Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Malignant Haematology > Flashcards

Malignant Haematology Flashcards

1
Q

why do you determine non lymphoid blood cells

A

(erythrocytes, platelets, granulocytes, macrophages)
MORPHOLOGY

cell surface antigens (glycophorin A = red cells) 
enzyme expression (myeloperoxidase= neutrophils)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how do you identify normal progenitor/ stem cells

A

IMMUNOPHENOTYPING (cell surface antigens e.g. CD34)

cell culture assays

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what characterises malignant haemopoiesis

A

increased number of abnormal and dysfunctional cells

loss of normal activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what types of cancers have a loss of normal haemopoiesis

A

acute leukaemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what cancers have loss of normal immune function

A

certain lymphomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what cell mechanisms cause malignant haemopoiesis

A

increased proliferation

lack of differentiation, maturation and apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the causative mechanisms of acute leukaemia

A

proliferation of ABNORMAL progenitor with block in differentiation/ maturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes acute myeloid leukaemia

A

neoplastic proliferation of blast cells derived from marrow myeloid elements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what causes chronic myeloproliferative disorders

A

proliferation of abnormal progenitors but NO differentiation/ maturation block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the aetiology of malignant haemotology

A

genetic
epigenetic
environment

somatic mutations in regulatory genes (driver mutations/ passenger mutations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are clones

A

populations of cells derived from a single parent cell
the parent cell has a genetic marker (driver mutation/ chromosomal change) that is shared by the daughter cells
clones can diversify but contain a similar genetic background

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do driver mutations and malignancy affect clones

A

driver mutations can select clones (be shared by entire lineage) : can confer growth advantage on the cells and are then selected during the evolution of the cancer

normal haemopoiesis is polyclonal
malignant haemopoesis is MONOCLONAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is a passenger mutation

A

do not confer a growth advantage but where present in an ancestor of the cancer cell when is acquired one of its drivers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how are haematological malignancies classified

A

based on lineage
based on developmental stage (precursor within lineage)
based on anatomical site involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the lineage classifications of malignancy

A

myeloid and lympoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the developmental stage classifications of malignancy

A

stem cells= chronic myeloid leukaemias/ myeloproliferative disorders
oligolineage progenitors: acute myeloid leukaemia/ acute lymphoblastic leukaemia
mature cells= lymphomas/ chronic lymphocytic leukaemia
plasma cells= myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the classifications of malignancy on anatomical site

A

blood= leukaemia

lymph node involvement with lymphoid malignancy= lymphoma

18
Q

what anatomical sites can chronic lymphocytic leukaemia involve

A

blood and lymph nodes

19
Q

what sites does myeloma involve

A

is a plasma cell malignancy in marrow

20
Q

which types of haem malignancy are most aggressive

A

acute leukaemias and high grade lymphomas (both histologically and clinical more aggressive than chronic leukaemias and low grade lymphomas)

21
Q

what makes a cancer histologically aggressive

A

large cells with high nuclear cytoplasmic ration
prominent nucleoli
rapid proliferation

22
Q

what makes a cancer clinically aggressive

A

rapid progression of symptoms

23
Q

how do acute leukaemias present

A

failure of normal bone marrow function

24
Q

define acute leukaemia

A

rapidly progressing clonal malignancy of the marrow/ blood with maturation defects (cancer of immature blast cells)
=an excess of blasts (>20%) in either the peripheral blood or bone marrow causing a decrease/ loss of normal haemopoietic reserve

25
Q

what are the types of acute leukaemia

A

acute myeloid

acute lymphoblastic

26
Q

what is the most common childhood cancer

A

acute lymphoblastic leukaemia

27
Q

what is acute lymphoblast leukaemia

A

malignancy of primitive lymphoid cells (lymphoblasts)

28
Q

what is the presentation of acute lymphoblastic leukaemia

A

usually in children
marrow failure= anaemia, infections, bleeding
leukaemic effects: high count with obstruction of circulation (DVT/PE), extramedullary involvement (CNS, testis)
bone pain

29
Q

what is the presentation of acute myeloid leukaemia

A

elderly (>60)
can be de novo or secondary
present similar to ALL (anaemia, bleeding, infections, extramedullary involvement, bone pain) + subgroups can cause: DIC, gum infiltration

30
Q

what Ix for acute leukaemia

A

blood count and film
coagulation screen
bone marrow aspirate: morphology and IMMUNOPHEONTYPING (required for definitive diagnosis)
cyto/moleular genetics (used in diagnosis and prognosis)
trephine (piece of bone)- enables better assessment of cellularity and helpful if aspirate sub optimal

31
Q

what is seen on a blood film in leukaemia IMPORTANT

A

reduction in normal cells
presence of abnormal cells: blasts with high nuclear: cytoplasmic ratio
ANUER rod in acute myeloid leukaemia

32
Q

how is immunophenotyping done

A

by flow cytometry (looks for lineage specific proteins on the cell surface)

33
Q

what is required for a definitive diagnosis of acute leukaemia

A

immunophenotyping

34
Q

what is the curative Tx for acute leukaemia

A 
multi agent chemo 
ALL- can last 2-3 years 
-can use different/ targeted Tx for different phases/ subsets
AML- normally intensive
-2-4 cycles 
-prolonged hospitalisation
35
Q

what is a hickman line

A

central venous catheter used for the administration of chemo therapy

36
Q

what problems can arise from marrow suppression

A

anaemia

neutropenia: infections
thrombocytopenia: bleeding

37
Q

what organisms pose a high risk to neutropenic patients

A

gram -ve bacteria (cause fulminant life threatening sepsis)

38
Q

what are the complications of chemotherapy

A 
Nausea and vomiting 
hair loss 
liver and renal dysfunction 
tumour lysis syndrome 
infections: bacterial, fungal, protozoal (e.g. PJP)

late effects: loss of fertility, cardiomyopathy with anthracylines

39
Q

how do you manage infections in chemo patients

A

bacterial: treat empirically with broad spectrum (esp covering gram -ves) AS SOON AS NEUTROPENIC FEVER

fungal (Tx as this if prolonged neutropenia and persisting fever unresponsive to antibacterial agents)

protozoal (more relevant in ALL)

40
Q

what are the usualy outcomes of AL treatment

A

many go into remission (<5% marrow blasts + normal haemopoiesis)
however many relaplse
some die of treatment related toxicity

cure rates:
childhood ALL >85-90% 
adult ALL ~30-40%
adult AML <60 ~40-50%
adult AML >60 ~10%/less
41
Q

what options other than chemo exists for AL

A 
targeted Txs (molecular targeting with kinase inhibitors) 
allogenic stem cell transplantation

Haematology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions