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42 Cards in this Set

  • Front
  • Back

Where are auer rods found

Myeloid lineage

Epidemiology of acute leukemia

Presence of blasts in bone marrow and peripheral blood


Anemia caused by bleeding and replacement of marrow components with leukemic blasts

Hallmark characterizations of acute leukemia

Symptoms of short duration


Mild to severe anemia low plts


Many immature forms >20%


Elevated leukocyte

Selecting appropriate treatment of leukemia relies on

Accurate diagnosis

FAB divides acute leukemia into 2 major divisions

Acute myeloid leukemia AML


Acute lymphoblastic leukemia ALL

Acute myeloid leukemia is divided into

M0 thru M7


Nine subtypes

Acute lymphoblastic leukemia is divided into

3 categories


L1 thru L3

WHO categories emphasize

Underlying common genetic characteristics as well as clinical signs and symptoms

Most common leukemia subtype

Acute myeloid leukemia

AML is characterized by

An increase in the number of immature cells in bone and arrest in their maturation

AML M0

Minimally differentiated


Almost all blasts

AML M1

Most common leukemia in <18 mnth


Typically occurs in middle age


Majority blasts


Auer rods

AML M2

Acute myeloblastic leukemia with maturation


Blasts with maturation stages

AML M3

Promyelocytes predominant cell


DIC risk is higher

AML M4

Proliferation of granulocytes and monocytes


Early myelogenous cells are predominant but appx 20% of the cells are monocytes

AML M5


Pure monocytic leukemia


2 forms M5A and M5B


Mostly monocytic


Monoblast, promono, monocytes

AML M5A

Most common in young adults 16

AML M5B

More common in middle age

Pure monocytic anemia constitutes less than what % of leukemia

Less than 15%

AML M6

Erythroleukemia


Erythroblasts and myeloblast


and myeloblast


Poik and aniso along with immature RBC

AML M7

Acute megakaryoblastic leukemia


50% or more of the blasts are from megakaryocyte lineage

Predominant type of leukemia in children 2-10 yrs old

Acute lymphoblastic leukemia

ALL 3 categories

L1: children


L2: older children and adults


L3: patients with leukemia secondary to burkitt lymphoma

WHO classification of ALL

B cell neoplasm


T cell neoplasm

B cell neoplasm

Secrete monoclonal proteins (immunoglobulin) inappropriately causing increased blood viscosity

T cell neoplasm

More aggressive


Involveme extranodal/extramedullary sites like skin CNS

Signs and symptoms as ALL infiltrates tissue

Joint and bone pain especially in extremities

Signs symptoms of ALL

Hepatomegaly and lymphadenopathy


Extramedullary hematopoiesis

Lab data of ALL

25% have leukopenia


50%of cells are blast and the rest are mostly lymphs and smudge cells

Differentiate AML and ALL PBS

AML: adults, >20% myeloblasts, auer rods


ALL: children, >20% lymphoblasts

Cytochemistry of AML

Positive peroxidase and SBB


Negative TdT

Cytochemomistry of ALL

Negative peroxidase and SBB


Positive TdT

Almost 50% of all leukemia patients demonstrate

Some form of chromosomal abnormality

Sudan black stain

Myeloblast ID


Detect cellular lipids


Black staining is pos

Myeloperixidase stain

Myeloblast ID


Peroxidase activity present in primary granules of myeloid and monocytic cells

Periodic acid Schiff stain

Lymphoblasts


Stains glycogen stores in cells

Non specific Esterase

differentiate myeloblast from monocyte


Monocyte strongly positive


Granules stain orange

Phosphatase stain

Cells of hair cell leukemia are strongly positive

Surface markers

Proteins on cell membrane that can be detected with immunologic reagents are extremely helpful in differentiating ALL

CALLA

Common ALL antigen is found on surface of lymphoblasts in 70% of patients with ALL

Life threatening emergencies of acute leukemia

Infections, bleeding, leukemic infiltration of organs, metabolic abnormalities, hyperleukocytosis

Treatment options of acute leukemia

Chemo, stem cell transplant, vaccines?, immunotherapy