Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Crit Care, Oncology & Hematology > Myeloid Leukemia > Flashcards

Myeloid Leukemia Flashcards

(50 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is used to diagnose leukemia?

A

Bone marrow aspirate & biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What age range is most common for AML?

A

≥65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are risk factors for AML?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Anemia
Thrombocytopenia
Neutropenia
TLS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What % blasts isolated in bone marrow autopsy indicates AML?

A

≥ 20% blasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What treatments could be used in refractory/relapse AML?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
A

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

25
Anthracyclines (used in AML) have what TWO major AEs?
Cardia toxicity Myelosuppression
26
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?
NEUROTOXICITY - must conduct “neuro checks”, observe motor skills CONJUCTIVITIS - treat w dexamethasone eye drops qty during and 3 days after
27
Gemtuzumab Ozogamicin has what AE that needs to be pretreated? What is its BBW?
AE: infusion related reactions - pretreat w APAP, Benadryl, Methylprednisolone **BBW: hepatotoxicity** including venous-occlusion
28
What are TWO AEs with low-intensity chemo in AML? Which needs to be premedicated?
Severe constipation (have standing bowel regimen meds ordered) Emetogenic (premedicate w/ ondansetron)
29
What is a major AE of venetoclax?
Significant myelosuppression
30
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?
Be cautious of POTENTIATING leukemia cells! AE: bone pain (bc GROWTH factor), use loratidine or hydroxyzine for management
31
In CML, translocation occurs between the ____ gene and ____ gene, causing a _______ ___________. The gene thus is eternally active, synthesizing more WBCs.
Translocation at BCR and ABL genes Creates Philadelphia chromosome
32
What does CML presentation look like?
MOSTLY ASYMPTOMATIC **Splenomegaly** (>50%) Anorexia, bone pain, fatigue
33
What are 3 key lab findings for diagnosis of CML?
Leukocytosis [WBC > 25 x 10^9/L] Thrombocytosis (+) Ph chromosome
34
What are the three phases of CML progression? What do we aim for?
Chronic, Accelerated, Blast phases Aim: chronic
35
What is the class of drug that controls chronic phase CML? Why are they so good?
Tyrosine Kinase Inhibitors (TKI) Oral tablet, specific cytogenetics targets
36
What are the available TKIs for CML?
1st gen: Imatinib 2nd gen: Dasatinib, Nilotinib 3rd gen: Bosutinib, *Ponatinib (for T31 mutation only)*
37
What mutation in CML is considered the most resistant, with poorer survival and increased disease progression?
T31-5I
38
What is a boxed warning on 2nd gen TKI Nilotinib?
QTc prolongation
39
What are the FDA approved indications of 3rd gen TKI Bosutinib?
Approved for: - new CML - Advanced disease with resistance/intolerance to other TKIs
40
If a CML patient has a LOW RISK score, what are first line therapies?
Any generation TKI
41
If a CML patient has a INTERMEDIATE/HIGH RISK score, what are first line therapies?
2nd or 3rd gen TKIs
42
What are 3rd line therapies for CML after 1st/2nd gen TKIs/Bosutinib?
Ponatinib - usually reserved for T315I mutation Aciminib - STAMP inhibitor, effective against T315I Omacetaxine mepesuccinate (off-market)
43
What are some BBWs for 3rd gen TKI Ponatinib? (3)
Vascular occlusion, HF, hepatotoxicity
44
What is the FDA indication for Asciminib?
STAMP inhibitor Approved for previously received 2+ TKIs or with T315I mutation
45
What are the most common AEs of each TKI?
Imagining = Edema/fluid retention Dasutinib = pleural effusions Nilotinib = QTc prolongation and CVD Bosutinib = GI effects
46
What are common side effects with Ponatinib (3rd get TKI)?
Elevated pancreatic enzymes HTN Skin toxicity Thrombotic events
47
What needs to be monitored periodically while using 2nd gen TKI Nilotinib?
Lipid profile
48
Which CML drugs should be taken on an empty stomach? Which requires an acidic environment (no H2RAs or PPIs)?
Empty stomach = Nilotinib, asciminib Need acidic environment = Dasatinib
49
What drugs are recommended for treatment of ACCELERATED phase CML?
2nd gen TKIs Consider allogenic transplant
50
What drugs are recommended for treatment of BLAST phase CML?
TKI + induction therapy or low intensity chemo (basically AML + CML treatment)

Crit Care, Oncology & Hematology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions