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Heme/Lymph 2 > Leukemias and Myeloid Disorders 1 > Flashcards

Leukemias and Myeloid Disorders 1 Flashcards

1
Q

Leukemia defined

A

Neoplastic proliferation of hematopoeitic cells

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2
Q

Lymphomas and leukemias

A

Can be caused by the same cell types

Lymphomas are solid neoplasms of lymphoid cells outside the marrow

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3
Q

Leukemia leading cause of cancer death

A

In children/young adults

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4
Q

Which are most common

A

Acute and chronic each half

AML most common acute, CLL most common chronic

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5
Q

Sex and luekemia

A

Male mostly

Especially Hairy cell leukemia and T cell ALL

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6
Q

Inherited genetic and chromosomal risk for leukemia

A

Down sydnrome

Fanconis anemia

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7
Q

Radiation and drugs and leukemia

A

Radiation - increased risk of all except CLL

Drugs - alkylating agents, topoisomerase inhibitors increase risk of acute

Smoking increase AML risk

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8
Q

Viral and leukemia

A

Human T cell leukemia virus and T cell leukemias/lymphomas

EBV or HHV-8

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9
Q

Immune and leukemia

A

Chronic immune stimulation and immunodeficiency associated with increased risk

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10
Q

Mutations (common)

A

t(9;22) - Philly - Most CML and some ALL

t(15;17) - in promyelotic AML (retinoic acid receptor fuses with PML…tx with trans-retinoic acid)

t(8;21) in AML with maturation (favorable)

in(16) in AML with myelomonocytic diff and abnormal eosinophils (favorable)

t(12;21) in favorable ALL

11q23 (MLL gene) infantile ALL t(4;11), some AML following topoisomerase inhibitors (bad prognosis)

Trisomy 8, momnosomey, of chromosomes 5 and 7 associated with AML and myelodisplastic disroders

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11
Q

Acute vs chonirc leukemia

A

Acute - fatal…at least 20% blast cells…sudden onset…marked cytopenias and more symtpoms

Chronic - greater cell maturation…better survival…more prominent splenomegaly…more gradual symptoms and mild cytopenias

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12
Q

Clinical manifestations

A

Bone marrow - neutropenia, thrombocytopenia, anemia

Organ infiltration

INcreased metab and cell lysis

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13
Q

Bone
Lymphadenopathy
Splenomegaly

Types of leukemias

A

Bone pain, espeically in acute

LAD - in lymphoctyic anemias, mostly CLL

Spleno - Mild to mod in acute, mod in CLL, most in CML

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14
Q

Hepato
CNS
Skin
Myeloid sarcomas and leuk

A

Hepato - most in CLL
CNS - espeically ALLs, some AMLs
Skin - T cell and monocytic leukemias
Mye Sarc- bone or soft tissue infiltrates in AML

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15
Q

Cytochemistry used for

A

AML for most part

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16
Q

Cytogenics used for

A

CML confirmatory…subtypes of acute

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17
Q

ALL types

A

Precursor B or T lymphoblastic leukemia

Same cell may cause lymphoma but if 25% or more lymphoblasts in marrow then leukemia

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18
Q

Most common patients with ALL

A

Children, adolescents (most common in childreN)

More in men

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19
Q

ALL subtype and flow cytometry…also symptoms

A

Bone pain, CNS< tests
May have low white count

Precurosr T (15%) - Mediastinal mass or lymphoma common )…more common in males

20
Q

Prognosis, morphology of ALL

A

95% of childrne into remission

Round and convoluted nuclei, small to medium with little cytoplasm, high grwoth rate

21
Q

AML primary population

A

Most adults and more male

22
Q

AML classifcation

A 
Need cytogenics 
Recurring cytogenic abn (8;21), t(15;17)
Mylodysplasia related changes
Therapy related
NOS
23
Q

AML onset

A 
Gum hyperplasia (esp in monocytic)
DIC in promyelocytic, may be aleukemic
24
Q

Morphology and flow cytometry and prognosis of AML

A

Auer rods…positive nezym estains

60% remission but most relapse

25
Q

Favorable and unfavorable AML

A

Favorable - t(8;21), promyelocytic t(15;17), inv(16), isolated NPM 1 mutation

Unfavorable - AML with myelodysplasia changes (del 5,7), therapy related AML, FLT3 mutations

26
Q

Acute promyelocytic leukemia

A

t(15;17)
Abnormal RAR…can lead to DIC

Look for multiple auer rods and intense granularity

ATRA is the therpay

27
Q

Acute leukemia of ambiguous lineage

A

Primitive acute leukemias showing either insufficienct evidence of lymphoid or myeloid differentiation OR showing both myeloid and lymphoid or bothB and T cell differentiation

Typically a poor prognosis

28
Q

B lymphoid-myeloid cases mutations

A

t(9;22) or 11q23 (MLL)

29
Q

CML mutation and ages

A

t(9;22) - Philly…c-abl transferred to bcr region of 22…increased tyrosine kinase activity…more cell division…doesn’t block differentiation

26-60

30
Q

Symptoms of CML and what to look for

A

Splenomegaly
Netutrophilia with less than 5% blasts and all stages of myeloid precursors…basophilia
100% cellular bone marrow with increased small MK but full granulocytic maturation
Thrombocytosis in 50%

31
Q

CML blast phase

A

After about 3 years.

Myeloid - 70%
Lymphoid - 30%

32
Q

Effect of MLL mutation, BCR-ABL mutation and RAR mutation

A

MLL - increased self renewal
BCR-ABL - increased growth and survival
RAR - differentiation blocked

33
Q

Philly chromosome mutation and what it causes

A

CML and ALL

BCR-ABL fusion protein from t(9;22) is tyr kinase that activates pro-growht and survival

34
Q

t(15;17) mutation

A

AML (promyelocytci)

PML-RARE fusion creates abnormal RAR

35
Q

Core binding factor mutations

A

Disrupt TF needed (usually good prognosis)
t(8;21) - AML with maturation
inv (16) - monocytic AML with abnormal eosino
t(12;21) - favorable ALL`

36
Q

MLL mutation

A

11q23
Poor
Histone modifying protein that allows prolif pathways to be turned on

37
Q

Mature B cell and plasma cell markers

A

Kappa and lambda light chains

38
Q

First tier of AML diagnosis

A

Cytogenics

39
Q

In a nutshell

A

Is it acute leukemia (more than 20% blasts)…if yes then myeloid or lymphoid (flow)…if lymphoid, B or T (flow)…if myeloid, does it have recurring CG abnormality)..if not, then is there associated dysplasia or histroy of chemo or XRT…if not, is there maturation

40
Q

Things for good diagnosis of precurosr B cell ALL

A

Hyperdiploidy
t(12;21) mutation
Age 2-10 with lower WBCs at diagnosis

41
Q

Poor prognosis of B cell ALL

A 
Hypodiploidy
Under 1 or over 10
Higher WBC
t(9;22) - BCR/ABL, Philly
t(4;11) - AF4/MLL
42
Q

AML with maturation

A

t(8;21) good prognosis

Core binding factor mutations

43
Q

Myelomonocytic AML

A

Inv (16) or t(16,16)

Abnormal eosinophils

44
Q

Monocytic AML

A

11q23 MLL abn

Poor prognosis

45
Q

Promyelocytic AML

A

t)15;17)
Distinctive granules with Auer rods and DIC

Good prognosis if treated

46
Q

NPM1, FLT-3 and CEBPA

A

In AML with normal CG, prognositc significance

FLT-3 duplication - bad 
NPM 1 - good
CEBPA - good
FLT3 plus NPM1 - IM
FLT3 plus CEPBA - ?
47
Q

Alkylating agent and toposiomerase related changes

A

Alkylating - chr 5,7 loss

Topo - 11q23

Heme/Lymph 2 (12 decks)

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