Lec 16 Flashcards

1
Q

what are myeloid cells

A

granulocytes
monocytes
erythrocytes also
and megakaryocytic cell lineages

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2
Q

the 2 types of myeloid leukemia u need to know

A
  • acute myeloid leuk
  • chronic myeloid leuk
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3
Q

official WHO classification system

A

20% blast cell count in either blood, or bvone marrow
chromosome translocations
dysplasia

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4
Q

which group is aml most common in

A

65+ yrs old

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5
Q

what are the 2 most ccommon AML genetic mutations

A
  • transloc between chrom 8 and 21 [t(8;21)]
  • transloc between chrom 15 and 17
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6
Q

what might be an exception to the WHO diagnosis

A

if you see the particular genetic abnormality (e.g. PML-RARA) you dont need the 20% blast count to diagnose

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7
Q

whats a non cytogenetic testing way to possibly identify a malignant cell under the microscope

A

Auer rods
an accumulation of a certain protein
this was useful pre cytogenetic tests

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8
Q

how does FAB classification work

A

based on morphology, visualising what stage the cell is at
goes from M0 to M7 (and has subcategories)

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9
Q

what is FAB class M3

A

acute promyelocytic leukemia (APML)

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10
Q

which translocation is M3 APML

A

15 to 17

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11
Q

APML: which gene is on chrom 15

A

promyelocytic leukaemia gene (PML)

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12
Q

APML: what gene is on chrom 17

A

retinoic acid receptor alpha gene (the gene from 15 fuses with this one to form fusion product)

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13
Q

APML: what does the fusion product do

A

blocks differentiation of the cells

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14
Q

what can M3 APML be treated with

A

all-transretinoic acid (ATRA)
degrades the fusion product
which induces differentiation

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15
Q

what is M2 AML

A

granulated blasts with Auer rods

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16
Q

what translocation is the M2 AML

A

8 and 21

17
Q

M2: what gene is on chrom 21 adn what does it do

A

AML1
- codes for alpha chain of a transcriptional apparatus called CORE BINDING FACTOR (CBF)
- critical for haemotpoietic development

18
Q

M2: what gene is on chrom 8

A

ETO gene

19
Q

M2: what happens when the translocation happens (effect of fusion gene)

A

Causes RUNX1 and RUNx1T1 to come together
which blocks transcription of genes needed for myeloid differeniation

20
Q

what type of thingy is RUNx1T1

A

a co repressor

21
Q

M2: what type of blasts usually seen in this disease

A

promeylocytes and myelocytes

22
Q

clinical features ofAML

A
  • anamia
  • thrombocytopenia
  • infections
  • skin inflitration
  • CNS disease
23
Q

process of diagnosing AML

A
  • full blood count
  • blood film
  • bone marrow smear
  • immunophenotyping
  • cytogenetics
24
Q

what are some supportive treatments of AML

A

Treatment of bone marrow failure
Episodes of fever

25
Q

what is chemotherapy divided into

A

induction (remission-reduction) and
consolidation (post induction) phases.

26
Q

what is aim of induction therapy

A

achieve a complete remission (<5% blasts in bone marrow, normal blood counts, clinical status)

27
Q

what is aim of consolidation

A

to eliminate any residual cells

28
Q

the main 2 types of induction chemotherapy drugs

A
  • cytarabine
  • antracycline
29
Q

what is M3 subtype treated

A

ATRA
combined with standard chemo

30
Q

what is consoldiation therapy based on

A

prognostic factors
changes the amount of lenght of consolodiation therapy

31
Q

what is CD33

A

a molecule expressed by meyeloid stem cells that can be used as a identifying marker

32
Q

name the Anti CD33 drug

A

mylotarg
now is used alongside the chemotherapy drugs mentioned before

33
Q

what is myelotoxicity side effect of cytotoxic drugs

A

limited selectivity between leukemic and normal marrow cells

can even lead to bone marrow failure

34
Q

2 types of stem cell transplantation

A

autologous
allogenic

35
Q

what is autologous stem cell transplant

A
  • patient’s own marrow
  • taken when theyre in remission
36
Q

what is allogenic transplantation

A

marrow from normal donor (usually someone related, with same tissue type)

37
Q

how does age affect prognosis

A
  • 50% of young adults and kids cna be cured
  • but less than 5% of over 65
38
Q
A