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Haematology > Concepts in Malignant Haematology > Flashcards

Concepts in Malignant Haematology Flashcards

1
Q

normal haemopoiesis?

A

stem cells > multipotent progenitors > oligolineage progenitors > mature cells

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2
Q

what kinetic events occur during haemopoiesis?

A 
self-renewal
proliferation
differentiation/lineage commitment
maturation
apoptosis
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3
Q

how can normal, mature non-lymphoid cells be identified?

A

via morphology

  • cell surface antigens (e.g glycophorin A = red cells)
  • enzyme expression (myeloperoxidase = neutrophils)
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4
Q

what are the non-lymphoid cells?

A

red cells (erythrocytes)
platelets
granulocytes (neutrophils, basophils, eosinophils)
macrophages

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5
Q

how can normal progenitor cells/stem cells be identified?

A

cell surface antigens (immunophenotyping eg CD34)
cell culture assay
animal models

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6
Q

malignant haemopoiesis is characterised by what?

A

increased numbers of abnormal and dysfunctional cells

loss of normal activity (loss of normal haemopoiesis in leukaemia or loss of immune function in certain lymphoma)

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7
Q

what problems can occur in haemopoiesis?

A

increased proliferation
lack of differentiation
lack of maturation
lack of apoptosis

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8
Q

describe bone marrow aspirate in acute leukaemia

A

proliferation of abnormal progenitors with block in differentiation/maturation

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9
Q

describe bone marrow aspirate in chronic myeloproliferative disorders (e.g chronic myeloid leukaemia)

A

proliferation of abnormal progenitors

but no block of differentiation/maturation

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10
Q

what causes haematological malignancy?

A

genetic, epigenetic and environmental interaction
somatic mutations in regulatory genes(driver/passenger genes)
recurrent cytogenic abnormalities (e.g deletions, chromosomal translocations etc) can contribute but not usually causal
usually multiple “hits” rather than single event

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11
Q

driver mutations can select “clones”, what are clones?

A

population of cells derived from a single parent cell
this parent cells has a genetic marker that is chared by all daughter cells
clones can diversify but contain similar genetic backbone

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12
Q

clones in normal haemopoiesis vs malignant haemopoiesis?

A 
normal = polyclonal
malignant = monoclonal
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13
Q

what is a driver mutation?

A

a mutation that gives a selective advantage to a clone in its microenvironment, through either increasing its survival or reproduction. Driver mutations tend to cause clonal expansions.

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14
Q

how do driver mutations cause cancer?

A

they confer a growth advantage on the cells and are selected during the evolution of the cancer

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15
Q

what is a passenger mutation?

A

AKA hitchhiker mutation
doesn’t confer a growth advantage but can still be associated with clonal expansion as it occurs on the same genome as the driver mutation

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16
Q

what are types of haematological malignancies based on?

A

lineage
developmental stage (precursor) within lineage
anatomical site involved

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17
Q

types of haematological malignancy based on lineage?

A

myeloid

lymphoid

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18
Q

examples of haematological malignancy based on developmental stage?

A

cancer of lymphocyte precursor = acute lymphoblastic anaemia
cancer of mature lymphocytes = chronic lymphocytic leukaemia
cancer of mature plasma cell (branch of B cell) = myeloma

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19
Q

types of haematological malignancy based on anatomical site involved?

A

blood involvement = leukaemia
lymph node involvement with lymphoid malignancy = lymphoma
(however chronic lymphocytic leukaemia can involve blood and lymph nodes)

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20
Q

which is more histologically and clinically more aggressive, acute leukaemias/high grade lymphomas or chronic leukaemias/low grade lymphomas?

A

acute leukaemias and high grade lymphomas

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21
Q

what features on histology indicate aggressive cancer?

A

large cells with high nuclear:cytoplasmic ratio
prominent nucleoli
rapid proliferation

22
Q

clinical features of aggressive cancer?

A

rapid progression of symptoms

acute leukaemias, in contrast to chronic, present with failure of normal bone marrow function

23
Q

what myeloid cancers occur at stem cell stage?

A

chronic myeloid leukaemia

chronic myeloproliferative disorders

24
Q

what myeloid cancers occur at multipotent progenitor stage?

A

acute myeloid leukaemia

25
Q

what lymphoid cancer can occur at multipotent progenitor stage?

A

acute lymphoblastic leukaemia

26
Q

what lymphoid cancer can occur at mature cell stage?

A

lymphomas
chronic lymphocytic anaemia
myeloma of plasma cells

27
Q

describe pathology of acute laeukaemia

A

rapidly progressive clonal malignancy of the marrow/blood with maturation defects
defined as an excess of “blasts” (>20%) in either the peripheral blood or bone marrow
decrease/loss of normal haemopoietic reserve

28
Q

types of acute leukaemia?

A

acute myeloid leukaemia (AML)

acute lymphoblastic leukaemia (ALL)

29
Q

ALL is a malignant disease of which cells?

A

primitive lymphoid cells (lymphoblasts)

30
Q

most common childhood cancer?

A

ALL

31
Q

clinical presentation of ALL?

A

features of marrow failure (anaemia, infection, bleeding)
leukaemic effects (high blood cell counts with obstruction of circulation, involvement of areas outside blood/marrow)
bone pain

32
Q

who is AML more common in?

A

elderly (>60)

can be de novo or secondary to something else

33
Q

presentation of AML?

A

similar to ALL

subgroups may have characteristic presentation (DIC, gum infiltration etc)

34
Q

investigations for acute leukaemia?

A

blood count and film
coagulation screen
bone marrow aspirate

35
Q

blood film in acute leukaemia?

A

reduction in normal cells

presence of abnormal cells (high nuclear:cytoplasmic ratio etc)

36
Q

characteristic feature found in cells in acute myeloid leukaemia on blood film?

A

auer rod (pale area/line/blob/slit? at edge of cell)

37
Q

what features do you look for on bone marrow aspirate?

A

morphology
immunophenotyping (are there lineage-specific proteins on cell surface?)
cyto/molecular genetics
trephine (piece of bone) - better assessment of cellularity and helpful if aspirate not great

38
Q

definitive diagnosis to differentiate between AML and ALL?

A

immunophenotyping

even though cells from AML and ALL look alike, they express lineage associated proteins

39
Q

curative treatment of acute leukaemia?

A

multi-agent chemo

other options include targeted treatments with kinase inhibitors and allogeneic stem cell transplant in select patients

40
Q

how is multi agent chemo given in ALL?

A

can last up to 2-3 years
different phases of treatment with different intensity
targeted treatment in certain subsets

41
Q

how is multi-agent chemo given in AML?

A

intensive
2-4 cycles (5-10 days chemo then 2-4 weeks recovery)
prolonged hospital stay
targeted treatments in subsets

42
Q

what is a hickman line?

A

long term IV line inserted through the chest and SVC > right atrium
has port for easy connection of drips and syringes

43
Q

problems with marrow suppression from chemo?

A

anaemia
neutropenia (main problem as can cause infections which are severe and long lasting)
thrombocytopenia (bleeding problems)

44
Q

what type of bacteria can cause fulminant life threatening sepsis in neutropaenic patients?

A

gram -ve

45
Q

other complications of chemo?

A 
nausea and vomiting
hair loss
liver/renal dysfunction
tumour lysis syndrome
infection
late effects such as infertility, cardiomyopathy in anthracyclines)
46
Q

how is bacterial infection in chemo managed (important)?

A

broad spectrum antibiotics as soon as neutropenic fever occurs
(cover gram -ves in particular)

47
Q

what suggests a fungal infection in chemo? (important)

A

prolonged neutropenia and persisting fever unresponsive to anti-bacterial agents

48
Q

how effective is treatment in acute leukaemia?

A

many people go into remission
however remission might not last depending on type of acute leukaemia and many relapse
some patients will also die of treatment related toxicity

49
Q

definition of remission?

A

<5% marrow blasts with recovery of normal haemopoiesis

50
Q

cure rates in acute leukaemia

A

childhood ALL = 85-90%
adult ALL = 30-40
adult AML = 40-50
elderly AML = 10% or less

Haematology (26 decks)

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