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← Acute Myeloid Leukaemia mini review

Acute Myeloid Leukaemia: MCQ bank

90 clinical-vignette questions in three levels: 30 basics, 30 applied and innovative, and 30 challenging (30 Diagnosis, 55 Treatment, 5 Survivorship; 4 built on schematic imaging, endoscopy or histology drawings). Practise question by question with instant marking, or take a timed mock test with a result summary by topic, level and section. You can also print the page as a booklet.

LevelScore 0 / 0 answered
Topic

Level 1 · Basics

Core facts for NEET-PG and USMLE Step 1–2: histology, risk factors, presentation, staging and first-line principles.

Q1DiagnosisLevel 1At a glance

About what share of acute leukaemias in adults is acute myeloid leukaemia (AML)?

  1. AAbout 50%
  2. BAbout 80%
  3. CAbout 20%
  4. DUnder 10%
  5. ENearly 100%
Show answer

Answer: B. AML is the commonest acute leukaemia of adults; median age at diagnosis is 65–68 in Western registries. In children under 10 it is under 10% of acute leukaemias, where ALL dominates.

Review: section 01

Q2DiagnosisLevel 1Presentation, traps & genetics

Which statement about the white count at diagnosis of AML is correct?

  1. AIt is always above 100,000/µL at diagnosis
  2. BIt is normal only in APL, never in other AML
  3. CA count under 5,000/µL rules out AML
  4. DIt is the test that makes the diagnosis
  5. EA normal or low count does not exclude AML
Show answer

Answer: E. A quarter to two-fifths of patients have fewer than 5,000 white cells (median about 15,000/µL). The smear, not the count, makes the diagnosis: blasts are seen in nearly all patients.

Review: section 02

Q3DiagnosisLevel 1ImageScreening, workup & staging

This schematic blood film is from a 55-year-old with fever and bruises. What is the pink rod-shaped inclusion marked by the arrow?

Schematic drawing · not a patient image
  1. AA Döhle body
  2. BA Howell-Jolly body
  3. CToxic granulation
  4. DA Russell body
  5. EAn Auer rod
Show answer

Answer: E. Auer rods are fused azurophilic granules in myeloblasts. They are pathognomonic of myeloid lineage; bundles of them ("faggot cells") are typical of APL.

Review: section 03

Q4DiagnosisLevel 1Screening, workup & staging

Which flow cytometry markers confirm myeloid lineage in a new acute leukaemia?

  1. ACD13, CD33, CD117 and MPO
  2. BCD20, CD5 and CD23
  3. CCD138 and CD38
  4. DCD3, CD7 and CD5
  5. ECD19, CD10, CD22 and CD79a
Show answer

Answer: A. Myeloid blasts express CD13, CD33, CD117 and MPO (often CD34). Flow also sets the baseline for measuring residual disease (MRD) later.

Review: section 03

Q5DiagnosisLevel 1Screening, workup & staging

For most AML without a defining genetic lesion, what marrow or blood blast count is needed for the diagnosis?

  1. A30% or more
  2. B20% or more
  3. C50% or more
  4. D5% or more
  5. E10% or more
Show answer

Answer: B. Most AML needs ≥20% blasts (also BCR::ABL1-positive AML). Defining lesions (APL, CBF fusions, KMT2A and others) need ≥10%, and NPM1-mutated AML any count under WHO. Myeloid sarcoma counts as AML at any marrow count.

Review: section 03

Q6DiagnosisLevel 1ImagePresentation, traps & genetics

This schematic drawing shows the gums of a 48-year-old with a new acute leukaemia. Which AML type does it suggest?

Schematic drawing · not a patient image
  1. AAML with t(8;21)
  2. BAcute promyelocytic leukaemia
  3. CPure erythroid leukaemia
  4. DMonocytic AML
  5. EChronic myeloid leukaemia in chronic phase
Show answer

Answer: D. Gum hypertrophy and violaceous skin nodules (leukaemia cutis) suggest monocytic AML. Patients are often sent to the dentist first: a blood count with a smear is the right test.

Review: section 02

Q7DiagnosisLevel 1Presentation, traps & genetics

Which is a recognised cause of AML?

  1. AEarlier infectious mononucleosis
  2. BEarlier alkylating chemotherapy
  3. CLong-term low-dose aspirin use
  4. DChronic hepatitis C infection
  5. ELong-standing iron deficiency
Show answer

Answer: B. Known risks are previous chemotherapy (alkylating agents, topoisomerase II inhibitors) or radiotherapy, an earlier MDS or MPN, benzene, smoking and obesity. Most AML arises from clonal haematopoiesis that gathers further mutations.

Review: section 02

Q8DiagnosisLevel 1Presentation, traps & genetics

A mass biopsied from the orbit shows sheets of myeloid blasts; the marrow has 6% blasts. How is this classified?

  1. AA lymphoma until proved otherwise
  2. BMDS, because marrow blasts are under 20%
  3. CA small round cell tumour of the orbit
  4. DAML (myeloid sarcoma), whatever the marrow
  5. EA benign reactive inflammatory lesion
Show answer

Answer: D. Myeloid sarcoma counts as AML at any marrow blast count and is treated as AML. It needs myeloid immunostains, because it is easily called a small round cell tumour or lymphoma.

Review: section 02

Q9TreatmentLevel 1Systemic therapy

A 26-year-old has gum bleeding, a low fibrinogen and many granular cells on the smear. When should ATRA be started?

  1. AAfter the bleeding has stopped
  2. BAfter the bone marrow report
  3. CAt once, the same day, on suspicion of APL
  4. DOnly if the white count is above 10,000/µL
  5. EOnly after PML::RARA is confirmed
Show answer

Answer: C. Bleeding with low fibrinogen and granular cells is APL until proved otherwise. ATRA is started on suspicion; confirmation by PCR or FISH comes later.

Review: section 06

Q10DiagnosisLevel 1At a glance

Which genetic lesion defines acute promyelocytic leukaemia (APL)?

  1. At(9;22) BCR::ABL1
  2. Bt(15;17) PML::RARA
  3. Cinv(16) CBFB::MYH11
  4. Dt(9;11) MLLT3::KMT2A
  5. Et(8;21) RUNX1::RUNX1T1
Show answer

Answer: B. PML::RARA is found in ≥95% of APL. It is confirmed by PCR or FISH and is also the marker followed to molecular remission.

Review: section 01

Q11TreatmentLevel 1Systemic therapy

What does "7+3" induction mean?

  1. A7 weeks of tablets followed by 3 weeks off
  2. B7 cycles of azacitidine with 3 of venetoclax
  3. C7 days of anthracycline with cytarabine on days 1–3 only
  4. D7 days of ATRA with 3 days of arsenic
  5. E7 days of cytarabine with an anthracycline on days 1–3
Show answer

Answer: E. 7+3 gives complete remission in about three-quarters of fit younger adults. Daunorubicin or idarubicin is the anthracycline.

Review: section 06

Q12TreatmentLevel 1Systemic therapy

A fit 45-year-old has AML with a FLT3 mutation. What is added to 7+3 induction?

  1. AImatinib or dasatinib
  2. BRituximab or obinutuzumab
  3. CMidostaurin or quizartinib
  4. DATRA or arsenic trioxide
  5. EVenetoclax or azacitidine
Show answer

Answer: C. Midostaurin (ITD or TKD) or quizartinib (ITD) is added to induction and continued in consolidation and maintenance. Every fit FLT3-mutated patient should get one.

Review: section 06

Q13TreatmentLevel 1Systemic therapy

Which drug is added to induction for CD33-positive core-binding-factor AML?

  1. AMidostaurin
  2. BBlinatumomab
  3. CArsenic trioxide
  4. DIvosidenib
  5. EGemtuzumab ozogamicin
Show answer

Answer: E. Gemtuzumab ozogamicin targets CD33, which nearly all CBF AML express. It gives fewer relapses and better 5-year survival, with the largest benefit in CBF AML (Hills 2014).

Review: section 06

Q14TreatmentLevel 1Systemic therapy

What is the standard first treatment for an older adult with AML who is unfit for intensive chemotherapy but not frail?

  1. AVenetoclax with azacitidine
  2. BImatinib
  3. CSupportive care only, with no drugs
  4. DATRA with arsenic trioxide
  5. E7+3 induction
Show answer

Answer: A. In VIALE-A, venetoclax with azacitidine improved survival over azacitidine alone. IDH1-mutated AML can be treated with ivosidenib plus azacitidine.

Review: section 06

Q15TreatmentLevel 1Systemic therapy

What is the preferred induction for low- or intermediate-risk APL (white count 10,000/µL or less)?

  1. AATRA with arsenic trioxide
  2. B7+3 without ATRA
  3. CAllogeneic transplant
  4. DATRA alone
  5. EVenetoclax with azacitidine
Show answer

Answer: A. ATRA plus arsenic trioxide gave 72-month event-free survival of about 97% in APL0406. Where arsenic is not available, ATRA with an anthracycline is used.

Review: section 06

Q16TreatmentLevel 1Systemic therapy

A patient on induction has a temperature of 38.6°C and neutrophils of 200/µL. What is the first step?

  1. AParacetamol now and review on the morning round
  2. BWait 24 hours for the blood culture results before antibiotics
  3. CGranulocyte transfusion before any antibiotic
  4. DStart an antifungal only, with no antibiotic
  5. ECultures, then an antipseudomonal beta-lactam within 60 min
Show answer

Answer: E. Neutropenic fever is an emergency: cultures, then an antipseudomonal beta-lactam within 60 minutes. Local resistance patterns guide the choice.

Review: section 06

Q17TreatmentLevel 1Systemic therapy

A breathless patient has a white count of 200,000/µL and haemoglobin of 6 g/dL. What should be avoided if possible?

  1. AStarting induction
  2. BIntravenous fluids
  3. CPlatelet transfusion if bleeding
  4. DHydroxyurea
  5. EA rapid red cell transfusion
Show answer

Answer: E. Red cells raise blood viscosity and can precipitate leukostasis. Cytoreduce first (induction, or hydroxyurea if induction is delayed) and transfuse slowly only if essential.

Review: section 06

Q18TreatmentLevel 1Systemic therapy

For a patient at high risk of tumour lysis, which drug is given with intravenous fluids, after checking for G6PD deficiency?

  1. AFurosemide
  2. BSodium bicarbonate
  3. CAllopurinol alone
  4. DRasburicase
  5. ECalcium gluconate
Show answer

Answer: D. High risk (in AML, WBC ≥100,000/µL): fluids plus rasburicase, which is avoided in G6PD deficiency. Intermediate risk: fluids plus allopurinol.

Review: section 06

Q19TreatmentLevel 1Systemic therapy

What happens to most patients in complete remission who receive no post-remission therapy?

  1. AThey are cured
  2. BHalf are cured without further treatment
  3. CThey relapse
  4. DThey develop MDS but not AML
  5. EThey develop CML
Show answer

Answer: C. Without consolidation or transplant almost everyone relapses. The choice depends on ELN risk, MRD, age and fitness.

Review: section 06

Q20TreatmentLevel 1Systemic therapy

A fit 40-year-old with adverse-risk AML reaches first complete remission. What is the usual next step?

  1. AAllogeneic transplant in first remission
  2. BTwo years of ATRA maintenance
  3. COral azacitidine maintenance alone
  4. DAutologous stem cell transplant
  5. ENo further treatment, with close follow-up
Show answer

Answer: A. Adverse risk: allogeneic HCT in CR1. Favourable risk: consolidation, with transplant only for persistent or rising MRD. Intermediate risk: decided on MRD, donor and transplant risk.

Review: section 06

Q21DiagnosisLevel 1Biomarkers

Which genetic finding places AML in the ELN 2022 favourable group?

  1. ATP53 mutation
  2. Bt(6;9) DEK::NUP214
  3. CA complex karyotype
  4. DMonosomy 7
  5. Et(8;21) RUNX1::RUNX1T1
Show answer

Answer: E. Favourable: t(8;21), inv(16)/t(16;16), NPM1 mutated without FLT3-ITD, and in-frame bZIP CEBPA. The others are adverse.

Review: section 04

Q22DiagnosisLevel 1Biomarkers

How is a TP53 mutation in AML best described?

  1. AAdverse in every risk model
  2. BCured by ATRA
  3. CWithout prognostic meaning
  4. DFavourable with intensive chemotherapy
  5. EFavourable with venetoclax
Show answer

Answer: A. TP53-mutated AML (about 8%, more in older and therapy-related cases) responds poorly to all current therapy; trials are preferred.

Review: section 04

Q23TreatmentLevel 1Systemic therapy

A patient on ATRA for APL develops fever, breathlessness and weight gain. Which drug is started at once?

  1. AHeparin
  2. BDexamethasone
  3. CFurosemide alone
  4. DErythropoietin
  5. EVancomycin alone
Show answer

Answer: B. Differentiation syndrome is treated with dexamethasone as soon as it is suspected ("dexamethasone first, questions later"), with cultures, antibiotics, oxygen and diuretics as needed.

Review: section 06

Q24SurvivorshipLevel 1Survivorship

Which is a recognised late effect of AML treatment?

  1. ALoss of hearing from daunorubicin
  2. BHeart damage from anthracyclines
  3. CDiabetes from 7+3
  4. DLiver cirrhosis from ATRA
  5. EChronic kidney stones from cytarabine
Show answer

Answer: B. Late effects include anthracycline heart damage, infertility, chronic graft-versus-host disease and infections after transplant, second cancers, fatigue and the financial toll of treatment.

Review: section 08

Q25SurvivorshipLevel 1Survivorship

In English data (2001–2006), what was the main factor by which 5-year survival from AML fell?

  1. AAge at diagnosis
  2. BBlood group
  3. CHeight
  4. DPlace of birth
  5. ESex
Show answer

Answer: A. 5-year survival was about 50% under 40, 33% at 40–59, 13% at 60–69 and 3% at 70–79. Results are better with favourable genetics and modern targeted and transplant care.

Review: section 08

Q26DiagnosisLevel 1Screening, workup & staging

Where is a bone marrow sample taken in suspected AML?

  1. AAnterior tibia, as in adults generally
  2. BSternum, for both aspirate and biopsy
  3. CPosterior iliac crest
  4. DA vertebral body, under CT guidance
  5. EThe femoral head, under anaesthesia
Show answer

Answer: C. A unilateral aspirate (500-cell count) and biopsy are taken from the posterior iliac crest; the sternum is acceptable for aspiration only. Warn the laboratory: fresh samples are needed for flow, karyotype, FISH and molecular tests.

Review: section 03

Q27TreatmentLevel 1Local therapy

When is a lumbar puncture done in an adult with newly diagnosed AML?

  1. AIn APL, on the first day
  2. BOnly after transplant
  3. COnly for neurological symptoms
  4. DBefore every cycle of chemotherapy
  5. EIn every patient at diagnosis
Show answer

Answer: C. There is no routine CNS prophylaxis in adult AML. Image first if there are focal signs; correct platelets and clotting; in APL defer the LP until the coagulopathy is corrected.

Review: section 05

Q28DiagnosisLevel 1Presentation, traps & genetics

In the Vellore series of 380 patients with non-APL AML, why did most not start standard treatment?

  1. AAdvanced age
  2. BLack of money
  3. CLack of a diagnosis
  4. DRefusal of transfusion
  5. EPreference for herbal medicine
Show answer

Answer: B. Only 29% started standard treatment, and 81% of the rest did not for lack of money. Median age was 40, symptoms had lasted a median of 4 weeks, and patients travelled a median of 580 km.

Review: section 02

Q29DiagnosisLevel 1Screening, workup & staging

Which tests are sent at once in every suspected case of AML to look for DIC?

  1. ASerum protein electrophoresis
  2. BHbA1c and a lipid profile
  3. CPT, aPTT, fibrinogen and D-dimer
  4. DTroponin and creatine kinase
  5. ESerum ferritin and transferrin
Show answer

Answer: C. DIC is common in APL and in monocytic AML with a high count. Results guide platelet and cryoprecipitate support and raise the suspicion of APL; recheck often in APL.

Review: section 03

Q30DiagnosisLevel 1Presentation, traps & genetics

A 35-year-old has had "viral fever" for 3 weeks with pallor and new bruises. What is the right test today?

  1. AA chest X-ray only
  2. BA dengue test and a review in a week
  3. CA complete blood count with a smear
  4. DAnother course of oral antibiotics
  5. EA vitamin B12 level only
Show answer

Answer: C. Fever with pallor, bruises or gum bleeding needs a CBC with a smear the same day. Fatigue and pallor often precede the diagnosis by months.

Review: section 02

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, risk scores, NNT), imaging and laboratory findings, reading trial results, sequencing traps.

Q31DiagnosisLevel 2Screening, workup & staging

A marrow shows 12% blasts with t(8;21) RUNX1::RUNX1T1. What is the diagnosis?

  1. AMDS/AML
  2. BMDS with excess blasts
  3. CAML
  4. DCML in blast phase
  5. EA reactive marrow after infection
Show answer

Answer: C. With a defining lesion (APL, CBF fusions, KMT2A, DEK::NUP214, MECOM, CEBPA), ≥10% blasts are enough for AML. t(8;21) occurs in 1–7% of adults (median age 25–30) and is favourable.

Review: section 03

Q32DiagnosisLevel 2Screening, workup & staging

A marrow has 8% blasts and an NPM1 mutation. How does the WHO 5th edition classify it?

  1. AClonal haematopoiesis only
  2. BAML with mutated NPM1
  3. CMDS with low blasts
  4. DA normal marrow for age
  5. EMDS/AML (ICC term)
Show answer

Answer: B. WHO accepts NPM1-mutated AML at any blast count; ICC 2022 asks for ≥10%. NPM1 without FLT3-ITD is favourable, and NPM1 transcripts can be followed by PCR.

Review: section 03

Q33DiagnosisLevel 2Screening, workup & staging

Under ICC 2022, how is a marrow with 15% blasts and no defining genetic lesion classified?

  1. AAcute leukaemia of ambiguous lineage
  2. BMDS/AML
  3. CMyeloproliferative neoplasm
  4. DMDS with low blasts
  5. EAML
Show answer

Answer: B. ICC calls 10–19% blasts MDS/AML; ≥20% is AML for most cases without a defining lesion.

Review: section 03

Q34DiagnosisLevel 2Presentation, traps & genetics

A patient with a white count of 250,000/µL has a potassium of 7.2 mmol/L but a normal ECG. What should you do first?

  1. AIgnore it, as high counts never affect potassium
  2. BGive insulin-dextrose and calcium at once
  3. CRecheck potassium on a heparinised plasma sample
  4. DGive a potassium binder and stop fluids
  5. EStart urgent haemodialysis
Show answer

Answer: C. Potassium leaks from cells in a clotted sample (pseudohyperkalaemia). A huge count also lowers glucose and oxygen in the tube; send the blood gas on ice.

Review: section 02

Q35DiagnosisLevel 2ImageScreening, workup & staging

This schematic blood film is from a 28-year-old with gum bleeding and a fibrinogen of 90 mg/dL. What is the immediate step?

Schematic drawing · not a patient image
  1. AInsert a central line for induction today
  2. BStart heparin for the clotting disorder
  3. CLumbar puncture to look for CNS disease first
  4. DStart ATRA now, before PML::RARA is confirmed
  5. EWait for FISH results before any treatment
Show answer

Answer: D. Abnormal promyelocytes with dense granules and bundles of Auer rods mean APL until proved otherwise. ATRA is started on suspicion; lines, lumbar puncture and heparin are avoided during induction.

Review: section 03

Q36TreatmentLevel 2Systemic therapy

Which transfusion targets are used during induction for APL?

  1. APlatelets only for bleeding; fibrinogen not measured
  2. BPlatelets ≥150,000/µL; fibrinogen >400 mg/dL
  3. CPlasma only, with no platelet transfusion at all
  4. DPlatelets ≥10,000/µL; no fibrinogen target needed
  5. EPlatelets ≥30,000–50,000/µL; fibrinogen >150 mg/dL
Show answer

Answer: E. Platelets and cryoprecipitate keep these targets; no heparin; antifibrinolytics only in selected patients. In Lucknow, 34% got less support than planned because of shortages.

Review: section 06

Q37TreatmentLevel 2Systemic therapy

APL is confirmed in a 32-year-old with a white count of 14,000/µL. Which induction fits?

  1. AATRA + arsenic alone, exactly as for low risk
  2. B7+3 alone, with ATRA kept for relapse only
  3. CHigh-risk treatment: ATRA with an anthracycline
  4. DVenetoclax with azacitidine as first induction
  5. EArsenic alone, without ATRA, until counts fall
Show answer

Answer: C. A white count >10,000/µL is high risk: ATRA with an anthracycline, or ATRA plus arsenic with hydroxyurea or an anthracycline for a rising count.

Review: section 06

Q38TreatmentLevel 2ImageSystemic therapy

On day 9 of ATRA and arsenic for APL, a patient has fever, breathlessness, a 6 kg weight gain and this schematic chest X-ray. What is the best plan?

RSchematic drawing · not a patient image
  1. ADexamethasone now; usually continue the drugs
  2. BStop ATRA and arsenic permanently today
  3. CIncrease ATRA to speed up differentiation
  4. DTreat as pneumonia with antibiotics alone
  5. EDiuretics only, and review again tomorrow
Show answer

Answer: A. Differentiation syndrome (≥3 features: fever, hypoxia, weight gain >5 kg, lung opacities or effusions, hypotension, kidney injury) needs dexamethasone at once. Pause ATRA or arsenic only if severe or not better in 24–48 hours.

Review: section 06

Q39TreatmentLevel 2Systemic therapy

A fit 66-year-old develops AML 5 years after chemotherapy for breast cancer (intermediate-risk genetics). Which induction is preferred?

  1. AATRA with arsenic
  2. B7+3 with gemtuzumab
  3. CLow-dose cytarabine
  4. DCPX-351
  5. EImatinib with 7+3
Show answer

Answer: D. For therapy-related or myelodysplasia-related AML with favourable or intermediate genetics, CPX-351 gave 5-year OS of 18% vs 8% with 7+3 in patients aged 60–75, with more patients reaching transplant.

Review: section 06

Q40DiagnosisLevel 2Presentation, traps & genetics

A 30-year-old with AML has a RUNX1 variant at about half the reads on NGS, and an aunt had leukaemia. A sibling is the planned donor. What must be done first?

  1. ACheck if the variant is germline; test the sibling
  2. BCancel transplant and give chemotherapy only
  3. CIgnore it, since RUNX1 variants are never inherited
  4. DProceed with the sibling as donor without tests
  5. EUse the patient's own stem cells (autologous)
Show answer

Answer: A. Familial disorders underlie 10–20% of AML/MDS in young adults. Clues: relatives with blood cancers, long-standing cytopenias, a germline-type variant (DDX41, RUNX1, GATA2, biallelic CEBPA). A sibling carrying it should not be the donor.

Review: section 02

Q41TreatmentLevel 2Systemic therapy

A 35-year-old with NPM1-mutated AML (no FLT3-ITD) is in remission with negative MRD. What is suggested?

  1. AOral azacitidine only, without consolidation
  2. BAllogeneic transplant in first remission for all
  3. CNo further treatment after induction
  4. DConsolidation; transplant only if MRD persists or rises
  5. EATRA maintenance for two years after induction
Show answer

Answer: D. Favourable risk: consolidation (intermediate-dose cytarabine suggested over high-dose for most). Transplant is kept for persistent or rising MRD.

Review: section 06

Q42TreatmentLevel 2Systemic therapy

For a 45-year-old with intermediate-risk AML in first remission, what decides between consolidation and transplant?

  1. AMRD, donor availability and transplant risk
  2. BSex and ABO blood group of the patient
  3. CThe number of transfusions in induction
  4. DThe white count at diagnosis, on its own
  5. EWhether Auer rods were seen on the film
Show answer

Answer: A. Intermediate risk is decided on MRD, donor and transplant risk. MRD-negative patients had 5-year OS of 68% vs 34% in a meta-analysis.

Review: section 06

Q43TreatmentLevel 2Systemic therapy

Who should be offered oral azacitidine maintenance after consolidation, as in QUAZAR?

  1. AOnly patients after allogeneic transplant
  2. BOnly patients with APL after arsenic
  3. CAll patients with favourable-risk AML
  4. DChildren with high-risk AML after induction
  5. EAge 55 or more, intermediate or adverse risk
Show answer

Answer: E. QUAZAR showed longer survival (median OS 25 vs 15 months). FLT3-mutated AML gets an FLT3 inhibitor after chemotherapy or after transplant instead.

Review: section 06

Q44TreatmentLevel 2Systemic therapy

A 72-year-old with ECOG 1, Charlson 1 and normal heart, lung, liver and kidney function has AML. Which is correct?

  1. ASupportive care is the only reasonable option
  2. BAge over 70 means lower-intensity therapy only
  3. CShe is frail by definition at this age
  4. DShe can be treated as fit for intensive therapy
  5. ETransplant is impossible at any age above 70
Show answer

Answer: D. Fitness (ECOG, Charlson or HCT-CI, organ function, cognition, wishes), not age alone, decides intensive versus lower-intensity therapy. Transplant eligibility also depends on organ function, not age.

Review: section 06

Q45TreatmentLevel 2Systemic therapy

An unfit 76-year-old has IDH1-mutated AML. Which combination improved survival in AGILE?

  1. AMidostaurin with 7+3
  2. BIvosidenib with azacitidine
  3. CQuizartinib with decitabine
  4. DGilteritinib with azacitidine
  5. EEnasidenib with cytarabine
Show answer

Answer: B. AGILE: overall survival 24 vs 8 months. Venetoclax with azacitidine is the other main option for unfit adults.

Review: section 06

Q46TreatmentLevel 2Systemic therapy

A patient on venetoclax with azacitidine is started on posaconazole prophylaxis. What follows?

  1. AVenetoclax dose is adjusted (azoles raise levels)
  2. BVenetoclax is replaced by 7+3 induction
  3. CPosaconazole must never be given with it
  4. DAzacitidine is stopped while on posaconazole
  5. ENo change is needed to either drug
Show answer

Answer: A. Azole antifungals raise venetoclax levels, so its dose is adjusted. The marrow is checked early in cycle 1 because responses are fast and counts may need time off venetoclax.

Review: section 06

Q47TreatmentLevel 2Systemic therapy

When is the marrow first checked on venetoclax or ivosidenib combinations?

  1. AOnly if the patient feels unwell
  2. BNever, because blood counts are enough
  3. CBefore each daily dose of venetoclax
  4. DEarly in cycle 1 (day 14–21)
  5. EOnly after 12 cycles of treatment
Show answer

Answer: D. Responses are fast and counts may need time off venetoclax, so an early marrow guides the schedule.

Review: section 06

Q48TreatmentLevel 2Systemic therapy

AML relapses 10 months after consolidation; FLT3-ITD is now present. Which drug improved survival over salvage chemotherapy?

  1. AImatinib
  2. BATRA
  3. CMidostaurin
  4. DIvosidenib
  5. EGilteritinib
Show answer

Answer: E. In ADMIRAL, gilteritinib gave median OS 9.3 vs 5.6 months. Genetics are repeated at relapse because clones evolve; the transplant team is involved at once.

Review: section 06

Q49TreatmentLevel 2Systemic therapy

Relapsed AML has an NPM1 mutation. Which class of drug is now FDA-approved for it?

  1. ABCR::ABL1 inhibitors
  2. BBTK inhibitors
  3. CMenin inhibitors
  4. DJAK2 inhibitors
  5. EAnti-CD20 antibodies
Show answer

Answer: C. Menin inhibitors are approved for NPM1-mutated AML and KMT2A-rearranged acute leukaemia. They cause differentiation syndrome and QT prolongation; Indian availability is to be confirmed.

Review: section 06

Q50TreatmentLevel 2Systemic therapy

Relapsed AML has an IDH2 mutation. Which targeted drug is used?

  1. AGilteritinib
  2. BEnasidenib
  3. CGemtuzumab ozogamicin
  4. DIvosidenib
  5. ERevumenib
Show answer

Answer: B. Enasidenib targets IDH2 (CR 19%, median OS 9 months); ivosidenib or olutasidenib target IDH1.

Review: section 06

Q51DiagnosisLevel 2Biomarkers

Why must the genetic tests be repeated when AML relapses?

  1. ARelapse is always a new, unrelated leukaemia
  2. BClones evolve, so the target may have changed
  3. CLaboratories require it for billing
  4. DThe first results expire after 6 months
  5. EGenetics never change, but staging does
Show answer

Answer: B. Relapse may come from the dominant clone gaining mutations or from a minor clone that survived treatment. A FLT3, IDH or NPM1 result at relapse can open a targeted option.

Review: section 04

Q52TreatmentLevel 2Local therapy

A patient with AML develops a new facial nerve palsy; CSF shows blasts. What is the right approach?

  1. AHigh-dose systemic chemotherapy during cranial RT
  2. BWait for nerve recovery before any CNS treatment
  3. CIntrathecal therapy alone, with RT only if it fails
  4. DCraniospinal RT as the first and only choice
  5. EPrompt cranial radiotherapy with intrathecal therapy
Show answer

Answer: E. Cranial nerve palsies need RT (for example 18–25 Gy to the brain, field down to C2), started as soon as CNS involvement is suspected, because recovery falls with delay. Cranial RT spares the marrow; avoid high-dose systemic chemotherapy around it.

Review: section 05

Q53TreatmentLevel 2Local therapy

A myeloid sarcoma compresses the spinal cord. Which management is right?

  1. AHydroxyurea alone, with RT kept for later relapse
  2. BObservation until the marrow relapses, then chemotherapy
  3. CSurgery alone, with no systemic therapy afterwards
  4. DSteroids, urgent MRI, RT and/or decompression, plus systemic therapy
  5. ESystemic therapy alone, with no RT or surgery at any stage of care
Show answer

Answer: D. Myeloid sarcoma is AML: systemic treatment is the main therapy. Add RT (about 20 Gy is generally enough) for compression of a vital structure or persistence after recovery from induction.

Review: section 05

Q54TreatmentLevel 2Systemic therapy

On day 5 of neutropenic fever a stable patient is still febrile on piperacillin-tazobactam with negative cultures. What next?

  1. AAdd an antifungal (4–7 days of unexplained fever)
  2. BAdd vancomycin routinely to the regimen
  3. CChange to meropenem because of the fever alone
  4. DStop all antibiotics while cultures are negative
  5. EGive a granulocyte transfusion today
Show answer

Answer: A. Do not change antibiotics for fever alone in a stable patient. Vancomycin is for line, skin or soft-tissue infection, pneumonia or instability.

Review: section 06

Q55TreatmentLevel 2Systemic therapy

Which antifungal prophylaxis is used during AML induction?

  1. AOral nystatin only, throughout induction
  2. BFluconazole, or a mould-active azole in second induction
  3. CNone until fever appears, then amphotericin for everyone
  4. DAmphotericin for every patient from day 1
  5. EAn echinocandin, but only after transplant
Show answer

Answer: B. Fluoroquinolone prophylaxis covers expected ANC <500/µL for >7 days; aciclovir for HSV-seropositive patients. In an Indian centre, fungal pneumonia was still diagnosed in 55% during induction.

Review: section 06

Q56TreatmentLevel 2Systemic therapy

A patient at high risk of tumour lysis has G6PD deficiency. Which drug must be avoided?

  1. ARasburicase
  2. BAllopurinol
  3. CCalcium gluconate for symptomatic hypocalcaemia
  4. DIntravenous saline
  5. EHydroxyurea
Show answer

Answer: A. Rasburicase is not given in G6PD deficiency (risk of haemolysis); check G6PD before using it. Allopurinol with fluids is the alternative.

Review: section 06

Q57TreatmentLevel 2Systemic therapy

AML is diagnosed at 9 weeks of pregnancy. What does the module advise?

  1. ADelay all treatment until delivery
  2. BStart ATRA only
  3. CLow-dose cytarabine throughout pregnancy
  4. DTermination of pregnancy, then treatment
  5. ELeukapheresis until term
Show answer

Answer: D. In the first trimester, termination followed by treatment is advised. Later in pregnancy, urgent induction is discussed against temporary measures such as leukapheresis.

Review: section 06

Q58SurvivorshipLevel 2Survivorship

A man in remission from NPM1-mutated AML has a rising NPM1 transcript level in blood on two tests. What next?

  1. ARepeat the test in 2 years
  2. BA marrow examination and plans for relapse
  3. CReassurance: blood MRD has no meaning
  4. DStop follow-up, as he is in remission
  5. EStart ATRA maintenance at once
Show answer

Answer: B. Some experts follow MRD in blood (NPM1, CBF fusions). A falling count or rising MRD needs a marrow, because NPM1 transcripts by PCR predict relapse.

Review: section 08

Q59TreatmentLevel 2Systemic therapy

In hyperleukocytosis where induction must be delayed, which measure lowers the white count?

  1. AHigh-dose steroids for three days
  2. BRed cell transfusion to dilute the blood
  3. CHydroxyurea
  4. DPlasma exchange, repeated daily
  5. ELeukapheresis alone, without any drug
Show answer

Answer: C. Fit patients start induction at once. Leukapheresis has no proven benefit on its own and is used with hydroxyurea only for symptomatic leukostasis when induction cannot start.

Review: section 06

Q60SurvivorshipLevel 2Survivorship

Which advice suits a person living after AML treatment?

  1. AReport fever only if it lasts a week
  2. BStay active and social, with sensible precautions
  3. CAvoid all other people for five years after treatment
  4. DSkip all vaccines after a transplant
  5. ENever exercise again after treatment
Show answer

Answer: B. Encourage activity and normal contact (sensible precautions while counts are low), follow the transplant team's vaccination schedule, and report fever, bleeding and new tiredness promptly.

Review: section 08

Level 3 · Challenging

DNB, DM and USMLE Step 3 level: landmark trials, newer targeted drugs and difficult decisions.

Q61TreatmentLevel 3Systemic therapy

In RATIFY (midostaurin with 7+3 for FLT3-mutated AML), what was median overall survival?

  1. A15 vs 10 months
  2. B26 vs 75 months
  3. C9.3 vs 5.6 months
  4. D75 vs 26 months
  5. E32 vs 15 months
Show answer

Answer: D. 4-year OS was 51% vs 44%. Midostaurin is used for ITD or TKD mutations; quizartinib for ITD.

Review: section 06

Q62TreatmentLevel 3Systemic therapy

In QuANTUM-First (quizartinib for FLT3-ITD AML), what was median overall survival?

  1. A24 vs 8 months
  2. B75 vs 26 months
  3. C15 vs 10 months
  4. D25 vs 15 months
  5. E32 vs 15 months
Show answer

Answer: E. Quizartinib is added to induction and continued in consolidation and maintenance, like midostaurin.

Review: section 06

Q63TreatmentLevel 3Systemic therapy

In the CPX-351 phase 3 trial (patients aged 60–75 with secondary AML), what was 5-year overall survival?

  1. A68% vs 34%
  2. B97% vs 77%
  3. C18% vs 8%
  4. D51% vs 44%
  5. E8% vs 18%
Show answer

Answer: C. More patients on CPX-351 reached transplant. TP53-mutated therapy-related AML responds poorly to all options; trials are preferred.

Review: section 06

Q64TreatmentLevel 3Systemic therapy

In VIALE-A, what were median overall survival and complete remission with venetoclax plus azacitidine versus azacitidine alone?

  1. AOS 10 vs 15 months; CR 18% vs 37%
  2. BOS 32 vs 15 months; CR 70% vs 40%
  3. COS 24 vs 8 months; CR 50% vs 10%
  4. DOS 15 vs 10 months; CR 37% vs 18%
  5. ENo survival difference
Show answer

Answer: D. Venetoclax combinations are standard for unfit adults. In VIALE-C, venetoclax was added to low-dose cytarabine for those unsuitable for an HMA.

Review: section 06

Q65TreatmentLevel 3Systemic therapy

In AGILE, what was median overall survival with ivosidenib plus azacitidine in IDH1-mutated AML?

  1. A12 vs 11 months
  2. B9.3 vs 5.6 months
  3. C24 vs 8 months
  4. D75 vs 26 months
  5. E15 vs 10 months
Show answer

Answer: C. AGILE compared ivosidenib plus azacitidine with azacitidine alone in unfit adults with IDH1 mutations.

Review: section 06

Q66TreatmentLevel 3Systemic therapy

In ADMIRAL (relapsed FLT3-mutated AML), which pair of results is correct for gilteritinib vs salvage chemotherapy?

  1. AMedian OS 9.3 vs 5.6 months
  2. BMedian OS 32 vs 15 months
  3. CMedian OS 5.6 vs 9.3 months
  4. DNo difference in survival
  5. EMedian OS 24 vs 8 months
Show answer

Answer: A. Gilteritinib is a bridge to allogeneic transplant, the only cure after relapse.

Review: section 06

Q67TreatmentLevel 3Systemic therapy

In APL0406, what was 72-month event-free survival with ATRA plus arsenic versus ATRA plus chemotherapy?

  1. A77% vs 97%
  2. B68% vs 34%
  3. C50% vs 30%
  4. D97% vs 77%
  5. E99% vs 98%
Show answer

Answer: D. ATRA-arsenic gave fewer relapses and no induction deaths in low/intermediate-risk APL. AML17 tested ATRA-arsenic in all risk groups.

Review: section 06

Q68TreatmentLevel 3Systemic therapy

In QUAZAR, what was median overall survival with oral azacitidine maintenance versus placebo?

  1. A75 vs 26 months
  2. B25 vs 15 months
  3. C48 vs 12 months
  4. D9 vs 6 months
  5. E15 vs 25 months
Show answer

Answer: B. It is for patients aged 55 or more with intermediate- or adverse-risk AML in remission after consolidation.

Review: section 06

Q69DiagnosisLevel 3Biomarkers

In the Short 2020 meta-analysis, what was 5-year overall survival with negative versus positive MRD?

  1. A34% vs 68%
  2. B50% vs 45%
  3. C18% vs 8%
  4. D90% vs 10%
  5. E68% vs 34%
Show answer

Answer: E. MRD negativity roughly doubled 5-year survival across ages, subtypes and methods. NPM1 and CBF fusions are followed by PCR; other AML by multiparameter flow.

Review: section 04

Q70DiagnosisLevel 3Biomarkers

Under ELN 2024 for venetoclax plus azacitidine, what was median survival in the favourable, intermediate and adverse groups?

  1. A5.5, 12.1 and 26.5 months
  2. B12.1, 26.5 and 5.5 months
  3. C36, 24 and 12 months
  4. D75, 26 and 15 months
  5. E26.5, 12.1 and 5.5 months
Show answer

Answer: E. Favourable (52%): no FLT3-ITD, RAS or TP53 mutation. Intermediate (25%): FLT3-ITD or RAS. Adverse (25%): TP53 mutated.

Review: section 04

Q71TreatmentLevel 3Systemic therapy

In PARADIGM (fit adults), how did azacitidine-venetoclax compare with 7+3?

  1. AMore remissions and transplants, similar survival
  2. BBetter overall survival by about 20% at three years
  3. CIdentical remission and transplant rates
  4. DFewer remissions but much less toxicity
  5. EMore early deaths and fewer transplants
Show answer

Answer: A. It is acceptable for selected intermediate- or adverse-risk patients; most experts await longer follow-up.

Review: section 06

Q72TreatmentLevel 3Systemic therapy

In relapsed IDH2-mutated AML (Stein 2017), which results are reported for enasidenib?

  1. ANo responses
  2. BCR 97%, median OS not reached
  3. CCR 19%, median OS 9 months
  4. DCR 34%, median OS 9.3 months
  5. ECR 70%, median OS 32 months
Show answer

Answer: C. Enasidenib, like other IDH inhibitors, can cause differentiation syndrome because it releases the differentiation block.

Review: section 06

Q73TreatmentLevel 3Systemic therapy

What did ziftomenib achieve in its approval study of 112 adults with relapsed NPM1-mutated AML?

  1. ACR + CRh 75%
  2. BCR 5%
  3. CNo responses
  4. DCR + CRh 21%
  5. ECR 97%
Show answer

Answer: D. Ziftomenib (approved 13 November 2025) and revumenib are menin inhibitors; both cause differentiation syndrome and QT prolongation.

Review: section 06

Q74TreatmentLevel 3Systemic therapy

What did the Hills 2014 meta-analysis show for gemtuzumab ozogamicin with induction?

  1. ABenefit only in adverse-risk AML, none in CBF AML
  2. BBenefit only in APL, with no gain in other AML
  3. CMore relapses and deaths with gemtuzumab added
  4. DNo survival benefit in any genetic risk group
  5. EFewer relapses and better survival, most in CBF AML
Show answer

Answer: E. Benefit was seen in favourable and intermediate cytogenetics and was largest in core-binding-factor AML, which is nearly always CD33-positive.

Review: section 06

Q75TreatmentLevel 3Systemic therapy

What did Fernandez 2009 show about induction in younger adults?

  1. AIdarubicin was harmful
  2. BAnthracyclines added nothing
  3. CHigher daunorubicin exposure improved outcomes
  4. DCytarabine for 3 days was as good as 7
  5. EInduction can be omitted with good-risk genetics
Show answer

Answer: C. 7+3 gives complete remission in about three-quarters of fit younger adults; anthracycline exposure matters.

Review: section 06

Q76DiagnosisLevel 3Presentation, traps & genetics

At AIIMS, 480 patients aged 8–60 treated with 3+7 and high-dose cytarabine had what induction mortality?

  1. A40%
  2. B60%
  3. C5%
  4. D18.4%
  5. E1%
Show answer

Answer: D. Multidrug-resistant infections drive induction deaths in India; local resistance data should guide empirical antibiotics.

Review: section 02

Q77TreatmentLevel 3Systemic therapy

In 102 patients with APL at SGPGIMS Lucknow (2014–2024), which finding is correct?

  1. AInduction mortality about 1%, as in clinical trials
  2. BAll deaths were caused by differentiation syndrome
  3. CInduction mortality 24.5%; support limited by shortages
  4. DNo patient received ATRA during induction
  5. EMedian age 65, with most patients at low risk
Show answer

Answer: C. Median age was 33, 47% were high risk, and it took a median of 18 days from symptoms to diagnosis. Deaths were mostly from bleeding and infection.

Review: section 06

Q78TreatmentLevel 3Systemic therapy

How do early deaths in APL compare between clinical trials with early ATRA and population registries?

  1. AAbout 1% in both
  2. BAbout 29% in trials vs 3.7% in population registries
  3. CAbout 3.7% in trials vs up to 29% in registries
  4. DAbout 50% in both
  5. ERegistries report fewer deaths than trials do
Show answer

Answer: C. The gap between trials and real life reflects delays in starting ATRA and in blood product support. ATRA on suspicion is the single most important step.

Review: section 06

Q79TreatmentLevel 3Systemic therapy

At an Indian tertiary cancer centre (Jain 2020), what proportion of AML patients grew multidrug-resistant organisms during induction?

  1. A55%
  2. BNone, with prophylaxis
  3. C15%
  4. D90%
  5. E5%
Show answer

Answer: A. Fungal pneumonia was also diagnosed in 55% despite prophylaxis. Local resistance data should drive empirical choices.

Review: section 06

Q80SurvivorshipLevel 3Survivorship

In England (2001–2006), what was 5-year survival from AML at age 70–79?

  1. AAbout 13%
  2. BAbout 50%
  3. CAbout 70%
  4. DAbout 3%
  5. EAbout 33%
Show answer

Answer: D. About 50% under 40, 33% at 40–59, 13% at 60–69 and 3% at 70–79. Newer drugs and transplant in older adults have improved this since.

Review: section 08

Q81DiagnosisLevel 3Screening, workup & staging

What did Ganzel 2021 find about CNS involvement at diagnosis of adult AML?

  1. AFound in about 1–3%; it does not by itself worsen outcome
  2. BIt always requires craniospinal RT
  3. CIt doubles the risk of death
  4. DFound in about half of patients
  5. EIt is an indication for routine prophylaxis in all adults
Show answer

Answer: A. MRI and lumbar puncture are done only for neurological symptoms. Leptomeningeal AML without deficits is treated with intrathecal therapy; deficits need RT.

Review: section 03

Q82DiagnosisLevel 3Biomarkers

According to TCGA 2013, about how many mutations does an AML genome carry on average?

  1. AAbout 1,000, most of them in AML genes
  2. BExactly one driver and no other change
  3. CAbout 13,000 across the genome
  4. DNone: only translocations drive AML
  5. EAbout 13, about five in AML genes
Show answer

Answer: E. Most cases grow out of age-related clonal haematopoiesis (DNMT3A, TET2, ASXL1) that gathers further mutations.

Review: section 04

Q83DiagnosisLevel 3Biomarkers

Why can IDH inhibitors cause differentiation syndrome?

  1. AThey destroy CD33-positive blasts very fast
  2. BThey lift the block caused by 2-hydroxyglutarate
  3. CThey inhibit FLT3 signalling in the blasts
  4. DThey release potassium from leukaemic cells
  5. EThey deplete fibrinogen and trigger DIC
Show answer

Answer: B. IDH1/2 mutations (about 20%) make the oncometabolite 2-hydroxyglutarate. Ivosidenib, olutasidenib and enasidenib release the block, so blasts mature, as with ATRA in APL.

Review: section 04

Q84TreatmentLevel 3Systemic therapy

About how often does differentiation syndrome occur with different drugs?

  1. AOnly with ATRA in APL, and never with other drugs
  2. BOnly after allogeneic transplant, whatever the drug
  3. CAbout 3% (APL), up to 20% (IDH/menin), about 25% (FLT3)
  4. DAbout 25% (APL), up to 20% (IDH/menin), about 3% (FLT3)
  5. EAbout 80% with every drug that causes differentiation
Show answer

Answer: D. Routine steroid prophylaxis is not suggested. Mimics include sepsis, heart failure, pulmonary embolism, alveolar haemorrhage and drug reactions.

Review: section 06

Q85DiagnosisLevel 3Biomarkers

Which MRD method suits NPM1-mutated AML, as shown by Ivey 2016?

  1. AQuantitative PCR
  2. BMonthly karyotype
  3. CPET-CT
  4. DSerum LDH trend
  5. EMarrow morphology alone
Show answer

Answer: A. NPM1 transcripts by PCR predicted relapse. CBF fusions are also followed by PCR; other AML by multiparameter flow.

Review: section 04

Q86TreatmentLevel 3Systemic therapy

How do myeloablative and reduced-intensity conditioning compare for AML transplant?

  1. AMyeloablative is better for relapse, deaths and survival
  2. BMyeloablative: fewer relapses, more deaths; similar survival
  3. CThey differ only in cost, not in any outcome
  4. DReduced intensity is never used for AML transplant
  5. EReduced intensity gives fewer relapses than myeloablative
Show answer

Answer: B. The choice follows age and comorbidity. Transplant in CR2 is myeloablative if fit.

Review: section 06

Q87TreatmentLevel 3Systemic therapy

After an ATO-containing regimen and molecular remission in APL, how often does relapse occur, and what is done?

  1. A5–10% (20–30% if high risk); ATRA + arsenic, then auto-HCT
  2. BAbout 1%; ATRA maintenance is then given for life
  3. CAbout 80%; palliative care is the usual approach
  4. DNever; no further PCR follow-up is ever needed
  5. EAbout 50%; allogeneic transplant in every relapsed case
Show answer

Answer: A. No maintenance is needed after an ATO-containing regimen with molecular remission; without ATO, intermittent ATRA maintenance is used. Gemtuzumab treats molecular relapse where available.

Review: section 06

Q88TreatmentLevel 3Systemic therapy

What did the CMC Vellore studies (Mathews 2006, 2010) show in newly diagnosed APL?

  1. AChemotherapy alone beats arsenic
  2. BATRA is ineffective in Indian patients
  3. CAPL cannot be cured without transplant
  4. DAPL is very rare in India
  5. EDurable remissions with arsenic alone
Show answer

Answer: E. Today ATRA plus arsenic is standard where both are available; where arsenic is not, ATRA with an anthracycline is used.

Review: section 06

Q89TreatmentLevel 3Local therapy

What is the evidence for leukapheresis in hyperleukocytosis (Oberoi 2014)?

  1. AIt prevents tumour lysis
  2. BIt halves early mortality
  3. CIt replaces induction chemotherapy
  4. DIt is mandatory above 50,000/µL
  5. ENo proven benefit on its own
Show answer

Answer: E. Leukapheresis is used with hydroxyurea only for symptomatic leukostasis when induction cannot start at once. Hyperleukocytosis occurs in 10–20% of new AML.

Review: section 05

Q90DiagnosisLevel 3Presentation, traps & genetics

In what proportion of AML/MDS in young adults may an inherited predisposition be the cause?

  1. AUnder 1%
  2. BAbout 50%
  3. CAll cases
  4. D10–20%
  5. EAbout 80%
Show answer

Answer: D. It is 5–10% in older adults. It matters when a sibling is the planned donor, so germline-type variants (DDX41, RUNX1, GATA2, biallelic CEBPA) need follow-up.

Review: section 02

Prepared and reviewed by Dr. Haritha Chiramana for teaching. Facts compiled from current guidelines, primary trials and evidence summaries, written in our own words; drawings are original schematics, not patient images; no doses are included.