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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