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Year 2 - MCD Cancer > CasaD - Leukaemia > Flashcards

CasaD - Leukaemia Flashcards

1
Q

What is leukaemia?

A

Cancer of the BLOOD

i.e. bone marrow disease

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2
Q

What occurs resulting in leukaemia?

A

Results from a series of mutations in a SINGLE

• LYMPHOID or MYELOID cell

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3
Q

What cells can be involved in leukaemia?

A
  • Pluripotent hematopoietic SC
  • Myeloid/lymphoid SC
  • Pro-/Pre- T/B lymphocyte
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4
Q

What is different about leukaemia to other cancers in terms of tumours?

A

Most cancers exist as solid tumours but it is unusual for leukaemia patients to have tumours
• more often they have leukaemia cells replacing normal bone marrow cells and circulating freely

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5
Q

What is different about leukaemia to other cancers in terms of the cells involved?

A

Haemopoietic & lymphoid cells behave DIFFERENTLY to other body cells

  • normal haemopoietic SC = circulate in the blood AND both the SCs & cells derived from them can enter tissues
  • normal lymphoid SCs RE-circulate betw. tissues and blood
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6
Q

What does the difference about leukaemia mean about invasion and metastasis?

A

Invasion/metastasis can NOT be applied normally
• if ‘benign’ are called CHRONIC

• if ‘malignant’ are called ACUTE (aggressive & quick death if untreated)

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7
Q

How to classify leukaemia?

A
  1. Acute OR chronic
  2. Lymphoid OR myeloid origin
  3. Lymphoid - can be B or T lineage

Myeloid - can be combination of granulocytic, monocytic, erythroid OR megakaryocytic

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8
Q

Final classes of leukaemia?

A

ALL - acute lymphoblastic leukaemia

AML - acute myeloid leukaemia

CLL - chronic lymphocytic leukaemia

CML - chronic meyrloid leykaemia

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9
Q

Why do people get leukaemia?

A

An acquired genetic disease, resulting from SOMATIC mutation

Arises because of a series of mutations in a:
• single stem cell
• some from oncogenic influences
• others random errors that accumulate over time

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10
Q

Important leukaemogenic mutations that have been recognised?

A

• Proto-oncogene mutation

• Novel gene creation
- e.g. a chimeric OR fusion gene

• Dysregulation of a gene
e.g. when translocation brings the gene under influence of a promotor or enhancer of another gene

• TSG loss of function
- deletion or mutation of both copies

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11
Q

Inherited or other constitutional abnormalities can also contribute to leukaemogenesis - give examples

A

Down’s syndrome

Chromosomal fragility syndromes

Defects in DNA repair

Inherited defects of TSGs

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12
Q

What is included in identifiable causes of leukaemogenic mutations

A
  • Irradiation
  • Anti-cancer drugs
  • Cigarette smoking
  • Chemicals - benzene
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13
Q

Explain AML?

A

Acute Myeloid Leukaemia

Cell continue to proliferate BUT they do not mature, leading to:
 Build-up of immature cells
 Failure of production of normal functioning end cells such as neutrophils, monocytes, platelets, etc.

o Responsible mutations usually affect TFs so transcription of multiple genes affected
o Often is due to the product of an oncogene affecting proteins

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14
Q

Explain CML

A

Chronic Myeloid Leukaemia

o Responsible mutations usually affect genes encoding proteins (membrane receptor or cytoplasmic proteins) involved in the signalling pathways from receptors

Cell kinetics & function are not as seriously affected as in AML
 BUT cell becomes independent of external signals, alterations in its interaction w. stroma, there is still reduced apoptosis and the cell progressively expands in population

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15
Q

Broad difference between AML & CML

A

AML
• FAILURE of production of cells

CML
• INCREASED production of cells

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16
Q

Difference between ALL & CLL

A

Acute/Chronic Lymphoid Leukaemia

Acute lymphoblastic leukaemia (ALL):
• Increase in very immature cells (lymphoblasts) with a failure of these to develop to mature B/T cells

Chronic lymphoid leukaemia (CLL):
• Leukaemic cells are mature but abnormal

17
Q

How does leukaemia cause the disease characteristics?

A 
Caused by an accumulation of abnormal cells leading to:
 • Leucocytosis
 • bone pain (acute)
 • hepatomegaly
 • splenomegaly
 • lymphadenopathy (if lymphoid)
 • thymus enlargement (if T lymphoid)
 • skin infiltration
18
Q

What are the metabolic effects of leukaemia cell prolifration?

A
  • Hyperuricaemia
  • Renal failure
  • Weight loss
  • Low grade
  • Fever
  • Sweating
19
Q

In leukaemia, what does crowding out of normal cells lead to?

A

• Anaemia
- e.g. fatigue, lethargy, pallor, dyspnoea

• Neutropenia
- e.g. fever & features of infection

• Thrombocytopenia
- e.g. bruising, petechiae, bleeding

20
Q

What does a CT Scan of a person with AML look like?

A

Shows

Intraventricular Haemorrhage

21
Q

What is a feature of CML?

A

Loss of normal immune fuction

• due to loss of normal T/B-cell function

22
Q

Which group of people does ALL affect most?

A

Disease of CHILDREN

23
Q

What does B-lineage ALL result from?

A

Delayed exposure to a common pathogen

OR, conversely

Early exposure to a pathogen protects
• e.g. study showed enterovirus infection gave protection

24
Q

Some leukaemias in children can also result from?

A
  • Irradiation in utero
  • In utero exposure to chemicals (e.g. Baygon, Dipyrone)
  • EBV
  • Rarely - exposure to a mutagenic drug
25
Q

Describe the clinical features of ALL resulting from accumulation of abnormal cells

A 
o Bone pain
o Hepatomegaly & splenomegaly
o Lymphadenopathy
o Thymic enlargement
o Testicular enlargement
26
Q

Describe the haematological features of ALL

A
  • Leucocytosis with lymphoblasts in the blood
  • Anaemia (normocytic, normochromic)
  • Neutropenia
  • Thrombocytopenia
  • Lymphoblasts replacing normal bone marrow cells
27
Q

Investigations done to see if someone has ALL

A
  • FBC with liver and renal function tests
  • Bone marrow aspirate

• Cytogenic/molecular analysis
 Immunophenotyping
– find the lineage of the cells
 These methods are useful for assessing the prognosis of the ALL
• Hyperdiploidy (many extra chromosomes) –> good prognosis
• T(4; 11) –> poor prognosis

• Chest x-ray

28
Q

Explain the leukaemogenic mechanisms of ALL

A

Mechanism:
• Formation of a fusion gene (e.g. ETV6-RUNX1)

  • Dysregulation of a proto-oncogene
  • Point mutation in a proto-oncogene
29
Q

How can the formation of a fusion gene be detected?

A

e.g. ETV6-RUNX1

Can be detected using cytogenic & molecular analysis - FISH
• Green probe for ETV6 and red for RUNX1
• Fused colours give yellow

30
Q

Example of dysregulation?

A

t(10;14) (q24;q11)

The TCL3 is dysregulated by proximity to the TCRA gene

31
Q

Treatment types for ALL?

A

SUPPORTIVE
• e.g. replace RBCs, platelets & Abs

SYSTEMIC CHEMOTHERAPY

INTRATHECAL CHEMOTHERAPY

32
Q

What type of treatment should be given for leukaemia and why?

A

Systemic

As leukaemis disseminates EARLY in the disease (similar to metastasis)

33
Q

Why does treatment for ALL vary?

A

ALL has many phenotypes depending upon mutation

Year 2 - MCD Cancer (14 decks)

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