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Path Week 2 > Ha - Acute Leukaemia > Flashcards

Ha - Acute Leukaemia Flashcards

1
Q

3 year old girl has splenomegaly, lymphadenopathy, low platelets, high WCC. Most likely diagnosis?

A

ALL

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2
Q

define acute leukaemia

A

neoplastic condition characterised by rapid onset, high mortality if untreated, blast cells and bone marrow failure

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3
Q

3 types of bone marrow failure and the sx they manifest

A

anaemia - pallor, SoB, fatigue
neutropenia - infections
thrombocytopaenia - bleeding

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4
Q

name monocyte cells

A

neutrophils
eosinophils

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5
Q

which cell gives rise to AML

A

multipotent myeloid stem cell or pluripotent stem cell

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6
Q

which cell gives rise to ALL

A

common lymphoid stem cell

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7
Q

what cell type is dominant in acute leukaemias

A

BLAST CELLS

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8
Q

granules on a cell indicate what

A

myeloid cell

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9
Q

age trend in AML

A

increased with age, except blip in first year of life

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10
Q

median age of AML

A

65-70

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11
Q

how does age affect prognosis of AML q

A

prognosis worse with icnreasing age

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12
Q

what % of adults cured of AML

A

40%

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13
Q

what causes AML

A

abberations in chromosome count / structure –> eg translocations, trisomy

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14
Q

which type of acute leukaemia gets abnormal regulation of genes

A

ALL

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15
Q

which leukaemia has creation of new genes involved

A

ALL and AML

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16
Q

is chromosomal duplication common in AML

A

yes

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17
Q

which chromosomes are most likely to be duplicated to cause AML

A

8 and 21

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18
Q

is chromosome loss / deletion common in AML

A

yes

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19
Q

which chromosomes are deleted / lost in AML

A

5 and 7

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20
Q

how does chromosome deletion / duplication cause AML

A

deletion - loss of TSG
duplication - more oncogenes

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21
Q

what type of molecular abnormalities can be seen in normal chromosomes in acute leukaemia

A

point mutations
loss of TSG
partial duplication
cryptic deletion

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22
Q

describe the cell development process that leads to AML formation

A

block in maturation of myelocyte cells so blast cells accumulate

23
Q

why do people get AML

A

familial / syndromic predisposition
irridation
anti cancer drugs
smoker
unknown !

24
Q

how many molecular insults are needed to cause leukaemia

A

at least 2

25
Q

what are type 1 abnormalities in AML

A

promote proliferation and survival

26
Q

what are type 2 abnormalities in AML

A

block differentiation (which normally preceeds apoptosis)

27
Q

for which specific type of AML is the mechanism understood and a cure available to patients

A

t(15;17)

28
Q

complication of t(15;17) AML

A

DIC

29
Q

what genes are fused in t(15;17) AML

A

PML and RARA

30
Q

is transcription factor disturbance enough to cause AML

A

no - need further genetic hit

31
Q

what cells have auer rods

A

myeloid cells

32
Q

what confirms AML vs ALL

A

immunophenotyping

33
Q

which stains are positive in AML but negative in ALL

A

myeloperoxidase
sudan black
non specific esterase

34
Q

how does immunophenotyping work

A

AB recognises specific antigen. AB is then flagged with a immunoflurescent dye to recognise it

35
Q

Sx of AML

A

anaemia, neutropenia, thrombocytopaenia
hepatosplenomegaly
lymphadenopathy / gum infiltration

36
Q

which type of AML has gum infiltration

A

acute monocytic leukaemia

37
Q

which type of AML gets CNS disease (eye palsy etc) more commonly than others

A

acute monocytic
also ALL

38
Q

what can bleeding in AML lead to

A

DIC

39
Q

what eye signs can be seen due to AML and why

A

papilloedema / retinal haemorrhages due to hyper-viscosity of blood

40
Q

how is AML diagnosed

A

blood film - diagnostic usually

41
Q

what is seen on blood film to diagnose AML

A

blasts / auer rods

42
Q

leukaemia Sx. No abnormal cells on film. What do you do?

A

bone marrow aspirate

43
Q

leukaemia Sx. No abnormal cells on film. likely dx?

A

aleukaemic leukaemia - blasts confined to bone marrow so cant see on film

44
Q

why are cytogenetoc / molecular studies done on AML pts?

A

prognostic value
selective tx targets

45
Q

which gene patterns convey the best prognosis of AML

A

t(15;17)
t(8;21)
inv(16) or t(16;16)

46
Q

which gene patterns convey the worst prognosis of AML

A

-5, del 5
-7, 3q-
complex

47
Q

supportive care Tx of AML

A

red cells
platelets
FFP
Abx
long line
allopurinol

48
Q

mx of AML

A

supportive care
chemo
targeted molecular therapy
transplant

49
Q

describe chemo regime of AML

A

cell cycle specific drugs
4-5 courses over 6 months
- remission induction x2
- consolidation x2 or 3

50
Q

give some examples of molecular therapies for acute promyelocytic leukaemia

A

all trans retinoic acid (ATRA)
arsenic trioxide

51
Q

molecular therapies for acute Ph+ leukaemia

A

tyrosine kinase inhibitors

52
Q

antibody tx for AML

A

gemtuzumab
ozogamicin

53
Q

what determines prognosis of AML

A

pt charactristics
morphology / immunophenotyping
response to tx

Path Week 2 (18 decks)

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