2nd Exam: Hematopathology Flashcards

1
Q

Pain after drinking alcohol, think:

A

Hodgkin Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Auer rods, think this:

A

AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Translocation t(8;14), think:

A

Burkitt’s Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lymphadenopathy may be due to:

A

reactive ( define) or neoplastic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ex’s of reactive conditions leading to lymphadenopathy:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Infections that can lead to lymphadenopathy:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ai disease that can lead to lymphadenopathy:

A

RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ex’s of malignancies that can lead to lymphadenopathy:

A

non-lymphoid, lymphoid-lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

metastatic carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T-cell zone of normal lymph node:

A

Parafollicular cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

B-cell zone of normal lymph node:

A

Lymphoid follicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptoms of lymphadenopathies depends on:

A

Node location, central vs. peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Palpable nodes:

A

peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Central nodes:

A

sup vena cava syndrome, obstruction of urethra or bowels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cancer that begins in lymphoid cells of immune system

A

lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lymphoma typically starts here:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

2 basic types of lymphoma:

A

hodgkin’s, non-h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Types of non-Hodgkin’s lymphomas:

A

indolent, aggressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define effacement:

A

normal structure replaced by tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2 types of leukemia:

A

lymphoid, myeloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Effects of BM infiltration:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical presentation of Hematologic Malignancies:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Low grade hematologic malignancy:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)