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703 > Leukemia > Flashcards

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?

A

IDH1

25
Q

What must be considered when giving venetoclax?

A

DDIs with -azole antifungals, CYP drugs

26
Q

What is the second line therapy given to those with refractory disease?

A

Azacitidine + Venetoclax (if not given venetoclax upfront)

27
Q

What are ADEs of quizartinib, especially with DDIs?

A

QTc prolongation
Cardiotoxicity

28
Q

T/F: Midostaurin is pretty well tolerated

A

FALSE: many patients throw up their doses

29
Q

Which drug is approved for FLT3 refractory disease but is BETTER TOLERATED than both quizartinib and midostaurin?

A

Gilteritinib

30
Q

Which IDH inhibitors have FDA approved indications?

A

Ivosidenib (new or refractory disease)
Enasidenib (refractory disease)

31
Q

What are the major ADEs of anthracyclines?

A
  • Myelosuppression
  • Cardiac toxicity

Reason why there is a lifetime maximum dose

32
Q

What are the major ADEs of cytarabine?

A
  • Neurotoxicity (neuro checks required before each dose)
  • Conjunctivitis (dexamethasone eye drops should be given x3 days after HiDAC)
33
Q

What do we do to prevent infusion-related reactions with GO treatment?

A

Premedication with
- APAP, Benadryl, methylprednisolone

34
Q

What is the BBW on GO?

A

Hepatotoxicity, including fatal veno-occlusive disease (VOD)

35
Q

What are the major side effects of low-intensity chemo (azacitidine + venetoclax)?

A

Extreme constipation (standing bowel medications should be given)
Low-moderate emetogenicity (premedicate with ondansetron)

36
Q

What are S/S of CML?

A
  • Most are symptomatic
  • Maybe abdominal pain from splenomegaly
  • Leukocytosis
37
Q

What is the major risk factor for CML?

A

Ionizing radiation

38
Q

Which lab finding is the hallmark sign of CML?

A

Ph+ chromosome (Philadelphia chromosome)

39
Q

What do we look for on labs in CML?

A
  • Leukocytosis (WBC >25)
  • Thrombocytosis
  • Hypercellular on bone marrow biopsy
  • Ph+ chromosome
40
Q

What characterizes chronic phase of CML?

A
  • <10% blasts
  • <20% peripheral blood basophils
41
Q

What characterizes blast phase of CML?

A

> 20% blasts in peripheral or bone marrow

42
Q

What comes in between chronic and blast phases of CML?

A

Accelerated phase

43
Q

Why was ponatinib only really used before asciminib was introduced?

A

T315I mutation (resistance mechanism)

44
Q

What are mechanisms of resistance to TKI drugs?

A
  • OCT1 transporter
  • P-gp efflux
  • Point mutations in ABL kinase domain (e.g. T315I)
45
Q

Which ADE is common in Imatinib and Dasatinib?

A

Edema (PDGFR-related)

Imatinib (peripheral)
Dasatinib (pleural)

46
Q

What is the BBW on nilotinib?

A

QTc prolongation

47
Q

Which TKI drugs need to be taken on an empty stomach?

A

Nilotinib and Asciminib

48
Q

Which 3rd generation TKI is grouped with Dasatinib and Nilotinib due to its disappointing performance?

A

Bosutinib

49
Q

What is the main side effect of Bosutinib?

A

Diarrhea

50
Q

What is the most tolerated TKI which ends up being first line unless a pleural effusion is developed?

A

Dasatinib

51
Q

Which TKI should not be used for intermediate-high risk patients?

A

Imatinib

52
Q

What should be done if a patient has BCR-ABL1 >10% after 6 months of therapy?

A

Switch to an alternate TKI

53
Q

Which drugs can be used for the T315I mutation?

A

Asciminib, Ponatinib, Allo HCT, Clinical trial drugs

54
Q

What are the ADEs possible with Ponatinib?

A
  • Heart attack
  • Stroke

BBW: Vascular occlusion, heart failure, hepatotoxicity

55
Q

What is the most important factor for TKI failure and relapse?

A

Poor adherence

56
Q

What stomach environment is needed for dasatinib?

A

Acidic - NO PPIS OR H2 BLOCKERS

57
Q

T/F: There is criteria that lets people discontinue TKIs if met

A

TRUE

58
Q

How is the blast phase of CML treated?

A

Basically AML chemotherapy + TKI followed by stem cell transplant

59
Q

T/F: Lower doses of TKIs should be used in the accelerated phase of CML

A

FALSE

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