2nd Exam: Hematopathology Flashcards Preview

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Flashcards in 2nd Exam: Hematopathology Deck (145)
1

Pain after drinking alcohol, think:

Hodgkin Disease

2

Auer rods, think this:

AML

3

Translocation t(8;14), think:

Burkitt's Lymphoma

4

Lymphadenopathy may be due to:

reactive ( define) or neoplastic conditions

5

Ex's of reactive conditions leading to lymphadenopathy:

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

6

Infections that can lead to lymphadenopathy:

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

7

Ai disease that can lead to lymphadenopathy:

RA

8

Ex's of malignancies that can lead to lymphadenopathy:

non-lymphoid, lymphoid-lymphoma

9

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

metastatic carcinoma

10

T-cell zone of normal lymph node:

Parafollicular cortex

11

B-cell zone of normal lymph node:

Lymphoid follicles

12

Symptoms of lymphadenopathies depends on:

Node location, central vs. peripheral

13

Palpable nodes:

peripheral

14

Central nodes:

sup vena cava syndrome, obstruction of urethra or bowels

15

Cancer that begins in lymphoid cells of immune system

lymphoma

16

Lymphoma typically starts here:

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

17

2 basic types of lymphoma:

hodgkin's, non-h

18

Types of non-Hodgkin's lymphomas:

indolent, aggressive

19

Define effacement:

normal structure replaced by tumor cells

20

2 types of leukemia:

lymphoid, myeloid

21

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

Leukemia

22

Effects of BM infiltration:

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

23

Clinical presentation of Hematologic Malignancies:

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

24

Low grade hematologic malignancy:

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

25

High grade hematologic malignancy:

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

26

TF? High grade hematologic malignancy is immunologically primitive.

F. (Difference between immunologically primitive and primitive)

27

Most common acute leukemia in children:

ALL

28

Classification is in regards to:

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

29

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

T

30

primitive marker:

CD34

31

5 lymphoid lineages:

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

32

4 categories of neoplastic proliferations of WBc's:

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

33

Types of precursor lymphoid neoplasms:

b-/ t-cell lymphoblastic leukemia/lymphoma

34

Blasts are associated w acute/ chronic.

acute

35

Markers of T-cell lineage:

CD1-8

36

markers for B-cell lineage:

CD10+

37

Marker shared by both T and B-cell lineages:

CD34, primitive marker

38

myelodysplastic vs. myeloproliferative:

inneffective vs effective hematopoiesis

39

Myeloproliferative neoplasms such as CML, high or low grade?

low

40

Types of hematopoeitic/ myeloid disorders:

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

41

myelodysplastic/myeloproliferative neoplasms, ineffective or effectve hematopoeisis?

both? (check)

42

ex of myeloproliferative neoplasm:

CML

43

87% of lymphomas are:

non-Hodgkin's

44

Almost 50% of leukemias are:

CLL (60+ men,)

45

There are more cases of AML than:

ALL + CML

46

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

B cell and T cell neoplasms

47

B cell neoplasms:

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

48

Ex of T cell neoplasm:

mycosis fungoides, cutaneous lymphoid, mushroom like appearance

49

CD for T lymphs:

3, 4, 5, 8

50

CD for B lymphs and surface Ig:

19, 20

51

CD for most granulocytes:

13

52

CD for granulocytes, R-S cells:

15

53

CD for stem cells, pleuripotent:

34

54

CD for all wbc's:

45

55

neoplastic cell in Hodgkins:

Reed Sternberg cells

56

Do low grade lymphomas divide?

no

57

Burkitt's lymphoma:

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

58

Tx for Burkitt's lymphoma:

chemo

59

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

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

60

Lymphoma belt:

wet, hot, malaria, infected with EBV, immunocompromised

61

most highly proliferative human tumor:

Burkitt's lymphoma

62

30% of all childhood lymphomas in US:

Burkitt's

63

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

abdomen

64

Burkitt's lymphoma, intra or extranodal?

extranodal

65

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

F. rarely

66

Pathology of Burkitt's lymphoma:

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

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

benign macrophages

68

Causes of Burkitt's lymphoma:

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

69

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

Africa

70

Translocation resulting in Burkitt's lymphoma involves:

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

71

c-myc:

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

72

What is translocated in Burkitt's lymphoma?

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

73

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

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

74

Most lymphomas and leukemias are assoc w:

molecular/ chromosomal abnormalities

75

2 moa for lymphomas and leukemia:

activate oncogenes, lose tsg's

76

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

variety of mechs

77

Etiologic and pathogenic factors in leukemias and lymphomas:

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

78

Virus that makes lymphs divide more frequently:

EBV

79

Cx man of Hodgkin's Disease:

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

80

Pel-Ebstein fever:

cyclically fever, usually 1-2wks

81

pruritis:

itchy skin wo rash

82

Lymphadenopathy:

abnormal number, size or consistency

83

early presentation of Hodgkins:

neck lymphadenopathy

84

Spread of Hodgkin's:

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

High grade Hodgkin's:

includes BM and liver

86

Types of Hodgkin's

nodular sclerosis and mixed cellular types

87

Nodular sclerosis type Hodgkin's:

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

Mixed cellular type Hodgkin's

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

89

Lymphadenopathy and splenomegaly w multiple nodules is assoc w:

Hodgkin's, splenomegaly is also assoc with AML

90

Malignant cell of Hodgkin's

Reed-Stenberg cell

91

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

mixed cellular type

92

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

F. in the right env

93

Genome found in some R-S cells:

EBV, esp mixed cellular type

94

Cell origin of R-S cells:

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

95

Cell origin of Hodgkin's cells:

B cells

96

granulocyte marker:

CD15

97

activation marker:

CD30

98

Subtype of R-S cell:

Lacunar cells, nodular sclerosis

99

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

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

100

Hodgkin's cells:

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

101

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

Hodgkin's

102

Large, clear cells in distinct space, think:

nodular sclerosis type Hodgkin's

103

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

Hodgkin's does not skip to distant nodes

104

System used to stage Hodgkin's Disease:

Ann Arbor System

105

Stage I Hodgkin's:

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

106

Stage II Hodgkin's:

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

107

Stage III Hodgkin's:

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

108

Stage IV Hodgkin's:

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

109

Stage I or II Hodgkins recurrence rate after 20 years:

less than 20%

110

Oral mani of lymphomas:

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

111

neck nodes are indicative of what tumor type?

all types

112

Oral lymphomas are usually of __ cell origin.

B

113

Oral lymphomas:

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

114

Complication of chemotherapy tx for oral lymphomas:

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

115

Oral lymphomas, 1' or 2'?

either, usually 2'

116

Pt w lymphoma is more likely to get this infection:

herpes zoster, oral manifestation

117

Pharyngeal tonsil is aka:

adenoid tonsil

118

Interrupted circle of protective lymphoid tissue:

Waldeyer's Ring

119

Location of Pharyngeal tonsils:

upper midline in nasopharynx

120

Location of tubal tonsils:

near opening of auditory tube

121

Location of palatine tonsils:

sides of oropharynx

122

Location of lingual tonsils:

under mucosa of pos 3rd of tongue

123

Tonsil that are part of Waldeyer's Ring:

Pharyngeal, tubal, palatine, lingual

124

Block in WBC differentiation/ maturation:

Acute leukemia

125

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

suppression of normal hematopoeisis, anemia, thrombocytopenia

126

Acute leukemia can spread to:

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

127

Meningeal infiltration is seen in:

Acute leukemia, children

128

BM aspiration is done here:

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

129

Normal BM is 50%:

fat

130

Leukemic BM is:

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

131

Heterogenous group of acute/ aggressive myeloid malignancies:

AML

132

AML:

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

splenomegaly is assoc with:

Hodgkin's and AML, CLL

134

% remission from AML w chemo:

60%, only 15% disease free after 5y

135

Pathologic findings of AML w granulocytic maturation:

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

Enzyme found in primary granules of AML w granulocytic maturation:

myeloperoxidase

137

# of blasts normally in peripheral blood:

none

138

Most common leukemia in US:

CLL

139

CLL:

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

140

Pathology of CLL:

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

How to determine type of leukemia:

CD 5, a T cell marker

142

BM of CLL pt:

hypercellular, no fat, almost all lymphos

143

When to tx CLL:

lymphadenopathy, hepatosplenomegaly, anemia, low platelets

144

Px of CLL:

good: 10-15 surival

145

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

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