Haematopathology MCQs: Blood Disorders & OmpathStudy

MOUNT KENYA UNIVERSITY — MEDICAL SCHOOL Programme: Bachelor of Medicine and Bachelor of Surgery — Department of Pathology Assessment: CAT 2 — End of Semester 2 Unit Code: MBML 3522 — Haematopathology --- Q1. Common myeloid progenitor (CMP) vs common lymphoid progenitor (CLP) — which transcription factor is MOST critical for commitment to myeloid over lymphoid lineage? A. GATA-2 — promotes lymphoid differentiation at the expense of myeloid B. PU.1 — upregulates myeloid gene programmes and suppresses lymphoid commitment C. PAX5 — required for commitment to the erythroid lineage D. Ikaros — required exclusively controls megakaryocyte differentiation E. C/EBPalpha — exclusively controls megakaryocyte differentiation Answer: B — PU.1 PU.1 is the master transcription factor tipping multipotent progenitors toward myeloid fate while suppressing lymphoid genes. The descriptions attached to the other options here are inaccurate distractors (PAX5 is actually essential for B-lymphoid commitment, not erythroid; GATA-2 supports early haematopoietic stem cell maintenance, not lymphoid-biased differentiation). Q2. 35-year-old woman, bone marrow trephine shows <10% cellularity, fat replacement, reduction of all three cell lines; serum erythropoietin markedly elevated. A. Myelofibrosis — replacement of marrow by reticulin fibrosis driven by megakaryocyte cytokines B. Aplastic anaemia — immune-mediated (T-cell) destruction of haemopoietic stem cells C. Myelodysplastic syndrome — clonal stem cell disorder with ineffective haemopoiesis D. Megaloblastic anaemia — impaired DNA synthesis causing intramedullary cell death E. Chronic lymphocytic leukaemia — marrow infiltration by clonal B-lymphocytes Answer: B — Aplastic anaemia Severely hypocellular marrow (<10%) with fat replacement, pancytopenia, and appropriately elevated EPO (compensatory response to anaemia) is the classic picture of aplastic anaemia, typically driven by autoimmune T-cell attack on haematopoietic stem cells. Q3. 28-year-old female, fatigue/pallor; Hb 85 g/L, MCV 110fL, hypersegmented neutrophils, oval macrocytes, low reticulocytes — mechanism of impaired DNA synthesis in megaloblastic anaemia? A. Impaired globin chain synthesis causes imbalanced haemoglobin production B. Deficiency of vitamin B12 or folate impairs thymidylate synthesis, blocking DNA replication C. Reduced EPO production from renal failure prevents erythroblast maturation D. Iron deficiency prevents haem synthesis, stalling erythroblast maturation E. Riboflavin deficiency impairs the electron transport chain in erythroblasts Answer: B — Deficiency of vitamin B12 or folate impairs thymidylate synthesis, blocking DNA replication B12/folate are essential cofactors for thymidylate (and thus DNA) synthesis; their deficiency causes nuclear-cytoplasmic asynchrony (large cells with immature nuclei) — the hallmark of megaloblastic change. Q4. 70-year-old with rheumatoid arthritis: Hb 96 g/L, MCV 78fL, serum ferritin 420 microg/L (elevated), serum iron low, TIBC low, transferrin saturation 12% — which finding best distinguishes anaemia of chronic disease (ACD) from iron deficiency anaemia (IDA)? A. Low MCV and microcytic film in ACD, versus low ferritin and high TIBC in IDA B. Elevated serum ferritin and low TIBC in ACD, versus low ferritin and high TIBC in IDA C. Reticulocyte count is always elevated in ACD D. Bone marrow iron stores are absent in both ACD and IDA E. Hepcidin levels are low in ACD, causing iron sequestration Answer: B — Elevated serum ferritin and low TIBC in ACD, versus low ferritin and high TIBC in IDA This is the classic distinguishing pattern: ACD shows normal/high ferritin (an acute phase reactant) with low TIBC due to hepcidin-mediated iron sequestration, while true IDA shows low ferritin with compensatory high TIBC. Q5. 22-year-old woman, fatigue, koilonychia, dysphagia; Hb 78 g/L, MCV 62fL, MCH 18pg, microcytic hypochromic cells, pencil cells, target cells, serum ferritin 4 microg/L — most appropriate INITIAL treatment? A. Intramuscular hydroxocobalamin injections B. Blood transfusion to immediately raise the haemoglobin C. Oral ferrous sulphate 200mg three times daily for 3-6 months D. Erythropoietin injections to stimulate red cell production E. Desferrioxamine to chelate excess iron stores Answer: C — Oral ferrous sulphate 200mg three times daily for 3-6 months This is classic Plummer-Vinson/Paterson-Brown-Kelly syndrome-type severe IDA (koilonychia, dysphagia); low ferritin confirms true iron deficiency, and oral iron replacement is standard first-line treatment unless there's haemodynamic instability requiring transfusion. Q6. 30-year-old Mediterranean male, mild anaemia, Hb 102 g/L, MCV 65fL, target cells; HbA 93%, HbA2 4.8%, HbF 1.5%, normal ferritin. Wife has similar findings — most important counselling point? A. Alpha-thalassaemia trait; risk to offspring is clinically insignificant B. Beta-thalassaemia trait; if his wife also has trait, there is a 25% chance of beta-t