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Path - Haem > Acute leukaemia > Flashcards

Acute leukaemia Flashcards

1
Q

auer rods are present in which leukaemia?

what other feature in the cell might you see?

A

AML

fine speckled granules

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2
Q

what is a feauture of aeur rods?

A

peroxidase positive

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3
Q

leukaemia of myeloBlasts and monoBlasts are?

A

AML

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4
Q

leukaemia of lymphoBlasts are?

A

ALL

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5
Q

list some symptoms of acute leukaemia and why they occur?

A
  1. Bone marrow infiltration = pancytopaenia =

Anemia - fatigue
neutropaenia - Infections
thrombocytopaenia - mucosal bleeding

  1. Multi-organ mets =
Hepatosplenomegaly
Headaches
Testicular enlargement
Bone pain eg tenderness over sternum !!
Generalised Lymphadenopathy - painless (as it is not an infection)
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6
Q

How does ALL present?

A

Headaches
Testicular enlargement
Skin

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7
Q

What diagnostic tests are conducted for acute leukamias?

A

Peripheral blood

Bone marrow biopsy + stain

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8
Q

what would be the findings from ivx of ALL?

A 
Peripheral blood:
Lymphoblasts - agranular, little cytoplasm, large nucleus to cytoplasm ratio
MCV - normo or macrocytic anaemia
Platelets low
WCC low or v high

Bone marrow:
Hypercellular balsts > 20%

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9
Q

What would be the findings from ivx of AML?

A

Peripheral blood:
Myeloblasts - Aeur rods, granular
Monoblasts

MCV - normo or macrocytic anaemia
Platelets low
WCC low or v high

Bone marrow:
Hypercellular balsts > 20%

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10
Q

what is the basic outline of treatment in acutee leukaemia’s?

youtube

A
  1. Induction phase -
    - eg to induce remission. give the following
    A - High dose chemo
    B - Myeloid growth factors (as chemo causes
    pancytopaenia = inc infections due to neutropenia)
    C - RBC, Platelets - if pancytopenia
  2. Consolidation phase
    • used in remission, to prolong remission

DNA microarrays - predict prognosis
CNS prophylaxis - intrathecal - in ALL

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11
Q

what is the most common cancer in kids?

A

ALL

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12
Q

Kids with down syndrome are predisposed to which cancer?

A

ALL

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13
Q

epidemiology of ALL?

A

mostly young kids but bimodal so older patients too

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14
Q

what aree the subtypes of ALL

A

WHO:

Pre-B : kids
Mature B
Pre-T: adults

lecture: B&T

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15
Q

with immunophenotyping, what would you find with ALL?

A

B & Pre-B ALL:
B cell antigens - CD20, 19, CD10

T cell:
CD3+ (can be 3-8)

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16
Q

Which translocations. might you find in B& Pre-B ALL?

prognosis? mnemonic?

A

Pre-B:
t9:22 -> philadelphia chromosome BCR ABL

t12:21 -> mirror, minor (kids), minor damage (good prognosis)

Mature B:
burkitts leukameia so t(8:14)

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17
Q

which factors are indicative of poor prognosis in ALL?

A 
Age > 60
WCC > 100,000
Mature B and pre-T
Philadelphia chromosome t9:22 (NOTE: in CML, this has good prognosis)
t4:11
18
Q

An individual aged 40-60 comes in with sx of leukaemia, which is it. most likely to be?

A

Myeloid lineage so AML, APML or CML

lecture : median age for AML 65-70

19
Q

An individual aged 60+ comes in with sx of leukaemia, which is it. most likely to be?

A

CLL

20
Q

AML can bee associated with which genetic abnormalities?

A

Kleinfelters
Downs syndrome
Turner’s

21
Q

List some important subclasses of AML

A

Based on myeloblast differentiation:

M2 - Myeloblastic with maturation - t(8:21) - most common

M3 - APML Acute promyeolocytic leukaemia - t(15:17) ->
associated with DIC.
good prognosis, unless they develop DIC

M5 - Monocytic AML

22
Q

what do auer rods look like?

A

needle shaped crystals

23
Q

what would immunohistochemistry show for

ALL
AML

A

ALL: Tdt+ PAS+

AML: Tdt- Myeloperoxidase+ (remember auer rods have these)

24
Q

list possible mechanisms for developmeent of acute myeloid leukaemias. give examples

A
  1. Chromosomal duplication
    • > chrom 8,21
    • > more proto-oncogenes
  2. Chromosomal deletion
    • > chrom 5/5q, 7/7q
    • > less tumour suppressor genes
    • > loss of DNA repair systems
  3. Molecular abnormalities in patients with apparently normal chromosomes:
    FLT3 - mutated in AML ‘Partial duplication’
25
Q

list risk factors for leukaemia?

A 
Familial or constitutional predisposition
Irradiation
Anticancer drugs - chemotherapy etc
Cigarette smoking
Unknown
26
Q

what are type 1 and 2 abnormalities in forming of leukaemia ?

A

Type 1 abnormalities
- promote proliferation & survival (anti-apoptosis)

Type 2 abnormalities
block differentiation and maturation
(by blocking transcription factor function)

this means we have blasts floating around

27
Q

what is core binding factor leukaemia?

A

core binding factor is a transcription factor

it is altered when some translocations occur eg t(8:21) inv16 or t16:16 causing leukaemia somehow

28
Q

what genes are involved in t15:17 in APML?

A

PML gene chromosome 15:
RARA gene chromosome 17:

there is the classical and thee variant type of this condition

Rara - retinoic acid receptor alpha
PML - promyelocytic leukaemia gene

29
Q

what are the local characteristics of monocytic AML/Acute monocytic leukaemia - M5?

A

Skin infiltration, gum infiltration -swelling & organomegaly

remember mouth is 5 letters - M5

30
Q

how does CNS disease infiltrate present in AML?

A

Cranial nerrve palsy
retinal exudate & haemorrhage
etc

31
Q

how could bone marrow failure present in severe and life threatening situations?

A

septic shock
renal failure
DIC

32
Q

how is AML treated?

lecture

A

Chemo

targetted molecular therapy

transplant - if poor prognosis

supportive care:
RBC, Platelets, Antibiotics,
Allopurinol, fluid + electrolyte balance
FFP if DIC

33
Q

in the treatment of APML, give examples of Molecularly targeted therapy?

A
  1. All-trans-retinoic acid (ATRA) - vit A ->
    remember in APML its the PML-Rara fusion gene
    Rara: retinoic acid receptor alpha
  2. A2O3
34
Q

is lymphadenopathy more common in ALL/AML?

A

ALL

35
Q

ALL in general has poor prognosis? true/false

A

false - depends on cytogenetic subtype

36
Q

what are the Leukaemogenic mechanisms in ALL?

A 
1. Proto-oncogene dysregulation:
chromosomal translocation causes:
Fusion genes
Wrong gene promoter
Dysregulation by proximity to T-cell receptor (TCR) or immunoglobulin heavy chain loci
  1. Unknown – hyperdiploidy
37
Q

the presence of hyperdiploidy in ALL has what prognosis ?

A

good one

38
Q

Why does cytogenetic/molecular genetic category matter in ALL?

A

Ph-positive need imatinib

39
Q

How is ALL treated?

A

same general principles as AML
+ CNS-directed therapy/prophylaxis -intrathecal

Freeze sperm in bank

the targeted molecular therapy is

  1. imatinib - Tyrosine kinase inhibitor: Ph+
  2. Rituximab CD20+
remission induction  (prednisolone + vincristine) -> consolidation (Methotrexate + cyclophosphamide)+ 
CNS rx (intrathecal methotrexate + radiation) -> intensification -> maintenance (methotrexate + 6MP)

stem cell transplant lalst resort

40
Q

compared to thee rest of AML, when does the block in cell maturation occur in APML?

A

later

41
Q

what does t(15:17) lead to?

A

arrested differentiation of the promyelocytes

abnormal retinoic acid metabolism (hence use of ATRA in rx)

42
Q

what should the normal % of blasts be in:

  1. the bone marrow
  2. periphery
A

Bone marrow - 5%

Periphery - 0%

Path - Haem (13 decks)

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