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Heme/Onc > Leukemia > Flashcards

Leukemia Flashcards

1
Q

What is the description of AML?

A

Blast cells 20% + on peripheral blood smear or bone marrow aspirate
Auer rods on peripheral smear

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2
Q

What age group is typically present with AML?

A

Adults

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3
Q

What is the typical initial treatment for AML?

A

7 + 3

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4
Q

What is AML?

A

Acute myelogenous leukemia

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5
Q

What is ALL?

A

Acute lymphoblastic leukemia

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6
Q

What is the description of ALL?

A

Blast cells 20%+ on peripheral blood smear on bone marrow aspirate

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7
Q

What age groups are typically affected with aLL?

A

Children and young adults

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8
Q

What are the types of initial treatments for ALL?

A

Induction
Consolidation
Interim maintenance
Maintenance

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9
Q

What is CML?

A

Chronic myelogenous leukemia

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10
Q

What is the description of CML?

A

Philadelphia chromosome (BCR-ABL1 fusion gene)

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11
Q

What are the typical age groups affected in CML?

A

Older adults

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12
Q

What is CLL?

A

Chronic lymphocytic leukemia

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13
Q

What is the description of CLL?

A

Presence of 5x10^9/L + B lymphocytes in peripheral blood

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14
Q

What age group is typically affected by CLL?

A

Older adults

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15
Q

What is the typical initial treatment of CLL?

A

“watch and wait” if asx

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16
Q

Is ALL or AML more common?

A

AML

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17
Q

What are RFs for acute leukemias?

A 
Prior chemotherapy
Genetics
SH
Viruses
Radiation
Chemicals
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18
Q

What chemotherapies are RFs for acute leukemias?

A

Alkylating agents
Anthrcyclines
Epipodophyllotoxins

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19
Q

What genetics syndromes are RFs for acute leukemias?

A

Down’s
Klinefelter’s
Neurofibromatosis type 1

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20
Q

What SH are RFs for acute leukemias?

A

Cigarette smoking

Maternal marijuana or ethanol use

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21
Q

What viruses are RFs for acute leukemias?

A

EBV
HTLV-1
HTLV-2

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22
Q

What chemicals are RFs for acute leukemias?

A

Herbicides
Pesticides
Benzenes

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23
Q

What defect is present in AML?

A

Defect in pluripotent stem cell or myeloid precursor

Defect probably occurs in earlier lineage cells in adults compared with children

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24
Q

What translocation occurs in APL?

A

t(15;17)

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25
Q

What defect is present in ALL?

A

Defect in lymphoblasts

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26
Q

For how long are patients symptomatic before presentation?

A

Sx for 1-3 months before presentation

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27
Q

What are sx in the first 1-3 months for acute leukemia?

A

Fatigue
Fever
Pallor

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28
Q

What are s/sx of acute leukemia?

A

Loss of normal functional blood cells replaced by immature leukemic cells cause sx
Splenomegaly, hepatomegaly, lymphadenopathy
DIC
Coagulopathy, bleeding, skin manifestations, bone pain

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29
Q

What is DIC?

A

Disseminated Intravascular Coagulation

May be in APL

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30
Q

What is the diagnosis of acute leukemias?

A

CBC w/diff, coagulation studies, blood chemistries
Peripheral blood smear
Bone marrow biopsy and aspirate
Screening lumbar puncture in ALL to assess CNS involvement

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31
Q

What is the classification of AML?

A

> 20% blasts in marrow or blood defines acute leukemia
AML w/recurrent genetic abnormalities (includes acute promyelocytic leukemia, APL)
AML myelodysplastic (MDS) - related changes/ multilineage dysplasia
Therapy-related myeloid neoplasms
AML not otherwise categorized

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32
Q

What are less favorable prognostic factors of AML?

A

Age > 60
Cytogenetic abnormalities
Molecular abnormalities
Co morbidities
More time/cycles needed to achieve complete remission
Elevated WBC, LDH, and/or uric acid may indicate higher tumor burden

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33
Q

What are cytogenic abnormalities with AML?

A

Complex karyotype

3+ clonal chromosomal abnormalities

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34
Q

What are molecular abnormalities in AML?

A

FLT3 ITD mutation

FMS-like tyrosine kinase 3 internal tandem duplication

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35
Q

What are AML co-morbidities?

A

Renal/liver dysfunction
Underlying MDS
Secondary leukemia

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36
Q

What is considered complete remission of AML?

A

Disappearance of clinical and bone marrow evidence
ANC > 1,000; plt > 100,000
Bone marrow blasts < 5%
Absence of auer rods
No residual evidence of extramedullary disease

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37
Q

What is considered cytogenic complete remission of AML?

A

Normal cytogenics, independent of transfusions

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38
Q

What is the goal in AML?

A

Induce remission and prevent relapse

Treat with curative intent in most patients unless considered unfit

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39
Q

What are the types of treatment for AML?

A

Induction

Post-remission

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40
Q

What is the 7+3 regimen for AML?

A

Cytarabine w/Daunorubicin

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41
Q

What are the induction regimens for AML?

A

7+3

HiDAC

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42
Q

What does the HiDAC regimen consist of?

A

Cytarabine with Idarubicin

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43
Q

What are the goals of post-remission/consolidation?

A

Eliminate residual leukemia cells to maintain remission and prevent recurrence

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44
Q

What are the options during post-remission/consolidation?

A

Same chemo given during induction, different agents, or higher doses
Clinical trial
Stem cell transplant

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45
Q

What is the option for older patients with comorbidities during post-remission/consolidation?

A

Lower intensity therapies, best supportive care

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46
Q

What is supportive care for AML treatment?

A

Tumor lysis syndrome
Infection prophylaxis
Myelosuppression (CSFs, transfusions)

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47
Q

What are supportive care regimens for HD cytarabine regimens with cerebellar dysfunction?

A

Increased risk w/renal dysfunction

Neurologic assessments necessary prior to each dose

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48
Q

What are supportive care regimens for HD cytarabine regimens with ocular toxicity?

A

May damage corneal epithelium

Saline/steroid eye drops

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49
Q

APL is a subtype of which acute leukemia?

A

AML

50
Q

What causes APL?

A

Fusion protein forms from translocation of PML gene and RAR alpha gene

51
Q

How can APL present?

A

DIC

Fibrinolysis

52
Q

What is the MOA of tretinoin?

A

Binds to t(15;17) gene product and induces maturation and apoptosis

53
Q

What is APL differentiation syndrome (or retinoic acid syndrome)?

A

Fever
SOB
Edema
Pleural/pericardial effusions

54
Q

If there is respiratory compromise after tretinoin administration, how is it treated?

A

Dexamethasone

55
Q

What is the induction option for APL?

A

Able to tolerate anthracyclines: tretinoin + idarubicin/daunorubicin +/- cytarabine
Not able to tolerate anthracyclines: tretinoin + arsenic trioxide

56
Q

What are options for post-remission/consolidation in APL?

A

May include tretinoin or arsenic trioxide

57
Q

What is the MOA of arsenic trioxide?

A

Not understood

May cause degradation of PML/RAR-alpha fusion protein

58
Q

What are AEs of arsenic trioxide?

A

APL differentiation syndrome

QT prolongation

59
Q

How do we monitor arsenic trioxide?

A 
EKG
K
Ca
Mg
SCr
60
Q

According to the NCI, what is a standard risk classification for ALL?

A

Age 1-10
WBC < 50
No karyotypes present

61
Q

According to the NCI, what is a high risk classification for ALL?

A

<1 or 10+
WBC 50+
Karyotypes t(9;22) or t(4;11)

62
Q

What is the goal of ALL treatment?

A

Induce clinical and hematologic remission (cure)

Once complete remission (CR) is achieved, goal is to maintain it. Therapy usually must be continued for maintenance

63
Q

When is a child considered cured of ALL?

A

After 5-10 years of CR

64
Q

What are the types of ALL treatment?

A

Induction therapy
Consolidation
Interim maintenance/delayed intensification
Maintenance

65
Q

What prophylaxis is included in all ALL phases?

A

CNS prophylaxis

66
Q

What is the goal of induction therapy for ALL?

A

Clear as many leukemic cells as possible from bone marrow

67
Q

What drugs are in the backbone of induction therapy for ALL?

A

Dexa/prednisone
Vincristine
Asparaginase/pegasparaginase

68
Q

What drugs may be added to ALL induction therapy?

A 
\+/- :
Daunorubicin
Cyclophosphamide
MTX
Cytarabine
Depends on pt RFs
69
Q

What do we add to induction ALL therapy if Philadelphia chromosome +?

A

TKI

70
Q

What are CNS therapy options?

A

Radiation
IT chemo
HD systemic chemo

71
Q

What are some IT agents?

A

MTX +/- cytarabine +/- hydrocortisone

72
Q

What is the goal of maintenance therapy in ALL?

A

Eliminate remaining leukemic cells, eradication of residual disease

73
Q

What are therapy options for consolidation/intensification of ALL?

A

Post-remission therapy, usually same drugs used to induce remission + other drugs
Pt may receive SCT

74
Q

What is the goal of maintenance therapy for ALL?

A

Prevent recurrence

75
Q

How long is maintenance therapy used in ALL?

A

2-3 years following consolidation

76
Q

What drugs are used for relapsed/refractory ALL?

A

Blinatumomab

Tisagenlecleucel

77
Q

What is blinatumomab?

A

Bispecific CD19 deirected T cell engager

78
Q

What are supportive therapies for ALL?

A

CSF
Infxn prophylaxis
Constipation prophylaxis for vincristine regimens
Corticosteroid AEs

79
Q

What are causes for CML?

A

Ionizing radiation, occupational exposure to benzene

Increased incidence in atomic bomb survivors

80
Q

What is the genetic cause of CML?

A

Translocation of the chromosome 22 (BCR) fused with chromosome 9 (ABL), resulting in philidelphia chromosome

81
Q

What does the BCR-ABL gene cause?

A

Increased tyrosine kinase activity which results in uncontrolled cellular division, proliferation, and inhibition of apoptosis causing an increase in the abnormal clone

82
Q

When can the philadelphia chromosome be present?

A

ALL
Some AML
CML

83
Q

What are the 3 phases of CML?

A

Chronic (stable)
Accelerated
Blast crisis

84
Q

What is the chronic phase of CML?

A

Usual phase for diagnosis
Disease managed with tx
< 10% blasts in peripheral blood or bone marrow

85
Q

What is accelerated phase of CML?

A

Occurs with loss of drug efficacy and disease control - Increased WBC count
10-19% blasts in peripheral blood or in bone marrow
Plts < 100,000 or > 1,000,000
Sx including splenomegaly, fever, night sweats, wt loss, bone pain

86
Q

What is the blast crisis phase of CML?

A

> 30% blasts in peripheral blood or bone marrow

Transformation to acute leukemia, rapid proliferation of blast cells, quick onset of sx and death w/o treatment

87
Q

What are the goals of CML management?

A

To induce hematologic, cytogenic, moleculare response/remission, delay progression to accelerated phase or blast crisis

88
Q

What is the only curative option for CML?

A

SCT

89
Q

What is a hematologic response?

A

Normalization of peripheral blood counts

90
Q

What is a cytogenetic response?

A

Percentage of Ph+ cells in a bone marrow biopsy

91
Q

Which type of response is the gold standard for CML?

A

Cytogenetic response

92
Q

What is a molecular response?

A

Based on quantificaiton of BCR-ABL mRNA transcripts

From peripheral blood

93
Q

What is the primary treatment of CML?

A

TKIs
Imatinib
Dasatinib
Nilotinib

94
Q

At what months do we follow up after primary treatment of CML?

A

3, 6, 12, 18

95
Q

What are we evaluating at the follow ups for CML?

A

Evaluate compliance/DDI

Mutation analysis

96
Q

What are the options after evaluation at follow up?

A

Increase TKI dose

Change TKI

97
Q

Which TKI do we administer with food?

A

Imatinib

98
Q

Which TKI do we avoid food with?

A

Nilotinib

99
Q

Which TKI does food not affect?

A

Dasatinib

100
Q

What are AEs of Imatinib?

A 
Edema
Fluid retention
Cardiomyopathy (pleural /pericardial effusion, ascites)
Rash
Myalgia
GI upset
101
Q

What are the AEs of Dasatinib?

A 
Pleural/pericardial effusion
Edema
Rash
GI upset
QT prolongation
102
Q

What are the AEs of nilotinib?

A 
QT prolongation**
Electrolyte abnormalities
LFT alterations
Rash
Myalgia
103
Q

What are the DDIs for Imatinib?

A

3A4 substrate and inhibitor

104
Q

What are the DDIs for Dasatainib?

A

3A4 substrate

H2RA and PPIs

105
Q

What are the DDIs of Nilotinib?

A

3A4 substrate and inhibitor
H2RA and PPI
Avoid QT prolonging drugs

106
Q

What are the supportive care treatments for leukocytosis?

A

Hydroxyurea
Apheresis
TKIs

107
Q

What are the supportive care treatments for thrombocytosis?

A

Hydroxyurea
Apheresis
Anagrelide

108
Q

What is the most common form of leukemia?

A

CLL

109
Q

What cells have mutations for CLL?

A

B cell
T cell
NK cell

110
Q

What is the pathophysiology of CLL?

A

Proliferation of CD5+ B-lymphocytes - accumulation of nonfunctional small lymphocytes in the lymph nodes, spleen, blood, liver, bone marrow, and other organs

111
Q

What are the s/sx of CLL?

A

Asx at presentation
Fever, malaise, and fatigue
Elevated WBC, small lymphocytes, lymphadenopathy, hepatomegaly, splenomegaly
Chronic infections

112
Q

What is the main diagnosis of CLL?

A

> 5 x 10^9 / L B lymphocytes in the pheripheral blood for minimum of 3 months

113
Q

What are the characteristics of a 0 Rai stage?

A

Lymphocytosis alone (in peripheral and bone marrow)

114
Q

What are the characteristics of a I-II Rai stage?

A

Lymphocytosis +/- lymphadenopathy, splenomegaly, hepatomegaly

115
Q

What are the characteristics of a III-IV Rai stage?

A

Lymphocytosis +/- lymphadenopathy +/- organ enlargement +/- hgb < 11 +/- plt < 100K

116
Q

What is the Richter’s syndrome?

A

Transformation of CLL to an aggressive diffuse large B-Cell non-hodgkin’s lymphoma

117
Q

What are unfavorable prognostic factors for CLL?

A

ZAP-70
CD38
Complex cytogenetic abnormalities

118
Q

Is CLL curable?

A

No

119
Q

What are the goals of CLL therapy?

A

Improve QOL and duration, slow CLL cell growth, provide long remissions

120
Q

What are treatment options for CLL?

A

Watch and wait

Chemotherapy dependent on age/genetics

121
Q

If a patient is < 65 yo with no genetic abnormalities and CLL, what are their chemo options?

A

Fludarabine, Cyclophosphamide and Rituximab
Fludarabine and Rituximab
Bendamustine +/- Rituximab
Ibrutinib

Heme/Onc (20 decks)

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