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Hematology > Hematology Week 2: Acute Myeloid Leukemia > Flashcards

Hematology Week 2: Acute Myeloid Leukemia Flashcards

1
Q

Myeloid vs Lymphoid lineages

A
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2
Q

AML cell

A

myeloblast

blast of the myeloid lineage

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3
Q

Myeloblast threshold for AML

A

>or=20% of the total nucleated cells in the blood or BM

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4
Q

AML Smear

A

Can see Auer rod which tells us myeloid lineage and are neoplastic

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5
Q

AML Key Diagnostic Findings

4 listed

A
  • Auer rod
  • MPO+
  • CD33+
  • CD34+
  • Blasts >=20%
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6
Q

AML BM Aspirate Morphology

A

Hypocellular BM taken over by sheets of blasts

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7
Q

Typical CBC findings and Differential in AML

A

Decreased Reflecting reduced BM production

  • RBCs
  • Platelets
  • Neutrophils

Can have high/low WBC counts

  • key is that blasts are >20%
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8
Q

Most Common Leukemia in Adults

A

AML

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9
Q

AML Survival Curve

A
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10
Q

Subtypes of AML

3 listed

A

Need BM biopsy to determine subtype

  • Low risk
  • Intermediate risk
  • High Risk
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11
Q

AML Risk Assesment tool

A
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12
Q

Low-Risk AML Genetic Findings

3 listed

A
  • t(15;17) PML-RARA fusion
  • t(8;21) RUNX1-RUNX1T1 fusion
  • t(16;16) or inv(16) CBFB-MYH11 fusion
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13
Q

Intermediate Risk AML Genetic Findings

A

Normal Karyotype

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14
Q

High-Risk AML Genetic Findings

3 listed

A
  • Complex Karyotype (>=3 abnormalities)
  • Monosomy for chromosome 7

or

  • 7q deletion
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15
Q

Treatment of AML

A
  • Induction Chemotherapy = 7+3
  • Consolidation Chemotherapy
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16
Q

AML left untreated is?

A

Universally fatal

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17
Q

7+3 Induction Chemotherapy

6 listed

A
  • 7 days Cytarabine + 3 days Anthracycline
  • Extremely toxic therapy
  • 7 days of chemo resulting in severe bone marrow suppression that may last several weeks
  • Called induction chemotherapy to try to induce remission
  • High risk of infection and bleeding during this time
  • May not be tolerated by elderly or patients with comorbidity
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18
Q

Consolidation Chemotherapy

2 listed

A
  • High Dose Cytarabine
  • Given 3-4 times after remission is achieved to consolidate that remission
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19
Q

Anthracycline key Toxicity

A

Cardiac Failure

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20
Q

Cytarabine Key Toxicities

A

Cerebellar Toxicity

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21
Q

Anything that ends in Rubicin is an?

A

Anthracycline

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22
Q

Doxorubicin AKA

A

Adriamycin

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23
Q

Doxorubicin MOA & Metabolism & Elimination

3 listed

A
  • Binds directly to DNA and intercalates interfering with DNA repair, transcription and replication which induces apoptosis
  • Widely distributed except in CNS
  • Metabolized in the liver and eliminated in the bile
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24
Q

Doxorubicin Classic Toxicity

A
  • Cardiotoxicity
  • (Tachycardia, arrhythmia, refractory CHF)
  • results from free-radical damage due to the low levels of free radical buffers in cardiac tissue
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25
Q

HSCT for AML?

2 listed

A
  • For high-Risk Subgroups in first remission or any patient in relapse
  • patient must have minimal or no disease before transplant
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26
Q

Treatment for patients >60 in AML

A

>60 unfit for high-dose therapy

so

use low-intensity therapy

  • 5-Azacytidine or decitabine (hypomethylating agents)
  • May require 3-4 cycles to see the response
  • may increase survival - effective but less toxic

Best supportive care

  • Transfusions
  • Antibiotics
27
Q

AMl and genetic components

A

Genetic mutations or translocations that increase cellular proliferation

+

Genetic mutations or translocations that blocks myeloid differentiation or maturation

=

AML

Both of these are needed for AML

28
Q

AML Class I Mutation description

A

A mutation that increases cellular proliferation

29
Q

AML Class I Mutation examples

A

FLT3 Mutation

30
Q

FLT3 Mutation Class?

A

Class I Mutation

31
Q

AML Class II Mutation Description

A

Alterations that impair cellular differentiation (often involve transcription factors)

32
Q

AML Class II Mutation Examples

3 listed

A
  • t(15;17) PML RARA
  • t(8;21) RUNX1-RUNX1T1
  • t(16;16) or inv(16) CBFB-MYH11
33
Q

t(15;17) PML RARA Mutation class?

A

Class II

34
Q

t(8;21) RUNX1-RUNX1T1 Mutation Class

A

Class II

35
Q

t(16;16) or inv(16) CBFB-MYH11 Mutation class

A

Class II

36
Q

AML Class III Mutation

A

Epigenetic Changes (affecting gene methylation)

37
Q

t(16;16) or inv(16) CBFB-MYH11 MOA

A

MYH11 protein binds onto CBFß-RUNX1 becomes a gene repressor

38
Q

t(8;21) RUNX1-RUNX1T1 MOA

A

RUNX1T1 binds to CBFß and RUNX1 to make it a repressor of genes necessary for genes of cellular differentiation

39
Q

Paths to AML

4 listed

A
  • Mutations over a lifetime
  • Genotoxic therapy
  • disease progression from myeloid neoplasm (e.g. MDS, MPN)
  • Inherited predisposition (e.g down syndrome)
40
Q

Midostaurin MOA

A
  • First in class multi-targeted kinase inhibitor
  • activity in FLT-3 mutated AML with significantly increased overall and event-free survival
  • Used in conjunction with standard induction chemotherapy
  • Significantly increases survival
41
Q

Pathway to AML matters

A
42
Q
A
  • Immature cells with many granules
  • multiple Auer Rods
  • Disseminated intravascular Coagulation
  • Schistocytes
    *
43
Q

M3 AKA

A

APL

44
Q

Histological findings in APL

A
  • Immature cells with many granules and multiple Auer rods
  • schistocytes on peripheral smear
  • can be in DIC
  • APL or M3 is same thing
45
Q

APL is a medical?

A

EMERGENCY typically because of the DIC

46
Q

What cell type is proliferating?

A

AML

47
Q

What cell type is proliferating?

A

CML

48
Q
A

APL

49
Q

APL AKA

A

Acute Promyelocytic Leukemia

50
Q

APL Genetics

A

t(15;17) fusion of PML-RARA

51
Q

APL Genetics testing

A

Karyotype or FISH

52
Q

APL MOA and ATRA therapy

A

kicks repressor off and overcomes blockade that was causing cells to be arrested in their development

53
Q

ATRA AKA

A

All-Trans-Retinoic-Acid

54
Q

APL Overview

A
55
Q

APL Treatment?

A

Highly curable with ATRA or arsenic trioxide and chemotherapy

56
Q

ATRA overcomes?

A

the differentiation blockade caused by (15;17)

57
Q

APL Histological features

A

BM packed with abnormal promyelocytes often with multiple Auer Rods

These are considered blast equivalents

58
Q

APL unique risk

A

Unique risk of fatal hemorrhage due to disseminated intravascular coagultion (DIC)

59
Q

Clinical aspects of APL

A
60
Q

Differentiation Syndrome?

A
61
Q

Keep in mind with APL

A
62
Q

AML Key Points

5 listed

A
63
Q

ATRA Toxicity

A

Differentiation Syndrome

Hematology (26 decks)

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