PY2.1-13 | Haematology — Gate Quiz

Correct! Normal Hb in adult males is 13–17 g/dL (WHO/ICMR). The cut-off for anaemia in males is <13 g/dL. Indian population data shows slightly lower values on average compared to Western norms, but the clinical cut-offs remain the same.

Key concept: Normal Hb values — Adult male: 13–17 g/dL; Adult female: 12–15 g/dL; Pregnant woman: >11 g/dL; Newborn: 16–22 g/dL (high fetal Hb). Anaemia in India is commonly iron-deficiency (IDA). PCV (haematocrit): M 40–54%, F 36–47%. RBC count: M 4.5–5.5 million/μL.

Incorrect. Normal Hb in adult males is 13–17 g/dL. Values <13 g/dL in males indicate anaemia.

Correct! In adults, erythropoiesis occurs in the red bone marrow of flat bones (sternum, ribs, vertebrae, iliac crest, skull). During fetal life, the liver and spleen are also sites of haemopoiesis (extra-medullary haemopoiesis), but in healthy adults only red marrow is active.

Key concept: Haemopoiesis sites by age — Yolk sac (first 2 months), liver/spleen (2–7 months fetal), red bone marrow (from 5th month, primary from birth). Adult flat bones active: sternum, ribs, vertebrae, skull, iliac crest. Long bone marrow becomes yellow (adipose) after age 5–7. Reactivated in haemolytic anaemias.

Incorrect. In healthy adults, RBCs are produced in red bone marrow of flat bones (sternum, ribs, vertebrae, iliac crest). Yellow marrow is adipose; the spleen/liver only in pathological states.

Correct! Iron deficiency impairs haemoglobin synthesis. RBCs are microcytic (MCV <80 fL), hypochromic (MCH <27 pg, wide central pallor), with pencil cells (elongated) and occasional target cells. Serum ferritin is low; TIBC is elevated.

Key concept: Anaemia classification by MCV — Microcytic (<80 fL): IDA, thalassaemia, sideroblastic; Normocytic (80–100 fL): haemolytic, aplastic, renal; Macrocytic (>100 fL): B12/folate deficiency, liver disease, hypothyroidism. IDA: low ferritin, high TIBC, low serum iron. Most common nutritional deficiency in India.

Incorrect. Iron-deficiency anaemia causes microcytic, hypochromic RBCs (MCV <80 fL, MCH <27 pg) with pencil cells and target cells on the blood smear.

Correct! Normal platelet count is 1.5–4 lakh per μL (150,000–400,000/μL). Thrombocytopaenia (<1 lakh) causes bleeding risk; spontaneous haemorrhage typically occurs below 20,000/μL. Thrombocytosis (>4 lakh) can predispose to thrombosis.

Key concept: Platelet count — Normal: 1.5–4 lakh/μL. Thrombocytopaenia: <1 lakh. Severe (<20,000) → spontaneous bleeding, intracranial haemorrhage risk. Causes in India: dengue (most common acute), ITP, hypersplenism, drug-induced. Thrombocytosis: >4 lakh (reactive or clonal).

Incorrect. Normal platelet count is 1.5–4 lakh per μL (150,000–400,000/μL).

Correct! HbA (adult) = 2α + 2β chains. It constitutes ~97% of adult haemoglobin. HbA₂ = 2α + 2δ (~2.5%). HbF (fetal) = 2α + 2γ. Each globin chain carries one haem group with iron (Fe²⁺) that reversibly binds one O₂ molecule.

Key concept: Haemoglobin types — HbA (α₂β₂, 97%), HbA₂ (α₂δ₂, 2.5%), HbF (α₂γ₂, <1% adult). HbF has higher O₂ affinity (shifts ODC left) — important for placental O₂ transfer. HbS (sickle cell): β chain Glu→Val substitution. Beta-thalassaemia: reduced/absent β chain synthesis.

Incorrect. HbA (adult haemoglobin) = 2α + 2β chains. HbF (fetal) has 2α + 2γ; HbA₂ has 2α + 2δ.

Correct! Increased 2,3-DPG (2,3-bisphosphoglycerate) shifts the ODC to the right (Bohr effect extension), DECREASING Hb-O₂ affinity and INCREASING O₂ release to tissues. 2,3-DPG binds to β chains of deoxyHb, stabilising the T (tense, deoxy) state.

Key concept: ODC right shift (↓affinity, ↑O₂ delivery) — ↑CO₂, ↓pH (Bohr effect), ↑temperature, ↑2,3-DPG. Left shift (↑affinity, ↓O₂ delivery) — ↓CO₂, ↑pH, ↓temperature, HbF, CO poisoning. P50 = pO₂ at 50% saturation (normal ~27 mmHg); right shift increases P50.

Incorrect. The ODC shifts RIGHT (lower O₂ affinity, more O₂ delivery) with: ↑CO₂, ↓pH (acidosis), ↑temperature, ↑2,3-DPG. Remember: "CADET, face Right!" (CO₂, Acid, DPG, Exercise, Temperature).

Correct! Group O negative has no A, B, or Rh(D) antigens on red cells, so it cannot be attacked by anti-A, anti-B, or anti-D antibodies in any recipient. It is the universal donor for red blood cells in emergency situations.

Key concept: ABO groups — A (antigen A, antibody anti-B), B (antigen B, antibody anti-A), AB (antigens A+B, no antibodies — universal recipient for RBCs), O (no antigens, antibodies anti-A + anti-B — universal donor for RBCs). Rh: if Rh-negative recipient gets Rh+ blood → sensitisation → haemolytic disease of newborn risk.

Incorrect. O negative blood lacks A, B, and Rh(D) antigens — it can be transfused to any recipient regardless of ABO or Rh group (universal donor for packed RBCs).

Correct! Warfarin inhibits vitamin K epoxide reductase, preventing regeneration of active vitamin K (KH₂). This impairs γ-carboxylation of Factors II (thrombin), VII, IX, X, and Proteins C and S. PT (extrinsic pathway) is prolonged first due to the short half-life of Factor VII.

Key concept: Vitamin K-dependent factors — II, VII, IX, X, Protein C, Protein S. Warfarin blocks vitamin K reductase. Heparin vs warfarin: Heparin = immediate, activates antithrombin III, inhibits thrombin (II) and Xa; APTT monitored. Warfarin = delayed (3–5 days), oral, inhibits synthesis of K-dependent factors; PT/INR monitored.

Incorrect. Warfarin inhibits synthesis of vitamin K-dependent clotting factors: II, VII, IX, X (and Proteins C and S). PT is prolonged because Factor VII (extrinsic pathway) has the shortest half-life (~6h).

Correct! Acute phase proteins (fibrinogen, immunoglobulins) reduce the negative charge (zeta potential) on RBCs, causing them to aggregate into rouleaux (stacks of coins). Rouleaux fall faster through plasma due to increased mass-to-surface-area ratio, elevating ESR.

Key concept: ESR elevated by: infection, inflammation, malignancy, pregnancy, anaemia, multiple myeloma (high immunoglobulins). ESR is low in: polycythaemia, sickle cell disease (abnormal shape prevents rouleaux), hypofibrinogenaemia. Westergren method: Normal ESR — Male <15 mm/hr, Female <20 mm/hr.

Incorrect. Elevated ESR is due to rouleaux formation — aggregation of RBCs into coin-stack formations — driven by increased fibrinogen and other acute phase proteins that reduce zeta potential.

Correct! G6PD deficiency is the most common enzyme defect in RBCs (~400 million people worldwide). Primaquine and other oxidant drugs (dapsone, nitrofurantoin) cause haemolysis because G6PD-deficient RBCs cannot regenerate NADPH to protect against oxidative stress, leading to Heinz body formation and haemolysis.

Key concept: G6PD deficiency — X-linked recessive (males affected), common in India, Africa, Mediterranean. Precipitants: primaquine, dapsone, nitrofurantoin, fava beans, infection. G6PD is the entry enzyme of the pentose phosphate pathway, generating NADPH for glutathione reduction. Heinz bodies = denatured Hb precipitates. Blood film: bite cells (macrophages remove Heinz bodies).

Incorrect. Drug-induced haemolysis after primaquine/dapsone/nitrofurantoin in a young male strongly suggests G6PD deficiency — the most common RBC enzyme disorder. It is X-linked, hence more severe in males.