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Block 3 > ACUTE LEUKEMIAS 1 > Flashcards

ACUTE LEUKEMIAS 1 Flashcards

1
Q

All pluripotent cells in the bone marrow proliferate into what 2 cells?

A

Myeloid and Lymphoid

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2
Q

Proliferate into their mature end cells within the bone marrow

A

Myeloid cells

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3
Q

Migrate to the lymphoid organs to complete maturation

A

Lymphoid precusors (T cells)

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4
Q

An uncontrolled proliferation of myeloid or lymphoid blasts

A

Acute leukemia

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5
Q

What is the mechanism that ensures that the cells remain proliferative and never mature so cancer progresses?

A

Cells are blocked at an early stage of differentiation and
have a proliferative advantage

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6
Q

Do acute leukemias metastisize and invade tissues and organs outside of the marrow?

A

Yes,
They can invade BM, blood and extramedullary sites

*They often replace normal haematopoietic cells in the BM, which causes life threatening cytopenias

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7
Q

Arise from multiple genetic mutations, both
unchecked proliferation and abnormal or no maturation

A

Acute leukemias

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8
Q

Most common type of acute leukaemia in adults, with the median age at presentation of 65 years

A

Acute Myeloid Leukemia

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9
Q

Patients are often younger

A

Acute promyelocyte anaemia

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10
Q

Common in children, with peak incidence between ages of 2
and 5 years.

A

Acute Lymphoid Leukemia

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11
Q

Name the cell that is not of myeloid origin
A. Erythroblast
B. Basophil
C. Natural killer cell
D. Neutrophil

A

Natural killer

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12
Q

The pathogenic genomic abnormalities in haematopoietic
stem and progenitor cells include:

A
  1. structural cytogenetic abnormalities
  2. mutations
    leading to abnormal proliferative advantage.
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13
Q

Acute leukemia Risk factors

A
  • Chromosomal abnormalities (e.g., Fanconi anaemia, Down
    syndrome etc.)
  • Germline predisposition
  • Drugs (i.e. chemotherapy) or benzene
  • Radiation
  • Other myeloid malignancies
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14
Q

List the symptoms of bone marrow failure

A
  • Anaemia; dyspnoea, palpitations, fatigue, headache etc.
  • Thrombocytopenia; mucocutaneous bleeding (easy bruising, petechiae, epistaxis, bleeding gums, menorrhagia etc.)
  • Neutropenia; infections
  • Tissue infiltration – gingival
    hyperplasia, lymphadenopathy,
    hepatomegaly, splenomegaly,
    CNS, scrotum etc.
  • Joint and bone pain (paediatric
    population) - limping or
    refusing to walk
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15
Q

Death within 30 days of
diagnosis

A

Acute Promyelocytic leukemia

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16
Q

What is the cause of sudden death following Acute Promyelocytic Leukemia (APL)?

A

Production of pro-coagulant granules by the (APL)»trigger the DIC»Leads to coagulation and clots forming throughout the microvasculature»>Platelets and clotting factors depleted»>Hermorhage and bleeding

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17
Q

The translocation unique to APL

A

t(15,17)

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18
Q

Describe how the t(15,17) mutation is derived

A

Involves the PML gene (promyelocytic leukaemia) on chr 15 and the RARa gene (retinoic acid receptor-alpha) on chr 17

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19
Q

What is a maturation block?

A

myeloid precursors unable to mature beyond the promyelocyte stage

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20
Q

A common finding in Acute Myeloid lukemia, which leads to increased blood viscosity

A

Hyperviscosity

*Seen with WBC counts >100 x 109/L

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21
Q

Describe the impact of high, immature leukemic myeloids in the blood

A

Intravascular accumulation of these quickly proliferating cells»increased viscosity of blood»thrombotic complications

22
Q

helpful in making a hyperviscosity diagnosis

A

Fundoscopic examination

23
Q

The PML-RARA fusion gene is the same as which
translocation?
A. t(15;17)
B. t(8;21)
C. t(9;22)
D. t(12;21)

A

A

24
Q

Can occur in all ages but has its peak incidence in the 7th
decade (70 yrs)

A

Acute myeloid leukemia

25
Q

Survival expectations remain age-dependent, with a 62%
estimated 5-year survival in patients diagnosed under the age of 50 years, 37% in 50–64 years, and only 9·4% in ≥ 65 years

A

AML

26
Q

An acute leukemia classified according to morphology

A

AML

27
Q

primarily a disease of childhood, ~75% of cases in children <10
years

A

ALL

28
Q

An acute leukemia presenting with good prognosis in children, >90% survive without disease in the long term. However, the outcome of older adults (≥40 years) and patients with relapsed or refractory disease remains poor.

A

ALL

29
Q

Which of the 2 lymphoblastic leukemias is more common? The B or T cell lymphoblastic leukemia?

A

B cell

30
Q

An acute lymphoblastic leukemia resulting to mediastinal mass

A

T cell

31
Q

organ involvement quiet seen with this kind of leukemia– splenomegaly,
hepatomegaly, LAD, testicular swelling, CNS etc

A

ALL

32
Q

Techniques or methods to carry out ALL diagnoses

A
  • Clinical history and examination
  • FBC, differential count and peripheral smear
  • CXR - lymphadenopathy or an enlarged thymus.
  • CEU, LFT’s, PT, PTT, LDH, Uric acid etc
33
Q

EXAMPLES OF IMPORTANT GENETIC FEATURES
IN ALL

A

Good prognosis
* Hyperdiploidy-> 50 < 66 chromosomes
* t(12;21)

Bad prognosis
* t(9;22)
* KMT2A gene rearrangement –11q23

34
Q

The full blood count for an AML

A
  • White cell count – low, high or normal
  • Haemoglobin – usually low (anaemia)
  • Platelets – usually low (thrombocytopenia)
     typically severe decrease in counts

Need to request a differential count, to check
WBC composition & neutrophils&raquo_space;>pancytopenia = neutropenia, anaemia and
thrombocytopenia.
* Peripheral smear – increase in BLASTS.
* Acute leukaemia ≥20% blasts in the blood or
BM but………
* Some acute leukaemia with specific genetic
abnormalities can be diagnosed with <20%
blasts.
- Auer rod -
AML

35
Q

Specific AML Investigation methods or techniques

A
  • Bone marrow aspirate and trephine biopsy
  • Flow cytometry
  • Conventional cytogenetics
  • FISH analysis
  • NGS
36
Q

This AML investigation method Uses antibodies directed against surface and cytoplasmic antigens

A

Flow cytometry

37
Q

An AML investigation method that detects large chromosomal abnormalities. Analysis of the number and structure of chromosomes

A

CONVENTIONAL CYTOGENETICS

38
Q

Allows analysis of chromosome
structure at a molecular level

A

FISH

39
Q
  • Able to detect multiple
    genetic abnormalities in
    a single test:
  • Mutations and translocations.
  • Diagnostic and prognostic significance.
A

NXT GENERATION SEQUENCING

40
Q

An Auer rod is seen in which type of acute leukaemia?
A. T lymphoblastic leukaemia
B. Acute myeloid leukaemia
C. B lymphoblastic leukaemia
D. Chronic lymphocytic leukaemia

A

B

41
Q

Which type of abnormality cannot be detected on
karyotype?
A. Mutation
B. Trisomy
C. Monosomy
D. Translocation

A

A

42
Q

FACTORS WHICH AFFECT AML PROGNOSIS ON VARIOUS PATIENTS

A
  • Age
  • Cytogenetic abnormalities
  • Additional mutations
  • Response to initial chemotherapy
  • CNS disease in ALL
  • Performance status
43
Q

EXAMPLES OF IMPORTANT GENETIC FEATURES
IN AML

A

Good prognosis
* t(8;21)
* Inversion 16

Bad prognosis
* Complex karyotype

44
Q

MANAGEMENT OF THE ACUTE LEUKEMIAS

A
  • Supportive therapy - should be initiated to correct
    haematologic, metabolic and infectious complications.
  • transfusions, antibiotics, fluids etc.
  • Specific therapy
  • Chemotherapy – systemic and CNS
  • Allogeneic haemopoietic stem cell transplantation
45
Q

Discuss chemotherapy

A
  • Work by impairing mitosis&raquo_space;targeting rapidly dividing cells.
  • They prevent mitosis by various mechanisms including damaging DNA.
  • Familiarity with the agents used is required to prevent or anticipate and treat toxicities timeously.
  • Many side effects are due to damage to normal cells that divide rapidly e.g. BM, digestive tract and hair follicles.
46
Q

Name the side effects of chemotherapy

A
  • Short term; hair loss, immunosuppression, cytopenias, nausea and
    vomiting, skin rash, mucositis etc.

Long term:
- Infertility – consider fertility preservation prior to chemotherapy.
- Secondary malignancies

46
Q

Basic Principles of Treatment

A

the goal is to completely eradicate blast cells through
intensive chemotherapy (induction phase)

Patient on chemo are at risk of infections and chemotherapy side effects

Consolidation phase – for patients in complete remission (CR) to eliminate residual leukaemic blasts and prevent relapse.
- better tolerated than induction therapy

Maintenance – to maintain remission, for up to 2 to 3 years.
CNS directed therapy
– in ALL, to prevent and treat CNS disease.
-given at all the phases of therapy.

47
Q

To see with response to chemotherapy

A
  • Complete remission – absence of extra-medullary disease (no LAD, hepatomegaly, splenomegaly etc.)
  • absolute neutrophil count > 1 x 109/L
  • platelet count >100 x 109 /L
  • <5% blasts in the bone marrow
48
Q

APL management

A
  • ATRA (All Trans Retinoic Acid) is required.
  • Helps with maturation of promyelocytes to
    granulocytes  reverses the coagulopathy associated
    with APL.
  • Should be given ASAP if any suspicion of APL – this is a
    medical emergency.
49
Q
A
50
Q
A

Block 3 (51 decks)

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