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Pathology > 2nd Exam: Hematopathology > Flashcards

2nd Exam: Hematopathology Flashcards

1
Q

Pain after drinking alcohol, think:

A

Hodgkin Disease

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2
Q

Auer rods, think this:

A

AML

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3
Q

Translocation t(8;14), think:

A

Burkitt’s Lymphoma

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4
Q

Lymphadenopathy may be due to:

A

reactive ( define) or neoplastic conditions

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5
Q

Ex’s of reactive conditions leading to lymphadenopathy:

A

infections, ai, malignant (non-lymphoid, lymphoid–lymphoma)

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6
Q

Infections that can lead to lymphadenopathy:

A

infectious mono, cat scratch disease, bacterial lymphadenitis, tubeculous lymphadenitits

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7
Q

Ai disease that can lead to lymphadenopathy:

A

RA

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8
Q

Ex’s of malignancies that can lead to lymphadenopathy:

A

non-lymphoid, lymphoid-lymphoma

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9
Q

Ex of non-lymphoid malignancy that can lead to lymphadenopathy:

A

metastatic carcinoma

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10
Q

T-cell zone of normal lymph node:

A

Parafollicular cortex

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11
Q

B-cell zone of normal lymph node:

A

Lymphoid follicles

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12
Q

Symptoms of lymphadenopathies depends on:

A

Node location, central vs. peripheral

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13
Q

Palpable nodes:

A

peripheral

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14
Q

Central nodes:

A

sup vena cava syndrome, obstruction of urethra or bowels

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15
Q

Cancer that begins in lymphoid cells of immune system

A

lymphoma

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16
Q

Lymphoma typically starts here:

A

lymph nodes (enlarged) or extra nodal lymphoid tissue (masses)

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17
Q

2 basic types of lymphoma:

A

hodgkin’s, non-h

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18
Q

Types of non-Hodgkin’s lymphomas:

A

indolent, aggressive

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19
Q

Define effacement:

A

normal structure replaced by tumor cells

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20
Q

2 types of leukemia:

A

lymphoid, myeloid

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21
Q

Malignant progressive, bone marrow produces inc # of immature or abnormal wbcs:

A

Leukemia

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22
Q

Effects of BM infiltration:

A

pain, weakness, shortness of breath, fatigue, CHF, neutropenia, anemia, thrombocytopenia, inc infection , bleeding, petechiae (bleeding into skin)

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23
Q

Clinical presentation of Hematologic Malignancies:

A

malaise, fatigue, w8 loss, fever, organ/ bm infiltration, lymphadenopathy, acute or chronic

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24
Q

Low grade hematologic malignancy:

A

mature appearing cells, low rate of proliferation, chronic, longer life expectancy untreated

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25
Q

High grade hematologic malignancy:

A

immature/ primitive cells, high mitotic rate, rapidly progressive, onset w/in wks, fast death (couple years) wo tx, may cure w aggressive therapy

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26
Q

TF? High grade hematologic malignancy is immunologically primitive.

A

F. (Difference between immunologically primitive and primitive)

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27
Q

Most common acute leukemia in children:

A

ALL

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28
Q

Classification is in regards to:

A

lineage, molecular chara, shape, immunophenotye, Cx syndromes, stage of differentiation

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29
Q

TF? lymphomas and lymphoid leukemias are classified into 1 classification system.

A

T

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30
Q

primitive marker:

A

CD34

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31
Q

5 lymphoid lineages:

A

precursor neoplasm, mature t-cell and b-cell neoplasm, Hodgkin’s lymphoma, post-transplant lymphoproliferative disorders

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32
Q

4 categories of neoplastic proliferations of WBc’s:

A

lymphoid lineage, histiocytic and dentdritic cell neoplasms (rare), hematopoeitic/ myeloid disorders, acute leuk’s of ambiguous origin

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33
Q

Types of precursor lymphoid neoplasms:

A

b-/ t-cell lymphoblastic leukemia/lymphoma

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34
Q

Blasts are associated w acute/ chronic.

A

acute

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35
Q

Markers of T-cell lineage:

A

CD1-8

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36
Q

markers for B-cell lineage:

A

CD10+

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37
Q

Marker shared by both T and B-cell lineages:

A

CD34, primitive marker

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38
Q

myelodysplastic vs. myeloproliferative:

A

inneffective vs effective hematopoiesis

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39
Q

Myeloproliferative neoplasms such as CML, high or low grade?

A

low

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40
Q

Types of hematopoeitic/ myeloid disorders:

A

myeloroliferateive neoplasms, myelodysplastic syndromes, myelodysplastic/myeloproliferative neoplasms, AML and related precursor neoplasms

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41
Q

myelodysplastic/myeloproliferative neoplasms, ineffective or effectve hematopoeisis?

A

both? (check)

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42
Q

ex of myeloproliferative neoplasm:

A

CML

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43
Q

87% of lymphomas are:

A

non-Hodgkin’s

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44
Q

Almost 50% of leukemias are:

A

CLL (60+ men,)

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45
Q

There are more cases of AML than:

A

ALL + CML

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46
Q

Non-Hodgkin’s lymphomas can be broken into these 2 branches:

A

B cell and T cell neoplasms

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47
Q

B cell neoplasms:

A

CLL/ small lymphocytic lymphoma, Diffuse large cell lymphoma, Burkitt’s lymphoma

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48
Q

Ex of T cell neoplasm:

A

mycosis fungoides, cutaneous lymphoid, mushroom like appearance

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49
Q

CD for T lymphs:

A

3, 4, 5, 8

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50
Q

CD for B lymphs and surface Ig:

A

19, 20

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51
Q

CD for most granulocytes:

A

13

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52
Q

CD for granulocytes, R-S cells:

A

15

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53
Q

CD for stem cells, pleuripotent:

A

34

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54
Q

CD for all wbc’s:

A

45

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55
Q

neoplastic cell in Hodgkins:

A

Reed Sternberg cells

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56
Q

Do low grade lymphomas divide?

A

no

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57
Q

Burkitt’s lymphoma:

A

Kids, endemic in Africa, extranodal, begins in man or max, esp in Africa, involves colon, adrenal, kidney, ovary, aggressive, high grade, poor prognosis, tx w chemo

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58
Q

Tx for Burkitt’s lymphoma:

A

chemo

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59
Q

TF? Burkitt’s lymphoma is a primitive B cell neoplasm.

A

F. not primitive, but it is a B cell neoplasm

60
Q

Lymphoma belt:

A

wet, hot, malaria, infected with EBV, immunocompromised

61
Q

most highly proliferative human tumor:

A

Burkitt’s lymphoma

62
Q

30% of all childhood lymphomas in US:

A

Burkitt’s

63
Q

Area affected in most US cases of Burkitt’s lymphoma:

A

abdomen

64
Q

Burkitt’s lymphoma, intra or extranodal?

A

extranodal

65
Q

TF? Burkitt’s lymphoma never begins in the lymph nodes.

A

F. rarely

66
Q

Pathology of Burkitt’s lymphoma:

A

B cell origin (not primitive, CD 19, 20), small-intermediate size lymphos, monotonous pop, round nuclei, prominent nucleoli, high mitotic rate, starry sky patter w macs, apoptosis of tumor cells

67
Q

pale area of starry sky pattern of Burkitt’s Lymphoma slide:

A

benign macrophages

68
Q

Causes of Burkitt’s lymphoma:

A

Latent EBV infection, translocation, t(8;14) (ebv related to mono, too) How does malaria play a role?)

69
Q

Cases of Burkitt’s Lymphoma are more commonoly assoc w latent EBV infection in U.S. or Africa?

A

Africa

70
Q

Translocation resulting in Burkitt’s lymphoma involves:

A

c-myc (8q24) and IgH gene (14q32), overexpression of c-myc

71
Q

c-myc:

A

regulates proliferation (of what, the B cells?), oncogene

72
Q

What is translocated in Burkitt’s lymphoma?

A

c-myc from q arm of #8 + p and rest of q from #14

73
Q

Genes effected in translocation that leads to Burkitt’s lymphoma:

A

H chain gene (antibody H chains?, H chain enhancer?) and c-myc

74
Q

Most lymphomas and leukemias are assoc w:

A

molecular/ chromosomal abnormalities

75
Q

2 moa for lymphomas and leukemia:

A

activate oncogenes, lose tsg’s

76
Q

How are oncogenes activiated or tsg’s lost, leading to lymphomas and leukemias?

A

variety of mechs

77
Q

Etiologic and pathogenic factors in leukemias and lymphomas:

A

molecular abnormalities, translocations, oncogenes, inherited genes, viruses, infection, chronic antigenic stimulation, immune dysfunction, environmental agents, chemo, radiation

78
Q

Virus that makes lymphs divide more frequently:

A

EBV

79
Q

Cx man of Hodgkin’s Disease:

A

Pel-Ebstein fever, night sweats, pruritis, painless cervical and mediastinal lymphadenopathy, except after alcohol

80
Q

Pel-Ebstein fever:

A

cyclically fever, usually 1-2wks

81
Q

pruritis:

A

itchy skin wo rash

82
Q

Lymphadenopathy:

A

abnormal number, size or consistency

83
Q

early presentation of Hodgkins:

A

neck lymphadenopathy

84
Q

Spread of Hodgkin’s:

A

to adjacent ln groups, orderly, begins in 1 ln, splenic involvement late in development, progression makes staging imp in prognosis, because it has to spread to the spleen via adjacent tissues

85
Q

High grade Hodgkin’s:

A

includes BM and liver

86
Q

Types of Hodgkin’s

A

nodular sclerosis and mixed cellular types

87
Q

Nodular sclerosis type Hodgkin’s:

A

75%, usually young women, cervical, mediastinal nodes, dx in Stage I-II usually, reactive, eosinophilic lymphos, lacunar cells, rarely R-S cells, birefringent bands of collagen dividing node into nodules

88
Q

Mixed cellular type Hodgkin’s

A

25%, men over 50, dx in Stage III-IV usually, many R-S cells and lymphocytes, eosinophils, inflammatory cells in background

89
Q

Lymphadenopathy and splenomegaly w multiple nodules is assoc w:

A

Hodgkin’s, splenomegaly is also assoc with AML

90
Q

Malignant cell of Hodgkin’s

A

Reed-Stenberg cell

91
Q

R-S cell is more abundant in this type of Hodgkin’s:

A

mixed cellular type

92
Q

TF? R-S cells are always diagnostic of Hodgkin’s.

A

F. in the right env

93
Q

Genome found in some R-S cells:

A

EBV, esp mixed cellular type

94
Q

Cell origin of R-S cells:

A

B cells, but does not express typical B cell markers, CD15 (granulocyte marker) and CD30 (activation marker), used to calsify lymphoma as Hodgkins

95
Q

Cell origin of Hodgkin’s cells:

A

B cells

96
Q

granulocyte marker:

A

CD15

97
Q

activation marker:

A

CD30

98
Q

Subtype of R-S cell:

A

Lacunar cells, nodular sclerosis

99
Q

How to differentiate bw nodular sclerosis type and mixed cellular type:

A

lacunar cells: nodular sclerosis, mixed: more R-S cells, EBV found in R-S cells

100
Q

Hodgkin’s cells:

A

binucleated, bilobated, mirror image, prominent nucleoli, owl-like appearance

101
Q

B-cell that does not mark w typical B cell markers, think:

A

Hodgkin’s

102
Q

Large, clear cells in distinct space, think:

A

nodular sclerosis type Hodgkin’s

103
Q

Major difference between Hodgkin’s disease and non-Hodgkin’s Lymphoma:

A

Hodgkin’s does not skip to distant nodes

104
Q

System used to stage Hodgkin’s Disease:

A

Ann Arbor System

105
Q

Stage I Hodgkin’s:

A

one ln or one ln group, 100% 5y survival

106
Q

Stage II Hodgkin’s:

A

2+ ln, same side of diaphragm, 87% 5y survival

107
Q

Stage III Hodgkin’s:

A

lns on both sides of diaphragm, 71% 5y survival

108
Q

Stage IV Hodgkin’s:

A

disseminated, non-nodal organ involvement, 45% 5y survival

109
Q

Stage I or II Hodgkins recurrence rate after 20 years:

A

less than 20%

110
Q

Oral mani of lymphomas:

A

involve palate, tonsils, Waldeyers ring (circle of lymphoid tissue in back of throat)

111
Q

neck nodes are indicative of what tumor type?

A

all types

112
Q

Oral lymphomas are usually of __ cell origin.

A

B

113
Q

Oral lymphomas:

A

older pts, usually secondary lymphoma, complication of chemo (low platelets, WBC count), infections likely (ie herpes zoster) the

114
Q

Complication of chemotherapy tx for oral lymphomas:

A

low platelets, WBC count, ulcers, fungal infections, herpes

115
Q

Oral lymphomas, 1’ or 2’?

A

either, usually 2’

116
Q

Pt w lymphoma is more likely to get this infection:

A

herpes zoster, oral manifestation

117
Q

Pharyngeal tonsil is aka:

A

adenoid tonsil

118
Q

Interrupted circle of protective lymphoid tissue:

A

Waldeyer’s Ring

119
Q

Location of Pharyngeal tonsils:

A

upper midline in nasopharynx

120
Q

Location of tubal tonsils:

A

near opening of auditory tube

121
Q

Location of palatine tonsils:

A

sides of oropharynx

122
Q

Location of lingual tonsils:

A

under mucosa of pos 3rd of tongue

123
Q

Tonsil that are part of Waldeyer’s Ring:

A

Pharyngeal, tubal, palatine, lingual

124
Q

Block in WBC differentiation/ maturation:

A

Acute leukemia

125
Q

Many immature WBCs (CD34+, primitive) in BM can lead to:

A

suppression of normal hematopoeisis, anemia, thrombocytopenia

126
Q

Acute leukemia can spread to:

A

liver, spleen, ln, various organs inc. meningeal infilatration

127
Q

Meningeal infiltration is seen in:

A

Acute leukemia, children

128
Q

BM aspiration is done here:

A

posterior superior iliac crest, through cortical bone, into marrow space bw spongy bone

129
Q

Normal BM is 50%:

A

fat

130
Q

Leukemic BM is:

A

hypercellular, much less fat, diffusely infiltrated, full of blasts

131
Q

Heterogenous group of acute/ aggressive myeloid malignancies:

A

AML

132
Q

AML:

A

wide age range, uncommon in kids, onset w/in wks-months, fatigue, fever, skin palor, swollen, bleeding gums (hypertropy, neoplastic cell infilatration), petechiae, hepatosplenomegaly

133
Q

splenomegaly is assoc with:

A

Hodgkin’s and AML, CLL

134
Q

% remission from AML w chemo:

A

60%, only 15% disease free after 5y

135
Q

Pathologic findings of AML w granulocytic maturation:

A

inc WBC in peripheral blood, many blasts, auer rods, round nuclei and azurophilic granules, reduced platelets (under 100,00), more than 30% blasts in BM, normally 3%, positive myeloperoxidase staining (enzyme in primary granules)

136
Q

Enzyme found in primary granules of AML w granulocytic maturation:

A

myeloperoxidase

137
Q

of blasts normally in peripheral blood:

A

none

138
Q

Most common leukemia in US:

A

CLL

139
Q

CLL:

A

men 60+, often no symptoms at dx (leukemic cells in peripheral blood), often involve lymph nodes (lymphoma), indolent/ painless course

140
Q

Pathology of CLL:

A

inc WBC in peripheral blood, 5,000+ abnormal (small, smooshed, broken) lymphos in peripheral blood that look normal, smudge cells indicate increased cell fragility, inc lymphos in BM, aggregates or clusters, mark with CD 19 and 20 (B cells) and CD 5 (T cell marker)

141
Q

How to determine type of leukemia:

A

CD 5, a T cell marker

142
Q

BM of CLL pt:

A

hypercellular, no fat, almost all lymphos

143
Q

When to tx CLL:

A

lymphadenopathy, hepatosplenomegaly, anemia, low platelets

144
Q

Px of CLL:

A

good: 10-15 surival

145
Q

TF? There is no lymphadenopathy with Burkitt’s lymphoma:

A

F. right? since it CAN start in lymph nods but usually does not (check)

Pathology (23 decks)

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