About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Most common acute leukaemia in adults — median age at diagnosis ~65 years. Incidence rises with age
- Diagnosis: ≥20% myeloblasts in bone marrow. Blood film: Auer rods (azurophilic rod-shaped inclusions) are pathognomonic
- Acute promyelocytic leukaemia (APML, t(15;17) PML-RARA): commonly presents with DIC — medical emergency. Treat with all-trans-retinoic acid (ATRA) + arsenic trioxide — cure rate >90%
- May arise de novo or secondary to myelodysplastic syndrome, prior chemotherapy/radiotherapy, or myeloproliferative disease
- Treatment: intensive induction (daunorubicin + cytarabine "3+7"), consolidation, ± allogeneic transplant. Overall 5-year survival ~25-30% in adults
Overview
Acute myeloid leukaemia (AML) is a heterogeneous group of aggressive haematological malignancies characterised by clonal expansion of myeloid precursor cells (myeloblasts) in the bone marrow and blood. Normal haematopoiesis is suppressed, leading to pancytopenia. AML is classified by the WHO system based on cytogenetics, molecular genetics, and morphology. It may arise de novo or evolve from a preceding myelodysplastic syndrome or myeloproliferative neoplasm, or occur secondarily to prior chemotherapy or radiotherapy.
Epidemiology
AML is the commonest acute leukaemia in adults with approximately 3,000 new cases per year in the UK. The median age at diagnosis is approximately 65 years, and incidence increases sharply with age. Risk factors include prior chemotherapy (especially alkylating agents and topoisomerase II inhibitors), radiation exposure, pre-existing haematological disorders (MDS, MPN), and genetic conditions (Down syndrome, Fanconi anaemia). Occupational exposures (benzene) are also a recognised risk factor.
Clinical Features
Symptoms
Fatigue, pallor, breathlessness (anaemia)
Recurrent infections, persistent fever (neutropenia)
Easy bruising, bleeding gums, epistaxis (thrombocytopenia)
Gum hypertrophy — characteristic of monocytic subtypes (AML-M4/M5)
Disseminated intravascular coagulation — particularly with APML (bleeding and/or thrombosis)
Bone pain (less common than in ALL)
Signs
Pallor, petechiae, bruising
Gum infiltration and hypertrophy (monocytic AML)
Hepatosplenomegaly (less prominent than in ALL)
Skin infiltration (leukaemia cutis) — violaceous nodules
Signs of DIC: widespread bleeding from venepuncture sites, mucosal surfaces
Leukostasis symptoms if WCC very high: confusion, visual disturbance, dyspnoea
Investigations
First-line
FBCUsually pancytopenia. WCC may be low, normal, or very high. Elevated WCC with circulating blasts
Blood filmMyeloblasts: larger cells than lymphoblasts, granular cytoplasm. AUER RODS are pathognomonic (rod-shaped azurophilic inclusions). Multiple Auer rods ("faggot cells") seen in APML
Coagulation screenDIC screen (prolonged PT/APTT, low fibrinogen, raised D-dimer) — URGENT if APML suspected
Second-line
Bone marrow aspirate and trephineDiagnostic: ≥20% myeloblasts. Morphology, immunophenotyping, cytogenetics, and molecular genetics
Cytogenetics and molecular geneticst(15;17) PML-RARA = APML (good prognosis). t(8;21), inv(16) = favourable risk. Complex karyotype, monosomy 5/7 = adverse risk. NPM1 mutation, FLT3-ITD — prognostic markers
ImmunophenotypingConfirms myeloid lineage: CD13+, CD33+, CD117+, MPO+
Specialist
HLA typingIf transplant candidate — begin donor search at diagnosis
Lumbar punctureNot routine in AML (unlike ALL) unless CNS symptoms present
Tumour lysis panelK+, urate, PO4, Ca2+, creatinine — before starting treatment
1
APML — medical emergency
- If APML suspected (AUER RODS + DIC): start ALL-TRANS-RETINOIC ACID (ATRA) IMMEDIATELY — do not wait for cytogenetic confirmation
- ATRA + arsenic trioxide (ATO) is now standard for non-high-risk APML — avoids conventional chemotherapy
- Aggressive correction of DIC: platelets, FFP, cryoprecipitate (maintain fibrinogen >1.5 g/L, platelets >30)
- APML is CURABLE: cure rate >90% with modern ATRA/ATO protocols
2
Intensive induction (fit patients)
- Standard "3+7" protocol: daunorubicin 3 days + cytarabine 7 days
- Midostaurin added if FLT3-mutated AML
- Aim: achieve complete remission (CR) — expect 4-6 weeks of marrow aplasia requiring intensive supportive care
- Repeat bone marrow at day 14 and recovery to assess response
3
Post-remission therapy
- Favourable risk: consolidation chemotherapy with high-dose cytarabine (3-4 cycles)
- Intermediate/adverse risk: allogeneic stem cell transplant in first CR
- Adverse-risk cytogenetics: transplant is the only potentially curative option
4
Non-intensive treatment (unfit/elderly)
- Azacitidine ± venetoclax — now standard of care for unfit patients
- Low-dose cytarabine as alternative
- Best supportive care with transfusions and hydroxyurea for symptom control if treatment not appropriate
Complications
- DIC: Particularly with APML — the major cause of early death. Start ATRA at first suspicion
- Tumour lysis syndrome: Aggressive hydration and rasburicase prophylaxis for high WCC
- Leukostasis: WCC >100 × 10⁹/L — hyperviscosity causing pulmonary and cerebral symptoms. Emergency leucoreduction needed
- Neutropenic sepsis: During treatment-induced aplasia — the major cause of treatment-related mortality
- Treatment-related mortality: Induction mortality ~5-10% in fit patients, higher in elderly
UKMLA Exam Tips
- 1Auer rods = AML. They are PATHOGNOMONIC. "Faggot cells" (multiple Auer rods) = APML
- 2APML + DIC = start ATRA IMMEDIATELY. Do not wait for genetic confirmation. This saves lives
- 3AML is the commonest acute leukaemia in ADULTS. ALL is the commonest in CHILDREN
- 4Gum hypertrophy = monocytic AML subtypes (M4, M5)
- 5t(15;17) = APML = EXCELLENT prognosis (>90% cure with ATRA + arsenic). t(8;21) and inv(16) = favourable
- 6De novo AML has better prognosis than secondary AML (from MDS or prior chemo/radiotherapy)
practicetest your knowledge on amlApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — haematology and beyond.
open q-bank