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Blood and Lymph > Leukemias and Lymphomas > Flashcards

Leukemias and Lymphomas Flashcards

1
Q

Acute Leukemia Types

A

1) Acute Myeloid Leukemia 2) Acute Lymphoblastic Leukemia

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2
Q

Symtoms of Acute Leukemia

A

Anemia (fatigue, pallor) Thrombocytopenia (easy bruising, petechiae) Neutropenia (infection)

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3
Q

What are the rare signs of Acute Leukemia?

A

Leukostasis, DIC, infiltration of WBCs in skin, gums, lymphs nodes

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4
Q

What is general Blast Marker?

A

CD34

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5
Q

Risk Factors of Acute Leukemia

A

Previous Chemo (aklylating agent, Topo II); Tobacco smoke, Radiation, Benzen, Down Syndrom, Bloom, Fanconi Anemia, ataxia-Telang

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6
Q

AML

A

Acute Myeloid Leukemia - neoplastic accumulation of myeloblasts in BM

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7
Q

ALL

A

Acute Lymphoblastic Leukemia - neoplastic accumulation of lymphoblasts in BM

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8
Q

Age of Diagnosis: AML vs ALL

A

AML: 65 YO; ALL:

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9
Q

Diagnosis of AML

A

> 20% myeloblasts in marrow and/or blood via smear or flow cytometry OR have cytogenetic abnormality

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10
Q

Diagnosis of ALL

A

Packed marrow with lymphoblasts - no set percentage

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11
Q

Markers for ALL vs AML

A

Both: CD34; AML: CD117(Ckit) or MPO; ALL: TdT

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12
Q

Remission/prognosis of AML

A

60% remission; consider HSC transplant for healthy pats with high risk of relapse

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13
Q

Remission/prognosis of ALL

A

95% remission; cure rate 80% in children; Adults 60-80% remission; 50% cure rate.

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14
Q

what factors decrease prognosis in ALL?

A

Under 1 or over 10 YO; high WBC, hypodiploidy, slow to respond to treatment

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15
Q

Types of AML

A

Congenital OR Therapy related

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16
Q

RUNX1-RUNX1T1 Translocation

A

t(8;21)

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17
Q

RUNX1

A

alpha subunit in Core Binding Factor is inactive; unable to differentiate homeostasis

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18
Q

RUNX1-RUNX1T1 AML

A

Mutation in alpha CBF; good prognosis

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19
Q

CBFB-MYH11 mutation

A

Inv 16 or t(16:16)

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20
Q

CBFB-MYH11 Presentation

A

Baso-Eos in BM: immature eosinophils with baso granules; mutation in CBF beta - for beta Core Binding Factor; Good prognosis

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21
Q

PML-RARA mutation

A

t(15:17); also known as APL

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22
Q

APL clinical Presentation

A

hypergranular with multiple Auer Rods; Retinoid Acid Receptor Alpha protein mutated (unable to differentiate); risk of DIC

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23
Q

APL treatment

A

All Trans Retioic Acid; not chemo

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24
Q

RBM15-MKL1 mutation

A

t(1;22)

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25
Q

RBM15-MKL1 Clinical Presentation

A

Slow megakaryoblastic differentiation; seen in infants with down syndrome; good prognosis

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26
Q

MLL abnormalities with 11q23

A

poor prognosis

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27
Q

Prognosis of Congenital vs. Therapy AML?

A

Congenital are usually good (except 11q23) while therapy is very bad prognosis

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28
Q

what therapies cause AML?

A

Alkylating agents, radiation, topo II inhibitors

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29
Q

What AML has 2-8 year latency?

A

Alkylating agents or radiation

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30
Q

What karyotype is associated with Alkylating Agent or radiation induced AML?

A

Complex karyotype with whole or partial loss of Ch5 and 7

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31
Q

what AML has 1-2 year latent period?

A

Topo II inhibitors

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32
Q

What karyotype is associated with Topo II inhibitor induced AML?

A

MLL with 11q23

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33
Q

Which therapy related AML has a more progressive path?

A

Topo II inhibitor induced

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34
Q

FLT3

A

Internal Tandem Repeat; has an extremely bad prognosis of AML - trumps all other factors

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35
Q

NPM1 mutation

A

Good prognosis for AML if negative for FLT3

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36
Q

CEBPA mutation

A

Good prognosis for AML if negative for FLT3

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37
Q

What factors influence prognosis of AML?

A

FLT-3, NPM1, CEBPA

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38
Q

types of ALL?

A

B-ALL and T-ALL

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39
Q

prevalence of Congenital vs. Therapy induced AML?

A

90% Congential

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40
Q

Prevalence of B-ALL vs T-ALL?

A

B-ALL is 80-85% of ALL cases

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41
Q

what markers distinguish B-ALL from T-ALL?

A

B-ALL: CD19, CD22, CD79a, lack CD20; T-ALL have CD2, CD3, CD7 (CD2-8)

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42
Q

BCR-ABL mutation

A

t(9:22); different fusion protein from CML (190 NTs) still on Philadelphia Chromosome

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43
Q

BCR-ABL Clinical Manifesation

A

Adults; poor prognosis

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44
Q

MLL Mutation

A

t(11q23)

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45
Q

MLL - clinical manifestation

A

Common in neonates and infants, poor prognosis

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46
Q

ETV6-RUNX1 mutation

A

t(12;21)

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47
Q

ETV6-RUNX1 Clinical Manifestation

A

Mostly in children; very favorable prognosis

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48
Q

T-ALL clinical manifestation

A

More in males; adolescents and young adults; mediastinal mass; worse prognosis than B-ALL

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49
Q

Myelodysplastic Syndrome

A

Clonal population from hematopoietic stem cell takes over; failure to make normal cells over one of more lineages

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50
Q

Risks of MDS?

A

Increased risk of progression to AML

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51
Q

MDS diagnosis

A

One persistent Cytopenia; Evidence of dysplasia, increased myeloblasts, clonal cytogenetic abnormalities (sideroblast, bilobed nuclei in nuetrophils, hypolobulated small megakaryocytes)

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52
Q

Pseudo-pelger-Huet Cells

A

bilobed nuclei in neutrophils; characteristic of MDS

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53
Q

What causes MDS?

A

Primary/idiopathic or Therapy Related

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54
Q

Primary MDS

A

Usually occurs in late adulthood with insidious onset; cytogenetic abnormalities

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55
Q

Cytogenetic abnormalities in primary MDS

A

Partial or whole deletion sof Ch5 and 7, Deletion of 5q, trisomy 8

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56
Q

Therapy MDS

A

due to non-neoplastic causes ( B12/Folate def, virus, toxin, heavy metal) or Neoplastic (chemo drugs or radiation that causes whole or partial deletions of Ch5 and/or 7)

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57
Q

Low Grade MDS basic definition

A

Myeloblasts are not increased in frequency;

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58
Q

High Grade MDS basic Definition

A

Myeloblasts increased in frequency; >5% in marrow; and/or >2% in periphery

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59
Q

Types of low grade MDS?

A

1) refractory cytopenia with unilineage dysplasia (RC_UD) 2) refractory cytosine with multilineage dysplasia (RC-MD) 3) MDS with isolated 5q deletion

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60
Q

RC-UD

A

Refractory cytopenia with unilineage dysplasia - low grade MDS; good prognosis; survival is >5 years with 2% progressing into AML; usually associated with refractory anemia and not thrombi or neutropenia

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61
Q

RC-UD

A

Refractory cytopenia with multilineage dysplasia; dysplasia in 2+ lineasge, whose prognosis than RC-UD; survival 2.5 years, 10% progression in AML

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62
Q

MDS with 5q deletion

A

anemia, increased platelets and marrow with small, round, non-lobulated nuclei in megakaryocytic

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63
Q

Types of high grade MDS

A

Refractory anemia with excess blasts-1 and 2

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64
Q

RAEB-1 vs. RAEB-2

A

both high grade MDS; 1: Blasts from 5-9% in BM and 2-4% in periphery 2: 10-19% in BM and 5-19% in periphery; 1 survival is 16 months with 25% transformation to AML; 2: survival 9 months with 33% progression to AML; 2) has small round non-lobulated nuclei

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65
Q

Myeloproliferative neoplasms

A

Too many (non-dysplastic) cells of one or more lineages

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66
Q

Age of MPS

A

late adulthood

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67
Q

Common signs of MPS?

A

high WBC, hypercellular marrow; Hepatosplenomegaly; BM fibrosis, Less able to transform into AML or MDS

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68
Q

What is more transformative MDS or MPN?

A

MDS into AML

69
Q

Types of MPN?

A

1) Chronic myelogenous leukemia 2) polycythemia Vera 3) Primary Myelofibrosis 4) Essential Thrombocytopenia

70
Q

CML

A

a type of MPN; with neoplastic proliferation of neutrophils and basophils; characteristic BCR-ABL translocation (210; Philadelphia Ch)

71
Q

CML Symptoms

A

Fatigue, weight loss, night sweats, splenomegaly, anemia occurs in 40-50 yo

72
Q

Initial Phase of CML?

A

also called chronic; neutrophilia, basophilia, increased platelets, hypercellular marrow, small megakaryocytic with round, non-lobulated nuclei, no dysplasia

73
Q

Blast Phase of CML?

A

> 20% of blasts in marrow/blood, usually myeloblasts sometimes lymphoblasts

74
Q

Treatment of CML?

A

Imatinib/Gleevec or Protein Tyrosine Inhibitors

75
Q

PolyCythemia Vera

A

Type of MPN with Increased RBC mass (associated with increase in neutrophils and platelets as well); JAK2 or V617F mutations

76
Q

PV - Symptoms

A

Hyperviscosity of blood: Headaches, dizziness,venous and arterial thrombosis, visual problems, parasthesia, plethora, itching, hepatosplenomegaly

77
Q

Plethora

A

flushed face due to congestion in PV

78
Q

why is there itching in PV?

A

due to increased histamine release from Mast cell overproduction

79
Q

Where do thromboembolic form in PV?

A

Mesenteric, portal and splenic Veins

80
Q

Treatment of PV?

A

Plebotomy to reduce clotting; aspirin, mild chemo

81
Q

Prognosis of PV?

A

good, survival 10-20 years

82
Q

Primary Myelofibrosis

A

type of MPN, proliferation of granulocyte and megakaryocytic lineaste (no erythrocytosis) and Marrow fibrosis; JAK2 mutation

83
Q

PMF stages

A

Prefibrotic: hypercellular marrow; large megakaryocytes; fibrotic: reticulin fibrosis of BM, leukoerythroblastosis, falling blood counts, dacrocytes, extramedually hematopoiesis in spleen (enlarged spleen)

84
Q

Prognosis of PMF

A

5 year survival, little AML transforamtion

85
Q

Essential Thrombocytopenia

A

Type of MPN, normocellular marrow, with large and bizzarre looking megakaryocytes; JAK2 mutation

86
Q

ET symtoms

A

usually asymptomatic, but increased risk of bleeding and thrombosis (transient ischemic attacks, digital ischemia with paresthesia, NO splenomegaly)

87
Q

ET prognosis

A

Indolent disease; survival of 10-15 years

88
Q

what MPN is associated with neutrophils?

89
Q

what MPN is associated with RBC?

90
Q

what MPN is associated with Granulocytes and megakaryocytes?

A

PFM (both) and ET( only megakaryocytic)

91
Q

what MPN does not have splenomegaly?

92
Q

what MPNs have JAK2 mutations?

A

PV, PMF, ET (all except CML)

93
Q

category of plasma neoplasms, NHL and HL?

A

neoplastic mature B- lymphoid cells that results in lymph node mass or extra nodal mass

94
Q

types of NHL

A

SLL/CLL, Follicular Lymphoma, Mantel Cell lymphoma, Burkitt Lymphoma, Diffuse Large B-cell Lymphoma

95
Q

SLL vs CLL

A

Pre or Post Germinal Center B cell. CLL: blood lymphocytosis with BM involvement, most common western society; SLL: is lymphocytosis in extrameduallary site (7% of NHL)

96
Q

Clinical Presentation of SLL/CLL?

A

Asymptomatic or with fatigue, infection, AIHA, hepatosplenomegaly, lymphadenopathy

97
Q

What population does SLL/CLL occur in?

A

Males and older adults

98
Q

Lab findings of SLL/CLL?

A

Lymphocytosis, small round dense nuclei, smudge and basket cells; pro lymphocytes with effaced nodes and pale proliferation centers

99
Q

Prolymphocytes

A

large cytoplasm with round, fine nuclei found in SLL and CLL

100
Q

Markers for SLL/CLL

A

CD5 and CD23 (most important) negative for CD10 and FMC7

101
Q

Molecular Defect associated with SLL/CLL?

A

13q14 deletion

102
Q

Follicular Lymphoma origin

A

germinal center

103
Q

Follicular lymphoma definition

A

Neoplastic proliferation of small B-cells that form follicle like nodules in lymph node

104
Q

Follicular Lymphoma clinical signs

A

painless lymphadenopathy in nodes, spleen, BM, waldeyer’s ring, GI

105
Q

Age of onset of Follicular lymphoma

A

late adulthood

106
Q

Lab Findings of Follicular Lymphoma

A

Crowded follicle in cortex and medulla, no matel zone, node effacement, homogenous follicle with no tangible body macrophages

107
Q

Markers of Follicular Lymphoma

A

Cd19, CD20, BCL2*, CD10, BCL6, negative for CD5 and CD23

108
Q

Molecular Defect in Follicular Lymphoma

A

t(14;18) causes overexpression of BCL2 an oncogene that inhibits apoptosis in the germinal center

109
Q

Mantel Cell lymphoma definition

A

Neoplastic Proliferation of small B-cells in mantel zone

110
Q

Mantel Cell lymphoma Clinical signs

A

painless lymphadenopathy in nodes, spleen, MB, GI, waldey’s, hepatosplenomegaly. ITs moderately agressive compared to follicular!

111
Q

Age of onset for Mantel cell lymphoma

A

late adulthood

112
Q

Lab findings of mantle cell lymphoma

A

Effaced node with small to medial cells with irregular nuclei

113
Q

Markers of Mantel Cell Lymphoma

A

Cd19, CD20, *CD5, *BCL1 negavie for CD10, and BCL6

114
Q

Molecular Defect with Mantel Cell lymphoma

A

t(11;14) overexpression of BCL1 to promote phosphorylation of RB and transition of G1 to S phase

115
Q

Burkitt Lymphoma definition

A

neoplastic proliferation of intermiate B-cells associated with EBV

116
Q

Various kinds of Burkitt Lymphoma

A

Edemic, Sporadic, Immunodeficient

117
Q

Endemic Burkitt

A

Occurs in 4-7 YO in africa, Mass on jaw and abdomen, +EBV

118
Q

Sporadic Burkitt

A

Children or young adults, ileoceccal mass; low association with EBC

119
Q

Immunodeficient Burkitt

A

HIV occurs with 25-40% EBV

120
Q

Prognosis of Burkitt Lyphoma

A

Highly agressive but 60% curable

121
Q

Lab findings with Burkitt Lymphoma

A

Medium cells with round neulei, basophilic city with lipid vacuoles, high mitotic index, starry sky appearance

122
Q

Markers of Burkitt Lymphoma

A

CD19, CD20, CD10, BCL6, *MYC, negative for CD5 and CD23

123
Q

Molecular Defect with Burkitt Lymphoma

A

t(8;14) to form c-myc an TF that promotes growth

124
Q

Diffusion Large B-cell lymphoma Definition

A

neoplastic proliferation of large B-cells great than a histiocyte nucleus or small lymphocyte that grow into sheets

125
Q

Clinical symptoms of Large-Bcell lymphoma

A

enlarged lymph or extra nodal mass; rapidly progressive; B-symtoms; potentially curable

126
Q

Age of onset of Large B-cell Lymphoma

A

late adulthood

127
Q

Lab Findings of large B-cell Lymphoma

A

Effaced nodes with necrosis and permeation into tissue, centroblasts with immunoblasts

128
Q

Markers for Large Bc ell lymphoma

A

CD19 and CD20

129
Q

Molecular Defect of Large B-cell lymphoma

A

sporadic mutation or transformation from lower grade lymphoma

130
Q

Types of Hodgkin Lymphoma

A

Nodule-Lymphocyte predominate hodgkins lymphoma or Classic HL

131
Q

Common characteristics of CHL

A

malignant cells are minority (

132
Q

Reed Sternberg Cells

A

characteristic of CHL; large up to 100 um, multi lobed nulcue, large eosinophilic nucleolus, ample cytoplasm

133
Q

Types of CHL

A

Nodular sclerosis, mixed cellularity, lymphocyte rich, lymphocyte depleted

134
Q

Nodular Sclerosis Clinical Pres

A

Most common type of CHL (50-80%); in young adults and femals; EBC not common; enlarged cervical and mediastinal nodes above diaphragm

135
Q

Morphology of Nodular Sclerosis

A

Thick lymph node with capsule and collagen sclerosis, RS in lacunar cells; background of small round lymphoctes, eos, plasma cells

136
Q

Mixed Cellularity Clinical Prognossi

A

20-30% of CHL cases, most prevalent in kids and elderly, highly associated with EBV; B-symtoms with nodes below or on both sides of diaphragm

137
Q

Morphology of Mixed Cellularity

A

Large cells that lack broad bands of collagen; abundant eosinophils

138
Q

Lymphocyte Rich Clinical Characteristics

A

5% of CHL, Best prognosis, with B-symptoms, enlarged nodes below or on both sides of diaphragm

139
Q

Morphology of Lymphocyte Rich

A

Lack broad collagen, RS cells are very rare

140
Q

Lymphocyte Depleted Clinical Pres

A

1% of CHL, most agressive, associated with elderly and HIV+ as well as EBV+

141
Q

Morphology of Lymphocyte depleted

A

NO lymphocytes, numerous RS cells that are anapestic and bizarre looking

142
Q

Dyscarsia

A

clonal proliferation of plasma cells that secrete single immunoglobulin that originates in BM and can present extramedually

143
Q

Types of Plasma cell Disorders

A

Plasma Cell myeloma, Monoclonal Gammaopathyof Undetermiend significance, Plasmcytoma

144
Q

PCM definition

A

malignant proliferation of Plasma cells in bone marrow with overproduction of IgG and IgA

145
Q

Clincical features of PCM

A

Asymptomatic to progressive; bone pain due to lesions or osteoporosis, weakness or tiredness due to anemia, hypercalcemia, increased risk of infection, AL amyloidosis

146
Q

Age group for PCM

A

older adult

147
Q

Diagnostic criteria of PCM

A

Elevated M protein (IgG or IgA) in serum or urine detectable by protein electrophoresis, BM clonal plasma cells, CRAB, sometimes peripheral plasma cells, Reuleaux

148
Q

CRAB

A

feature unique to PCM; Hypercalcemia, renal insufficiency, Anema/AL amyloidosis, Bone lesions

149
Q

MGUS Definition

A

Increased serum or urine M-spike without myeloma, amyloidosis, or lymphoprolifeative disorder

150
Q

MGUS Clinical Features

A

Most common in late adulthood; Precursor for PCM

151
Q

MGUS diagnostic criteria

A

Increased M component, but less than with PCM, Marrow Plasmacytosis

152
Q

Types of Plasmactoma

A

Solitary plasmacytoma of bone and Extraosseous/Extramedually plasmcytoma

153
Q

Solitary Plasmacytoma of Bone Definition

A

Loca tumor of bone with myeloma like cells

154
Q

Solitary Plasmacytoma of Bone Diagnostic Criteria

A

Single bone lesion, NO CRA; low to normal Mprotein

155
Q

Extraosseous/Medually plasmacytoma definiation

A

PCM-cell mass lesions outside of bone in soft tissue; most commonly respiratory

156
Q

Extraosseous/Medually plasmacytoma clinical age

A

2/3 are male; middle age

157
Q

Extraosseous/Medually plasmacytoma Diagnostic criteria

A

similar to solitary: single lesion, NO CRA, low to normal Mprotein

158
Q

Plasmacytoma vs. PCM?

A

PCM has multiple bone lesions and CRAB, Plasmacytoma has a single lesion and NO CRA

159
Q

MGUS vs PCM

A

MGUS: no bone lesions or PCM symptomes, but increased IgG or IgA

160
Q

which CHL are associated with EBV?

A

Mixed and lymphocyte depleted

161
Q

What CHL have B-symptoms?

A

Mixed and Lymphocyte rich

162
Q

what CHL have nodes blow diaphrgam?

A

Mixed and Lymphocyte rich

163
Q

what NHL are positive fo CD10 and BCL6?

A

Follicular and Burkitt

164
Q

high grade

A

means acute; rapidly enlarging mass, high WBC count, almost complete replacement of normal cells.

165
Q

treatment of high grade leukemia

A

radiation, stem cell transplant, palliative treatment, rarely surgery

166
Q

Low grade leukemia

A

chronic; midly enlarged lymph nodes for extensive period of time, increased WBC count, often will die with the disease rather than from it.

167
Q

Treatment of low grade leukemia

A

no therapy, treat symptoms or survelliance

168
Q

Chronic Leukemia

A

usually CLL or CML; increased WBC due to normal, but clonal WBC population. Grandual onset. Natural disease progression with small risk of transformation into high grade.

Blood and Lymph (6 decks)

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