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Crit Care, Oncology & Hematology > Myeloid Leukemia > Flashcards

Myeloid Leukemia Flashcards

1
Q

What are some differentiating factors between ACUTE and CHRONIC leukemia?

A

Acute: rapid onset, highly symptomatic, made of ONLY immature blasts!
Chronic: slow, mostly asymptomatic, mix of immature blasts and mature leukocytes

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2
Q

What is used to diagnose leukemia?

A

Bone marrow aspirate & biopsy

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3
Q

What age range is most common for AML?

A

≥65

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4
Q

What are risk factors for AML?

A

≥65
Prior chemo (secondary AML, harder to treat)
Radiation therapy
Smoking
Benzene/pesticide/petrochemical exposure

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5
Q

What are major signs/symptoms of AML? (4)

A

Anemia
Thrombocytopenia
Neutropenia
TLS

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6
Q

Hyperleukocytosis is a common AE of AML. What is a classic presentation? What drug may be used to temporarily decrease leukocyte count?

A

“Blood sludging” - SoB, stupor, vision changes, stroke, respiratory failure, renal failure, ischemia, retinal hemorrhage

Hydroxyurea used for count control, use until induction therapy can be started

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7
Q

What are some common ADEs of the drug used to treat hyperleukocytosis in AML?

A

Hydroxyurea AEs: N/V/D, TLS
Long-term toxicity = cutaneous ulcerations, mucositis, Alopecia/hyperpigmentation
use acutely for count control before induction therapy ONLY!

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8
Q

What % blasts isolated in bone marrow autopsy indicates AML?

A

≥ 20% blasts

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9
Q

What is a major prognostic marker to look for in AML?

A

Cytogenetics - predicts favorability of remission, risk of relapse, overall survival

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10
Q

What is the major cytogenetic target for AML? What are TWO mutations that could occur?

A

FMS-Like Tyrosine Kinase (FLT3)
Mutations:
- Internal Tandem Duplication (ITD) [worse prognosis]
- Tyrosine Kinase Domain (TKD) point mutations

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11
Q

Other than FLT3, what are two other molecular mutations in AML?

A

Isocitrate dehydrogenase (IDH)
DNA methyltransferase 3A (DNMT3A) [no drugs for this yet]

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12
Q

What determines if an AML patient can get aggressive induction chemo?

A

Age (<60?)
- if >60, must have NO comorbidities/end organ dysfunction
Performance status (can the walk?)

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13
Q

What is the “7+3” gold standard for induction chemo in AML?

A

Cytarabine infusion x 7 days
+
Daunorubicin/idarubicin x 3 days

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14
Q

What are additional induction therapies other than 7+3 that can be used in AML? Which one is nasty and most people throw up?

A

Quizartinib (FLT3-ITD target)
Midostaurin (FLT-TKD target) - nasty one, most pts dont tolerate
Gilteritinib (dual FLT/AXL inhibitor) approved for refractory AML
Gemtuzumab Ozogamacin (GO) [favorable/intermediate cytogenetics]
Liposomal daunorubicin + cytarabine

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15
Q

AML patients usually become “leukemia-free” by day ____ after induction therapy. Complete remission is usually around day ____.

A

Leukemia free = day 14
Complete remission = day 28

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16
Q

Once an AML pt finishes induction chem, what post-remission therapy can be used?

A

High dose cytarabine (HiDAC) x 3 doses + filgrastim
Liposomal daunorubicin + cytarabine
Use only in favorable cytogenetics and young!

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17
Q

Who should be considered for allogeneic stem cell transplant in AML?

A

Intermediate/poor cytogenetic risk
Secondary AML (after prior chemo)
Done after INDUCTION + 1 CYCLE CONSOLIDATION

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18
Q

If an AML candidate is not fit to receive induction chemo, they can trial what therapies?

A

“Low intensity chemo”
Gemtuzumab O
Target therapies (quizartinib, Midostauron, etc)

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19
Q

What are some “low intensity chemo” treatments for AML?

A

Hydromethylating agents (Decitabine/Azacitidine) + venetoclax
Low-dose cytarabine [LDAC] + venetoclax
Ivosidenib + venetoclax
(LDAC + gladegib, but glasdegib is not great)

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20
Q

What is the MOA of venetoclax (low intensity chemo adjunct)?

A

Inhibits anti-apoptotics (allows for apoptosis of cells infected with leukemia)

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21
Q

What treatments could be used in refractory/relapse AML?

A

NOT induction therapy!
HiDAC + mitoxantrone (like daunorubicin)
GO
“Low-intensity chemo” (venetoclax-based therapies)
target therapy if mutation present

22
Q

Name the 3 FLT3 mutation-targeting drugs. Which is the best tolerated? What are its FDA approved indications?

A

Quizartinib (FLT3-ITD)
Midostaurin (cannot be used in relapse AML)
Gilteritinib (FDA approved for relapse AML! BEST TOLERATED)

23
Q

Name the two IDH inhibitors (AML target therapy). Which targets IDH1 and which targets IDH2? What are its FDA approved indications?

A

Ivosidenib = IDH1 target (“I” = 1 in Roman numeral)
- FDA approved for new and refractory AML
Enasidenib = IDH2
- FDA approved for refractory only
(All end in -sidenib)

24
Q

What are some supportive care measures in AML?

A

Blood transfusions
Infection prophy while neutropenic (often febrile neutropenia)
TLS treatment allopurinol/rasburicase, hydration, etc refer to TLS)

25
Q

Anthracyclines (used in AML) have what TWO major AEs?

A

Cardia toxicity
Myelosuppression

26
Q

Cytarabine has what TWO major AEs? What is the test that must be done before each dose? What drug can treat one of the AEs?

A

NEUROTOXICITY
- must conduct “neuro checks”, observe motor skills
CONJUCTIVITIS
- treat w dexamethasone eye drops qty during and 3 days after

27
Q

Gemtuzumab Ozogamicin has what AE that needs to be pretreated? What is its BBW?

A

AE: infusion related reactions
- pretreat w APAP, Benadryl, Methylprednisolone
BBW: hepatotoxicity including venous-occlusion

28
Q

What are TWO AEs with low-intensity chemo in AML? Which needs to be premedicated?

A

Severe constipation (have standing bowel regimen meds ordered)
Emetogenic (premedicate w/ ondansetron)

29
Q

What is a major AE of venetoclax?

A

Significant myelosuppression

30
Q

Growth factors like filgrastim and sargramostim are used in AML in severe infections/neutropenia.
What should be we cautious of? What is a major AE and what can we treat it with?

A

Be cautious of POTENTIATING leukemia cells!
AE: bone pain (bc GROWTH factor), use loratidine or hydroxyzine for management

31
Q

In CML, translocation occurs between the ____ gene and ____ gene, causing a _______ ___________. The gene thus is eternally active, synthesizing more WBCs.

A

Translocation at BCR and ABL genes
Creates Philadelphia chromosome

32
Q

What does CML presentation look like?

A

MOSTLY ASYMPTOMATIC
Splenomegaly (>50%)
Anorexia, bone pain, fatigue

33
Q

What are 3 key lab findings for diagnosis of CML?

A

Leukocytosis [WBC > 25 x 10^9/L]
Thrombocytosis
(+) Ph chromosome

34
Q

What are the three phases of CML progression? What do we aim for?

A

Chronic, Accelerated, Blast phases
Aim: chronic

35
Q

What is the class of drug that controls chronic phase CML? Why are they so good?

A

Tyrosine Kinase Inhibitors (TKI)
Oral tablet, specific cytogenetics targets

36
Q

What are the available TKIs for CML?

A

1st gen: Imatinib
2nd gen: Dasatinib, Nilotinib
3rd gen: Bosutinib, Ponatinib (for T31 mutation only)

37
Q

What mutation in CML is considered the most resistant, with poorer survival and increased disease progression?

A

T31-5I

38
Q

What is a boxed warning on 2nd gen TKI Nilotinib?

A

QTc prolongation

39
Q

What are the FDA approved indications of 3rd gen TKI Bosutinib?

A

Approved for:
- new CML
- Advanced disease with resistance/intolerance to other TKIs

40
Q

If a CML patient has a LOW RISK score, what are first line therapies?

A

Any generation TKI

41
Q

If a CML patient has a INTERMEDIATE/HIGH RISK score, what are first line therapies?

A

2nd or 3rd gen TKIs

42
Q

What are 3rd line therapies for CML after 1st/2nd gen TKIs/Bosutinib?

A

Ponatinib - usually reserved for T315I mutation
Aciminib - STAMP inhibitor, effective against T315I
Omacetaxine mepesuccinate (off-market)

43
Q

What are some BBWs for 3rd gen TKI Ponatinib? (3)

A

Vascular occlusion, HF, hepatotoxicity

44
Q

What is the FDA indication for Asciminib?

A

STAMP inhibitor
Approved for previously received 2+ TKIs or with T315I mutation

45
Q

What are the most common AEs of each TKI?

A

Imagining = Edema/fluid retention
Dasutinib = pleural effusions
Nilotinib = QTc prolongation and CVD
Bosutinib = GI effects

46
Q

What are common side effects with Ponatinib (3rd get TKI)?

A

Elevated pancreatic enzymes
HTN
Skin toxicity
Thrombotic events

47
Q

What needs to be monitored periodically while using 2nd gen TKI Nilotinib?

A

Lipid profile

48
Q

Which CML drugs should be taken on an empty stomach? Which requires an acidic environment (no H2RAs or PPIs)?

A

Empty stomach = Nilotinib, asciminib
Need acidic environment = Dasatinib

49
Q

What drugs are recommended for treatment of ACCELERATED phase CML?

A

2nd gen TKIs
Consider allogenic transplant

50
Q

What drugs are recommended for treatment of BLAST phase CML?

A

TKI + induction therapy or low intensity chemo (basically AML + CML treatment)

Crit Care, Oncology & Hematology (18 decks)

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