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Renal, Hematological, and Cardiovascular Organ Systems > Hematologic Malignancies Total!!! > Flashcards

Hematologic Malignancies Total!!! Flashcards

1
Q

When did cytogentics studies beging?

A

1970

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2
Q

What did reed and sternberg do and when?

A

1898 and 1902
found a cell/ histoloic correlation with Hodgkins lymphoma, R/S cells
-large binucleated cells

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3
Q

What are 5 morphologic characteristics of a blast cell?

A

1) big cell
2)high nuclear / cytoplasmic ratio
3) immuature chromatin
4) big nucleus
5) bunch of cells that look alike
(may not have all 5)

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4
Q

What should the ratio of myeloid cells to erythroid prcursors be?

A

2:1

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5
Q

what is the percentage of Blast cells that should be in the PB?

A

<5%

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6
Q

What can BM biopsies give you an indication of?

A

iron stores

erythroid, myeloid, adn megakaryocyte lineages

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7
Q

What are the B-Cell markers?

A 
CD45
CD79a
CD20
Kappa Light chain
or
Lamba light chain
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8
Q

What are the T-cell markers?

A 
CD45
CD3 (TCR)
CD7
CD4 
or 
CD8
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9
Q

What does the expression of CD34 mean?

A

BLSAT CELL!

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10
Q

What does the expression of CD33 mean?

A

Granulocytes– myeloid blasts

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11
Q

What is routien cytogenetics?

A

identify an enumerate the chrs present in dividing cells

  • use growth medium and arrest cells in mitosis
  • squash cells onto slide
  • stain
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12
Q

What is the philadelphia CHR and what does it mean?

A

abnormal CHR 22

  • t(9;22) characteristic of CML
  • founded by Janette Rowely 1973
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13
Q

What is Florescent in situ Hybridization?

A

protease digestion

  • red or green tag
  • prob to a specific gene and or chr
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14
Q

What are class I mutations?

A 
promoting proliferation 
ext AML: 
-FLT3-TID
FLT3-TKD
Kit
RAS
PTRNII
Jak2
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15
Q

What are class II mutations?

A 
inhibiting differentiation 
exp: AML
-PML-RARA
RUNX1-RUNX1T1
CBFB-MYHII
MLL Fusion
CEBOA
NPM1
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16
Q

What are acute Leukemias?

A

rapidly proliferating clones of BLAST cells in marrow and ofen in blood stream

  • can arise from myeloid, erythroid, MEGs, or lymphocyte lineages
  • look normal but ^ in #
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17
Q

What are myeloproliferative diseases?

A

chronically proliferating clones which differnetate for circulating blood cells

  • can arise from myeloid, erythroid, MEGs, or lymphocyte lineages
  • look normal but ^ in #
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18
Q

What are Myelodysplastic syndromes (MDS)?

A

Poorly functioning clones

  • can arise from myeloid, erythroid, MEGs, or lymphocyte lineages
  • look normal but ^ in #
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19
Q

What cells are likely to defferentiate adn go toward AL?

A

myeloproliferative and myleodysplastics

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20
Q

What cell lineage does AML arise from?

A

myeloid leange of rapidly prolerating clones: BLASTs in marow and oftern blood stream
-can also arise from megs, erythroids, and meyloid

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21
Q

What cell lineage does ALL arise from?

A

-lymphocytes (naive) rapid proliferating clones: blasts in marrow and often in blood stream

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22
Q

What cell lineage doe Acute undifferentiated Leukemia arise from?

A

heamtopoietic stem cells– very rare!

-rapidly proliferating clones: BLASTS in marrow and often, bloodstream

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23
Q

What is the arbitrary count that implies AL when in the marrow?

A

Blast # of 70%

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24
Q

What are the cell markers for myeloid blasts?

A

CD34 and CD33

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25
Q

What are the surface markers for lymphoid blasts?

A

CD19 and CD10

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26
Q

What is the common AML genetic translocation?

A 
t(15;17) (q22;q12) 
PML-RARA
t(8;21) (q22;q22) 
RUNX1-RUNXT1
inv16
cytogenetics - with FLT3 mutation
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27
Q

What are the common ALL translocations?

A

t(12;21) (q13;q22)

TEL-AML1

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28
Q

What are the things that go into makting a diagnosis?

A

1) blast coundt
2) blast morphology
3) immunophenotype
4) genetics

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29
Q

What is Gilland’s Hypothesis?

A

2 mutations needed to get cancer

1 from Class I and 1 from Class II

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30
Q

What are the characteristics of AML with t(8;21) (q22;q22) mutation?

A

Runx1-Runx1T1

  • fusion protin of 2 TF (5% of AML cases)
  • Dominant - repressor of myeloid maturation (class II muation)
  • requires a class I mutation also
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31
Q

What are the clinical presentations of AML with t(8;21) (q22;q22) mutation?

A

younger pts (kids)

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32
Q

What are the cellular morphlogy of AML with t(8;21) (q22;q22) mutation?

A

some maturation to myelocytes

ocassional cyrstalization of granulocyte contents (auer rods- myeloperoxidase percipitates)

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33
Q

What is the immunophenotype of AML with t(8;21) (q22;q22) mutation?

A

CD34+
HLA-DR+
CD13+
CD33 weak!

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34
Q

What is the prognosis of AML with t(8;21) (q22;q22) mutation?

A

Good response to chemo!

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35
Q

What are the characteristics of AML with t(15;17) (q22;q12) mutation?

A

PML-RARA
-fusion of PML (TF) with RARA (TF -retinocic acid R)
-5-8% of AML cases
results in dominant - blockade of normal RARA, and inhibits granulocte differentiation
-requires a class I mutation

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36
Q

How can AML with t(15;17) (q22;q12) mutation be treated?

A

using an RA analoque to block PML-RARA itself using All trans retinoci acid (ATRA)

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37
Q

What are the clinical presentations of AML with t(15;17) (q22;q12) mutation?

A

DIC

Sever thrombocytopenia

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38
Q

What are the cellular mophologies of AML with t(15;17) (q22;q12) mutation?

A

big blast cleaved “Bat wing” nuclei
many cytoplasmic graules
Auer rods in stacks

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39
Q

What is the immunophenotype of AML with t(15;17) (q22;q12) mutation?

A

weak/absent CD34
HLA-DR
CD13
CD33

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40
Q

What is the prognosis of AML with t(15;17) (q22;q12) mutation?

A

good if make diagnosis

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41
Q

what are the B cell development markers?

A

CD34 and TdT are stem cells
CD19 and CD10 are lymphoid precursors
Cyto adn uCD20 are pre-B-cell
-they can also express myeloid markers CD13 and CD33

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42
Q

what are the main 2 TF that regulate early B-cell development?

A

IKZF1 and PAX5

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43
Q

What is TdT?

A

a marker for VDJ recombination of B and T cells

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44
Q

what are the genetic markers for ALL?

A 
t(9;22) (q34;q11.2) BCR-ABL1
t(v;11q23) MLL rearranged
t(12;21)(q13;q22) TEL-AML1 
t(5;14) (q131;q32) IL3-IgH
t(1;19) (q23;p13.3) E2A-PBx1
Hperdiploid (>50 chr) good prognosis
Hyodiploid (<40 Chrs) poor prognosis
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45
Q

What are the characteristics of ALL with t(9;22) (q34;q11.2) mutation?

A
  • BCR-ABL1
  • fusion protein of part of a serine threonine kinase (BCR) to a tyrosine kinase (ABL1)
  • class I mutation
  • different size than seen in CML!!!!! so not a Philadelphia chromosome!
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46
Q

What are the clinical presentations of ALL with t(9;22) (q34;q11.2) mutation?

A 
older adults (25% ALL cases)
kides <1 (2-4 % of all peds ALL)
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47
Q

What is the cellular morphology of ALL with t(9;22) (q34;q11.2) mutation?

A

big agranular blasts

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48
Q

What is the immunophenotype of ALL with t(9;22) (q34;q11.2) mutation?

A

CD10+
CD19+
TdT

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49
Q

What is the prognosis of ALL with t(9;22) (q34;q11.2) mutation?

A

Poor :(

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50
Q

What are the characteristics of ALL with t(v;11q23) rearranged mutation?

A
  • MLL rearranged
  • fusion of a T regulator (histone methyl transferase) to any several partners
  • inhibit differentiation
  • class II mutation
  • FLT3 mutation -20% of cases in ALL
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51
Q

What are the clinical presentations of ALL with t(v;11q23) rearranged mutation?

A

most common leukemia in kids <1

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52
Q

What is the cellular morphology of ALL with t(v;11q23) rearranged mutation?

A

big agranular blasts

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53
Q

What is the immunophenotype of ALL with t(v;11q23) rearranged mutation?

A

CD10-
CD19+
TdT+

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54
Q

What is the prognosis of ALL with t(v;11q23) rearranged mutation?

A

Poor :(

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55
Q

What are the characteristics of ALL with t(12;21) (p13;q22) mutation?

A
  • TEL-AML1 (ETV6-RUNx1)
  • fusion protein that acts as a dominant negative TF
  • inhibits differentiation (class II)
  • 23% show a PAX5 deleation - predictited to inhibit differentation
56
Q

What are the clinical presentations of ALL with t(12;21) (p13;q22) mutation?

A

kids 25% of pediatric B-ALL

57
Q

What is the celllular morphology of ALL with t(12;21) (p13;q22) mutation?

A

big a granular blasts

58
Q

What is the immunophenotype of ALL with t(12;21) (p13;q22) mutation?

A

TdT+
CD34+
CD20+

59
Q

What is the prognosis and txment of ALL with t(12;21) (p13;q22) mutation?

A

good :)!!!
90% cure rate
give loads of chemo!!!!!!

60
Q

What are most of the T-ALL genetic muations?

A

a translocation of an ocogene to a T-cell receptor promoter

example: TCR-alpha;HOX11 t(14q11;10q24)

61
Q

What is a common motife for lymphoid maligancies?

A

oncogene»» IG or TCR promoters

62
Q

What are the clinical presenations of T-ALLs?

A

kides-25% of pedeatric B-ALLs

often with thymic mass or lymph node, spleen involments

63
Q

What are the cellular morphologies of T-ALL

A

big agranular blasts

64
Q

What is the immunophenotype of T-ALL

A

TdT+
CD3+
CD5++
-can express myeloid or B-cell antigens

65
Q

What are myeloproliferative diseases?

A

from chronically proliferating clones which differentiate to circulating blood cells

66
Q

What is CML?

A

Chronic Myelogenous Keukemia, from high WBC; All stages of granulocytes maturation ends up in blood

67
Q

What is CMML?

A

chronic myelomonocytic leukemia
myleodysplastic/myleoproliferative
-high WBC monocytes, promonocytes, weird hybrids btn monocytes adn granulocytes

68
Q

What do increased eosinophils cause?

A

chronic eosinophilic leukemia or PDGFT neoplasm

69
Q

What do increased mature neutrophils cause?

A

chronic neutrophilic leukemia (quite rare)

70
Q

What do increased mast cells cause?

A

mastocytosis (primarily tissue targeted)

-bone marrow usually involved

71
Q

What is polycythemia vera?

A

elevated RBC count from the erythroid lineage

72
Q

What is Essentail thrombocytopeina or primary myelofibrosis?

A

Elevated platelets from megs

73
Q

What is the differance btn sepsis and myeloproliferative disease?

A
  • both have ^ WBCs with lots of granulocytes
  • toxic granulation and a left shit– Sepsis (infection) (bands>metamyelocytes> myelocytes
  • pts with ^ WBCs but! not toxic granuations and mor myelocytes than meta myelocytes (myeloid bulge)–> myeloproliferatve neoplasm
74
Q

What is important about sample testing for CML?

A

you should be sending more sample with - than + b/c it is an easy thing to identify and to treat if diagnosed!!!

75
Q

How should a clinician work up a pt?

A

WL and night sweats–>CDC and maunal diff–> suspect CML–> TR-PCR of PS for BCR-ABL1–> BM biposy

76
Q

What are the phases of CML?

A

chronic phase–>acclerated phase–> acute leukemia (myeloid or lymphoid)

77
Q

What is common about myeloproliferative disease genetics?

A

Tyrosine Kinase RULE!!!

-many of these disease have a defect in an TK making it hyperactive

78
Q

What are activating translocations of TKs, and what disease do they correcpond too?

A 
BCR-ABL (CML)
FIP1L1-PDGFRA (CEL)
-vPDGFRB (5q33) (mastocytosis)
(above respond to imatinib)
vPDGFRB (3 partners identified) (CMML)
--no response to imatinib
79
Q

What are the activating pt. mutations and what disease do the correlate with?

A

Jak2 or MpI (ET in 5% of cases)

Jak2 (P.Vera in 95% of cases)

80
Q

How does Jak 2 work?

A

it acts down stream of TK in megakaryocytes, and the thrombopoietin receptor (MpI) and mutation in MpI have been found to minic effect of Jak 2 mutations
-also downstream of EPOR, so cells can have EPO response with out EPO

81
Q

What is mastocytosis?

A

mast cells are similar to basophils- but live loner,a nd non-circulatory

  • main funtion is to release histamine, when their Fc receptor binds to IgE antigen complex
  • A mitogen called SCF plays a big role in their growth and migration
  • neoplasems of mast cells usually present as a benign cutaneous lesion in kids (urticaria pigmentosa)
  • usually dont spread beyond skine (except when they do…..WHAT)
  • in cases that release a lot of histamine and other mediators causeing systemic symptoms (flushing abd pain, tachycardia, hypotension) can confuse clinician
  • bone marrow is most common site of systemic involvement, but multiple organs (lymph nodes, spleen liver) can e involved
82
Q

What are the bone marrow findings in mastocytosis?

A

bland looking cells, round or spindle shaped

-30% are associated w/ a second hematolgic maligancy

83
Q

What are the genetic of mastocytosis?

A

either cKit mutation or PDGFRA activation (FIP1 tranlocation)

84
Q

What are the clinical presentations of mastocytosis?

A

variable and confusing

85
Q

What are the cellular morphologies of mastocytosis?

A

aggregates of bland looking cells round or spindle shaped sometimes with eosinophila

86
Q

What are the immuniophenotypes of mastocytosis?

A

tyrytase
CD117 (cKit, the SCF receptor)
CD25+

87
Q

What is the prognosis of mastocytosis?

A

highly variable; depends on a complex subclassification scheme

88
Q

What is plycythemia vera?

A

its pathologenesis is poorly understood

  • Jak2 mutation in >95% of cases
  • detectable in PBleukocytes
89
Q

What is the clinical presentation of p. vera?

A

thrombosis/ hypertension/stroke or MI

^ RBCs- due to lung disease

90
Q

What is the morphology of p. vera?

A

hypercellular marrow
erythroid hyperplasia
^ megs

91
Q

what is the immunophenotype of p. vera?

A

no known features

92
Q

What is the prognosis of p. vera?

A

> 10 yr survival is common
can progress to myelofibrosis
MDS
acute leukemia

93
Q

What is the difference btn reactive and neoplastic?

A
  • W^ RBCs
  • Chest X-ray
  • Hypoxic- not likely to be neoplastic
  • EPO levels (^ if reactive)
  • Jak 2 is distal to EPOR
94
Q

What are the differential diagnosis for P.vera?

A

^RBCs

hypertension and thrombosis

95
Q

What are the differential diagnosis for ET?

A

^ Platelets

Thrombosis

96
Q

What are the differential diagnosis for Priamry myelofibroiss?

A

^ platelets

Thrombosis

97
Q

What is essentail thrombocythemia?

A

pathogenesis poorly understood
Jak2 mutation in ~50% of cases
(decteable in PB leukocytes)

98
Q

What can also cause an increase in platelets?

A

iron deficenty, infection, and chronic inflammation along iwth ET and Primary myelofibrosis

99
Q

What are the cellular morphology in ET?

A

^ Megs – they are large!!! (2x size) and weird looking, even for megs, and tend to clusters

100
Q

what are the immunophotypic markers for ET?

A

No known

101
Q

What is the prognosis of ET?

A

> 10 yr survival is common

-can progress to myelofibrosis, MDS, AL

102
Q

What is primary myelofibrosis?

A 
previously agnogenic myeloid metaplasia
pathogenesis poorly understood
-Jak 2 mutation in ~50% of cases 
- detectable in PB leukocytes
-Diagnostic criteria in dispute!!!
103
Q

What is the clinical presentation of primay myelofibrosis?

A

thromboisis and thrombocytosis and or leukoerythroblastic picture

104
Q

What is the celluar morphology in primary myelofibrosis?

A

^ meg- bizzare shape adn clusters

-fibrosis

105
Q

What are the immunophenotypic markers for primary myelofibrosis?

A

No known!!! (like of the myloproliferative disesase)

106
Q

What is the prognosis for primary myelofibrosis?

A

usually shorter survival tahn ET

-can progress to marrow failure, AL

107
Q

What is myelodysplasia?

A
  • poorly understood entities
  • lumped together b/c similar presentations
  • some have high risk to progress to AL
  • poorly functioning cells
108
Q

What are usually unexplaned in myelodysplasia?

A

cytopenia
bicytopenia
pancytopenia

109
Q

What are the key diagnositic feature of myelodysplasias?

A

abnormal “dyspoietic” BM morpholies
abnormal “dyspoietic” immunophenotypes of maturing precursors
Abnormal cytogenetics
^ morphologic blasts (75%,<20%) with normal cytogenetis (if cytogenetics –AL)

110
Q

What are the 5 mj. adut forms (best to worst)?

A

!)refractory cytopenia with unilineage dysplasia

2) refreactor anemia with ring sideroblasts
3) myelodysplastic syndrome with isolated del (5q)
4) refractory cytopenia with multilineage dysplasia
5) refreactory anemia with excess blasts

111
Q

What is refractory cytopenia with unileange dysplasia?

A
  • diagnosis depends on morphologic findings
  • non specific cytogeneti abnormalities (trisomies and monosomines)
  • hard if cytogenetics are normal
112
Q

What are the clinical presentations of refractory cytopenia with unileange dysplasia?

A

unexplaned cytopeina

usually elderly pts. (>65yo)

113
Q

What is the cellular morphology of refractory cytopenia with unileange dysplasia?

A
  • weird looking precursors
  • binucleation or irregular nuclei
  • can show fibrosis high or low cellularity
  • megaloblastoid features
114
Q

What are the immunophontype markers of refractory cytopenia with unileange dysplasia?

A

-can show abnormal acquistion on surface markers

115
Q

What is the prognosis of refractory cytopenia with unileange dysplasia?

A

survival not clearly less than normal for age rearely progress of AML

116
Q

What is refractory anemia with ring sideroblasts?

A

diagnosis depends on morphologic finding and iorn staining results
nonspecific cytogenetic abnormaliteis (tir and monosomies) maybe present

117
Q

What are the clinical presentations of refractory anemia with ring sideroblasts?

A
  • unexplained cytopenieas

- usually elderly pts. (>65)

118
Q

What is cellular morphology of refractory anemia with ring sideroblasts?

A

rig sideroblasts, usually with dyspoietic features (in red cell series only)

119
Q

What are the immunophenotic markers in refractory anemia with ring sideroblasts?

A

-can show abnormal acquistion on surface markers

120
Q

What is prognosis of refractory anemia with ring sideroblasts?

A

survival not clearly less than normal for age rarely progress to AML

121
Q

What is MDS with isolated del (5q)?

A
  • all the meakaryocytes are monocuclear

- cytogenetis chow only loss of the 1q arem of chr 5

122
Q

What is clinical presentation of MDS with isolated del (5q)?

A

Anemia - often severe

-usually elderly pts (>65yo) - more often than women

123
Q

What is cellular morphology of MDS with isolated del (5q)?

A

all the megs are mononuclear

124
Q

What is immunophenotype of MDS with isolated del (5q)?

A

no known markers

125
Q

What is prognosis of MDS with isolated del (5q)?

A

good median survial
txable iwth Lenalidomide!!!
10% progress to AML

126
Q

What is refractory cytopenia with multilenage dysplasia?

A

-2 or more lineages show dysplastic changes

~1/2 show nonspecific cytogenetic abnormalities

127
Q

What is the clinical presentation of refractory cytopenia with multilenage dysplasia?

A 
anemia - often severe
usually elderly (>65yo)- more often wo
128
Q

What is the cellular morphology of refractory cytopenia with multilenage dysplasia?

A

granulocytes (if affected) dont granulate normally

neucli doint lobulate normally

129
Q

What is the immunophenotype of refractory cytopenia with multilenage dysplasia?

A

can show abnomral auistion of surface markers

130
Q

What is prognosis of refractory cytopenia with multilenage dysplasia?

A

mean survial 20 mo

10% progress to AML in 2 yrs

131
Q

What is refractory anemia with excess blasts?

A

-5%-9% morpholoigic blasts (RAEB-1)
-10-19% morphologic blasts (RAEB-2)
~1/2 show nonspecific cytogenetic abnormalites

132
Q

What is the clinical presentation of refractory anemia with excess blasts?

A

cytopenia

usually elderly pts (>65 yo)

133
Q

What is cellular morphology of refractory anemia with excess blasts?

A

Blasts and dyspoietic maturation

134
Q

What is immunophenotype of refractory anemia with excess blasts?

A

blast proluation os CD34+ or CD117+

usually evidant

135
Q

What is prognosis of refractory anemia with excess blasts?

A

RAEB-1 25% progress of AML
RAEB-2 33%
POOR :(

Renal, Hematological, and Cardiovascular Organ Systems (9 decks)

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