Day 2-Hematology Slides
October 20, 2013
This disease can be mild to serious and it represents the heterozygous form of B-thalassemia.
This form of the disease can be asymptomatic and the patient may have a mild anemia which is rarely
severe. The patient will exhibit splenomegaly and the peripheral blood will present itself as
hypochromic. The RBC abnormality is proportional to the degree of anemia. Under the microscope one
will observe increased target cells, microcytic hypochromic RBCs, basophilic stippling. Many cases first
thought to be iron deficiency anemia however patients don’t respond to iron. The serum iron
concentration will be normal or increased, there will be decreased iron binding capacity and increased
iron stores. There will be an increase of RBCs to 2x the normal amount, which is an indication of
This is present when there are two thalassemia genes which is the homozygous representation.
This is the most severe form of the B-thalassemia disease. Cooley’s or Mediterranean anemia is present.
Under the microscope one will observe severe hypochromic anemia, polychromasia or increased
reticulocytes, normoblasts, howell-jolly bodies, increased target cells, leukocytosis, and basophilic
stippling. The patient often has splenomegaly, bone changes (extreme erythroid hyperplasia of bone
marrow), decreased survival of RBCs (usually 60 days), increased serum iron concentration, increased
bilirubin, and is often fatal in childhood.
In hemolytic anemia’s there are many potential causes for abnormal RBC morphology.
Spherocytes can be seen when the cause is transfused blood rejection, warm antibody hemolytic
anemia, or hereditary spherocytosis. Schistocytes can be seen when the cause is microangiopathy,
target cells will be seen when the cause is hemoglobinopathies such as sickle cell disease, HgbC disease
or thalassemias. Sickled cells will be seen when the cause is sickle cell diseases, Heinz bodies will be seen
with G6-PD deficiency, or oxidation of Hgb. Polychromasia will be seen as a result of thalassemia major.
Autoimmune Hemolytic Anemia-
These types of anemia occur by 2 mechanisms. The first is intravascular hemolysis where an Ab
attaches to RBC and activates complement causing direct cell lysis. The other mechanism for abnormal
morphology of RBCs is caused by extravascular hemolysis of the spleen, where an Ab coats the RBC and
it’s removed by the MPS. In this type of anemia we may be spherocytes because the spleen recognizes
Ab on RBC membrane and tries to remove it and removes some of the membrane. SC Disease-
Also known as microdrepanocytic disease, these patients will exhibit a severe hemolytic anemia.
Under the microsc