Myelocytic Leukemias Flashcards
Most common type of adult leukemia (incidence increases with age)
AML
Involves a defect of HSC (CD34+)
AML
condensed primary granules
Auer Rods
due to increased cell turnover
Hyperuricemia
due to cell lysis
Hyperphosphatemia
due to progressive bone destruction
Hypokalemia
Hyperuricemia due to increased cell turnover
Hyperphosphatemia due to cell lysis
Hypokalemia due to progressive bone destruction
These are all signs of tumor lysis syndrome- a group of metabolic complications that can occur in patients with a malignancy
abnormal hyperproliferation of bizarre granulocyte and/or monocyte precursors
Dysmyelopoiesis
found in children and adults younger than 60 years old
AML w/ t(8;21) (q22:q22)
Blasts are large with abundant, dysplastic cytoplasm and numerous primary granules and auer rods. Sometimes exhibit pseudo-pelger huet
MBO & SBB 1+
PAS neg
SE +
+/- auer rods
AML w/ t(8;21) (q22:q22)
Eosinophilia with dysplastic changed
AML w/ inv(16)(p13.1p22)
good prognosis
AML w/ t(8;21) (q22:q22)
AMLs and occurs at any age (usually young)
AML w/ inv(16)(p13.1p22)
Abnormal hypergranular promyelocytes with Auer rods
AML w/ t(15;17) (q22;q12)- Acute promyelocytic leukemia (APL)
AML w/ t(15;17) (q22;q12)-
Acute promyelocytic leukemia (APL)
Leukemic cells also have defective retinoic acid receptor (RARa gene), so can be treated with ATRA
APL t(15;17)
Strongly associated with DIC
APL
A promyelocytes primary granules are rich in thromboplastin-like substances… which trigger a
bleeding diathesis
cells look agranular if only light microscopy used in what variant?
Microgranular APL
Prolonged clotting time tests
⬇ plt. Count (because plts. Used up making clots)
MPO and SBB= 2+ pos. (increased primary granules)
PAS neg
SE pos
Frequently auer rods, can be in bundles (so-called “faggot cells”)
Both NSEs neg
Both variants of APL
hypergranulation and “coin-on-coin” nucleus
APL
Bundles of Auer Rods
Faggot cell
MBO and SBB still +
Both NSEs now start to be + (monos)
SE still +
PAS still (-)
+/- Auer rods (depending on the myelocytic cells involved)
CD 11b, CD 4, CD 36, and CD 64
AMML
20% monos 20% granulocytes
AMML
Usually CD4 and CD64 pos (“gold std.”)
AMoL
When >80% leukemic cells are monocytic
AMoL
<20% granulocytes
AMoL
MPO and SBB +/- (most frequently NEG)
Both NSEs pos (NBE 3+!)
Fluoride inhibition step (Neg)
PAS pos (finally)
Very rare Auer rods (most frequently NEG)
AMoL
marked erythroid precursor hyperplasia!!
AEL
Makes up only 3% of AMLs
AEL
Can evolve further into AML
AEL
abnormal proliferation of bizarre RBC precursors, with reverse M:E ratio due to huge # of abnormal erythroblasts, and even a few ringed sideroblasts
dyserythropoiesis
Lots of myeloblasts
AEL
- > 50% bizarre, multinucleated, megaloblastoid nRBCs!!
- Some abnormal megakaryocytes
AEL
“dry tap” upon bone marrow aspiration due to myelofibrosis
AMegL
⬆ #s of megakaryocyte precursors, include megakaryoblasts, atypical megakaryocytes (with “blebbing”), and giant platelets
dysmegakaryopoiesis
May plt.- specific receptors, such as GPIIb/IIIa receptor + (for fibrinogen)
AMegL
ACP positive
AMegL
also in T-cell ALL
