Leukaemia: AML, ALL, CML, CLL Flashcards

1
Q

Define leukaemia?

A

Group of malignant cancers characterised by overproduction of immature and abnormal mature leukocytes, which suppress formation of other blood cells

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2
Q

Leukaemia is a cancer of what blood cell lineage?

A

Leukocytes (WBCs)

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3
Q

How does leukaemia characteristically affect formation of other blood cell lineages?

A

Suppresses formation of other blood cell types

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4
Q

Why is leukaemia classed as either myeloid or lymphoid?

A

Classed as myeloid (originates from myeloid cell lineage)

or

lymphoid (originates from lymphoid cell lineage)

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5
Q

How many main types of leukaemia are there, and what are they called?

A

4 main types:

Acute Myeloid Leukaemia (AML)

Chronic Myeloid Leukaemia (CML)

Acute Lymphoblastic/Lymphocytic Leukaemia (ALL)

Chronic Lymphoblastic/Lymphocytic Leukaemia (CLL)

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6
Q

Why is leukaemia classed as either acute or chronic?

A

Classed as acute (predominantly originates from immature cells)

or

chronic (predominantly originates from mature cells)

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7
Q

Define CLL, in terms of classification?

A

Chronic Lymphoblastic/Lymphocytic Leukaemia (CLL): Characterised by clonal proliferation of mature B-lymphocytes

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8
Q

What is the most common type of leukaemia?

A

CLL

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9
Q

At what age does CLL typically present?

A

Over 70 yrs old

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10
Q

Describe the speed of progression of CLL?

A

Usually progresses slowly

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11
Q

Does a patient with CLL typically present as symptomatic or asymptomatic, and why?

A

Asymptomatic

Because it generally progresses slowly

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12
Q

In the clinical presentation of symptomatic CLL, what are the 4 characteristic findings?

A

Lymphadenopathy

Splenomegaly

Symptoms of anaemia eg. pallor, TATT

Symptoms of thrombocytopenia eg. easily bruises or bleeds

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13
Q

How is CLL usually initially diagnosed during investigation?

A

Incidental lymphocytosis finding on FBC

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14
Q

If a patient has lymphadenopathy but no lymphocytosis on the FBC, can this still be diagnosed as CLL?

A

No, CLL must have lymphocytosis finding

Diagnosed as a Small Lymphocytic Lymphoma (SLL), which is a low-grade Non-Hodgkin lymphoma

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15
Q

What are the 2 hallmark findings for CLL on a blood film?

A

Lymphocytosis (lymphocytes with large nucleus and very thin cytoplasm border)

Smudge/smear cells (ruptured lymphocytes with irregular cytoplasm border)

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16
Q

What is immunophenotyping?

A

Lab test that uses a monoclonal antibody with an attached fluorescent maker to identify different antigens

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17
Q

What lab investigation is used to confirm CLL diagnosis?

A

Immunophenotyping

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18
Q

What is the hallmark finding of CLL, on immunophenotyping?

A

Co-expression of CD5 (T-cell antigen) and CD19 (B-cell antigen)

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19
Q

When do you start treatment for a patient with CLL?

A

Only treat patient when they become symptomatic, otherwise watch and wait

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20
Q

What are the most common medications used to treat CLL?

A

Combination of cytotoxic chemotherapy and monoclonal antibodies

eg. Rituximab + fludarabine + cyclophosphamide

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21
Q

What new drug class can be used to treat CLL, and give 2 examples?

A

B-cell signaling inhibitor tablets

e.g. ibrutinib, venetoclax

22
Q

Define CML, in terms of classification?

A

Chronic Myeloid Leukaemia (CML): Characterised by clonal proliferation of mature granulocytes

23
Q

What is the pathophysiology of CML?

A

Philadelphia chromosome translocation between chromosomes 9 and 22 causes BCR-ABL protein (tyrosine kinase) to switch on myeloid cell production

24
Q

Does a patient with CML typically present as symptomatic or asymptomatic, and why?

A

Usually asymptomatic, as the chronic phase progresses slowly

25
Q

Compare the clinical presentation of symptomatic CML to CLL?

A

Similar presentation of splenomegaly, lymphadenopathy, anaemia, thrombocytopenia, neutropenia symptoms and signs

CML presents also with night sweats and weight loss

26
Q

How is CLL usually initially diagnosed during investigation?

A

Incidental lymphocytosis finding on FBC

27
Q

Other than neutrophilia, what are 3 findings on a FBC of a patient with CML?

A

Thrombocytosis
Eosinophilia
Basophilia

28
Q

What is the blood film hallmark for CML?

A

Neutrophilia

29
Q

Which 2 lab investigations are used to confirm a CML diagnosis?

A

FISH

Bone marrow aspirate

30
Q

What will the FISH investigation show to confirm CML?

A

Philadelphia translocation

31
Q

What will the bone marrow aspirate show to confirm CML?

A

Excess myeloid cells

32
Q

What is the FISH investigation, and why is it useful for diagnosing CML?

A

FISH (Fluorescent In-Situ Hybridisation) identifies specific chromosome translocations by providing fusion signal (yellow coloured)

Will identify Philadelphia translocation

33
Q

How does the bone marrow aspirate from a patient with CML correlate to their progression?

A

Shows state of progression between chronic and acute phase

34
Q

When do you start treatment for a patient with CML?

A

Immediately after diagnosis

Otherwise could progress to AML

35
Q

What is the first-line drug class for CML treatment, and how long must the patient take these for?

A

Tyrosine Kinase Inhibitors (TKI) eg.imatinib

Taken daily for rest of life

36
Q

How can TKIs treat CML, and how is this monitored?

A

Patient aims to have very low BCR-ABL protein as TKI blocks it

Monitored using PCR of blood

37
Q

Define ALL, in terms of classification?

A

Acute Lymphoblastic/Lymphocytic Leukaemia (ALL): Characterised by clonal proliferation of lymphoblasts (lymphocyte precursors)

38
Q

Define AML, in terms of classification?

A

Acute Myeloid Leukaemia (AML):Characterised by clonal proliferation of myeloblasts (myeloid cell precursors)

39
Q

Compare the epidemiologies of ALL and AML?

A

ALL: More common in children

AML: More common in adults and elderly

40
Q

Compare the clinical presentation of ALL and AML?

A

Both present with symptoms of pancytopenia: Lethargy, fever and infections, easily bleed and bruise, symptoms of anaemia

ALL patients can sometimes present with hepato-splenomegaly

41
Q

Compare the speed of onset of ALL and AML?

A

Speed of onset is usually fast, as history is short

42
Q

Why is hepato-splenomegaly less common in acute leukaemia than chronic leukaemia?

A

Hepato-splenomegaly is an adaptation so can take time to occur

43
Q

What must a blood film show to confirm an acute leukaemia diagnosis?

A

Over 20% blast cells

44
Q

Why is blood film not reliable to distinguish between ALL and AML?

A

Lymphoid and myeloid blasts both have high nuclear:cytoplasmic ratio and distinct nucleoli

45
Q

What lab investigation is used to distinguish between ALL and AML?

A

Immunophenotyping

46
Q

What blood film finding can indicate AML instead of ALL?

A

Auer rods

47
Q

What is meant by cancer remission, and is this absolute?

A

Cancer is not detected

Patients still have risk of cancer returning: Relapse

48
Q

What is the correlation between curative chemotherapy for acute leukaemias and patient age?

A

The more elderly a patient is, the less likely they are to tolerate curative chemotherapy

49
Q

Give one benefit and one disadvantage of intensive chemotherapy?

A

Chance of cure but is very toxic and has life-threatening complications associated

50
Q

Give one benefit and one disadvantage of low-intensity chemotherapy?

A

Prolongs life but not curative, still is toxic

51
Q

When palliative care is the chosen treatment for acute leukaemia, what is the main focus?

A

Symptom control with minimal time in hospital