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Hematology II > Myelocytic Leukemias > Flashcards

Myelocytic Leukemias Flashcards

1
Q

Most common type of adult leukemia (incidence increases with age)

A

AML

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2
Q

Involves a defect of HSC (CD34+)

A

AML

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3
Q

condensed primary granules

A

Auer Rods

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4
Q

due to increased cell turnover

A

Hyperuricemia

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5
Q

due to cell lysis

A

Hyperphosphatemia

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6
Q

due to progressive bone destruction

A

Hypokalemia

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7
Q

Hyperuricemia due to increased cell turnover
Hyperphosphatemia due to cell lysis
Hypokalemia due to progressive bone destruction

A

These are all signs of tumor lysis syndrome- a group of metabolic complications that can occur in patients with a malignancy

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8
Q

abnormal hyperproliferation of bizarre granulocyte and/or monocyte precursors

A

Dysmyelopoiesis

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9
Q

found in children and adults younger than 60 years old

A

AML w/ t(8;21) (q22:q22)

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10
Q

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

A

AML w/ t(8;21) (q22:q22)

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11
Q

Eosinophilia with dysplastic changed

A

AML w/ inv(16)(p13.1p22)

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12
Q

good prognosis

A

AML w/ t(8;21) (q22:q22)

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13
Q

AMLs and occurs at any age (usually young)

A

AML w/ inv(16)(p13.1p22)

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14
Q

Abnormal hypergranular promyelocytes with Auer rods

A

AML w/ t(15;17) (q22;q12)- Acute promyelocytic leukemia (APL)

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15
Q

AML w/ t(15;17) (q22;q12)-

A

Acute promyelocytic leukemia (APL)

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16
Q

Leukemic cells also have defective retinoic acid receptor (RARa gene), so can be treated with ATRA

A

APL t(15;17)

17
Q

Strongly associated with DIC

A

APL

18
Q

A promyelocytes primary granules are rich in thromboplastin-like substances… which trigger a

A

bleeding diathesis

19
Q

cells look agranular if only light microscopy used in what variant?

A

Microgranular APL

20
Q

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

A

Both variants of APL

21
Q

hypergranulation and “coin-on-coin” nucleus

A

APL

22
Q

Bundles of Auer Rods

A

Faggot cell

23
Q

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

A

AMML

24
Q

20% monos 20% granulocytes

A

AMML

25
Q

Usually CD4 and CD64 pos (“gold std.”)

A

AMoL

26
Q

When >80% leukemic cells are monocytic

A

AMoL

27
Q

<20% granulocytes

A

AMoL

28
Q

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)

A

AMoL

29
Q

marked erythroid precursor hyperplasia!!

A

AEL

30
Q

Makes up only 3% of AMLs

A

AEL

31
Q

Can evolve further into AML

A

AEL

32
Q

abnormal proliferation of bizarre RBC precursors, with reverse M:E ratio due to huge # of abnormal erythroblasts, and even a few ringed sideroblasts

A

dyserythropoiesis

33
Q

Lots of myeloblasts

A

AEL

34
Q
  • > 50% bizarre, multinucleated, megaloblastoid nRBCs!!
  • Some abnormal megakaryocytes
A

AEL

35
Q

“dry tap” upon bone marrow aspiration due to myelofibrosis

A

AMegL

36
Q

⬆ #s of megakaryocyte precursors, include megakaryoblasts, atypical megakaryocytes (with “blebbing”), and giant platelets

A

dysmegakaryopoiesis

37
Q

May plt.- specific receptors, such as GPIIb/IIIa receptor + (for fibrinogen)

A

AMegL

38
Q

ACP positive

A

AMegL

also in T-cell ALL

Hematology II (8 decks)

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