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YR2: MCD Cancer > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

What is the most common cancer in the 15-24 age group?

A

Cancers of the blood

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2
Q

What is the literal meaning of leukaemia?

A

White blood

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3
Q

Where does the problem exist in leukaemia?

A

Bone marrow (not all patients have abnormal cells in the blood)

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4
Q

What does leukaemia result from? What are the consequences to the progeny of the mutated cell?

A

A series of mutations in a single lymphoid or myeloid stem cell
Progeny show abnormalities in proliferation, differentiation or cell survival leading to steady expansion of the leukaemic clone

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5
Q

Which cells can be affected in leukaemia?

A 
Pluripotent haematopoietic stem cell 
Myeloid stem cell  
Lymphoid stem cell  
Pre B lymphocyte  
Pro T lymphocyte
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6
Q

What are the equivalent terms for ‘benign’ and ‘malignant’ in terms of leukaemia?

A 
Benign= CHRONIC
Malignant= ACUTE– very aggressive
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7
Q

What are the four main types of leukaemia?

A

Acute lymphoblastic leukaemia
Acute myeloid leukaemia
Chronic lymphocytic leukaemia
Chronic myeloid leukaemia

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8
Q

Explain the significance of the terms acute lymphoblastic leukaemia and chronic lymphocytic leukaemia.

A

ALL: cells are immature (lymphoblasts)- fail to develop into mature T or B cells
CLL: cells are abnormal mature lymphocytes

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9
Q

What are the important leukaemogenic mutations that have been recognised?

A

Mutation in a known proto-oncogene
Creation of a novel gene e.g. chimeric or fusion gene
Dysregulation of a gene when translocation brings it under the influence of a promoter or enhancer of another gene

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10
Q

State 4 inherited or other constitutional abnormalities that can contribute to leukaemogenesis.

A

Down syndrome
Chromosomal fragility syndromes/ tendency to increased chromosomal breaks
Defects in DNA repair mechanisms
Inherited defects in tumour suppressor genes

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11
Q

State 4 identifiable causes of leukaemogenic mutations

A

Irradiation
Anti-cancer drug
Cigarette smoking
Chemicals e.g. benzene

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12
Q

What type of cell is seen in abundance in acute myeloid leukaemia?

A

Immature myeloid cells: cells continue to proliferate but no longer mature so there is a build up of immature cells (myeloblasts) in the bone marrow, which spread to the blood

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13
Q

Explain how acute myeloid leukaemia leads to bone marrow failure.

A

Leukaemic cells crowd out normal cells in bone marrow leading to a decrease in the production of normal functioning end cells e.g. neutrophils, monocytes, platelets

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14
Q

What do the responsible mutations normally affect in AML?

A

Transcription factors: transcription of multiple genes is affected
Often the product of an oncogene prevents normal function of the protein encoded by its normal homologue
Leads to changes in cell kinetics + cell functions

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15
Q

What do the responsible mutations normally affect in CML?

A

A gene encoding a protein in the signalling pathway between a cell surface receptor + the nucleus
The protein encoded may be a membrane receptor or a cytoplasmic protein

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16
Q

Describe the nature of the leukaemic cells in CML.

A

Mature lymphocytes (cell kinetics + function are not as seriously affected as in AML) but cells become independent of external signals, there are alterations in the interaction with stroma + there is reduced apoptosis so cells survive longer + the leukaemic clone expands progressively

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17
Q

How is the production of end cells affected in AML and CML?

A

AML: Failure in production of end cells
CML: increase in production of end cells

18
Q

What are 5 metabolic effects of leukaemic cell proliferation?

A 
Hyperuricaemia  
Renal failure  
Weight loss  
Low grade fever  
Sweating
19
Q

Which type of leukaemia increases the risk of intraventricular haemorrhage and why?

A

Acute promyelocytic leukaemia (APML): associated with DIC so platelet count + fibrinogen are low leading to increased risk of fatal haemorrhage

20
Q

How can leukaemia cause proliferation of the gums?

A

Infiltration of leukaemic cells + monocytes can lead to inflammation of the gums
Small haemorrhages due to thrombocytopenia

21
Q

What does epidemiology suggest that B lineage acute lymphoblastic leukaemia may result from?

A

Delayed exposure to a common pathogen or that early exposure to pathogens protect

22
Q

What 4 factors that relate to risk of leukaemia?

A

Family size
New towns
Socio-economic class
Early social interactions

23
Q

What can leukaemias in infants and young children result from?

A

Irradiation in utero

In utero exposure to certain chemicals

24
Q

What are 6 clinical features of acute lymphoblastic leukaemia? What do they result from?

A 
Bone pain  
Hepatomegaly  
Splenomegaly  
Lymphadenopathy 
Thymic enlargement  
Testicular enlargement  
All result from the accumulation of abnormal cells
25
Q

What are 3 clinical features that result from the crowding out of normal cells in acute lymphoblastic leukaemia?

A

Anaemia: fatigue, lethargy, pallor, breathlessness
Neutropenia: fever + other features of infection
Thrombocytopenia: bruising, petechiae, bleeding

26
Q

What investigations are performed in acute lymphoblastic leukaemia?

A 
Blood count + film  
Check of liver function, renal function + uric acid  
Bone marrow aspirate  
Cytogenetic/ molecular analysis  
Chest X-ray
27
Q

What are the uses of cytogenetic and molecular genetic analysis in ALL?

A

Managing the individual patient because it gives info. about prognosis
Permits the discovery of leukaemogenic mechanisms

28
Q

What are the implications of hyperdiploidy in in the cytogenetic analysis of ALL?

A

Good prognosis

29
Q

What features of the cytogenetic analysis are associated with a poor prognosis?

A

Chromosomal translocations resulting in formation of a bad fusion gene

30
Q

What technique is used to detect the fusion genes in ALL?

A

Fluorescence in situ hybridisation (FISH)

31
Q

What are the treatment options for ALL?

A

Supportive: red cells, platelets, antibiotics
Systemic chemotherapy
Intrathecal chemotherapy (to stop residual cells that cross BBB)

32
Q

How is the presence of leukaemia different from most cancers?

A

Most cancers exist as solid tumours

Leukaemia cells replace normal bone marrow cells + circulate freely in the blood

33
Q

How do normal haemopoietic and lymphoid stem cells behave?

A

Haematopoeitic: circulate in blood, both the stem cells + their derivatives can enter tissues
Lymphoid: recirculate between tissues + blood

34
Q

How can lymphoid leukaemias be further classified?

A

B or T lineage

35
Q

How can myeloid leukaemias be further classified?

A

Granulocytic
Monocytic
Erythroid
Megakaryocytic

36
Q

Other than the overcrowding caused by leukaemia cells, why may platelet count be low in patients with AML?

A

There may be DIC

Platelets consumed by coagulation in bloodstream

37
Q

What is the difference between acute and chronic lymphoid leukaemias?

A

ALL: Increase in very immature cells (lymphoblasts), with failure to develop into mature T + B cells
CLL: Leukaemic cells are mature, though abnormal T + B cells

38
Q

What 7 leukaemic disease characteristics does accumulation of abnormal cells cause?

A 
Leukocytosis
Bone pain
Hepatomegaly
Splenomegaly
Lymphadenopathy
Thymic enlargement
Skin infiltration
39
Q

What causes a loss of normal immune function in chronic lymphoid leukaemia?

A

Loss of normal T or B cell function

40
Q

Who is largely effected by acute lymphoblastic leukaemia?

A

Children

41
Q

What are 5 haematological features of acute lymphoblastic leukaemia?

A

Leukocytosis with lymphoblasts in the blood
Anaemia (normocytic, normochromic)
Neutropenia
Thrombocytopenia
Replacement of normal bone marrow cells by lymphoblasts

42
Q

What technique can be used to determine cell lineage in acute lymphoblastic leukaemia?

A

Immunophenotyping

YR2: MCD Cancer (18 decks)

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