MCQ: High-Yield MCQs — Haematology (All Topics)

Question 1

The main site of haematopoiesis in a healthy adult is

Accepted Answer

Red bone marrow — Red bone marrow in flat bones (sternum, vertebrae, pelvis) is the primary haematopoietic site in adults; liver and spleen are fetal sites. ---

Question 2

Which cytokine is the primary stimulator of megakaryocyte and platelet production?

Accepted Answer

Thrombopoietin — Thrombopoietin (TPO) is produced mainly by the liver and acts on megakaryocytes to drive platelet production. ---

Question 3

On a peripheral blood film, which cell has a bilobed nucleus connected by a thin strand and prominent pink granules?

Accepted Answer

Eosinophil — Eosinophils have characteristically bilobed nuclei and large orange-pink granules; they are elevated in allergies and parasitic infections. ---

Question 4

Target cells on a peripheral blood film are seen in all of the following EXCEPT

Accepted Answer

Hereditary spherocytosis — Hereditary spherocytosis produces spherocytes, not target cells; target cells reflect excess membrane relative to cell content. ---

Question 5

A peripheral blood film shows hypersegmented neutrophils ( 5 lobes). The most likely underlying deficiency is

Accepted Answer

Vitamin B12 or folate — Vitamin B12/folate deficiency impairs DNA synthesis, causing nuclear maturation delay and hypersegmentation of neutrophils. ---

Question 6

Erythropoietin is produced mainly by

Accepted Answer

Adrenal cortex — Peritubular interstitial cells in the renal cortex sense hypoxia via HIF-1α and release EPO to stimulate red cell production. ---

Question 7

The normal lifespan of a red blood cell is approximately

Accepted Answer

120 days — 120 days is the normal RBC lifespan; senescent RBCs are phagocytosed by splenic and hepatic macrophages. ---

Question 8

Which haemoglobin is predominant in a normal adult?

Accepted Answer

HbA — HbA (α2β2) constitutes approximately 96–98% of adult haemoglobin; HbA2 is ~2.5% and HbF <1%. ---

Question 9

The Bohr effect describes

Accepted Answer

Decreased O₂ affinity with rising CO₂ and falling pH — Rising CO₂ and acidosis shift the oxygen-dissociation curve rightward, promoting O₂ release to tissues — the physiological Bohr effect. ---

Question 10

In intravascular haemolysis, which urine finding is most specific?

Accepted Answer

Haemosiderin — Haemosiderinuria occurs when free haemoglobin is filtered and reabsorbed by tubular cells; iron deposits detected by Prussian blue stain are specific for intravascular haemolysis. ---

Question 11

The MCV in iron deficiency anaemia is

Accepted Answer

Low — Low MCV (microcytic anaemia) occurs because insufficient iron limits haemoglobin synthesis, reducing RBC size. ---

Question 12

Which iron study pattern is seen in anaemia of chronic disease?

Accepted Answer

High ferritin, low serum iron, low TIBC — Inflammation sequesters iron in macrophages (high ferritin as acute phase reactant), reduces serum iron, and decreases TIBC — distinguishing it from iron deficiency. ---

Question 13

A patient has MCV 110 fL, hypersegmented neutrophils, and serum B12 of 80 pg/mL. The most likely diagnosis is

Accepted Answer

Megaloblastic anaemia — Megaloblastic anaemia from B12 deficiency causes macrocytosis and hypersegmented neutrophils due to impaired DNA synthesis. ---

Question 14

The most common cause of macrocytic anaemia in the developed world is

Accepted Answer

Alcohol excess — Alcohol causes macrocytosis through direct toxic effects on the bone marrow and poor nutrition; it is the most common cause overall in many populations. ---

Question 15

Schilling test was used to diagnose

Accepted Answer

Pernicious anaemia (B12 malabsorption) — Pernicious anaemia involves lack of intrinsic factor; the Schilling test showed B12 malabsorption corrected by intrinsic factor supplementation. ---

Question 16

Beta-thalassaemia major is caused by

Accepted Answer

Mutations causing absent or reduced beta-globin chains — Mutations in the beta-globin gene reduce (β+) or abolish (β0) beta-chain production, causing excess unpaired alpha chains that damage RBCs. ---

Question 17

HbA2 3.5% on HPLC is diagnostic of

Accepted Answer

Beta thalassaemia trait — Beta thalassaemia trait causes compensatory upregulation of delta-globin chains, raising HbA2 above 3.5%. ---

Question 18

In sickle cell disease, sickling is promoted by all of the following EXCEPT

Accepted Answer

High fetal haemoglobin — HbF inhibits HbS polymerization by disrupting the deoxygenated HbS polymer structure; high HbF is protective, not a trigger. ---

Question 19

The direct antiglobulin test (DAT/Coombs) detects

Accepted Answer

Antibodies or complement on the RBC surface — DAT detects IgG or complement (C3d) already bound to red cells, confirming immune-mediated haemolysis. ---

Question 20

Hereditary spherocytosis is most commonly due to deficiency of

Accepted Answer

Spectrin or ankyrin — Spectrin/ankyrin deficiency destabilizes the RBC membrane skeleton, causing membrane loss and spherocyte formation with reduced osmotic resistance. ---

Question 21

G6PD deficiency causes haemolytic episodes triggered by

Accepted Answer

Oxidative stress (drugs, infections, fava beans) — Oxidative stress depletes glutathione in G6PD-deficient cells (cannot regenerate NADPH), causing Heinz body formation and haemolysis. ---

Question 22

The Philadelphia chromosome results from translocation

Accepted Answer

t(9;22) — BCR-ABL fusion — t(9;22) creates the BCR-ABL fusion gene encoding a constitutively active tyrosine kinase, the hallmark of CML. ---

Question 23

A 45-year-old presents with fatigue, splenomegaly, WBC 120×10⁹/L with full myeloid spectrum on film. BCR-ABL is positive. Diagnosis

Accepted Answer

Chronic myeloid leukaemia — CML presents with very high WBC, full myeloid spectrum (including basophilia), splenomegaly, and positive BCR-ABL/Philadelphia chromosome. ---

Question 24

Blast crisis in CML is defined as blasts exceeding what percentage in bone marrow?

Accepted Answer

20% — ≥20% blasts in blood or bone marrow defines blast crisis (transformation to acute leukaemia) per WHO criteria. ---

Question 25

The first-line treatment for CML that targets BCR-ABL is

Accepted Answer

Imatinib (tyrosine kinase inhibitor) — Imatinib revolutionized CML treatment by selectively inhibiting the BCR-ABL tyrosine kinase, achieving molecular remission in most patients. ---

Question 26

Chronic lymphocytic leukaemia (CLL) is characterized by accumulation of

Accepted Answer

Mature monoclonal B lymphocytes — CLL is a clonal proliferation of functionally incompetent mature B cells (CD5+, CD23+, CD19+) that accumulate in blood, marrow, and lymph nodes. ---

Question 27

Smudge (smear) cells on peripheral blood film are characteristic of

Accepted Answer

CLL — CLL cells are fragile and rupture during film preparation, creating characteristic smudge/smear cells. ---

Question 28

Reed-Sternberg cells are pathognomonic of

Accepted Answer

Hodgkin lymphoma — Reed-Sternberg cells (large binucleated cells with prominent "owl-eye" nucleoli) are the hallmark of Hodgkin lymphoma. ---

Question 29

The most common chromosomal translocation in follicular lymphoma is

Accepted Answer

t(14;18) — BCL2 overexpression — t(14;18) juxtaposes BCL2 with the IGH locus, causing BCL2 overexpression and resistance to apoptosis in follicular lymphoma. ---

Question 30

Burkitt lymphoma is associated with which translocation causing MYC overexpression?

Accepted Answer

t(8;14) — t(8;14) places the MYC oncogene under control of the IGH enhancer, driving rapid B-cell proliferation in Burkitt lymphoma. ---

Question 31

Multiple myeloma is diagnosed by the presence of all of the following EXCEPT

Accepted Answer

Reed-Sternberg cells — Reed-Sternberg cells are seen in Hodgkin lymphoma, not myeloma. Myeloma diagnosis requires plasma cell proliferation with end-organ damage. ---

Question 32

Bence Jones proteins in urine represent

Accepted Answer

Free monoclonal light chains (kappa or lambda) — Free light chains filtered by the kidney form Bence Jones proteins; they cause tubular damage and cast nephropathy in myeloma. ---

Question 33

In acute myeloid leukaemia (AML), Auer rods are

Accepted Answer

Pathognomonic crystalline azurophilic inclusions in myeloblasts — Auer rods are fused lysosomal granules forming needle-like inclusions specific to myeloid blasts; their presence confirms AML over ALL. ---

Question 34

AML M3 (acute promyelocytic leukaemia) is associated with

Accepted Answer

t(15;17) — PML-RARA — t(15;17) creates PML-RARA fusion, blocking myeloid differentiation; ATRA (all-trans retinoic acid) induces differentiation and is curative. ---

Question 35

The most feared complication of AML-M3 at presentation is

Accepted Answer

Disseminated intravascular coagulation — DIC occurs because promyelocytic granules release procoagulants; it must be treated urgently with ATRA before chemotherapy. ---

Question 36

The hallmark laboratory finding in acute lymphoblastic leukaemia (ALL) is

Accepted Answer

Lymphoblasts positive for TdT (terminal deoxynucleotidyl transferase) — TdT positivity marks immature lymphoid cells; it distinguishes ALL blasts from mature lymphocytes and myeloid blasts. ---

Question 37

The coagulation cascade's final common pathway begins with activation of

Accepted Answer

Factor X — Factor Xa combines with Factor Va (prothrombinase complex) to convert prothrombin to thrombin — the start of the common pathway. ---

Question 38

Prothrombin time (PT) primarily measures

Accepted Answer

Extrinsic and common pathway (VII, X, V, II, fibrinogen) — PT/INR tests the extrinsic pathway via tissue factor/Factor VII; it is used to monitor warfarin therapy. ---

Question 39

APTT is prolonged in deficiency of all EXCEPT

Accepted Answer

Factor VII — Factor VII is part of the extrinsic pathway only; its deficiency prolongs PT but not APTT. ---

Question 40

A patient has prolonged APTT, normal PT, normal platelet count, and recurrent haemarthroses. Diagnosis

Accepted Answer

Haemophilia A (Factor VIII deficiency) — Haemophilia A causes isolated APTT prolongation and deep bleeding (haemarthroses, muscle haematomas) due to Factor VIII deficiency. ---

Question 41

Von Willebrand factor (vWF) has two main functions

Accepted Answer

Platelet adhesion to subendothelium and Factor VIII carrier — vWF bridges platelet GPIb receptors to exposed collagen and protects Factor VIII from degradation in plasma. ---

Question 42

In type 1 Von Willebrand disease, laboratory findings show

Accepted Answer

Normal PT, prolonged APTT, reduced vWF antigen and activity — Reduced vWF quantity causes mildly prolonged APTT (low Factor VIII), prolonged bleeding time, and reduced ristocetin cofactor activity. ---

Question 43

Disseminated intravascular coagulation (DIC) laboratory profile includes

Accepted Answer

Low fibrinogen, high D-dimer, prolonged PT and APTT, thrombocytopaenia — Systemic clotting consumes fibrinogen, factors, and platelets while fibrinolysis elevates D-dimers; both PT and APTT are prolonged. ---

Question 44

D-dimer is a degradation product of

Accepted Answer

Crosslinked fibrin (by Factor XIIIa) — D-dimer is released when plasmin cleaves crosslinked fibrin; it is elevated in DIC, DVT, PE, and any thrombotic state. ---

Question 45

Heparin works primarily by

Accepted Answer

Activating antithrombin III to inhibit thrombin and Factor Xa — Heparin binds antithrombin III, accelerating its inhibition of thrombin (IIa) and Factor Xa by ~1000-fold. ---

Question 46

Warfarin anticoagulation is monitored using

Accepted Answer

INR (PT ratio) — INR standardizes PT measurement across laboratories; therapeutic range is 2.0–3.0 for most indications. ---

Question 47

Immune thrombocytopaenic purpura (ITP) is caused by

Accepted Answer

Anti-platelet IgG antibodies causing splenic destruction — ITP involves autoantibodies (usually anti-GPIIb/IIIa) that coat platelets, leading to premature splenic macrophage destruction. ---

Question 48

A patient develops thrombocytopaenia 5–10 days after starting heparin with new thrombosis. The diagnosis is

Accepted Answer

Heparin-induced thrombocytopaenia (HIT) — HIT is caused by IgG antibodies against heparin-PF4 complex, activating platelets and causing paradoxical thrombosis despite low platelet count. ---

Question 49

Thrombotic thrombocytopaenic purpura (TTP) is caused by

Accepted Answer

ADAMTS13 deficiency causing large vWF multimers — ADAMTS13 deficiency prevents cleavage of ultra-large vWF multimers, causing platelet aggregation in microvasculature and microangiopathic haemolytic anaemia. ---

Question 50

The pentad of TTP includes all EXCEPT

Accepted Answer

Lymphadenopathy — Lymphadenopathy is not part of TTP. The pentad is: MAHA, thrombocytopaenia, fever, renal impairment, and neurological symptoms. ---

MCQ: High-Yield MCQs — Haematology (All Topics)

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