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Hematology, oncology > Acute Myeloid Leukemia > Flashcards

Acute Myeloid Leukemia Flashcards

1
Q

Medications that are RF’s for therapy-related AML

A

Topoisomerase inhibitors
Alkylating agents

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2
Q

Variables used to classify AML

A

cytogenetics (chromosomal translocations) + molecular characteristics

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3
Q

Signs/symptoms

A

bruising/bleeding, constitutional symptoms (fever, fatigue), DOE.

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4
Q

diagnostic criteria

A

Blasts (of myeloid lineage) from marrow OR peripheral blood >*20% OR presence of specific chromosomal abnormalities (t(15;17), t(8;21), inv(16), t(16;16))

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5
Q

general treatment approach

A

induction therapy (tumor debulking) –> BMB for response assessment –> await for counts to recover –> repeat BMB –> consolidation therapy –> maintenance therapy (for some types)

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6
Q

management of patient with aplastic marrow following induction therapy

A

await count recovery and consider growth factor support. Then repeat BMB.

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7
Q

when do you evaluate for CR

A

7 to 10 days after completion of induction chemotherapy (demonstrate adequate elimination of leukemia cells) + then repeat again after cell line recovery to document remission status

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8
Q

definition of morphologic CR

A

marrow blasts less than 5%, no auer rods, no persistence of extramedullary disease

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9
Q

definition of cytogenetic CR

A

normal cytogenetics in patients who had abnormal cytogenetics

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10
Q

definition of incomplete CR (CRi)

A

CR with persistence of cytopenia (usually thrombocytopenia)

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11
Q

Selection of consolidation therapy depends…

A

Depends on favorable vs intermediate vs. poor risk AML but usually cytarabine (standard vs. intermediate vs. high dose)

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12
Q

treatment options for relapse

A

ASCT
Clinical trial followed by ASCT
Salvage chemotherapy followed by ASCT
Supportive care

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13
Q

classic AML patient in terms of age and demographic

A

Male in his mid 60s (male predominance)

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14
Q

What does a myeloblast look like?

A

Immature cells with large nuclei, usually with prominent nucleoli, and a variable amount of pale blue cytoplasm (sometimes with faint granulation) after staining with Wright Giemsa

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15
Q

Image of myeloblast

A

https://www.google.com/search?q=myeloblast&sxsrf=ALeKk003-G0eW2csR836edRbQJjlGnBsFw:1601909565760&source=lnms&tbm=isch&sa=X&ved=2ahUKEwj6kISV2p3sAhUPUa0KHRxkDY4Q_AUoAXoECBkQAw&biw=1117&bih=509#imgrc=RWwfVxY1u9X22M

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16
Q

Bone marrow appearance in AML

A

usually hypercellular due to a partial or almost total replacement of the normal cellular components of the marrow by immature or undifferentiated cells, although AML can sometimes present with a hypocellular marrow.

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17
Q

What is the general basic science goal of diagnosis in AML?

A

To determine that clonal population of cells is of myeloid origin

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18
Q

What is a myeloblast?

A

Unipotent stem cell which differentiates into the effectors of the granulocyte series.

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19
Q

Typical regimen for induction chemo

A

7-day continuous infusion of cytarabine along with anthracycline treatment on days 1 to 3 (so-called “7+3” regimens),
AND targeted agent if leukemia has specific mutation

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20
Q

Cure rate after induction chemo

A

60 to 80 percent of younger adults achieve a CR with such regimens, but only about one-third of patients overall are ultimately cured of AML.

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21
Q

Management of patient who doesn’t achieve CR after induction chemo

A

Second, shorter course of remission induction therapy

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22
Q

How is response to therapy classified?

A

1) Complete remission (CR)
2) Complete remission (CRi) with incomplete recovery of normal neutrophil or platelet counts
3) Partial remission (PR)
4) Resistant disease (sometimes called refractory)

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23
Q

What is the goal of post remission therapy?

A

Eliminate residual, undetectable disease and achieve long-term disease control and cure

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24
Q

What is consolidation therapy in general?

A

intensive treatment that follows soon after the attainment of CR

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25
Q

what is HiDAC therapy?

A

infusions of high dose cytarabine

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26
Q

Options for consolidation therapy in AML

A

1) one or more courses of chemotherapy (usually infusions of high dose cytarabine, so-called HiDAC therapy)
2) autologous hematopoietic cell transplantation (HCT)
3) allogeneic HCT.
- Depending on medical fitness and whether transplant candidate

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27
Q

Which type of transplant is preferred in AMl and WHY?

A
  • allogeneic HCT
  • Induces an important graft-versus-leukemia effect that is not provided by other approaches but is complicated by short- and long-term toxicities)
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28
Q

Role of maintenance therapy in AML

A

Not necessary for most types of AML, certain categories of AML may benefit from maintenance therapy following recovery from consolidation therapy.

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29
Q

Labs in AML

A

Leukopenia or leukocytosis + retic normal or decreased + variable degree of normocytic anemia + variable degree of thrombocytopenia.

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30
Q

When is BMB typically performed

A

7 to 10 days after completion of induction chemotherapy to demonstrate adequate elimination of leukemia cells. Repeated after recovery of neutrophils and platelets to document remission status. The first marrow after induction therapy may be inconclusive and lead to a repeat marrow examination 7 to 10 days later.

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31
Q

Age cutoff typically used to differentiate management

A

60

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32
Q

What is a chimeric oncogene?

A

oncogene formed by chromosomal translocation, which generates a fusion oncogene

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33
Q

CBC in AML

A

neutropenia
thrombocytopenia
Can see leukocytosis (due to circulating blasts)

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34
Q

Clinical features of leukostasis in AML

A

respiratory and/or neurologic distress in AML patient + myeloblasts >50K

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35
Q

TLS labs

A

Hyperkalemia
Hyperphosphatemia
Hyperuricemia
hypocalcemia

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36
Q

Risk categories of AML

A

Favorable
Intermediate
Poor/Adverse

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37
Q

Post-remission therapy means

A

Two phases: consolidation and maintenance therapy

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38
Q

Options for consolidation in AML

A

HiDAC
Autologous HCT
Allogeneic HCT

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39
Q

HiDAC is

A

High dose cytarabine

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40
Q

Preferred consolidation therapy for patients with intermediate or unfavorable prognosis AML

A

HCT

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41
Q

Preferred transplant type for patients with intermediate or unfavorable prognosis AML + why

A

Allogeneic (induces graft-versus-leukemia effect

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42
Q

Induction therapy for AML if prior history of MDS

A

vyxeos

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43
Q

vyxeos is

A

daunorubicin and cytarabine

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44
Q

Ven-FLAG regimen

A

Venetoclax
Fludarabine
Ara-C Cytarabine
G-CSF

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45
Q

NPM1 risk category (with FLT3)

A

Mutated without FLT3 = favorable
Mutated with FLT3 = intermediate
Wild type = poor

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46
Q

Relapsed AML options

A

1) Second allograft
2) salvage chemo
3) glasdegib
4) clofarabine
5) targeted agents
6) clinical trial

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47
Q

Targets of molecular therapies in AML

A

IDH1
FLT3

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48
Q

FLT3 inhibitor drug

A

midostaurin
giltertinib

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49
Q

when to do BMB after induction therapy

A

Controversial – same say 7 days, others say wait until ANC of 0, which makes more sense to me

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50
Q

when BMB is repeated

A

typically 14 days after counts start recovering

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51
Q

management of residual disease found on BMB after induction therapy

A

typically repeat induction

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52
Q

when consolidation is typically started

53
Q

IDH inhibitors

A

Enasidenib and ivosidenib

54
Q

5 year survival

55
Q

Survival depends highly on

A

1) age
2) performance status
3) cytogenetics

56
Q

what are topoisomerase inhibitors

A

anthracyclines
etoposide

57
Q

Cell surface markers that are negative in APL (board question)

A

CD34 and HLA-DR (confirm)

58
Q

RUNX1 – favorable or unfavorable

A

unfavorable

59
Q

-5, -7, inv(3), complex cytogenetics – favorable or unfavorable

A

unfavorable

60
Q

CEBPA — Bialleliic, dual mutant - favorable or unfavorable

61
Q

t(15;17) – risk stratification

62
Q

Inv(16) or t(8;21) – favorable or unfavorable

63
Q

KIT mutation – favorable or unfavorable

A

Generally unfavorable

64
Q

general prognosis of APML

A

do very well with ATRA based therapy

65
Q

lower intensity treatment options for less fit patients

A

LDAC (low dose cytarabine)
HMA (hypomethylating agents)
Targeted agents

66
Q

what are the hypomethylating agents

A

azacitidine
decitidine

67
Q

FDA approved treatment for therapy-related AML

A

CPX-351 (vyxeos)

68
Q

FDA approved treatment for CBF-AML

A

intensive chemo + gemtuzumab

69
Q

transplant timing for unfavorable

A

ASAP (immediately after induction or more realistically after 1-2 HIDAC cycles)

70
Q

New maintenance therapy that will likely become standard of care

A

Oral azacitidine

71
Q

monoclonal AB approved for AML + indication

A
  • Gemtuzumab
  • intermediate but most benefit is in favorable risk w/ CEBPA
72
Q

Relapse risk is predicated now on…

73
Q

What are the MRD categories?

A

MRD-negative
MRD-positive

74
Q

Hallmark genetic feature of therapy-related AML

A

MLL rearrangement

75
Q

Most common drugs causing therapy-related AML

A

Topoisomerase inhibitors
Alkylating agents

76
Q

Preferred induction regimen at UMass

A

Mitoxantrone + cytarabine

77
Q

consolidation for AML

A

IF moderate or high risk – allo transplant
Favorable risk – HIDAC

78
Q

FDA approved maintenance treatment of AML

A

Oral azacitidine

79
Q

Molecular targets for AML

A

IDH1 or IDH2, FLT3, CD22

80
Q

IDH1 or IDH2 targeted agents

A

ivosidenib, enosidib

81
Q

FLT3 targeted agents

A

midostaurin, gitleritinib

82
Q

Prognostic significance of therapy-related AML

A
  • confers worse prognosis (higher likelihood of high risk genetic features)
83
Q

schedule for 7+3 regimen

A

seven-day continuous infusion of cytarabine along with anthracycline treatment on days 1 to 3 (so-called “7+3” regimens),

84
Q

Favorable gene abnormalities

A

1) t(8;21)
2) inv(16)
3) t(16;16)
4) Mutated NPM1 without FLT3
5) Biallelic mutated CEBPA
IDH2 (confim)

85
Q

Blast immunophenotype in AML

86
Q

Why DAH happens in induction therapy with AML

A

blasts invade lung, when killed by chemo, they cause alveolar inflammation and hemorrhaging

87
Q

Management of patient with CRi and not able to be taken to transplant

88
Q

management of cerebellar toxicity with HiDAC

A

Discontinuation of HiDAC. Never rechallenge.

89
Q

timeframe of therapy related AML after treatment with topoisomerase inhibitors

A

1-3 years after exposure

90
Q

Difference between topoisomerase inhibitor therapy-related AML and alkylating agent-associated therapy-related AML

A

topoisomerase inhibitor - rarely preceded by MDS + shorter latency period

91
Q

Clinical features of therapy related AML

A
  • rapidly progressive leukemia + high white blood cell counts
92
Q

Markers expressed by AML M7 (megakaryocytic AML)

A

CD41 and CD61

93
Q

marker associated with erythroid leukemia

94
Q

markers associated with monocytic leukemia

A

CD11c, CD14 and CD64

95
Q

risk stratification system used in AML

A

European LeukemiaNet (ELN) risk stratification system

96
Q

Classification of cytogenetics

A

Favorable
Intermediate
Adverse

97
Q

Significance of low FLT3-ITD

A

low allelic ratio

98
Q

intermediate risk genetic abnormalities

A

1) mutated NPM1 and FLT3-ITD (High)
2) Wild-type NPM1 without FLT3-ITD or with FLT3-ITD (low)
3) t(9;11)
4) cytogenetic abnormalities not classified as favorable or adverse

99
Q

adverse genetic abnormalities

A

t(6;9)
t(v;11q23.3)
t(9;22)
inversion(3)(q21.3q26.2) or t(3;3)(q21.3;q26.2)
-5 or del(5q); -7; -17/abn(17p)
monosomal karyotype
wild-type NPM1 and FLT3-ITD (High)
mutated RUNX1
Mutated ASXL1*
Mutated TP53

100
Q

Caveat about RUNX1 or ASXL1 mutation classification

A
  • should not be used as an adverse prognostic marker if they co-occur with favorable-risk AML subtypes
101
Q

Hypoplasia definition with response assessemnt

A

Cellularity less than 20% of which residual blasts are less than 5%

102
Q

Extramedullary manifestation of acute leukemia is referred to as? Term for skin manifestation?

A

1) Myeloid sarcomas
2) leukemia cutis

103
Q

Management of myeloid sarcomas

A
  • systemic chemotherapy with 3+7 regimen (considered manifestations of systemic disease)
104
Q

Allo conditioning regimens per boards

A
  • IV busulfan + cyclophosphamide
  • IV busulfan + fludarabine
105
Q

normal cytogenetics risk stratification

A

intermediate risk

106
Q

Risk factors for cerebellar toxicity with high-dose Ara-C

A

elderly + renal dysfunction

107
Q

management of pregnant patient diagnosed with AML

A

3+7 (38% risk of fetal demise) but can’t treat pregnant mother otherwise

108
Q

what are the myeloid lineage markers

A

CD13 and CD33

109
Q

Gene defect implicated in therapy related AML due to topoisomerase inhibitors

A

MLL rearrangement

110
Q

Latency period for therapy related AML with topoisomerase inhibitors

111
Q

Latency period for therapy related AML from alkylating agents

112
Q

Giltertinib target

A

FLT3 positive

113
Q

7 + 3 dosing + schedule

A

200 mg/m2 continuous infusion cytarabine for 7 days OR daily + idarubicin 12 mg/m2 or daunorubicin 60-90 mg/m2 x 3 days

114
Q

How is gemtuzumab administered for CD33 positive patients?

A

single dose on day 1 of 7+3

115
Q

consolidation for favorable risk

A

Hi-DAC (3 gm/m2 BID) x 3-4 cycles, TIW x 4 doses

116
Q

consolidation for therapy related AML

A

Allo-transplant (carries poor prognosis)

117
Q

Favorable mutation in AML

A

NPM1 mutation (think of scene)

118
Q

Advantages and disadvantages of umbilical cord blood for transplants

A

*Single cord transplants have stem cells so can’t be used in patients with higher BMI.
- single cord is associated with better OS as compared to double cord

119
Q

what are standard and high doses of daunorubicin

A

45 mg/m2 = standard dose
90 mg/m2 = high dose

120
Q

When is high dose daunorubicin indicated for?

A
  • No benefit in patients above age 65.
121
Q

highest risk mutation in AML

122
Q

Blast cutoff in AML

A

Greater than 10% + recurrent genetic abnormalities

123
Q

Other favorable mutations for AML

A

bZIP
AMl1-ETO
CBFB-MYH11

124
Q

AML Maintenance for patients who are transplant ineligible

A

oral azacitadine

125
Q

Cytogenetic abnormalities conferring poor prognosis and warranting transplant

A

1) inv (3)
2) t(6;9)
3) del(5q)
4) del(7p)
5) chromosome 17 abnormalities
6) complex karyotype

126
Q

Clinical features of AML with myelodysplasia-related changes (AML-MRC)

A

AML + multilineage dysplasia + MDS related cytogenetic changes

127
Q

What cytogenetics are seen in MDS?

A

Deletion chromosome 7 and 5

128
Q

Treatment of AML with myelodysplasia-related changes

A

liposomal daunorubicin and cytarabine (vyxaneos)

Hematology, oncology (218 decks)

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