PE26.1-17 | Hemato-Oncology — Practice Quiz

Mentzer index >13 favours IDA; this child has 11, but low ferritin (< 12 ng/mL) and diet history strongly confirm IDA. In clinical practice, ferritin is the discriminating test — thalassaemia trait has normal/high ferritin.

Use serum ferritin (<12 ng/mL diagnostic of IDA) over Mentzer index alone; Mentzer is a screening tool only. Treat IDA with elemental iron 3–6 mg/kg/day in 2 divided doses for 3 months after Hb correction.

Thalassaemia trait (A) gives Mentzer index <13 and normal ferritin. Lead poisoning (C) causes microcytic anaemia with basophilic stippling. Sideroblastic anaemia (D) has ringed sideroblasts and elevated serum iron.

Therapeutic dose for IDA is 3–6 mg/kg/day of elemental iron. For 20 kg: 3×20=60 to 6×20=120 mg/day. 60 mg/day (3 mg/kg/day) is the lower acceptable end and minimises GI side effects while achieving haematopoietic response.

Elemental iron for IDA: 3–6 mg/kg/day in 2 divided doses. Given between meals for absorption. Expect reticulocytosis in 5–10 days and Hb rise of 1 g/dL per week. Continue 3 months beyond Hb correction.

20 mg (1 mg/kg/day) is inadequate for treatment — it is roughly a supplementation dose. 120 mg (6 mg/kg/day) is acceptable but at the upper end. 200 mg exceeds 6 mg/kg/day and is potentially toxic.

When both B12 and folate deficiency coexist, always replace B12 before or simultaneously with folate. Starting folic acid alone in B12-deficient patients can precipitate or worsen subacute combined degeneration of the cord by driving folate-dependent pathways that further deplete functional B12.

In megaloblastic anaemia with BOTH B12 and folate deficiency, always administer B12 before or simultaneously with folic acid to prevent precipitating subacute combined degeneration of the cord.

Folic acid alone (A) risks precipitating subacute combined degeneration. B12 alone (B) is adequate when only B12 is deficient, but here both are low — combined replacement is needed. Iron (D) treats microcytic, not macrocytic anaemia.

Acute splenic sequestration is characterised by sudden massive splenomegaly, severe anaemia (Hb drop >2 g/dL), and hypovolaemia in children <5 years with sickle cell disease. It is life-threatening and requires urgent transfusion.

Acute splenic sequestration crisis in sickle cell disease: sudden spleen enlargement, Hb drop >2 g/dL, hypovolaemia in children <5 years. Treat with immediate transfusion. Recurrence risk is high — splenectomy is considered after recovery.

Vaso-occlusive crisis (A) causes pain with no acute Hb drop. Aplastic crisis (B) has reticulocytopenia and no splenomegaly. Haemolytic crisis (D) shows jaundice, reticulocytosis, and elevated LDH — not the picture here.

G6PD deficiency leads to impaired regeneration of NADPH, leaving RBCs vulnerable to oxidative stress. Oxidant haemoglobin damage causes Heinz bodies (denatured Hb precipitates); macrophages remove these inclusions, creating bite cells on the smear.

G6PD deficiency (X-linked recessive): oxidant triggers (fava beans, primaquine, dapsone, infections) → Heinz bodies and bite cells on smear → haemolysis. Management: remove trigger, supportive transfusion. Avoid oxidant drugs lifelong.

G6PD is X-linked recessive (A), so males are predominantly affected. Splenectomy (B) is not primary treatment for acute episodes — remove oxidant trigger and supportive transfusion as needed. G6PD offers protection against malaria (D), not bacterial infections.

Serum ferritin >1,000 ng/mL in a chronically transfused thalassaemia patient indicates transfusional iron overload requiring chelation. Desferrioxamine (SC infusion) or oral deferasirox are standard chelators to prevent iron-mediated cardiac, hepatic, and endocrine damage.

In transfusion-dependent thalassaemia major, start iron chelation when serum ferritin >1,000 ng/mL (typically after 10–15 transfusions). Target pre-transfusion Hb 9–10 g/dL. Monitor for iron-mediated end-organ damage annually.

Increasing transfusion frequency (A) will worsen iron overload without chelation. Erythropoietin (C) is ineffective in thalassaemia major where the primary defect is defective haemoglobin synthesis. Splenectomy (D) may reduce transfusion requirements but is not the immediate priority with ferritin at 3,800.

Post-viral isolated thrombocytopenia in a well-looking child with normal WBC/Hb, reduced platelets only, and no splenomegaly is classic ITP. Management: observation for platelet count >20,000 with no/minimal bleeding; IVIG (0.8–1 g/kg single dose) or corticosteroids for mucosal bleeding or count <10,000.

ITP: isolated thrombocytopenia in a well child, commonly post-viral. Exclude ALL (normal WBC, no organomegaly). Observe if platelets >20,000 with minimal bleeding. IVIG (0.8–1 g/kg) or prednisolone for severe thrombocytopenia with mucosal bleeding.

Acute leukaemia (A) presents with lymphadenopathy, hepatosplenomegaly, and abnormal WBC/RBC. Aplastic anaemia (C) causes pancytopenia. Meningococcal septicaemia (D) presents with fever, ill appearance, non-blanching rash, and haemodynamic instability.

The pattern — X-linked bleeding in males (maternal uncles affected), haemarthrosis after minor trauma, prolonged aPTT with normal PT and platelets — is classic haemophilia A (factor VIII deficiency, the commonest haemophilia at 80%). Haemophilia A and B are clinically identical; factor assay differentiates them.

Haemophilia A (Factor VIII, X-linked, 80% of haemophilia) and B (Factor IX, 15%) are clinically identical — differentiate by factor assay. Key management rules: NO IM injections, NO aspirin/NSAIDs. Treat bleeds with factor concentrate (FVIII or FIX) promptly.

Haemophilia B (B — Factor IX deficiency) is clinically identical to A but constitutes ~15% of haemophilia. Von Willebrand disease (B) prolongs bleeding time and often aPTT, affecting both sexes. ITP with factor deficiency (D) is a contrived combination — ITP gives low platelets, not prolonged aPTT with normal platelet count.

ALL is the commonest childhood cancer (80% of all childhood leukaemia). In high-risk ALL (high WBC, young age), tumour lysis syndrome is most dangerous in the first week of induction chemotherapy when rapid cell death releases intracellular contents (hyperuricaemia, hyperkalaemia, hyperphosphataemia, hypocalcaemia). Prophylaxis with hydration and allopurinol is mandatory.

ALL: commonest childhood cancer, peak 2–5 years, B-cell lineage (80%). >80% cure with modern protocols. Monitor for TLS in week 1 of chemotherapy: hyperhydration, allopurinol, electrolyte monitoring. No IM injections during thrombocytopenia.

ALL is the COMMONEST childhood cancer (not rarest) with >80% cure rate (A). Bone marrow biopsy is part of standard diagnosis and staging (C). Steroids (prednisolone/dexamethasone) are a cornerstone of ALL induction therapy (D).

Reed-Sternberg cells (large binucleate cells with 'owl-eye' nucleoli) are pathognomonic for Hodgkin lymphoma. HL is the commonest lymphoma in adolescents. B symptoms (fever >38°C, drenching night sweats, >10% weight loss) indicate Stage B disease and worse prognosis.

Hodgkin lymphoma: Reed-Sternberg cells, adolescent peak, cervical/mediastinal nodes, B symptoms = fever/night sweats/>10% weight loss. Highly curable (>85%) with ABVD. NHL (Burkitt): c-MYC, starry-sky, rapid progression, endemic EBV association.

Burkitt lymphoma (A) is a high-grade NHL characterised by c-MYC translocation and starry-sky appearance, not Reed-Sternberg cells. B symptoms indicate Stage B (not Stage I) disease (C). Hodgkin lymphoma has MORE frequent mediastinal involvement than NHL (D).