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This blog has a No Live Tissue policy in regards to its images. In addition, the views in this blog do not necessarily reflect those of my employers.
Anon left asks about this in rapid succession, so I guess that is my cue to talk about megaloblastic anemia, haha.
Megaloblastic anemia is a non-hemolytic anemia, usually attributed to either B12 deficiency (impaired absorption because of a gastrectomy, pernicious anemia, inflammation, or transcobalamin deficiency) or Folate deficiency (dietary, drug related impairment of use, loss though kidney). Both are cofactors in DNA synthesis, especially of thymidine. The result is nuclear cytoplasmic asynchrony wherein the nucleus matures slower than the cytoplasm, and you can see all the cells are a little off looking as a result.
In your smear, you won’t see much in the way of retics, but there will be extensive hypersegmentation of neutrophils, large platelets, huge macrocytes/macroovalocytes, tear cells, schistocytes, pancytopenia, and howell-jolly bodies. A few giant bands and metamyelocytes much sneak into the circulation too. Things are generally just. Big.
The bone marrow will have very distinct megaloblastic changees. The myeloid:erythroid ratio will be decreased but the marrow is almost always hypercellular. Very early erythroid precursors predominate over late precursors because of ineffective erythropoiesis. In contrast to the comically large myeloid precursors, megakaryocytes are small and hypolobated because they have so much DNA they are affected the most by impaired synthesis.