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STEP1 > Heme Onc > Flashcards

Heme Onc Flashcards

1
Q

Left supraclavicular lymphadenopathy

A

Abdominalmalignancy especially gastric cancer

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2
Q

Right supraclavicular lymphadenopathy

A

-chest cavity malignancy especially lung cancer

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3
Q

Mediastinaltymphadenopathy

A

Lymphoma

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4
Q

Reed sternbergcells

A

Hodgkin lymphoma
Owl eye

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5
Q

Auer rods

A

AML

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6
Q

Apml genetics

A

Translocation15,17

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7
Q

Apml tx

A

All-trans retinoicacid
Note that traditional chemo will cause di c due to release of coagulants in granuleswhen cells die

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8
Q

AML genemutation with worst px

A

11q23

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9
Q

AML m 0

A

Minimal different-tas
All blasts
No aver rods or granules

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10
Q

AML M1

A

Some differentiation
All blasts
Aver rods andgranuls

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11
Q

AML m2

A

More differentiation
Still at least 20% blasts since it’s Am l but more mature cells as well

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12
Q

AML m3

A

A P M L

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13
Q

AML my

A

Myelomonocytic
NS E orwright-giesma stain

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14
Q

AML m5

A

Monoblastic/ monocytic “
Oftenextramedullary eg C N S because of the monocytes

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15
Q

AML m6

A

Pure erythroid
Also myeloblasts…

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16
Q

AMC m7

A

Megakaryoblastie
Need flow not just microscopy

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17
Q

Therapies that may cause AML

A

Chemo-alkylating andtopossomerase 2 inhibitors

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18
Q

Alkylating agents e.g.

A

Busulfan
Cydophosph amide
Is of amide

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19
Q

Topoisomeraseinhibstorse eg.

A

E topside
Doxorubicin

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20
Q

TopoisomeraseinhibitorAML

A

Faster thanaltylatingagents
1-3 year latency
No MDs phase
Chromosome 11 and mll gene

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21
Q

Alkylatingagent AML

A

5-7 year latency often preceded by MDs,
Chromosomes 5 and 7

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22
Q

MDs

A

Myelodysplasticsyndrome ‘
Pancytopenia due to take over of dys plasticmydlaid cells in bm
Often evolves toaml

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23
Q

Aggressive tx of MDs

A

’ Stem cell transplant
Generallyreserved forjounger pts with high risk of conversion

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24
Q

Prussian blue

A

Stains iron

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25
Q

Ring syderoblasts

A

R BC dysplasia seen in MDs Amons others

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26
Q

Tdt

A

Terminal deoxynucteo tidy transferase
All and generallylymphoblast marker

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27
Q

B-all

A

Better prognosis
Bone marrow first
Most commonchildhood leukemia

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28
Q

T-all

A

Textbook presentation is teenage boy withmediastinallymphadenpatly
Because thymus is there
Peripheral involvement first

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29
Q

Cd10

A

B-all markerthatconfers good prognosis if present
Not seen in all b-all

30
Q

PhiladelphiaAhromasome

A

t(9;22)
Mostly a CML marker
May be seen in ALL, poor prognosis if so

31
Q

Cml mutation

A

Philadelphia t (9:22) r
Permanently ontyrosine kinase

32
Q

Cell linecml

A

Neutrophilsand their blasts

33
Q

Polycythemia Vera mutation

A

Jak 2
Constitutiveproliferation signal

34
Q

CMl clinical

A

’ Insidious
Splenomegaly and abd fullness
Fatigue
Weight loss

35
Q

Cml course

A

Chronicthen accelerated then terminal blast crisis

36
Q

Polycythemiavera S x

A

Headache
Visual disturbances
Ruddy face
PruRitis esp.after hot shower
Thrombosis risk

37
Q

Cml tx

A

Imatinib and other tyr k inhibitors

38
Q

Primary myelofibrosis histology

A

Dacrocytesaka teardrop cells

39
Q

Secondarypolycythemia

A

Due to excess E PO
Generallydue to hypoxia, altitude, or smoking i.e. Chronically low O 2 sat

40
Q

Pv tx

A

’ Phlebotomy
Hydroxyvrea, antimetabolite
Possiblymyelaosuppressive drugs

41
Q

Reactivethrombocytosis

A

Various causes
Infection surgery malignancy chronic inflammation post splenectomy blood loss iron deficiency

42
Q

Essentialthrombocyto sis tx

A

Low dose aspirin if clotting
Hydroxyureaifhigh risk

43
Q

Chronic myelufiboosis

A

Pan-myeloidproliferation
Then bm fibrosis
Then extramedullaryhematopoeisis including massivesplenomegaly

44
Q

Chronic mydlofibrosis peripheral smear

A

Dacryocytes - cells get squished intoteardrop shape trying to corner out of fibrotic marrow

45
Q

Chronic myelofibrosis ex

A

, Bm transplant it nigh risk
Ruxolitinib jak2 inhibitor

46
Q

Smudge cells

A

Lymphocytefragments seen in smear fr cl l and other lymph malignan;

47
Q

Cl l cell type

A

Usually Bsometionest

48
Q

Immunophenotype CLL/SLL

A

’ B cells w/ CD 5
I.e. Cd19 cd20 CD 5 +

49
Q

Richtertransformation

A

Conversion o CLL/SLL to DLBCL

50
Q

Immunophenotype hairy cells

A

Cd20 cd25 Cd 103 Cd 11C

51
Q

Hairy cell mutation

A

Bra f v6o0e

52
Q

Hcl physical exam

A

Massive splenomegaly
Sometimes hepatomegoly
Rarely lyipladenopathy

53
Q

Pel-ebstein fever

A

Cyclical fever1-2 weeks Hodgkintymplome

54
Q

Follicularlymphone genes

A

Mostly t(14:18)
Constitutive igh promoter to bcl-2

55
Q

Cell type follicularlymphoma

A

Germinal follicle B cells
Cd10 cd19 cd20

56
Q

Follicular lymphoma prognosis

A

Good
Worse ifconstittional S x

57
Q

Malt lymphoma risk fx

A

Preexisting conditions esp H pylori and siorgen rsyndrome

58
Q

Malt lymphoma tx

A

Antibiotics only if H pylori will usually kill cancer
Otherwisechems and radiation

59
Q

Mycosisfungoidest sezavi six histoloss

A

Cerebriformnueli. In blood
Also skin lesions

60
Q

Mf/ss cell type

A

T cell cutaneouslymphona

61
Q

Pautrier microabscesses

A

Mf/ss
Sezari cells infiltrated epidermis

62
Q

Mantle cell lymphoma gene

A

T (11;14) ‘
Bcl-l gene cyclin d1 protein to promoter igh

63
Q

Mantle cell lymphoma prognosis

A

Bad compared to other non-hodgkinlymphomas
5-7 years

64
Q

Starry sky

A

Burk it lymphoma

65
Q

Gene burkitt

A

Myc often t 8, 14

66
Q

When to start burkitt tx

A

Within 48h

67
Q

Burkitt virus

A

Eb v
Also associatedwith malaria

68
Q

N odular sclerosis

A

Subset ofhodgieinlymphora
Excellent prognosis
Lacunae cells

69
Q

M spike

A

Common inand diagnostic of multiple myloma

70
Q

Cause of deathmyclomo

A

Usually infection

71
Q

Crab

A

Clinical myeloma
High Ca renal anemia bone pain

72
Q

T 9,22

A

Cml
Philadelphia

STEP1 (15 decks)

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