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Leukemia Flashcards

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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
What defect is present in ALL?
Defect in lymphoblasts
26
For how long are patients symptomatic before presentation?
Sx for 1-3 months before presentation
27
What are sx in the first 1-3 months for acute leukemia?
Fatigue Fever Pallor
28
What are s/sx of acute leukemia?
Loss of normal functional blood cells replaced by immature leukemic cells cause sx Splenomegaly, hepatomegaly, lymphadenopathy DIC Coagulopathy, bleeding, skin manifestations, bone pain
29
What is DIC?
Disseminated Intravascular Coagulation | May be in APL
30
What is the diagnosis of acute leukemias?
CBC w/diff, coagulation studies, blood chemistries Peripheral blood smear Bone marrow biopsy and aspirate Screening lumbar puncture in ALL to assess CNS involvement
31
What is the classification of AML?
> 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
32
What are less favorable prognostic factors of AML?
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
33
What are cytogenic abnormalities with AML?
Complex karyotype | 3+ clonal chromosomal abnormalities
34
What are molecular abnormalities in AML?
FLT3 ITD mutation | FMS-like tyrosine kinase 3 internal tandem duplication
35
What are AML co-morbidities?
Renal/liver dysfunction Underlying MDS Secondary leukemia
36
What is considered complete remission of AML?
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
37
What is considered cytogenic complete remission of AML?
Normal cytogenics, independent of transfusions
38
What is the goal in AML?
Induce remission and prevent relapse | Treat with curative intent in most patients unless considered unfit
39
What are the types of treatment for AML?
Induction | Post-remission
40
What is the 7+3 regimen for AML?
Cytarabine w/Daunorubicin
41
What are the induction regimens for AML?
7+3 | HiDAC
42
What does the HiDAC regimen consist of?
Cytarabine with Idarubicin
43
What are the goals of post-remission/consolidation?
Eliminate residual leukemia cells to maintain remission and prevent recurrence
44
What are the options during post-remission/consolidation?
Same chemo given during induction, different agents, or higher doses Clinical trial Stem cell transplant
45
What is the option for older patients with comorbidities during post-remission/consolidation?
Lower intensity therapies, best supportive care
46
What is supportive care for AML treatment?
Tumor lysis syndrome Infection prophylaxis Myelosuppression (CSFs, transfusions)
47
What are supportive care regimens for HD cytarabine regimens with cerebellar dysfunction?
Increased risk w/renal dysfunction | Neurologic assessments necessary prior to each dose
48
What are supportive care regimens for HD cytarabine regimens with ocular toxicity?
May damage corneal epithelium | Saline/steroid eye drops
49
APL is a subtype of which acute leukemia?
AML
50
What causes APL?
Fusion protein forms from translocation of PML gene and RAR alpha gene
51
How can APL present?
DIC | Fibrinolysis
52
What is the MOA of tretinoin?
Binds to t(15;17) gene product and induces maturation and apoptosis
53
What is APL differentiation syndrome (or retinoic acid syndrome)?
Fever SOB Edema Pleural/pericardial effusions
54
If there is respiratory compromise after tretinoin administration, how is it treated?
Dexamethasone
55
What is the induction option for APL?
Able to tolerate anthracyclines: tretinoin + idarubicin/daunorubicin +/- cytarabine Not able to tolerate anthracyclines: tretinoin + arsenic trioxide
56
What are options for post-remission/consolidation in APL?
May include tretinoin or arsenic trioxide
57
What is the MOA of arsenic trioxide?
Not understood | May cause degradation of PML/RAR-alpha fusion protein
58
What are AEs of arsenic trioxide?
APL differentiation syndrome | QT prolongation
59
How do we monitor arsenic trioxide?
``` EKG K Ca Mg SCr ```
60
According to the NCI, what is a standard risk classification for ALL?
Age 1-10 WBC < 50 No karyotypes present
61
According to the NCI, what is a high risk classification for ALL?
<1 or 10+ WBC 50+ Karyotypes t(9;22) or t(4;11)
62
What is the goal of ALL treatment?
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
When is a child considered cured of ALL?
After 5-10 years of CR
64
What are the types of ALL treatment?
Induction therapy Consolidation Interim maintenance/delayed intensification Maintenance
65
What prophylaxis is included in all ALL phases?
CNS prophylaxis
66
What is the goal of induction therapy for ALL?
Clear as many leukemic cells as possible from bone marrow
67
What drugs are in the backbone of induction therapy for ALL?
Dexa/prednisone Vincristine Asparaginase/pegasparaginase
68
What drugs may be added to ALL induction therapy?
``` +/- : Daunorubicin Cyclophosphamide MTX Cytarabine Depends on pt RFs ```
69
What do we add to induction ALL therapy if Philadelphia chromosome +?
TKI
70
What are CNS therapy options?
Radiation IT chemo HD systemic chemo
71
What are some IT agents?
MTX +/- cytarabine +/- hydrocortisone
72
What is the goal of maintenance therapy in ALL?
Eliminate remaining leukemic cells, eradication of residual disease
73
What are therapy options for consolidation/intensification of ALL?
Post-remission therapy, usually same drugs used to induce remission + other drugs Pt may receive SCT
74
What is the goal of maintenance therapy for ALL?
Prevent recurrence
75
How long is maintenance therapy used in ALL?
2-3 years following consolidation
76
What drugs are used for relapsed/refractory ALL?
Blinatumomab | Tisagenlecleucel
77
What is blinatumomab?
Bispecific CD19 deirected T cell engager
78
What are supportive therapies for ALL?
CSF Infxn prophylaxis Constipation prophylaxis for vincristine regimens Corticosteroid AEs
79
What are causes for CML?
Ionizing radiation, occupational exposure to benzene | Increased incidence in atomic bomb survivors
80
What is the genetic cause of CML?
Translocation of the chromosome 22 (BCR) fused with chromosome 9 (ABL), resulting in philidelphia chromosome
81
What does the BCR-ABL gene cause?
Increased tyrosine kinase activity which results in uncontrolled cellular division, proliferation, and inhibition of apoptosis causing an increase in the abnormal clone
82
When can the philadelphia chromosome be present?
ALL Some AML CML
83
What are the 3 phases of CML?
Chronic (stable) Accelerated Blast crisis
84
What is the chronic phase of CML?
Usual phase for diagnosis Disease managed with tx < 10% blasts in peripheral blood or bone marrow
85
What is accelerated phase of CML?
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
What is the blast crisis phase of CML?
> 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
What are the goals of CML management?
To induce hematologic, cytogenic, moleculare response/remission, delay progression to accelerated phase or blast crisis
88
What is the only curative option for CML?
SCT
89
What is a hematologic response?
Normalization of peripheral blood counts
90
What is a cytogenetic response?
Percentage of Ph+ cells in a bone marrow biopsy
91
Which type of response is the gold standard for CML?
Cytogenetic response
92
What is a molecular response?
Based on quantificaiton of BCR-ABL mRNA transcripts | From peripheral blood
93
What is the primary treatment of CML?
TKIs Imatinib Dasatinib Nilotinib
94
At what months do we follow up after primary treatment of CML?
3, 6, 12, 18
95
What are we evaluating at the follow ups for CML?
Evaluate compliance/DDI | Mutation analysis
96
What are the options after evaluation at follow up?
Increase TKI dose | Change TKI
97
Which TKI do we administer with food?
Imatinib
98
Which TKI do we avoid food with?
Nilotinib
99
Which TKI does food not affect?
Dasatinib
100
What are AEs of Imatinib?
``` Edema Fluid retention Cardiomyopathy (pleural /pericardial effusion, ascites) Rash Myalgia GI upset ```
101
What are the AEs of Dasatinib?
``` Pleural/pericardial effusion Edema Rash GI upset QT prolongation ```
102
What are the AEs of nilotinib?
``` QT prolongation** Electrolyte abnormalities LFT alterations Rash Myalgia ```
103
What are the DDIs for Imatinib?
3A4 substrate and inhibitor
104
What are the DDIs for Dasatainib?
3A4 substrate | H2RA and PPIs
105
What are the DDIs of Nilotinib?
3A4 substrate and inhibitor H2RA and PPI Avoid QT prolonging drugs
106
What are the supportive care treatments for leukocytosis?
Hydroxyurea Apheresis TKIs
107
What are the supportive care treatments for thrombocytosis?
Hydroxyurea Apheresis Anagrelide
108
What is the most common form of leukemia?
CLL
109
What cells have mutations for CLL?
B cell T cell NK cell
110
What is the pathophysiology of CLL?
Proliferation of CD5+ B-lymphocytes - accumulation of nonfunctional small lymphocytes in the lymph nodes, spleen, blood, liver, bone marrow, and other organs
111
What are the s/sx of CLL?
Asx at presentation Fever, malaise, and fatigue Elevated WBC, small lymphocytes, lymphadenopathy, hepatomegaly, splenomegaly Chronic infections
112
What is the main diagnosis of CLL?
> 5 x 10^9 / L B lymphocytes in the pheripheral blood for minimum of 3 months
113
What are the characteristics of a 0 Rai stage?
Lymphocytosis alone (in peripheral and bone marrow)
114
What are the characteristics of a I-II Rai stage?
Lymphocytosis +/- lymphadenopathy, splenomegaly, hepatomegaly
115
What are the characteristics of a III-IV Rai stage?
Lymphocytosis +/- lymphadenopathy +/- organ enlargement +/- hgb < 11 +/- plt < 100K
116
What is the Richter's syndrome?
Transformation of CLL to an aggressive diffuse large B-Cell non-hodgkin's lymphoma
117
What are unfavorable prognostic factors for CLL?
ZAP-70 CD38 Complex cytogenetic abnormalities
118
Is CLL curable?
No
119
What are the goals of CLL therapy?
Improve QOL and duration, slow CLL cell growth, provide long remissions
120
What are treatment options for CLL?
Watch and wait | Chemotherapy dependent on age/genetics
121
If a patient is < 65 yo with no genetic abnormalities and CLL, what are their chemo options?
Fludarabine, Cyclophosphamide and Rituximab Fludarabine and Rituximab Bendamustine +/- Rituximab Ibrutinib

Heme/Onc (20 decks)

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