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Heme - Amanda > Heme Malignancies I > Flashcards

Heme Malignancies I Flashcards

1
Q

t(11:14)

A

Mantle cell lymphoma (Non-Hodgkin’s Lymphoma)

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2
Q

Which leukemia highly associated with DIC?

A

APL

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3
Q

“Core binding factor” leukemia and it’s associated cytogenetics

A

Acute myelomonocytic leukemia - inv(16:16)

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4
Q

Gingival hyperplasia

A

AML

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5
Q

Heart-shaped/bat wing nuclei?

A

APL

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6
Q

Arsenic MOA?

A

Breaks down PML-RARalpha fusion protein

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7
Q

BBW for Arsenic?

A

CV - QT prolongation, AV block, etc

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8
Q

CD14+/CD11b+

A

Acute myelomonocytic leukemia

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9
Q

Definition of class I hypothesis

A

Fusion gene causes constitutively active pro-proliferation gene

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10
Q

Definition of class II hypothesis

A

Fusion gene acts as a corepressor, inhibiting differentiation

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11
Q

AML translocations fit under class ___ hypothesis

A

II (inhibits differentiation of myelocytes)

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12
Q

AML associated with eosinophilia?

A

Acute myelomonocytic leukemia

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13
Q

Epidemiology of hairy cell leukemia?

A

Middle aged (~40yo) male

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14
Q

Most common cutaneous lymphoma and its cell?

A

Mycoses fungoides - Sezary cell

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15
Q

Which AML does NOT have CD34+ immunophenotype?

A

APL

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16
Q

Which method used to asses immunophenotype?

A

Flow cytometry

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17
Q

First step in workup of any heme disease

A

PBS

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18
Q

Five criteria to classify something as a blast

A
  1. Big cell 2. Increased cytoplasm:nuclear ratio 3. Immature chromatin 4. Large nucleus (may be >1 nucleus) 5. Bunch of cells that look alike
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19
Q

3 steps in bone marrow aspiration

A
  1. Half cc of bloody aspirate 2. 5-20 cc in same spot for special studies 3. Core biopsy from different site
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20
Q

Purpose of core biopsy in new spot

A

Will not contain blood if you draw from same site where aspirate was done

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21
Q

Normal range of myeloid:erythroid precurors

A

2:1 - 5:1 (myeloid should always outnumber erythroid precursors)

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22
Q

How to estimate cellularity of bone marrow

A

100-age (rest is fat)

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23
Q

Hapten

A

Site where an antigen binds (so a CD is a hapten)

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24
Q

Flow is a weak method for detecting ____ cells. Why?

A

Erythroid precursors - they’re lysed before flow so they’re underrepresented on scatter plots

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25
Q

Side scatter measures ____; front scatter measures _____.

A

Side scatter measures complexity (granules, seg nuclei); front scatter measures size.

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26
Q

On flow scatter plot, x-axis is generally ___, while y-axis is ____.

A

X-axis = CD45 (on almost all stem cells in different concentrations) Y-axis - SSC

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27
Q

Two immunophenotypes associated with AML’s

A

CD33+(marker for granulocytes)/CD34+(marker for HSC) = myeloid blasts! **Remember: APL NOT assc. with CD34

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28
Q

Reed-Sternberg/”owl eyes” cells

A

HL

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29
Q

CD15+/CD30+

A

RS cell = HL

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30
Q

t(9:22) causes what fusion protein?

A

BCR/ABL in CML

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31
Q

MOA of ATRA

A

Drives differentiation of blasts; tx for PML

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32
Q

In which stage of cell cycle must cells be for karyotyping? FISH?

A

Karyotyping = metaphase FISH = interphase

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33
Q

Red probe hybridized to chr9; green probe to chr22. What would CML look like on this FISH?

A

Yellow (t9:22)

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34
Q

Acute leukemias vs. myeloproliferative disorders

A

Acute leukemias = RAPIDLY proliferating BLASTS Myeloproliferative = CHRONICALLY proliferating DIFFERENTIATED blood cells

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35
Q

Which lineages can be involved in acute leukemias?

A

Myeloid, erthyroid, megakaryocyte

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36
Q

What is a myeloid sarcoma?

A

Acute myeloid LEUKEMIA with monocyte-like features that presents as solid tumors in bone or connective tissue (blasts outside marrow)

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37
Q

CD10/CD19 found on:

A

Lymphoid blasts

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38
Q

(T/F): Immunophenotype strongly correlated with response to tx.

A

False

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39
Q

(T/F): Genetics strongly correlated with response to tx.

A

True

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40
Q

Runx1-Runx1T1 is class I or II mutation?

A

II (AML t8:21)

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41
Q

FLT3-ITD is class I or II mutation?

A

!

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42
Q

Inv(16) results in what fusion protein?

A

CBFB-MYH11 *remember: acute myelomonocytic leukemia is core binding factor leukemia

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43
Q

(T/F): Dominant negative t8:21 sufficient to cause AML

A

False. Must have class I mutation, too.

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44
Q

Leukemia associated with thrombocytopenia?

A

APL (DIC!!!!)

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45
Q

AML prognosis: NPM1 + or CEBPA + and FLT3-ITD -

A

Poor; HSCT doesn’t help

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46
Q

AML prognosis: FLT3-ITD+

A

Good; HSCT helps

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47
Q

AML prognosis: NPM1 - and CEBPA - and FLT3-ITD -

A

Good; HSCT helps

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48
Q

How could one immunophenotypically tell apart the B cell ALLs?

A

t(9:22) = has CD10/19 and TdT t(11:19) = MISSING CD10 t(12:21) = CD34+

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49
Q

Imatinib could be used for which of the ALLs?

A

B cell ALL t(9:22); confers tyrosine kinase activity (class I mutation)

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50
Q

Most common ALL in very young pts?

A

t(11:19)

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51
Q

Fusion protein of B cell ALL t(11:19)? Prognosis?

A

MLL (histone methyltransferase = class II) Bad

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52
Q

Gilliand hypothesis doesn’t support which ALL?

A

B-ALL t(12:21)

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53
Q

Pax5 mutation seen in which ALL?

A

B-ALL t(12;21)

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54
Q

TRAP stain

A

Hairy cell leukemia (B-ALL)

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55
Q

Only leukemia w/o lymphadenopathy

A

Hairy cell (B-ALL)

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56
Q

Fusion gene of hairy cell leukemia

A

BRAF-V600

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57
Q

Rituximab is tx for which leukemia

A

Hairy cell (CD20+)

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58
Q

IFN2-a,b used for:

A

Hairy cell leukemia (B-ALL)

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59
Q

Dry bone marrow

A

Hairy cell leukemia (B-ALL)

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60
Q

Thymic mass + lymphadenopathy + splenomegaly

A

T-ALL

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61
Q

CD3+

A

T-ALL

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62
Q

Genetic abnormality of T-ALL

A

Translocation of oncogene to Ig or TCR promoter of chromosome 14

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63
Q

Morphology of every ALL (except hairy cell)

A

Big agranular blasts

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64
Q

WHO classification of AML

A

Blasts > 20%

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65
Q

(T/F): CD13/34 only found in myelogenous malignancies.

A

False - lymphoid malignancies may also express myeloid markers.

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66
Q

75% of ALL presents in pts < ____ yo

A

6

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67
Q

Class II mutation in B-ALL t(9:22)

A

IKZF1

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68
Q

t(9:22) in B-ALL vs. CML

A

B-ALL = p190 CML = p210 *Gene cleaved at different sites

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69
Q

Prognosis B-ALL t(9:22)

A

BAD

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70
Q

t(9:22) more common in adult or pediatric ALL?

A

20% adult ALL; 2-4% of pediatric ALL

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71
Q

Most common leukemia in kids <1 yo

A

B-ALL t(11:19)

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72
Q

B-ALL with class I mutation?

A

t(9:22); others are class II

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73
Q

Prognosis B-ALL t(12;21)

A

Good! ~90% cure rate!

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74
Q

Pax5 deletion (B-ALL t9:22) is a class ___ mutation.

A

II

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75
Q

Adolescent male with mediastinal mass:

A

T-ALL (thymic mass!!)

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76
Q

Relapse of ALL often presents in:

A

CNS and testis

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77
Q

Appearance of granules in lymphocytic leukemias:

A

ABSENT (agranular cells)

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78
Q

Most responsive leukemia to tx?

A

ALL

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79
Q

PML = M___

A

3

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80
Q

85% of MALTs associated with:

A

H. pylori

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81
Q

Starry sky

A

Burkitt’s t(8:14)

82
Q

Kid with mass on jaw

A

Burkitt’s t(8:14)

83
Q

Ruddy complexion

A

Polycythemia ruba vera

84
Q

Increased RBC mass with hypovolemia

A

Polycythemia

85
Q

“4 H’s” of polycythemia

A
  1. Hyperviscosity 2. Hypovolemia 3. Histaminemia 4. Hyperuricemia
86
Q

Blasts + myeloperoxidase positive

A

AML

87
Q

Tryptase+

A

Mastocytosis (myeloproliferative)

88
Q

Benzene exposure predisposes to:

A

CML

89
Q

CML usually ends in:

A

Blast crisis

90
Q

Progression of CML

A

Chronic phase –> Accelerated phases –> Blast phase

91
Q

AML blasts vs CML blast crisis blasts

A

AML blasts will have auer rods

92
Q

Tx for chronic phase CML

A

Imatinib

93
Q

Most common overall leukemia

A

CLL

94
Q

Myelogenous leukemias present in which age bracket?

A

Middle age

95
Q

Lymphocytic leukemias present in what age brackets?

A

Young and eldery ALL usually in kids CLL usually in eldery

96
Q

Basophilia

A

CML

97
Q

What is a leukomoid reaction?

A

Normal WBC with left shift; high leukocyte alk phos

98
Q

Low leukocyte alk phos (LAP):

A

CML (non-functional leukocytes)

99
Q

Affected cell type in CML

A

Pluripotent stem cell (myelogenous or lymphocytic)

100
Q

Which myeloproliferative disorder associated with possible eosinophilia?

A

Mastocytosis

101
Q

CKiT mutation:

A

Mastocytosis (myeloproliferative)

102
Q

CD25+:

A

Mastocytosis

103
Q

Tear drop cells:

A

Primary myelofibrosis (myeloproliferative); tear drop PLATELETS

104
Q

Jak2 mutation on chr9 short arm is cause of which three disorders?

A

Myelofibrosis or polycythemia or thrombocythemia

105
Q

Difference in JAK2 mutation of myelofibrosis vs polycythemia

A

Myelofibrosis = tyrosine kinase activity Polycythemia = increased growth factor effects

106
Q

What causes myelofibrosis?

A

Abnormal megs secrete cytokines –> type THREE collagen deposition in BM –> extramedullary hematopoeisis

107
Q

60 yo with thombosis, bone pain, muscle wasting, splenomegaly

A

Myelofibrosis (myeloproliferative)

108
Q

Which lineage most affected in polycythemia?

A

Erythroid

109
Q

How to tell essential polycythemia from secondary polycythemia?

A

Essential = DECREASED EPO (trying to reduce the # of RBCs being cranked out by BM) Secondary = increased EPO (trying to compensate for, as an example, high altitude)

110
Q

Generalized pruritis after hot shower:

A

Polycythemia (heat causes histamine release from excess # of mast cells in polycythemic pt)

111
Q

Prognosis of polycythemia

A

Progresses to MDS, AML, myelofibrosis

112
Q

Tx of polycythemia

A

Phlebotomy to deplete iron = less RBC production

113
Q

Cause of thrombocythemia

A

Excess of dysplastic/abnormal platelets from megs

114
Q

Tx thrombocythemia

A

Hydoxyurea (ribonucleotide reductase inhibitor)

115
Q

EPO and platelet levels in thrombocythemia

A

EPO = normal Platelet = extremely elevated

116
Q

Bone marrow with large, multilineage cells

A

CML

117
Q

Disease that is both a leukemia and a myeloproliferative disorder

A

CML

118
Q

How do you know when CML pt is in blast crisis?

A

Smear with >20% blasts. This will occur in all untreated patients eventually.

119
Q

How to tell CML vs leukomoid reaction

A

Leukomoid will much more elevated LAP (leukocyte alk phos)

120
Q

Tx for CML? Cure?

A

Tx = imatinib Cure = allogenic HSCT

121
Q

What’s the fusion gene in CML? Class I or II?

A

BCR-ABL conferring tyrosine kinase activity (why imatinib works). Class I (proliferation).

122
Q

Will CML blasts have auer rods?

A

NO! Feature of AML!

123
Q
A

AML

124
Q

There is one leukemia associated with eosinophiia and one myeloproliferative disorder. Name them.

A

Leukemia = Acute myelomonocytic (inv 16)

Myeloproliferative = Mastocytosis

125
Q

Three heme malignancies associated with JAK2 mutations.

A

Primary myelofibrosis

Essential thrombocythemia

Polycythemia vera

126
Q

Why muscle wasting in primary myelofibrosis?

A

Cytokine-like symptom

127
Q

What type of collagen is deposited in bone marrow in primary myelofibrosis? What kind of stain is used?

A

Type 3 collagen

Reticulin stain for fibers

128
Q

Heme malignancy with decreased EPO?

A

Polycythemia vera

129
Q

Bone marrow with large, clustered megs

A

Essential thrombocythemia

130
Q

TPO level in essential thrombocythemia

A

Normal (megs are pumping out more platelets, not TPO response)

131
Q

What is CMML? Cell type? Labs?

A

Chronic myelomonocytic leukemia; this is a cross between myeloproliferative and myelodysplastic syndrome

Monocytes, myelocytes, weird hybrids between the two

Leukocytosis

132
Q

PDGF-R mutation

A

Mastocytosis or CMML

133
Q

Does mastocytosis often present in bone marrow, lymph nodes, or tissues?

A

Tissues (although the bone marrow is also involved in most cases - cool story, Strom)

134
Q

What “cell” is elevated: PV? ET? Myelofibrosis?

A

PV = RBC

ET = platelet

Myelofibrosis = platelet

135
Q

Two patients with leukocytosis, fatigue, weight loss, night sweats. How can tell which has an infection and which has a myeloproliferative disorder?

A

Infection = toxic granulations and left shift with progressively fewer immature cells

MPD = More myelocytes than metamyelocytes (“myeloid bulge”); possible cytogenetic findings (i.e. t9:22 = CML)

136
Q

WBC: 40 K/ul

PMNS: 35

Metas: 15

Myelos: 5

Sepsis or MPD?

A

Sepsis

Left shift

137
Q

WBC: 40 K/ul

PMNs: 26

Metas: 10

Myelos: 20

Sepsis or MPD?

A

MPD

Myeloid bulge

138
Q

What’s going on during the accelerated phase of CML?

A

Increased number of blasts

(but not quite as bad as blasts phase, which is like an acute leukemia)

139
Q

Once CML confirmed via RT-PCR analysis of BCR-ABL protein, why must a bone marrow biopsy still be performed?

A

Must make sure CML is not progressing to accelerated or blast phase

140
Q

Why does a mutation in JAK2 cause problems with RBCs and platelets?

A

TPO and EPO are upstream of the JAK2 pathways. So, for example, if the MPL thrombopoeitin receptor of megs is mutated, the same phenoytpe is observed as when JAK2 is mutated (ET).

141
Q

Which MPDs are caused by translocations?

A

CML, Mastocytosis, CMML

142
Q

Which MPDs are caused by point mutations?

A

ET, PV

143
Q

What is SCF?

A

A mitogen involved in mast cell growth and migration

144
Q

Most common presentation of mastocytosis

A

Urticaria pigmentosa (itchy skin lesions) in a kid

145
Q

What is tryptase?

A

Mediator secreted by normal and hyperactive mast cells

(Tryptase level elevated in mastocytosis)

146
Q

(T/F): Mastocytosis usually spreads to bone marrow, the most common site of systemic involvement.

A

False - would be true but mastocytosis usually does NOT spread beyond the skin (urticaria pigmentosa)

147
Q

Kid presents with hypotension, skin lesions, flushing, and itchy skin. What test would you order?

A

Tryptase levels for mastocytosis

(or flow looking for CD117,CD25)

148
Q

CD117

A

Mastocytosis - this is the SCL receptor (remember: SCL is involved in mast cell growth and migration)

149
Q

Man presents with ruddiness, hypertension, and stroke. Dx if EPO low? If EPO high?

A

If EPO low, PV

If EPO high, secondary polycythemia

150
Q

How to tell PV from ET/myelofibrosis?

A

PV will have elevated RBCs rather than platelets and will have HTN in addition to thrombosis

ET/myelofibrosis have weird looking megs, PV does not

151
Q

How to tell ET from myelofibrosis?

A

Myelofibrosis will have more reticulin fibers on reticulin stain than ET

152
Q

WTF is agnogenic myeloid metaplasia?

A

Another (awful) name for primary myelofibrosis

153
Q

MDS: young or old?

A

Old

154
Q

del(5q)

A

MDS

155
Q

Binucleated RBCs

A

Refractory cytopenia with unilineage dysplasia

156
Q

Prognosis: refractory cytopenia with unilineage dysplasia

A

Normal for age (usually >65yo)

157
Q
A

APL (note many granules + lots of auer rods)

158
Q
A

Acute myelomonocytic leukemia (note large leukemic blasts with very large nucleoli and heavily vacuolated cytoplasm

159
Q
A

CML (note many different cell types that are abnormally large)

160
Q
A

CML

161
Q
A

CML accelerated phase (more blasts)

162
Q
A

CML blast crisis (many lineages with excess blasts)

163
Q
A

ET (lots of platelets and jacked up megs)

164
Q
A

Primary myelofibrosis (tear drops)

165
Q
A

Primary myelofibrosis (reticulin stain of type 3 collagen)

166
Q
A

Primary myelofibrosis (tear drops, type III collagen in BM, reticulin fibers)

167
Q

Why do patients with myelofibrosis have hepatosplenomegaly?

A

Fibrosis of BM necessitates extramedullary hematopoeisis

168
Q

Mononuclear megs

A

MDS (del 5q)

169
Q

MDS more common in men or women? Tx?

A

Women

Lenalidomide

170
Q

Lobulated granulocytes

A

Refractory cytopenia with multilineage dysplasia

171
Q

RAEB1 vs RAEB2

A

RAEB1 = blasts 5-9%

RAEB2 = blasts 10-19%

(blasts > 20% would be an acute leukemia)

172
Q
A

Polycythemia vera (excessive RBCs)

173
Q

Immunophenotype of refractory anemia with excessive blasts (RAEB)

A

CD34+/CD117+

174
Q

RAEB vs acute leukemia

A

Acute leukemia due to translocation, while RAEB due to expansion of cell with mutation that takes over as new cell line

175
Q

Where does iron reside in refractory anemia with ring sideroblasts?

A

Mitochondria, which make a circle around nucleus

176
Q

Prognosis: Refractory cytopenia with multilineage dysplasia

A

Poor, ~30 months

177
Q

Prognosis: RAEB

A

Poor (“pre-leukemia”)

178
Q

FAB classification:

AMLs vs ALLs

A

AMLs = M0-M7

ALLs = L1-L3

179
Q

ALL most common between ages __ - __ and falls off around age __ with a secondary rise around age ___

A

3-7

10

40

180
Q

As well as having constitutively active pro-proliferative genes and a block in differentiation, leukemic cells also have:

A

Reduced apoptosis

181
Q

M0

A

Undifferentiated

182
Q

M1

A

Without maturation

183
Q

M2

A

Granulocyte maturation

184
Q

M3

A

APL

185
Q

M4

A

Granulocytic and monocytic maturation

186
Q

M5

A

Monoblastic (M5a) or monocytic (M5b)

187
Q

M6

A

Erythroleukemia

188
Q

M7

A

Megakaryocytic

189
Q

L1

A

Blasts with high nuclear to cytoplasmic ratio; uniform

190
Q

L2

A

Larger blasts, lower nuclear to cytoplasmic ratio (more cytoplasm)

191
Q

L3

A

Vacuolated blasts, basophilic cytoplasm

192
Q

HLA-DR+

A
193
Q

Bleeding gums

A

AML

194
Q

MPO+

A

AML

195
Q

AMLs with good prognosis

A

t(8:21)

t(15:17)

inv16

71% 5 year survival

196
Q

AMLs with intermediate risk

A

Normal cytogenetics

46% 5 year survival

197
Q

AMLs with poor prognosis

A

3+ chromosomal abnormalities

Monosomies

16% 5 year survival

198
Q

Tx shown efficacious in older AML patients

A

Azacitidine

199
Q

ALLs with worst prognosis

A

BCR-ABL = t(9:22)

MLL-AF4

200
Q

ALLs with good prognosis

A

Hyperdiploidy

E2A-PBX

TEL-AML

201
Q

ALL cure rate better in adults or children? Why?

A

Children

Adults can’t handle high dose CTX that is part of curative tx for pediatric ALL

Heme - Amanda (3 decks)

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