Figure 3.14 Elliptocyte.
tinct morphologies have several recognizable differences (Fig. 3.14). Ovalocytes are egg shaped and capable of many variations of hemoglobin distribution. These cells may appear macrocytic, hypochromic, or normochromic. Ovalocytes—more specifically, macrooval-ocytes—may be observed in the megaloblastic process. Normochromic ovalocytes are typically seen in thal-assemic syndromes. Elliptocytes, on the other hand, are a distinct morphology derived from abnormal spectrin and protein 4.1 component, both red cell membrane proteins. In the primary condition, hereditary elliptocy-tosis, elliptocytes are the predominant morphology, yet this condition is fairly benign with little consequence to the red cell. The other two genotypes of this disorder, hereditary pyropoikilocytosis and spherocytic hereditary elliptocytosis, are a much more serious morphology with severe anemia and are discussed in a subsequent chapter. Elliptocytes may also be present in the peripheral smear of iron-deficient individuals as well as in patients with idiopathic myelofibrosis.
Target cells appear in the peripheral smear as a bull's eye-shaped cell. They are seen in the peripheral blood due to three mechanisms: (a) as an artifact, (b) due to decreased volume because of loss of hemoglobin, and (c) due to increased red cell surface membrane (Fig. 3.15). As cholesterol increases in the plasma, the red cell surface expands, resulting in increased surface area. Target cells appear as hypochromic with a volume of hemoglobin rimming the cells and a thin layer of hemoglobin located centrally, eccentrically, or as a thick band. As a morphology, target cells appear in iron deficiency anemia, hemoglobin C disease and associated conditions, liver disease, and post splenectomy. When hemo globin is affected qualitatively, target cells will appear (Fig. 3.16).
The fragmented cells represent a group of variant morphologies ranging from the schistocytes to the helmet cell. Regardless of the pathophysiology, these cells appear fragmented; indeed, pieces of the red cell membranes have been sheared and hemoglobin leaks through the membranes, causing anemia. Physiological events that may cause this situation are the formation of large inclusions (Heinz bodies) or the predispositions of thrombi. Heinz bodies are large inclusions formed in the red cell as a result of oxidative stress, usually in patients with glucose-6-phosphate dehydrogenase deficiency (see Chapter 7). As the inclusion-rich red cells try to negotiate the spleen, the inclusion-rich cell is pitted, leaving a helmet cell (Fig. 3.17). Schistocytes may be encountered as a result of shear stress from systemic thrombin disposition resulting from disseminated intravascular coagulation or thrombotic thrombocytopenic purpura.8 They may also occur in burn patients or in individuals with heart valve surgery. Burr cells, on the other hand, are usually seen in conditions of uremia or dehydration, both conditions that result from a change in tonicity of circulating fluids (Fig. 3.18). Additionally, burr cells may occur as artifacts in blood smears that have forced to dry through repeated shaking.
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