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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
Ring syderoblasts
R BC dysplasia seen in MDs Amons others
26
Tdt
Terminal deoxynucteo tidy transferase All and generallylymphoblast marker
27
B-all
Better prognosis Bone marrow first Most commonchildhood leukemia
28
T-all
Textbook presentation is teenage boy withmediastinallymphadenpatly Because thymus is there Peripheral involvement first
29
Cd10
B-all markerthatconfers good prognosis if present Not seen in all b-all
30
PhiladelphiaAhromasome
t(9;22) Mostly a CML marker May be seen in ALL, poor prognosis if so
31
Cml mutation
Philadelphia t (9:22) r Permanently ontyrosine kinase
32
Cell linecml
Neutrophilsand their blasts
33
Polycythemia Vera mutation
Jak 2 Constitutiveproliferation signal
34
CMl clinical
' Insidious Splenomegaly and abd fullness Fatigue Weight loss
35
Cml course
Chronicthen accelerated then terminal blast crisis
36
Polycythemiavera S x
Headache Visual disturbances Ruddy face PruRitis esp.after hot shower Thrombosis risk
37
Cml tx
Imatinib and other tyr k inhibitors
38
Primary myelofibrosis histology
Dacrocytesaka teardrop cells
39
Secondarypolycythemia
Due to excess E PO Generallydue to hypoxia, altitude, or smoking i.e. Chronically low O 2 sat
40
Pv tx
' Phlebotomy Hydroxyvrea, antimetabolite Possiblymyelaosuppressive drugs
41
Reactivethrombocytosis
Various causes Infection surgery malignancy chronic inflammation post splenectomy blood loss iron deficiency
42
Essentialthrombocyto sis tx
Low dose aspirin if clotting Hydroxyureaifhigh risk
43
Chronic myelufiboosis
Pan-myeloidproliferation Then bm fibrosis Then extramedullaryhematopoeisis including massivesplenomegaly
44
Chronic mydlofibrosis peripheral smear
Dacryocytes - cells get squished intoteardrop shape trying to corner out of fibrotic marrow
45
Chronic myelofibrosis ex
, Bm transplant it nigh risk Ruxolitinib jak2 inhibitor
46
Smudge cells
Lymphocytefragments seen in smear fr cl l and other lymph malignan;
47
Cl l cell type
Usually Bsometionest
48
Immunophenotype CLL/SLL
' B cells w/ CD 5 I.e. Cd19 cd20 CD 5 +
49
Richtertransformation
Conversion o CLL/SLL to DLBCL
50
Immunophenotype hairy cells
Cd20 cd25 Cd 103 Cd 11C
51
Hairy cell mutation
Bra f v6o0e
52
Hcl physical exam
Massive splenomegaly Sometimes hepatomegoly Rarely lyipladenopathy
53
Pel-ebstein fever
Cyclical fever1-2 weeks Hodgkintymplome
54
Follicularlymphone genes
Mostly t(14:18) Constitutive igh promoter to bcl-2
55
Cell type follicularlymphoma
Germinal follicle B cells Cd10 cd19 cd20
56
Follicular lymphoma prognosis
Good Worse ifconstittional S x
57
Malt lymphoma risk fx
Preexisting conditions esp H pylori and siorgen rsyndrome
58
Malt lymphoma tx
Antibiotics only if H pylori will usually kill cancer Otherwisechems and radiation
59
Mycosisfungoidest sezavi six histoloss
Cerebriformnueli. In blood Also skin lesions
60
Mf/ss cell type
T cell cutaneouslymphona
61
Pautrier microabscesses
Mf/ss Sezari cells infiltrated epidermis
62
Mantle cell lymphoma gene
T (11;14) ' Bcl-l gene cyclin d1 protein to promoter igh
63
Mantle cell lymphoma prognosis
Bad compared to other non-hodgkinlymphomas 5-7 years
64
Starry sky
Burk it lymphoma
65
Gene burkitt
Myc often t 8, 14
66
When to start burkitt tx
Within 48h
67
Burkitt virus
Eb v Also associatedwith malaria
68
N odular sclerosis
Subset ofhodgieinlymphora Excellent prognosis Lacunae cells
69
M spike
Common inand diagnostic of multiple myloma
70
Cause of deathmyclomo
Usually infection
71
Crab
Clinical myeloma High Ca renal anemia bone pain
72
T 9,22
Cml Philadelphia

STEP1 (15 decks)

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