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Leukemia Flashcards

1
Q

How is AML diagnosed?

A

Bone marrow biopsy

20% myeloid blasts in either peripheral blood or bone marrow
OR
Cytogenic abnormalities regardless of blast count

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2
Q

What can cause therapy related AML (much worse outcomes)?

A
  • Anthracyclines
  • Alkylators
  • Topoisomerase inhibitors
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3
Q

What are S/S of AML?

A
  • Anemia
  • Thrombocytopenia
  • Neutropenia
  • TLS
  • CNS involvement (rare)
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4
Q

T/F: AML patients presenting with hyperleukocytosis generally have better outcomes

A

FALSE
Poor prognosis, high risk of CNS involvement and TLS

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5
Q

What is hyper-viscosity syndrome?

A

“Blood sludging” caused by hyperleukocytosis
Complications: stroke, respiratory failure, eye problems, renal failure

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6
Q

What does hydroxyurea do in hyperleukocytosis?

A

Gets blood counts under control so chemotherapy can be started
(Ribonucleotide reductase inhibitor)

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7
Q

What are common side effects of hydroxyurea?

A
  • N/V
  • Mouth sores
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8
Q

Which patients need stem cell transplant in AML?

A

Intermediate and poor risk patients

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9
Q

Which patients are candidates for high-intensity chemotherapy for AML?

A
  • Most patients <60
  • Patients >60 without significant comorbidities or organ dysfunction
  • Aggressive disease course
  • Candidates for allogenic stem cell transplant
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10
Q

What is 7+3 induction therapy for AML?

A

Cytarabine 100mg/m^2 IV QD x7 days

Daunorubicin 60mg/m^2 QD x3 days
OR
Idarubicin 12mg/m^2 QD x3 days

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11
Q

Which drug is the standard of care for ITD patients (with 7+3)?

A

Quizartinib (watch out with -azole antifungal drug interactions)

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12
Q

Which drug can be used as add-on to 7+3 for TKD patients?

A

Midostaurin

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13
Q

Which add-on drug has evidence in favorable risk patients?

A

Gemtuzumab + Ozogamicin (GO)

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14
Q

Which drug has good evidence for SECONDARY leukemias?

A

Vyxeos

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15
Q

What is Vyxeos?

A

Liposomal Daunorubicin + Cytarabine
1:5 optimal ratio to stay in the marrow longer and have more potent effects

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16
Q

What is criteria for CR?

A

On day 28+
- <5% blasts
- ANC >1000/mcL
- Platelets >100k/mcL

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17
Q

What is the post-induction treatment that is ONLY given to CR patients?

A

High dose cytarabine (HiDAC)
1.5-3g/m^2 IV BID x6 doses every 28 days for 3-4 cycles

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18
Q

If you receive GO in induction, when is it given again?

A

ONLY cycles 1 + 2 of post-remission therapy if they received GO in induction

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19
Q

What additional drug should be given with post-remission therapy for FLT3+ patients?

A

Midostaurin

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20
Q

What MUST be given with post-remission therapy due to its high intensity?

A

Growth-factor support

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21
Q

What do we give to patients who ARE NOT candidates for aggressive induction chemotherapy?

A

HMA + Venetoclax
Low-dose cytarabine + Venetoclax
Ivosidenib + Venetoclax
LDAC + Gladegib

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22
Q

What are the hypomethylating agents (HMAs)?

A

Decitabine
Azacitidine

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23
Q

What is the standard of care for low-intensity chemotherapy?

A

Azacitidine + Venetoclax

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24
Q

Which mutation must be present to consider ivosidenib + venetoclax in low-dose chemotherapy?

25
What must be considered when giving venetoclax?
DDIs with -azole antifungals, CYP drugs
26
What is the second line therapy given to those with refractory disease?
Azacitidine + Venetoclax (if not given venetoclax upfront)
27
What are ADEs of quizartinib, especially with DDIs?
QTc prolongation Cardiotoxicity
28
T/F: Midostaurin is pretty well tolerated
FALSE: many patients throw up their doses
29
Which drug is approved for FLT3 refractory disease but is BETTER TOLERATED than both quizartinib and midostaurin?
Gilteritinib
30
Which IDH inhibitors have FDA approved indications?
Ivosidenib (new or refractory disease) Enasidenib (refractory disease)
31
What are the major ADEs of anthracyclines?
- Myelosuppression - Cardiac toxicity Reason why there is a lifetime maximum dose
32
What are the major ADEs of cytarabine?
- Neurotoxicity (neuro checks required before each dose) - Conjunctivitis (dexamethasone eye drops should be given x3 days after HiDAC)
33
What do we do to prevent infusion-related reactions with GO treatment?
Premedication with - APAP, Benadryl, methylprednisolone
34
What is the BBW on GO?
Hepatotoxicity, including fatal veno-occlusive disease (VOD)
35
What are the major side effects of low-intensity chemo (azacitidine + venetoclax)?
Extreme constipation (standing bowel medications should be given) Low-moderate emetogenicity (premedicate with ondansetron)
36
What are S/S of CML?
- Most are symptomatic - Maybe abdominal pain from splenomegaly - Leukocytosis
37
What is the major risk factor for CML?
Ionizing radiation
38
Which lab finding is the hallmark sign of CML?
Ph+ chromosome (Philadelphia chromosome)
39
What do we look for on labs in CML?
- Leukocytosis (WBC >25) - Thrombocytosis - Hypercellular on bone marrow biopsy - Ph+ chromosome
40
What characterizes chronic phase of CML?
- <10% blasts - <20% peripheral blood basophils
41
What characterizes blast phase of CML?
>20% blasts in peripheral or bone marrow
42
What comes in between chronic and blast phases of CML?
Accelerated phase
43
Why was ponatinib only really used before asciminib was introduced?
T315I mutation (resistance mechanism)
44
What are mechanisms of resistance to TKI drugs?
- OCT1 transporter - P-gp efflux - Point mutations in ABL kinase domain (e.g. T315I)
45
Which ADE is common in Imatinib and Dasatinib?
Edema (PDGFR-related) Imatinib (peripheral) Dasatinib (pleural)
46
What is the BBW on nilotinib?
QTc prolongation
47
Which TKI drugs need to be taken on an empty stomach?
Nilotinib and Asciminib
48
Which 3rd generation TKI is grouped with Dasatinib and Nilotinib due to its disappointing performance?
Bosutinib
49
What is the main side effect of Bosutinib?
Diarrhea
50
What is the most tolerated TKI which ends up being first line unless a pleural effusion is developed?
Dasatinib
51
Which TKI should not be used for intermediate-high risk patients?
Imatinib
52
What should be done if a patient has BCR-ABL1 >10% after 6 months of therapy?
Switch to an alternate TKI
53
Which drugs can be used for the T315I mutation?
Asciminib, Ponatinib, Allo HCT, Clinical trial drugs
54
What are the ADEs possible with Ponatinib?
- Heart attack - Stroke BBW: Vascular occlusion, heart failure, hepatotoxicity
55
What is the most important factor for TKI failure and relapse?
Poor adherence
56
What stomach environment is needed for dasatinib?
Acidic - NO PPIS OR H2 BLOCKERS
57
T/F: There is criteria that lets people discontinue TKIs if met
TRUE
58
How is the blast phase of CML treated?
Basically AML chemotherapy + TKI followed by stem cell transplant
59
T/F: Lower doses of TKIs should be used in the accelerated phase of CML
FALSE

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