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- Y6 Haematology > Leukaemia (AML, ALL, CML, CLL) > Flashcards

Leukaemia (AML, ALL, CML, CLL) Flashcards

1
Q

What are acute leukaemias?

A
  • Neoplastic conditions with rapid onset
  • Characterised by the presence of immature cells (blasts) in the blood and bone marrow
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2
Q

What are the clinical effects of acute leukaemias?

A

They cause bone marrow failure:

  1. Anaemia (↓ Hb): fatigue, pallor, breathlessness
  2. Neutropenia (↓ neutrophils): recurrent infections
  3. Thrombocytopenia (↓ platelets): bleeding and easy bruising
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3
Q

Describe how a blood stem cell splits.

A
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4
Q

What is the best investigation for differentiating lymphoid from myeloid leukaemias?

A

Immunophenotyping - shows antigens

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5
Q

What is the pathogenesis of acute myeloid leukaemia? What causes it?

A

Defect in the step which converts blast cell (myeloblast) to granulocytes (eosinophils, basophils, neutrophils). There is clonal explansion of myeloid blast cells in bone marrow, peripheral blood or extra-medullary tissues.

Aetiology: unknown

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6
Q

What investigations are used for diagnosing leukaemias?

A

Cytogenetic analysis

FISH - chromosome translocations identified

Molecular genetic analysis

Immunophenotyping

Histology

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7
Q

What is the management of AML?

A

Supportive e.g. RBC, plt, FFP, abx, allopurinol

Chemotherapy

Targeted molecular therapy

Transplantation

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8
Q

What are the risk factors for AML?

A
  • Down’s
  • Irradiation
  • Anti-cancer drugs
  • Age (incidence increases with age)

Common in the elderly population.

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9
Q

What are the clinical features of AML? How do you diagnose it?

A
  • Bone marrow failure - bleeding, infections, anaemia, hyperviscosity
  • Splenomegaly, hepatomegaly
  • Gum infiltration
  • Skin/CNS palsies
  • Lymphadenopathy

Diagnosis: Auer rods on blood film, myeloblast cells (10-19%)

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10
Q

What is promyelocytic leukaemia?

A

An AGGRESSIVE subtype of AML

aka APML

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11
Q

What is the cause of promyelocytic leukaemia? What is a common complication?

A

t(15;17)

Associated with DIC

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12
Q

What is the pathogenesis of acute lymphoblastic leukaemia?

A
  • Defect is in the lymphoblast to B/T/NK cell pathway.
  • –> uncontrolled proliferation of lymphoblasts
  • 3/4 are B cell ALL (acute lymphoblastic leukaemia)
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13
Q

What are the clinical features of ALL?

A
  • Child - 75% under 6 years old
  • Bone marrow failure - anaemia, infection, bleeding
  • Lymphadenopathy
  • Splenomegaly, hepatomegaly
  • Sanctuary sites - testes and CNS
  • Thymic enlargement → stridor
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14
Q

What are the histological features of ALL?

A
  1. Bloods: high WCC, low Hb, low Plt
  2. Bone marrow film: >20% lymphoblasts
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15
Q

What is the management of ALL?

A
  • Systemic 2-3yrs of therapy (boys treated longer as lymphoblasts accumulate in testes) e.g. imatinib for Ph+ve
  • CNS-specific therapy (all patients)
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16
Q

What is the pathogenesis of chronic lymphocytic leukaemia?

A

Accumulation of mature incompetent lymphocytes (unable to undergo apoptosis) that are able to self-renew. So bone marrow becomes infiltrated.

17
Q

What are the histological features of CLL? What other investigation can be done?

A
  1. Cells are fragile –> break when smeared on a blood film–> smear/smudge cells
  2. Bloods - ↑ lymphocytes, ↓ Hb, ↓ neutrophils, ↓ platelets

Flow cytometry is useful

Most diagnosed on FBC for unrelated reason

18
Q

What mutations may cause CLL to progress to a more aggressive type?

A

Richter transformation - risk is 1% a year

19
Q

What are the clinical features of CLL?

A

Median age 72yrs at diagnosis

Lymphoctyes can infiltrate lymphatic tissues and haemopoietic organs such as liver, spleen and bone marrow

  • Lymphadenopathy
  • Splenomegaly in 50%
  • SOB
  • Fatigue
20
Q

What two syndromes is CLL associated with?

A
  • Can be associated with autoimmune thrombocytopenia + anaemia = Evan’s syndrome
  • Can transform to aggressive NHL = Richter’s syndrome
21
Q

What is the management of CLL?

A

Supportive - vaccination, prophylactic abx

Immunotherapy - BCR kinase inhibitor (e.g. ibrutinib), BCL2 inhibitors (e.g. venetoclax)

Chemotherapy

Allogeneic SCT

22
Q

Under what type of lymphoma does CLL fall?

A

NHL (B cell type) - indolent

23
Q

What is the pathophysiology of chronic myeloid leukaemia?

A

Uncontrolled proliferation of granulocyte precursors in BM but slower proliferation than AML (myeloblast to granulocyte step that leads to basophil /eosinophil /neutrophil production)

Malignant clonal disorder of haemopoietic stem cell that results in marked myeloid hyperplasia in the bone marrow. AKA chronic granulocytic leukaemia

24
Q

When does CML usually present? What is a known risk factor?

A

Usually presents at age 53

Exposure to ionising radiation is the only known risk factor

25
Q

What are the clinical features of CML?

A
  • Hypermetabolism - weight loss, malaise, sweating, gout
  • Hyperviscosity - visual disturbance, headaches, thrombotic event
  • MASSIVE hepatosplenomegaly
  • Bone marrow failure- lethargy, dyspnoea, easy bruising/epistaxis (NB: plt and Hb normal or raised)

Massive splenomegaly in 90% (splenomegaly does not have time to form in acute leukaemias)

26
Q

How do you diagnose CML? How can the disease course change?

A

FBC with differential - raised WCC (myelocytes, basophilia, neutrophilia)

Philadelphia chromosome (>80%)

+/-

t(9, 22) forming BCR-ABL rearrangement in peripheral blood or bone marrow cells. This encodes an active TK receptor –> continuous cell proliferation

<5% blasts - only myelocytes, all mature

Can transform into accelerated phase (10-19% blasts) or into acute leukaemia phase (>20% blasts)

27
Q

What mutation causes CML?

A

Chromosomal translocation BCR-ABL

PhChr +ve (9;22)

28
Q

What was the prognosis for CML before imatinib?

A

chronic phase → new mutation → blast crisis

29
Q

How do you monitor therapy in CML?

A

RQ-PCR amplification and detection of % of BCR-ABL transcripts

30
Q

What is the prognosis with CML?

A
  • 1/3 never progress
  • 1/3 Progress, respond to CLL Rx (death from unrelated disorder)
  • 1/3 Progress, require multiple lines of Rx, refractory disease, death from CLL
31
Q

Give a buzzword for each type of leukaemia.

A
  1. AML: Auer rods
  2. ALL: children <6 years
  3. CML: Philadelphia chromosome t(9;22), BCR-ABL gene
  4. CLL: smear/smudge cells

- Y6 Haematology (22 decks)

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