French SUBGROUP - American - British (FAB) classification AML Flashcards
M0
AML, Minimally Differentiated
β Blasts having CD13, CD33, CD34 and CD117
β No Evidence of Cellular Maturation of Blasts
M0 (AML, Minimally Differentiated)
β Auer Rods (-), Myeloperoxidase (-), Sudan Black B (-)
β Less than 5% of All AML
M0 (AML, Minimally Differentiated)
Patients are usually infants or older adults
M0 (AML, Minimally Differentiated)
M1
(AML, Without Maturation)
β Blasts having CD13, CD33, CD34 and CD117 similar with those of M0
β 90% of Cells in BM are BLASTS
β Found in All Age Groups with Highest Incidence in Adults
M1 (AML, Without Maturation)
β Has No Male or Female Predominance
M1
β 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
M1 (AML, Without Maturation)
β Auer Rods (+), Myeloperoxidase (+), Sudan Black B (+)
β Chloroacetate Esterase (+), Acetate Esterase (-)
M1 (AML, Without Maturation)
β Greater than 20% Type I and II Blasts in Bone Marrow
β At least 10% Granulocyte @ Various Stages of Maturation
β Distinguished from M1 by Presence of Granulocytic Cells At or Beyond the Promyelocytic Stage of Maturation
M2 (AML, With Maturation)
β CharacteristicGINGIVALBLEEDING
β Pseudo-Pelger-Huet (+) - Rod-Shaped or Dumbbell-Shaped or Nonsegmented Nuclei
M2 (AML, With Maturation)
β Hypogranular Neutrophils (+) - Leads to Deficient Phagocytosis,
Deficient Microbial Killing and Deficient Chemotaxis
M2 (AML, With Maturation)
β Auer Rods (+), MPO (+) and SBB (+)
β Aspects of Dysplasia are present
M2 (AML, With Maturation)
β AKA Hypergranular Promyelocytic Leukemia
β Found in all age groups similar to M1 and M2
β Greater Predilection for Males
β Frequently more associated with DIC
M3 (Acute Promyelocytic Leukemia)
β Abnormal Promyelocytes with Heavy Granulation
β Presents with Leukopenia
β Auer Rods (+) and Intensely Positive for MPO and SBB
β Faggot Cells (+)
β Reniform or Bilobed Nuclei
M3 (Acute Promyelocytic Leukemia)
M3
(Acute Promyelocytic Leukemia)
(Acute Promyelocytic Leukemia)
M3
Subunit of M3
M3m (Microgranular Promyelocytic Leukemia)
β numerous granules present but can only be detected by electron microscopy hence the term βMICROGRANULARβ
β Has Worse Prognosis than M3 due to Initial High Blast Counts
M3m (Microgranular Promyelocytic Leukemia)
Caused by a Chromosomal Translocation t(15;17)
M3m (Microgranular Promyelocytic Leukemia)
M4
(Acute Myelomonocytic Leukemia)
β AKA Naegeli Monocytic Leukemia
β Positive for Myeloid Antigens - CD13 and CD33
β Positive for Monocytic Antigens - CD4, 11b, 11c, 14, 36, 64
M4 (Acute Myelomonocytic Leukemia)
β Auer Rods (+), MPO (+), SBB (+), Specific and Non-Specific Esterases (+)
β Lysozyme - Muramidase > Contained in Larger Amounts in Monocytes > Excreted in Large Amounts in Urine when there is M4 Leukemia
M4 (Acute Myelomonocytic Leukemia)
β Serum or Urine Lysozyme = Diagnostically Important forββ- Leukemia
β 3x the Upper Limit is Significant
β Caused by a Problem in Chromosome 16
M4 (Acute Myelomonocytic Leukemia)
M4 (Acute Myelomonocytic Leukemia) sub unit?
M4eo (Acute Myelomonocytic Leukemia w/ Eosinophilia)
β IncreasedMarrowEosinophils
β Cells exhibit Large Basophilic Granules mixed with Smaller Eosinophilic Granules
M4eo (Acute Myelomonocytic Leukemia w/ Eosinophilia)
βUniquely exhibits Distinct Chloroacetate Esterase and
PAS (+) which differentiates it from normal eosinophil
M4eo (acute myelomonocytic leukemia with eosinophilia )
M5
Acute Monocytic Leukemia
M5 Acute Monocytic Leukemia sub unit
M5a (Acute Monocytic Leukemia, Poorly Differentiated)
M5b (Acute Monocytic Leukemia, Well Differentiated)
β AKASchillingLeukemia
β Presents w/ Highest Incidence of Organomegaly and Organ
Involvement of all AMLs
β Greater than 80% of Marrow Cells are Monoblasts, Promonocytes or Monocytes
M5 (Acute Monocytic Leukemia)
β Auer Rods (+), MPO (-), SBB (-), Specific Esterase (-)
β Associated with problems in Chromosome 11, t(9;11)
β Divided into M5a (Poorly Differentiated) and M5b
(Well Differentiated)
M5 (Acute Monocytic Leukemia)
M5a
Acute Monocytic Leukemia, Poorly Differentiated
β 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)
More than 80% of Monocytic Compartment Predominance are Blasts
M5a
(Acute Monocytic Leukemia, Poorly Differentiated)
M5b Acute Monocytic Leukemia, Well Differentiated
β Characterized by Presence of ALL STAGES OF MONOCYTE DEVELOPMENT (Monoblasts, Promonocytes and Monocytes)
β Predominant Cell in BM Promonocyte
β Associated with DIFFUSE ERYTHEMATOUS SKIN RASH (differentiates it from M5a clinically)
M5b Acute Monocytic Leukemia, Well Differentiated
M6
(Acute Erythroleukemia)
β DiGuglielmoβs syndrome
β Variable WBC Count and Pancytopenia occurs
β Presence of Numerous Nucleated RBCs
M6 (Acute Erythroleukemia)
-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)
Auer Rods (+)
Defect in Chromosome 5 and 7
M6 (Acute Erythroleukemia)
M7
(Acute Megakaryocytic Leukemia)
Distinct Feature of M7
Myelosclerosis
Previously Classified as Undifferentiated Leukemia since
MPO (-), SBB (-) and Esterase (-)
M7 (Acute Megakaryocytic Leukemia)
Alpha-Naphthyl Acetate Esterase (+),
Alpha-Naphthyl Butyrate Esterase (-)
- Unique Cytochemistry for Megakaryoblasts
M7 (Acute Megakaryocytic Leukemia)
β PAS (+)
β CD41, CD42b and CD61
β Defect in Chromosome 21
M7 (Acute Megakaryocytic Leukemia)
Treatment for AML
β Chemotherapy
β Radiation Therapy
β Immunotherapy
Chronic granulocytic leukemia
Chronic myelogenous leukemia
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
Chronic myelogenous leukemia (CML) findings
Increase WBC
PMNs
MATURE WBC
Chromosome 9 and 22
translocation
Philadelphia chromosome ( CML)
Translocation of c-abl, from chromosome 9 to location of bcr on chromosome 22 to form fusion gene bcr-abl
active tyrosine kinase
β’ Splenomegaly
β’ Constitutional symptoms
- fatigue, malaise, LG fever, weight loss, excess sweating
β’ Anemia
β’ Bleeding
β’ pruritis
CML: Chronic myelogenous leukemia
β’ Investigation
- leukopenia
- basophila
- low RBC ct.
β’ Diagnosis
- evidence of BCR-ABL fusion product or presence of Philadelphia chromosome
CML: Chronic myelogenous leukemia
-excessive leukocytic response in the peripheral blood
-a result of severe infection, inflammation, metabolic disease or malignancy
Leukemoid reaction
-used to distinguish LR (leukemoid revtion) from CML
-Uses KAPLOWβs METHOD
Leukocyte (neutrophil) Alkaline Phosphatase(LAP) test
Normal Kaplowβs score
β20 β 100