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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
what lymphoid cancer can occur at multipotent progenitor stage?
acute lymphoblastic leukaemia
26
what lymphoid cancer can occur at mature cell stage?
lymphomas chronic lymphocytic anaemia myeloma of plasma cells
27
describe pathology of acute laeukaemia
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
types of acute leukaemia?
acute myeloid leukaemia (AML) | acute lymphoblastic leukaemia (ALL)
29
ALL is a malignant disease of which cells?
primitive lymphoid cells (lymphoblasts)
30
most common childhood cancer?
ALL
31
clinical presentation of ALL?
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
who is AML more common in?
elderly (>60) | can be de novo or secondary to something else
33
presentation of AML?
similar to ALL | subgroups may have characteristic presentation (DIC, gum infiltration etc)
34
investigations for acute leukaemia?
blood count and film coagulation screen bone marrow aspirate
35
blood film in acute leukaemia?
reduction in normal cells | presence of abnormal cells (high nuclear:cytoplasmic ratio etc)
36
characteristic feature found in cells in acute myeloid leukaemia on blood film?
auer rod (pale area/line/blob/slit? at edge of cell)
37
what features do you look for on bone marrow aspirate?
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
definitive diagnosis to differentiate between AML and ALL?
immunophenotyping | even though cells from AML and ALL look alike, they express lineage associated proteins
39
curative treatment of acute leukaemia?
multi-agent chemo | other options include targeted treatments with kinase inhibitors and allogeneic stem cell transplant in select patients
40
how is multi agent chemo given in ALL?
can last up to 2-3 years different phases of treatment with different intensity targeted treatment in certain subsets
41
how is multi-agent chemo given in AML?
intensive 2-4 cycles (5-10 days chemo then 2-4 weeks recovery) prolonged hospital stay targeted treatments in subsets
42
what is a hickman line?
long term IV line inserted through the chest and SVC > right atrium has port for easy connection of drips and syringes
43
problems with marrow suppression from chemo?
anaemia neutropenia (main problem as can cause infections which are severe and long lasting) thrombocytopenia (bleeding problems)
44
what type of bacteria can cause fulminant life threatening sepsis in neutropaenic patients?
gram -ve
45
other complications of chemo?
``` nausea and vomiting hair loss liver/renal dysfunction tumour lysis syndrome infection late effects such as infertility, cardiomyopathy in anthracyclines) ```
46
how is bacterial infection in chemo managed (important)?
broad spectrum antibiotics as soon as neutropenic fever occurs (cover gram -ves in particular)
47
what suggests a fungal infection in chemo? (important)
prolonged neutropenia and persisting fever unresponsive to anti-bacterial agents
48
how effective is treatment in acute leukaemia?
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
definition of remission?
<5% marrow blasts with recovery of normal haemopoiesis
50
cure rates in acute leukaemia
childhood ALL = 85-90% adult ALL = 30-40 adult AML = 40-50 elderly AML = 10% or less

Haematology (26 decks)

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