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Physiology · Blood and immunity: nuclear-cytoplasmic dissociation
Sample itemA marrow film shows large erythroid precursors with open, immature nuclear chromatin although the cytoplasm is well haemoglobinised. Which biochemical lesion explains this nuclear-cytoplasmic asynchrony?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Impaired thymidylate and DNA synthesis, with RNA and protein synthesis intact
In vitamin B12 or folate deficiency, thymidylate synthesis fails, so DNA replication and nuclear maturation lag. RNA and haemoglobin synthesis continue, so the cytoplasm matures normally and the nucleus looks immature, giving megaloblasts and macrocytes.
Option by option
A. Impaired thymidylate and DNA synthesis, with RNA and protein synthesis intact (correct)
Correct. DNA synthesis lags while cytoplasmic maturation proceeds.
B. Reduced globin chain output from gene deletion
Reduced globin output also gives small hypochromic cells, as in thalassaemia.
C. Excess erythropoietin driving early release of immature cells
Erythropoietin excess shortens maturation and does not delay nuclear development.
D. Defective haem synthesis with preserved DNA synthesis
Defective haem synthesis gives small, poorly haemoglobinised cells.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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