is possible that symptoms of severe malnutrition ordinarily supposed to be the cause of the anemia, may really be the earlier symptoms of the disease itself, as an entity caused by developmental defect in the spleen and red bone marrow. It was once considered to be a specific entity in children under the age of three.