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Hematalogy Lecture > Unit 2: Myeloid Leukemias > Flashcards

Unit 2: Myeloid Leukemias Flashcards

1
Q

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

A

Acute Myeloid Leukemia

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2
Q

True or false:

All myeloid leukemias are rapidly fatal if left untreated.

A

true

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3
Q

Acute myeloid leukemia involves a defect of __________.

A

HSC (CD34+)

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4
Q

In some AMLs you can find Auer rods = condensed to primary granules. This means cells are…

SBB and MPO+ in

A

myeloblasts or promyelocytes

SBB/MPO + (in mature myelocytes)

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5
Q

What are the two Non-specific Esterase stains (NSEs) – for monocytes?

A
  1. α-Naphthyl Butyrate Esterase (NBE)
  2. α-Naphthyl Acetate Esterase (NAE)
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6
Q

Specific Esterase Stains – stains for myeloid
cytoplasmic granules…used to separate monocyte
precursors from granulocyte precursors

A

Napthol AS-D Chloroacetate Esterase (NASD)

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7
Q

Diagnosis of acute myeloid leukemia begins with

A

Peripheral blood and bone marrow examination

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8
Q

WBC count could be variable in AML but most range from…

A

1 x 109/L - 200 x109/L

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9
Q

AML:

myeloblasts present in ___% of patients

A

90

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10
Q

Clinical presentation with AML?

A
  • Anemia
  • Neutropenia
  • Thrombocytopenia
  • Possible splenomegaly
  • Bone marrow is hypercellular with >20% blasts
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11
Q

What AML clinical presentations lead to pallor, fatigue, bruising, bleeding, and fever?

A
  • Neutropenia
  • Thrombocytopenia
  • Possible splenomegaly
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12
Q

AML Lab Findings:

_____________ due to increased cell turnover

A

Hyperuricemia

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13
Q

AML Lab Findings:

_____________ due to cell lysis

A

Hyperphosphatemia

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14
Q

AML Lab Findings:

__________________ due to progressive bone destruction.

A

Hypokalcemia

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15
Q

Hyperuricemia, Hyperphosphatemia, and Hypocalcemia are signs of what syndrome?

A

Tumor Lysis Syndrome – a group of metabolic
complications that can occur in patients with a malignancy

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16
Q

Generalizations for AMLs:

  • Many of these are due to mutations activating inappropriate __________ factors
  • All of these exhibit variable degrees of dysmyelo-poiesis
    (along with all of their other morphological abnormalities!)
A

transcription

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17
Q

abnormal hyperproliferation of bizarre
granulocyte &/or monocyte precursors

A

Dysmyelopoiesis

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18
Q

FAB Classification for AMLs:

Acute Myeloblastic (with Minimal Differen-
tiation) (of nucleus)

A

Mo

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19
Q

FAB Classification for AMLs:

Acute Myeloblastic w/o Maturation (of cytoplasm)

A

M1

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20
Q

FAB Classification for AMLs:

Acute Myeloblastic with Maturation (of cytoplasm)

A

M2

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21
Q

FAB Classification for AMLs:

Acute Promyelocytic

A

M3

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22
Q

FAB Classification for AMLs:

Acute Myelomonocytic

A

M4

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23
Q

FAB Classification for AMLs:

Acute Myelomonocytic w/Eosinophilic variant

A

M4(Eo)

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24
Q

FAB Classification for AMLs:

Acute Monocytic

A

M5

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25
FAB Classification for AMLs: Poorly differentiated =
M5a
26
>20% blast count not required if __________ found in AML
genetic mutations
27
Makes up 5% of AMLs; found in children and adults younger than 60 yo
AML with t(8;21)(q22;q22)
28
t(8;21) = ______ prognosis
good [ “It’s 2 good 2 have t(8;21).” ]
29
AML with t(8;21)(q22;q22): WBCs have what functional problems?
with phago-cytosis & chemotaxis
30
AML with t(8;21)(q22;q22): Lab findings?
Blasts are large with abundant, dysplastic cytoplasm and numerous primary granules and Auer rods. Sometimes exhibit pseudo-Pelger-Huet.
31
AML with t(8;21)(q22;q22): * MPO & SBB _____ * PAS ______
1+ negative
32
AML with t(8;21)(q22;q22): SE ___ ____ Auer rods
+ +/-
33
* Rare: 5-8% of all AMLs and occurs at any age (usually young) * Myeloblasts, monoblasts, and promyelocytes observed * Also eosinophila with dyplastic changes
AML with inv(16)(p13.1p22)
34
AML with inv(16)(p13.1p22): Remission rate is good but only _____ are cured
half
35
- Makes up 8% of AMLs - Characterized by a differentiation block in the promyelocyte stage
AML with t(15;17)(q22;q12) – Acute Promyelocytic Leukemia (APL)
36
Abnormal hypergranular promyelocytes with Auer rods * Granules can obscure nucleus with abundant cytoplasm & variable nuclear size & shape.
AML with t(15;17)(q22;q12) – Acute Promyelocytic Leukemia (APL)
37
AML with t(15;17)(q22;q12) – Acute Promyelocytic Leukemia (APL): Leukemic cells also have defective retinoic acid receptor (RARα gene), so can be treated with...
TRA (All Trans Retinoic Acid, a vit. A derivative)
38
How ATRA treatment work?
pushes pros into finishing maturation, thus causing remission! (Then attacked with chemo. – a very successful combination.)
39
Acute Promyelocytic Leukemia (APL) is strongly associated with _______.
DIC -A promyelocyte’s primary granules are rich in thromboplastin - like substances . . .which trigger a “bleeding diathesis”.
40
What is the variant subtype of APL?
microgranular APL (cells look agranular if only light microscopy used)
41
Lab Findings FOR BOTH APL VARIANTS: MPO & SBB = PAS ____
2+ negative
42
Lab Findings FOR BOTH APL VARIANTS: SE ____ Both NSE _____
positive negative
43
Lab Findings FOR BOTH APL VARIANTS: * Frequent Auer rods, can be in bundles (so-called “faggot cells”). * ↓ plt. count because...
Plts. used up making clots
44
Acute Myelomonocytic Leukemia (aka. AMML) lab findings: peripheral blood absolute monocytosis (>___%); many circulating blasts, pros, immature granulocytes & monos! * >20% monos AND >20% granulocytes
20
45
Acute Myelomonocytic Leukemia (aka. AMML) lab findings: -MPO and SBB still _____ -Both BSEs now start to be ______
positive positive
46
Acute Myelomonocytic Leukemia (aka. AMML) lab findings: - SE still _____ - PAS still ______ -_____ Auer rods
positive negative +/-
47
Acute Myelomonocytic Leukemia (aka. AMML) lab findings: CD...
CD 11b, CD 4, CD 36, and CD 64
48
AMML clinical symptoms are the common ones, PLUS...
* CNS & soft tissue involvement * Ex., gum hypertrophy & skin lesions
49
Acute Monocytic Leukemia (aka. AMoL) -Makes up _____% of AMLs -When _____% leukemic cells are monocytic
5-8 >80
50
Acute Monocytic Leukemia (aka. AMoL): Usually CD ___ and CD ___ pos. (“gold std.”)
4 64
51
Acute Monocytic Leukemia (aka. AMoL) is usually t(____)
t(8;16)
52
clinical symptoms of AMoL?
Similar to AMML (with CNS & soft tissue involvements.)
53
Why is there Increased serum & urinary lysozyme with AMoL?
Bc. this enzyme found in greatest amount in monos
54
With AMoL, bone marrow shows some granulocytes, but majority composition is monoblasts, promonocytes, & monocytes. * <___% granulocytes
20
55
AMoL: MPO and SBB _________
+ / - (most frequently NEG.)
56
Are there Auer rods with AMoL?
Very rare Auer rods (most frequently NEG.)
57
AMoL: PAS __________
positive
58
AMoL: Both NSEs ________ (NBE ___)
positive 3+
59
Acute Erythroid leukemia (AEL) only makes up ___% of AMLs.
3 -Can evolve further into AMLs
60
Only AML with marked erythroid precursor hyperplasia!!
Acute Erythroid leukemia (AEL)***
61
Acute Erythroid leukemia (AEL) is Frequently preceded by a ____________ syndrome.
myelodysplastic syndrome (MDS, aka. Refractory Anemia).
62
Acute Erythroid leukemia (AEL) lab findings: bone marrow shows ____________ (Atlas pp. 178-79) = abnormal proliferation of bizarre RBC precursors, with reverse M:E ratio due to huge # of abnormal erythroblasts, & even a few ringed sideroblasts.
dyserythropoiesis
63
Peripheral blood findings with Acute Erythroid leukemia (AEL)?
nRBCs with mkd. aniso, poik. & schistocytosis (due to the dyserythropoiesis)
64
Acute Erythroid leukemia (AEL) Lab Findings: * Lots of myeloblasts * Some abnormal _____________
megakaryocytes
65
Acute Erythroid leukemia (AEL): > ____% bizarre, multinucleated, megaloblastoid nRBCs!! (with few ringed sideroblasts.)
50
66
Acute Erythroid leukemia (AEL): MPO/SBB ______. Why?
negative, Defect here is mostly dyserythropoiesis, not so much dysmyelo- poiesis.
67
Acute Erythroid leukemia (AEL): * Both NSEs _______ * PAS __________
positive positive
68
Acute Erythroid leukemia (AEL): Early, abn. erythroblasts are PAS + in “granular” or “blocky” pattern. Later, abnormal erythroblasts + in "_______" pattern.
diffuse
69
Acute Erythroid leukemia (AEL): Normal RBC precursors ---> PAS ______
not PAS + at all!
70
Rarest form of AML!! (Makes up < 1% of AMLs.)
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL)
71
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL) is frequently associated with ________ syndrome.
Down's Syndrome
72
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL): Common leukemia symptoms + "dry tap" upon bone marrow aspiration due to ____________. What other leukemia has "dry tap"?
myelofibrosis Hairy Cell Leukemia
73
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL) * Lab Finding: bone marrow shows primarily...
dysmegakaryopoiesis: ↑ #s of megakaryocyte precursors, including megakaryoblasts, atypical megakaryocytes (with "blebbing"), & giant plts. (Atlas pp. 182-83)
74
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL): Few myeloblasts can look...
lymphoid or undifferen-tiated.
75
Does AMegL show dyserythropoises?
Little accompanying dyserythropoiesis
76
AMegL can be associated with t(____) & t(____).
t(3;21) & t(1;22)
77
AMegL: AMP and SBB ______. Why?
negative, so few myeloid elements
78
AMegL: NBE _____ but NAE ______. (unique to megakaryo-blasts)!
negative, positive
79
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL): PAS ________ Plt. peroxidase _____
positive postive
80
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL): CD 41, 42, 61 ______
+/-
81
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL): May plt.-specific receptors, such as _______________ + (for fibrinogen)
GPIIb/IIIa receptor
82
Acute Megakaryocytic/ Megakaryoblastic Leukemia (AMegL): Acid phosphatase _____ What other leukemia is acid phosphatase +
positive but this isn’t spe-cific for megakaryoblasts! In what other specific leukemia was acid phos. stain pos.? ---> T-cell ALL

Hematalogy Lecture (35 decks)

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