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Disease and Defense > AML/ALL > Flashcards

AML/ALL Flashcards

1
Q

AML – Acute myeloid leukemia

A

leukemic cells resemble cells of one or more myeloid lineages

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2
Q

ALL – Acute lymphoblastic leukemia

A

Leukemic cells - resemble precursor/immature lymphocytes

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3
Q

Etiology acute leukemia

A

Chromosomal abnormality, in PCR - block ability to differentiate/increase autonomy of growth signalling pathway

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4
Q

Risk factors for acute leukemia

A

Chemo (alkylating agent, topoisomerase II), ionizing, tabacco smoke, benzene, genetic syndrome

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5
Q

Acute leukemia clinical presentation

A

Anemia (fatigue, malaise, pallor, dyspnea)
Thrombocytopenia (brusing, petechiae, hemorrhage)
Neutropenia (fever, infection)
Rare: thrombotic events, DIC, skin/gum/tissues

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6
Q

___% of cases of ALL occur in children less than ___ y/o

A

75%; 6 y/o

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7
Q

Immaturity markers

A

CD34

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8
Q

Common immature lymphoblasts markers

A

TdT

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9
Q

B cell linage markers

A

CD19, CD22

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10
Q

T cell lineage markers

A

CD3, CD7

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11
Q

B cell mature markers

A

CD20, surface immunoglobulin

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12
Q

B-ALL accounts for _______ % of ALL, typically ALL of ____(age)___

A

80-85; childhood

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13
Q

BCR-ABL1 B-ALL

cytogenetics, distribution, prognosis

A

t(9;22) - philadelphia chromosome
“Ph+ALL”
25% of adult ALL, 2% childhood ALL
Poor prognosis

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14
Q

B-ALL MLL

A

translocation 11q23
Neonates/young infants
poor prognosis

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15
Q

B-ALL ETV6-RUNX1

A

t(12;21)
25% childhood B-ALL
Favorable prognosis

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16
Q

T-ALL traits

A 
25% of ALL
Adolescent/young adults
Mediastinal mass
High WBC
Favors males
17
Q

T-ALL prognosis general trends in children vs adults

A 
Good - kids
>95%, cure80%
Poor adults
Remission 60-80
Cure<50%
18
Q

Poor ALL prognosis factors

A 
< 1 y/o; >10 y/o
Very high WBC
T-lymphoblastic hypodiploidy
Slow response to rx
Min residual disease
19
Q

AML - Acute myeloid leukemia occurs in what age?

A

adults (65 avg); 10% of childhood leukemia are AML

20
Q

AML diagnosis

A

> 20% myeloblasts in marrow/peripheral blood

  • morphologic appearance
  • flow cytometric
  • immunohistochemistry
21
Q

Common myeloid markers

A

CD117 (C-Kit)

Myeloperoxidase

22
Q

AML/APL - PML-RARA/M3 AML

A 
t(15;17)
Blocked at promyeloctyes (not at blasts)
Hypergranular morphology
Auer rods
DIC
23
Q

APL treatment

A
  1. RARA - retinotic acid receptor alpha protein - does not signal well –> accumulation of promyelocyte
    Give high doses of ATRA to overcome
24
Q

AML RUNX1-RUNX1T1

A

t(8;21)
5% AML - younger patient
Good prognosis

25
Q

APL secondary risk

A

Disseminated intravascular coagulation (DIC)

26
Q

AML CBFB - MYH11

A 
inv(16) or t(16;16)
5-10% AML
Younger patients
Baso Eos
Good prognosis
27
Q

AML RBM15 - MKL 1

A

Megakaryoblastic differenation
Infants with downs
Good prognosis

28
Q

AML MLL - 11q23

A

abnormalities of MLL - some monocytic differentiation

Poor prognosis

29
Q

t-AML alkylating agent latency

A

2-8 years

30
Q

t-AML alkylation agent cytogenetics

A

whole/partial deletion of 5 and 7

31
Q

t-AML topoisomerase inhibitor

A

1-2 years

MLL 11q23 rearrangement

32
Q

NOS

A

Not otherwise specified

33
Q

AML NOS subtype

A

undifferentiated - myeloblasts
Myelomonocytic
Monoblasts/monocytic -> skin/gum lesion
Megakaryoblastics –> marrow fibrosis

34
Q

AML NOS molecular abnormality

A

FLT3 - poor
NPM1 - good
CEBPA - good

35
Q

Hematopoietic stem cell transplant depends on

A

Younger patient
High risk disease
Relapse disease
Current health standing

36
Q

which t-AML will be de novo?

A

topoisomerase II

37
Q

Prognosis of t-AML?

A

very poor

38
Q

Auer Rodes are?

A

fused azurophilic granules

Disease and Defense (10 decks)

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