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Haematology > The Acute Leukaemias > Flashcards

The Acute Leukaemias Flashcards

1
Q

Define leukaemia

A

Leukaemia: malignancy arising from bone marrow stem cells. Leukaemic cells replace most of BM (crowding out normal haematopoiesis – bleeding, fatigue, infections), enter the peripheral blood and metastatise throughout the body

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2
Q

Auer rods?

A

In AML
Peroxidase positive

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3
Q

Risk factors for acute leukaemias

A

Genetic & environmental

Antineoplastic agents
Ionising radiation
Hodgkin’s lymphoma
Benzene
MM

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4
Q

Define acute leukaemia

A

Monoclonal disorders of early haematopoietic stem cells

Cells lose their ability to differentiate, but retain their ability to replicate

Defined as >20% blasts in the bone marrow

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5
Q

FBE in acute leukaemia

A

Normocytic or macrocytic anaemia (due to folate def)

Platelets < 100

WBC <10 - >100
Blasts - myeloblasts (more granules, auer rods), monoblasts (less granules, no auer rods), lymphoblasts

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6
Q

Bone marrow biopsy findings acute leukaemia

A

Hypercellular
Blasts > 20%
Usually completely replaced by blast cells

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7
Q

LAB tests for acute leukaemia

A
  • Morphologic analysis
  • Cytogenic studies (karyotype)
  • Molecular markers
  • Cell surface (CD) markers - flow cyto and immunophenotyping
  • Cytochemical analysis (PAS, peroxidase, esterase, sudan black stains
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8
Q

Treatment of acute leukaemias

A

INDUCTION PHASE:

  1. Induce remission with high dose chemotherapy –> suppresses all clel lines –> patient prone to infections due to neutropenia
  2. Myeloid growth factors: reduces length of hospitalisations (by shortening neutropenic state) but do NOT increase survival
  3. Give RBCs and platelets

CONSOLIDATION PHASE (so the cancer doesn’t come back)
Once WCC normalise i.e. remission

  1. Consolidation therapy: prolongs remission, increases survival
    - Sometimes can use gene expression profiling (DNA microarrays) to predict prognosis and guide therapy
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9
Q

Dangers of tumour lysis syndrome

A
  • Cardiac arrhythmias (from electrolyte derangement) –> death
  • Severe renal failure due to uric acid crystal deposition
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10
Q

Prevention of tumour lysis syndrome

A

Prophylactic allopurinol until neutrophils <0.5

Or if high risk, rasburicase instead

Continuous fluids (i.e. 8 hourly bags) with close monitoring of fluid balance

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11
Q

Treatment of florid TLS

A

3-5% will develop TLS despite appropriate prophylaxis

Renal POV:
- Continuous urine output recording
- Aggressive fluids, diuresis to wash out obstructing UA crystals
- Renal consult
- CRRT if required

Cardiac POV:
- ECG and cardiac monitoring
- Monitor electrolytes, cr, uric acid, LDH, every 4-6 hours
> treat hyperK, hypoC, hyperPhos
- Rasburicase (once only if used prophylactically, can have repeat doses if not)
-

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12
Q

What is the most common type of acute leukaemia?

A

AML

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13
Q

What diseases may progress to AML?

A

MDS, MPNs, PNH, aplastic anaemia, clonal haematopoiesis of indeterminate prognosis (CHIP), clonal cytopenia of unknown significance (CCUS)

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14
Q

What happens when a myeloid precursor cell becomes malignant?

A

Clones of abnormal cells that can proliferate, but cannot differentiate into mature blood cells or undergo apoptosis

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15
Q

Clinical features of AML (symptoms)

A
  • Anaemia: SOB, weakness, dyspnoea
  • TCP: bleeding/bruising
  • Neutropenia: fever/infections

Headache/focal neurology due to CNS haemorrhage or leukaemic meningitis

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16
Q

Clinical features of AML (examination)

A

Pallor, bruising., bleeding

Occasionally splenomegaly/hepatomegaly or soft tissue mass (myeloid sarcoma). Lymphadenopathy is rare.

17
Q

AML - blood results

A
  • Low mature red cells, neutrophils and/or platelets
  • May have leukocytosis (due to blasts)
  • TLS features
  • Other metabolic complications assoc with hyperleukocytosis and leukostasis
18
Q

What is APML?

A

Acute promyelocytic leukaemia - distinctive syndrome that should be suspected in patients with: bleeding/bruising, TCP, leukaemia blasts with coarse cytoplasmic granules, low WCC, hypofibrinogenaemia and/or few circulating leukaemic cells.

It is a medical emergency that requires urgent management

19
Q

What is the risk with APML?

A

DIC

20
Q

Complications/emergencies with AML:

A
  • Pancytopenia
  • Hyperleukocytosis / leukostasis
  • Metabolic abnormalities: TLS, renal failure
  • Coagulation disorders: DIC from sepsis, drugs, AML or APML
  • Involvement of CNS or eyes
21
Q

What is hyperleukocytosis /leukostasis?

A

AML with myeloblasts >100,000/microL

Or myeloblasts >50,000/microL, with respiratory or neurological distress

22
Q

Diagnosis of AML?

A

Bone marrow or peripheral blood blasts >20% with characteristic morphological, cytochemical, immunophenotypic and molecular features

23
Q

Typical chromosomal / molecular abnormalities of AML

A

inv(16), t(16;16), t(8;21), t (15;17) or PML-RARA gene

24
Q

DDc for cytopenias (aside from AML/ALL/CML)

A

In some cases, AML presents with cytopenias, with few circulating blasts.

DDx include: aplastic anaemia, myelofibrosis, MDS< medications, nutritional deficiencies, BM suppression (alcohol, infection), sequestration from organomegaly, autoimmune (felty), HLH

25
Q

Prognostic factors for AML (

A

Clinical risk factors. Promising factors: age < 50, good ECOH, MDR-1 negative phenotype, no previous MPN/MDS or radiotherapy,

Cytogenetic and molecular features (guided by ELN stratification)

26
Q

Bad AML mutations

A

FLT3/ITD mutation
MLL partial tandem duplication
BAALC over-expansion
Mutations in IDH1 or IDH2

27
Q

How do we categorise risk of AML tumours?

A

Favourable, intermediate and adverse risk

Based on genetic abnormalities/mutations

Look up European LeukaemiaNet stratification

28
Q

Therapy related AML?

A

Prior exposure to chemo or radiation. Often has high risk genetic features and poor prognosis

29
Q

What is usually the goal of treatment for AML?

A

If deciding that tx is appropriate, aim for complete remission (<5% blasts) — necessary for cure.

Should also consider HLA typing for transplant

60-80& of younger adults will achieve CR post chemo, but only 1/3 will be cured…

30
Q

When do we marrow patients post treatment for AML?

A

BMA/biopsy 7-10 days post induction chemo ?adequate response with marrow hypoplasia

And again after count recovery to document remission status

31
Q

What are the possible outcomes following induction chemo?

A

Complete remission (CR)
Complete remission with incomplete count recovery (CRi)
Partial remission
Resistant/refractory disease

32
Q

Post remission therapy?

A

Nearly all patients will relapse unless post-remission therapy is given

Goal is to eliminate residual, undetectable disease to achieve long-term control

Has two phases: consolidation and maintenance

33
Q

What is ‘consolidation’ therapy?

A

Post remission treatment (to achieve long term cure/control post induction) – includes more chemo, and allogeneic stem cell transplant (if higher risk)

34
Q

What is ‘maintenance’ therapy?

A

Nonmyelosuppressive treatment with chemo and/or targeted drug, given over months to years

35
Q

Management of hyperleukocytosis/leukostasis?

A

Causes death mainly by lung / CNS involvement

Management: rapidly lower WCC. Options: induction chemo, hydroxyurea, leukapharesis.. Where induction chemo is likely to be delayed (i.e. the instances I’ve observed - start with leukapharesis)

Supportive - don’t give product support until blast crisis resolved, rasburicase/allopurinol and TLS monitoring, coag monitoring

36
Q

Which patients do we give FML eye drops to 2 hourly 24 hours before chemo and why?

A

Patients having high dose cytarabine (HiDAC)
Cytarabine-induced keratoconjunctivitis

Haematology (8 decks)

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