MLT GlobeHematology: RBC morphology & inclusions – page 3
89 Hematology MCQs on RBC morphology & inclusions with answers and explanations.
A red cell with two horn-like projections forms when:
Keratocytes (horn cells) form when a vacuole near the edge ruptures, often in microangiopathic states such as DIC. Removal of a Heinz body by the spleen produces a bite cell.
A patient with severe burns shows small, dense spherical red cells and budding fragments. The mechanism is:
Heat above about 49°C damages spectrin, causing fragmentation and microspherocytes soon after the burn. The DAT is negative, so antibodies are not the cause.
Target cells form when:
Excess membrane (e.g. cholesterol loading in liver disease) or reduced hemoglobin (thalassemia) leaves extra membrane that folds into a target shape. A decreased surface-to-volume ratio produces spherocytes instead.
Red cells appear in clumps on a wet preparation. After adding saline, the clumps disperse. This indicates:
Rouleaux are caused by high plasma proteins and break up when plasma is replaced or diluted with saline. True agglutination is antibody-mediated and persists after saline replacement.
A smear from a patient with a strong cold agglutinin shows large red cell clumps. The best way to prepare a readable smear is to:
Cold agglutinins disperse at body temperature, so warming the sample and slides reduces clumping. Refrigeration increases cold agglutination.
Red cells on a smear show sharp-edged, bright refractile areas that change with the fine focus. The stain methanol was left uncovered in humid air. These are most likely:
Water in the fixative or stain produces refractile, sharply outlined areas that shine when focusing, unlike true inclusions. Pappenheimer bodies are small dark granules that do not glisten.
An inclusion on top of a red cell has a clear halo around it and lies in a slightly different focal plane. It is most likely:
A platelet lying on a red cell often has a surrounding halo and a different focal plane, and may show granules. True inclusions lie within the cell in the same plane as the hemoglobin.
On a Wright-stained smear, red cells are bright orange-red and white cell nuclei are pale and poorly stained. The most likely cause is:
An acidic buffer favors the eosin dye, giving red cells a bright red color and weak nuclear staining. An alkaline buffer or overstaining makes the whole smear too blue.
Many round red cells without central pallor are seen only at the extreme feathered edge of an otherwise normal smear. The best interpretation is:
Cells at the feathered edge are flattened and lose central pallor, mimicking spherocytes. True spherocytes are seen throughout the proper reading area.
In a person with sickle cell trait who is well, the peripheral smear usually shows:
HbS below about 40% does not polymerize under normal oxygen levels, so sickle cells are not seen in trait. Irreversibly sickled cells are a feature of sickle cell disease.
A patient with advanced alcoholic cirrhosis has hemolytic anemia with many red cells showing irregular spiny projections. This is known as:
In severe liver disease, abnormal lipoproteins load the red cell membrane with cholesterol, forming acanthocytes (spur cells) that are removed by the spleen. Pyruvate kinase deficiency causes echinocytes, mainly after splenectomy.
A jaundiced group O mother's group A newborn has a weakly positive DAT. The smear most likely shows:
In ABO hemolytic disease of the newborn, IgG anti-A partly removes membrane in the spleen, producing microspherocytes. Target cells are not a feature of immune hemolysis.
A smear shows two distinct red cell populations: normocytic normochromic cells and hypochromic microcytes. Which situation best explains this dimorphic picture?
After iron therapy, new normal cells mix with the old hypochromic microcytes, giving two populations. Thalassemia trait produces a single, uniform microcytic population.
Rouleaux form in multiple myeloma mainly because the increased plasma proteins:
Red cells normally repel each other because of their negative surface charge. High globulin or fibrinogen lowers this zeta potential, so cells stack like coins; binding to specific antigens would cause agglutination instead.
An untransfused child with beta-thalassemia major would be expected to show which smear picture?
Severe ineffective erythropoiesis gives marked microcytic hypochromic poikilocytosis, target cells, basophilic stippling and numerous nucleated red cells. Isolated spherocytes or macrocytes do not fit.
Basophilic stippling on a Wright-stained smear represents aggregated:
Stippling is precipitated ribosomal RNA, seen when ribosome breakdown is impaired, as in lead poisoning. Denatured hemoglobin forms Heinz bodies, iron granules are Pappenheimer bodies and DNA remnants are Howell-Jolly bodies.
Mature trophozoites stretched across normal-sized red cells as bands, and schizonts with about 8 merozoites in a rosette, suggest:
Band-form trophozoites and rosette ('daisy-head') schizonts in normal or small red cells are typical of P. malariae. P. vivax enlarges the red cell and its schizonts have 12–24 merozoites.
Infected red cells are oval, slightly enlarged, with ragged (fimbriated) edges and coarse red dots (James dots). The species is most likely:
P. ovale typically makes the infected cell oval with fimbriated ends and Schüffner-type (James) dots. P. malariae does not enlarge or distort the cell.
Coarse, irregular red-purple dots (Maurer clefts) in red cells containing larger trophozoites are characteristic of:
Maurer clefts are membrane structures in red cells infected with P. falciparum. P. vivax shows fine Schüffner dots instead, and Babesia produces no stippling.
In P. falciparum infection, usually only ring forms and gametocytes are seen in peripheral blood because:
Knobs on infected red cells make them adhere to endothelium (sequestration), so mature trophozoites and schizonts stay in deep capillaries. Seeing schizonts in the blood suggests heavy, severe infection.