Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

OS Hematology/Oncology > Path/Leukemia > Flashcards

Path/Leukemia Flashcards

1
Q

Immunomarkers for AML

A

MPO
CD33 (myeloid transmem receptor)
CD13
HLA-DR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Immunomarkers for ALL

A

TdT
CD10 (Neprilysin/ CALLA)
CD19
CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

AML inv(16) prognosis?

A

Good, use induction + ARA-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

AML t(8;21) ETO-AML prognosis?

A

good, use induction + ARA-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AML t(9;11) prognosis?

A

intermediate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

AML t(9;22) prognosis?

A

poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AML t(15;17) PML-RARa treatment?

A

ATRA +/- ARA-C –> induction +/- arsenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

5- or 7- AML prognosis?

A

poor risk, start induction and allograft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

FLT3-ITD+ mutation AML - prognosis and treatment?

A

poor, start allograft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

FLT3-ITD- AML prognosis?

A

ARA-C (Cytarabine) and then allograft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

t(9;22) BCR-ABL ALL prognosis?

A

poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MLL-AF4 ALL prognosis?

A

poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

E2A-PBX ALL prognosis?

A

good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TEL-AML ALL prognosis?

A

good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Remission induction treatment for ALL?

A 
VCR
L-Asp
ARA-C
DEX or PRED
\+/- Daunorubicin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Consolidation treatment for ALL?

A 
Daunorubicin
ARA-C
Etoposide
Etoposide
Thioguanine or 6-MP
Cyclophosphamide,
L-ASP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Maintenance therapy for ALL

A

6-MP
MTX
Prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TdT is a marker for these cells

A

Early B cells in marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

These markers are expressed continuously throughout B cell development

A

CD19, CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 5 criteria for defining a blast?

A

Big, high nucleus:cytoplasm, smudgy chromatin, large nucleolus, all look alike

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is basophilic stippling?

A

Dark dots of RNA left behind in RBCS; always pathological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What should a normal bone marrow aspirate show?

A

Blasts below 4.5%; myeloid:erythroid precursor ratio at least 2:1

myeloid being granulocyte + monocyte

23
Q

What is the relationship between cellularity of BM and age?

A

100% - Age = Normal % cells

24
Q

What CD marker is on both B and T cells?

25
Q

WHat is a weakness of flow cytometry?

A

cannot assess erythroid line malignancies because RBCs are lysed

26
Q

What does forward scatter measure?

27
Q

How do you plot flow results initially?

A

CD45 (aka all lymphocytes) vs SSC

28
Q

What marker is used for maturing granulocytes in flow?

29
Q

What marker is best for HSCs in flow?

30
Q

What are two advantages of IHC over flow?

A

Stain background lightly allows you to still see cell types

Better for larger cells

31
Q

What is a requirement for doing cytogenetics? (not FISH)

A

cell must be dividing

32
Q

Advantage of FISH?

A

Cells can be in interphase

33
Q

Normal myeloid blasts would have this immunophenotype

A

CD33+ CD34+

34
Q

Normal lymphoid blasts would have this phenotype

A

CD10 CD19+

35
Q

What is the best way to categorize/prognosticate AML types?

36
Q

What are Class I mutations?

A

Proliferation and survival advantages

37
Q

What are Class II mutations?

A

Impaired differentiation/apoptosis

38
Q

What is Gilliland’s hypothesis?

A

Both a Class I and II mutation are needed to generate a neoplasm

39
Q

Way to remember the AMLs that only need genetic analysis for diagnosis (4)

A

MYH INVerted Pml RUNs away

RUNX1-RUNX1T1
inv(16)
CBFB-MYH1
PML-RARA

40
Q

Almost all of the AMLs we talked about are caused by these mutation types

A

Class II + I (Gilliland fulfilled)

41
Q

t(8;21) AML - everything

A

Inhibited myeloid differentiation, aka backup

Gilliland fulfilled
Kids/young adults
Pancytopenia
Blast diff blocked!
CD13+ CD33+ CD34+
Auer rods, lots of blasts, Smudgy
Good to chemo

t(8;21) is ETO-AML1 (RUNX1-RUNX1t1) - the blasts are “running and running” but can’t go any further down the road, so they just keep multiplying like rabbits in the summer (8/21)

42
Q

APL

A

t(15;17)
PML-RARA fusion protein with TF+retinoic acid receptor causes INHIBITED GRANULOCYTE DIFFERENTIATION

How fix? Help it grow! –> ATRA induction
Arsenic if necessary

Presents w/ thrombocytopenia, DIC!!

CD34- (no blasts!)
HLA-DR
CD13+ CD33+ (myeloid blast markers)

BAT WING nuclei
Big blasts, few bc all are myeloid now
Auer rods
Cytoplasmic granules

43
Q

Acute myelomonocytic leukemia

A

inv(16) or t(16;16) CBFB-MYH11

Inhibited myeloid maturation

Younger/kids

Mixed granulo/mono morphology
Inc eosinophilia

CD14+ CD11 = monocyte
CD13+ CD33+ = granulocyte

ARA-C otherwise poor prog

44
Q

AML normal cytogenetics

A

Any age; pediatric is uncommon

Gingival hypertrophy

Molecular genetics > cytogenetics
CD34+

Lots of blasts
Undifferentiated

May affect any non-lymphatic cell type

45
Q

Tell me about stratifying cytogenetically normal AML to predict helpfulness of BMT

A

NPM1+ or
[CEBPA+,FLT3-ITD-]
–> BMT doesn’t help

FLT3-ITD+ or
[NPMN1-,CEBPA-,FLT3-ITD-]
–> BMT helps

So remember [all negative ] means BMT and [FLT3+] also means BMT, otherwise BMT is not helpful

46
Q

Markers of early B cell development

47
Q

Markers of middle B cell development

48
Q

Markers of late B cell development

49
Q

TFs involved in early B cell development from stem cell

A

SPI1

IKZF1

50
Q

TF involved in middle B cell development

51
Q

ALL t(9;22) (B cell)

A

BCR-ABL1 fusion of two kinases (Class I)
IKZF1 TF inhibition (Class II)

Older adults + kids

(early b cell immunophenotype)
CD10+
CD19+
TdT+

Large agranular blasts

Poor prognosis
Anthracycline+Vinc+Prednisone induction
MTX + 6MP maintenance

52
Q

t(v 11q23) ALL

A

Rearranged MLL–>decrease diff

Kids <1 yr

CD10- (helps diff between t(9;22)
CD19+
TdT+

53
Q

ALL t(12;21)

A

TEL-AML1

Class II - inhib diff
Doesn’t support Gilliland

Kids

Big agranular blasts

Tdt+
CD20-
CD34+

Good prognosis 90% cure

54
Q

T-ALL

A

Usually oncogene translocates to TCR promoter

Kids - thymus/lymph nodes/spleen involved

Big agranular blasts

TdT+
CD5+/CD3+ (T cell markers)

High risk

OS Hematology/Oncology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions