French SUBGROUP - American - British (FAB) classification AML Flashcards

(56 cards)

1
Q

M0

A

AML, Minimally Differentiated

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2
Q

● Blasts having CD13, CD33, CD34 and CD117
● No Evidence of Cellular Maturation of Blasts

A

M0 (AML, Minimally Differentiated)

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3
Q

● Auer Rods (-), Myeloperoxidase (-), Sudan Black B (-)
● Less than 5% of All AML

A

M0 (AML, Minimally Differentiated)

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4
Q

Patients are usually infants or older adults

A

M0 (AML, Minimally Differentiated)

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5
Q

M1

A

(AML, Without Maturation)

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6
Q

● Blasts having CD13, CD33, CD34 and CD117 similar with those of M0
● 90% of Cells in BM are BLASTS
● Found in All Age Groups with Highest Incidence in Adults

A

M1 (AML, Without Maturation)

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7
Q

● Has No Male or Female Predominance

A

M1

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8
Q

● Nuclear:Cytoplasmic Maturational Asynchrony
β—‹ Morphologically - Nucleus appears more immature than Cytoplasm
β—‹ Functionally - Leukemic Blasts exhibits Phagocytosis w/c is a property only of a Mature WBC

A

M1 (AML, Without Maturation)

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9
Q

● Auer Rods (+), Myeloperoxidase (+), Sudan Black B (+)
● Chloroacetate Esterase (+), Acetate Esterase (-)

A

M1 (AML, Without Maturation)

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10
Q

● Greater than 20% Type I and II Blasts in Bone Marrow
β—‹ At least 10% Granulocyte @ Various Stages of Maturation

● Distinguished from M1 by Presence of Granulocytic Cells At or Beyond the Promyelocytic Stage of Maturation

A

M2 (AML, With Maturation)

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11
Q

● CharacteristicGINGIVALBLEEDING
● Pseudo-Pelger-Huet (+) - Rod-Shaped or Dumbbell-Shaped or Nonsegmented Nuclei

A

M2 (AML, With Maturation)

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12
Q

● Hypogranular Neutrophils (+) - Leads to Deficient Phagocytosis,
Deficient Microbial Killing and Deficient Chemotaxis

A

M2 (AML, With Maturation)

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13
Q

● Auer Rods (+), MPO (+) and SBB (+)
● Aspects of Dysplasia are present

A

M2 (AML, With Maturation)

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14
Q

● AKA Hypergranular Promyelocytic Leukemia
● Found in all age groups similar to M1 and M2
● Greater Predilection for Males
● Frequently more associated with DIC

A

M3 (Acute Promyelocytic Leukemia)

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15
Q

● Abnormal Promyelocytes with Heavy Granulation
● Presents with Leukopenia
● Auer Rods (+) and Intensely Positive for MPO and SBB
● Faggot Cells (+)
● Reniform or Bilobed Nuclei

A

M3 (Acute Promyelocytic Leukemia)

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16
Q

M3

A

(Acute Promyelocytic Leukemia)

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17
Q

(Acute Promyelocytic Leukemia)

A

M3

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18
Q

Subunit of M3

A

M3m (Microgranular Promyelocytic Leukemia)

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19
Q

● numerous granules present but can only be detected by electron microscopy hence the term β€œMICROGRANULAR”
● Has Worse Prognosis than M3 due to Initial High Blast Counts

A

M3m (Microgranular Promyelocytic Leukemia)

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20
Q

Caused by a Chromosomal Translocation t(15;17)

A

M3m (Microgranular Promyelocytic Leukemia)

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21
Q

M4

A

(Acute Myelomonocytic Leukemia)

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22
Q

● AKA Naegeli Monocytic Leukemia
● Positive for Myeloid Antigens - CD13 and CD33
● Positive for Monocytic Antigens - CD4, 11b, 11c, 14, 36, 64

A

M4 (Acute Myelomonocytic Leukemia)

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23
Q

● Auer Rods (+), MPO (+), SBB (+), Specific and Non-Specific Esterases (+)

● Lysozyme - Muramidase > Contained in Larger Amounts in Monocytes > Excreted in Large Amounts in Urine when there is M4 Leukemia

A

M4 (Acute Myelomonocytic Leukemia)

24
Q

β—‹ Serum or Urine Lysozyme = Diagnostically Important forβ€”β€”- Leukemia
β—‹ 3x the Upper Limit is Significant
● Caused by a Problem in Chromosome 16

A

M4 (Acute Myelomonocytic Leukemia)

25
M4 (Acute Myelomonocytic Leukemia) sub unit?
M4eo (Acute Myelomonocytic Leukemia w/ Eosinophilia)
26
● IncreasedMarrowEosinophils ● Cells exhibit Large Basophilic Granules mixed with Smaller Eosinophilic Granules
M4eo (Acute Myelomonocytic Leukemia w/ Eosinophilia)
27
●Uniquely exhibits Distinct Chloroacetate Esterase and PAS (+) which differentiates it from normal eosinophil
M4eo (acute myelomonocytic leukemia with eosinophilia )
28
M5
Acute Monocytic Leukemia
29
M5 Acute Monocytic Leukemia sub unit
M5a (Acute Monocytic Leukemia, Poorly Differentiated) M5b (Acute Monocytic Leukemia, Well Differentiated)
30
● AKASchillingLeukemia ● Presents w/ Highest Incidence of Organomegaly and Organ Involvement of all AMLs ● Greater than 80% of Marrow Cells are Monoblasts, Promonocytes or Monocytes
M5 (Acute Monocytic Leukemia)
31
● Auer Rods (+), MPO (-), SBB (-), Specific Esterase (-) ● Associated with problems in Chromosome 11, t(9;11) ● Divided into M5a (Poorly Differentiated) and M5b (Well Differentiated)
M5 (Acute Monocytic Leukemia)
32
M5a
Acute Monocytic Leukemia, Poorly Differentiated
33
● Characterized by Large Blast Cells with Delicate, Lacy Chromatin in both blood and bone marrow β—‹ 1-3 Large, Prominent Vesicular Nucleoli are present β—‹ Voluminous Cytoplasm with 1 or More Pseudopods
M5a (Acute Monocytic Leukemia, Poorly Differentiated)
34
More than 80% of Monocytic Compartment Predominance are Blasts
M5a (Acute Monocytic Leukemia, Poorly Differentiated)
35
M5b Acute Monocytic Leukemia, Well Differentiated
● Characterized by Presence of ALL STAGES OF MONOCYTE DEVELOPMENT (Monoblasts, Promonocytes and Monocytes) ● Predominant Cell in BM Promonocyte
36
● Associated with DIFFUSE ERYTHEMATOUS SKIN RASH (differentiates it from M5a clinically)
M5b Acute Monocytic Leukemia, Well Differentiated
37
M6
(Acute Erythroleukemia)
38
● DiGuglielmo’s syndrome ● Variable WBC Count and Pancytopenia occurs ● Presence of Numerous Nucleated RBCs
M6 (Acute Erythroleukemia)
39
-Mixed Populations of Hypochromic and Normochromic RBCs -Leukemia frequently progresses to M1, M2 or M4 Leukemia M6 -Erythroblasts = Alpha-Naphthyl Acetate Esterase (+)
M6 (Acute Erythroleukemia)
40
Auer Rods (+) Defect in Chromosome 5 and 7
M6 (Acute Erythroleukemia)
41
M7
(Acute Megakaryocytic Leukemia)
42
Distinct Feature of M7
Myelosclerosis
43
Previously Classified as Undifferentiated Leukemia since MPO (-), SBB (-) and Esterase (-)
M7 (Acute Megakaryocytic Leukemia)
44
Alpha-Naphthyl Acetate Esterase (+), Alpha-Naphthyl Butyrate Esterase (-) - Unique Cytochemistry for Megakaryoblasts
M7 (Acute Megakaryocytic Leukemia)
45
● PAS (+) ● CD41, CD42b and CD61 ● Defect in Chromosome 21
M7 (Acute Megakaryocytic Leukemia)
46
Treatment for AML
● Chemotherapy ● Radiation Therapy ● Immunotherapy
47
Chronic granulocytic leukemia
Chronic myelogenous leukemia
48
An MPN that originates in the abnormal pluripotent bone marrow stem cell and is consistently associated with the BCR-ABL(1) fusion gene located in the Philadelphia chromosome
Chronic myelogenous leukemia CML
49
Chronic myelogenous leukemia (CML) findings
Increase WBC PMNs MATURE WBC
50
Chromosome 9 and 22 translocation
Philadelphia chromosome ( CML)
51
Translocation of c-abl, from chromosome 9 to location of bcr on chromosome 22 to form fusion gene bcr-abl
active tyrosine kinase
52
β€’ Splenomegaly β€’ Constitutional symptoms - fatigue, malaise, LG fever, weight loss, excess sweating β€’ Anemia β€’ Bleeding β€’ pruritis
CML: Chronic myelogenous leukemia
53
β€’ Investigation - leukopenia - basophila - low RBC ct. β€’ Diagnosis - evidence of BCR-ABL fusion product or presence of Philadelphia chromosome
CML: Chronic myelogenous leukemia
54
-excessive leukocytic response in the peripheral blood -a result of severe infection, inflammation, metabolic disease or malignancy
Leukemoid reaction
55
-used to distinguish LR (leukemoid revtion) from CML -Uses KAPLOW’s METHOD
Leukocyte (neutrophil) Alkaline Phosphatase(LAP) test
56
Normal Kaplow’s score
❖20 – 100