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PATHOLOGY > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

NEOPLASIA DEFINITION

A

abnormal mass of tissue that’s growth exceeds the surrounding normal tissue and grows without stimuli

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2
Q

Benign Neoplasm Definition

A

neoplasm which lacks the ability to invade, destroy tissue and metastasize

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3
Q

Malignant Neoplasm Definition

A

A neoplasm that possesses the ability to invade, destroy tissue and metastasize

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4
Q

Cancer definition

A

referring to all types of malignant neoplasms.

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5
Q

Urothelium

A

Transitional epithelium, lining majority of GU tract

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6
Q

Squamous stratified epithelium

A

multilayered flattened epithelial cells arranged on a basement membrane (mitosis occurs near BM)

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7
Q

Polyp

A

mass arising from a mucous membrane protruding into the lumen of a hollow viscus

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8
Q

Poly origin

A

epithelial cell origin

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9
Q

Sessile polyps

A

flat, arising directly from the mucosal epithelial layer

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10
Q

Pedunculated polyps

A

extending from the mucosa through a fibrovascular elongated stalk + surrounding epithelium

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11
Q

Cyst

A

outer capsule + inner surface lined with epithelium, hollow-cavity filled with mucin

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12
Q

Pseudocyst

A

lacks inner epithelial lining

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13
Q

Adeno-

A

glandular epithelial origin

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14
Q

Squamo-

A

flat, scale-like epithelial origin

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15
Q

Papillary

A

epithelial growth that extend outward as small nipple-like structure or protuberance

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16
Q

Papillo-

A

referring to a epithelial polyp

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17
Q

Myxo-

A

mucin producing mesenchymal origin

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18
Q

Rhabdomyo-

A

skeletal muscle mesenchymal origin

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19
Q

Leiomyo-

A

smooth muscle mesenchymal origin

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20
Q

Hemangio-

A

blood vessel mesenchymal origin

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21
Q

Lymphangio-

A

lymph vessel mesenchymal origin

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22
Q

Lympho-

A

lymphoid organ origin

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23
Q

Myelo-

A

myeloid origin: part of marrow- eosinophil, basophil, neutrophil, and monocyte

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24
Q

-oma

A

Benign neoplasm suffix

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25
Q

Carcinoma

A

malignant epithelial-derived cancer cells

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26
Q

Sarcoma

A

malignant mesenchymal-derived cells

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27
Q

Lymphoma

A

ALL are malignant lymphoid-derived cells

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28
Q

Myeloma

A

ALL are malignant marrow-derived cells

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29
Q

Leukemia

A

ALL are malignant hematologic-derived cells

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30
Q

Melanoma

A

Malignant neoplasm of melanocytic origin

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31
Q

Nevi

A

small benign melanocytic neoplasia

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32
Q

Myelodysplastic syndromes

A

hematologic dysplastic neoplasm

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33
Q

Plasmacytomas

A

discrete, solitary mass of plasma cells extramedullary or in bone

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34
Q

plasma cell dyscrasias

A

expansion of the number of monoclonal bone marrow plasma cells

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35
Q

Heterotopia

A

NOT NEOPLASTIC; congenital growth of microscopically normal cells or tissues in an abnormal location

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36
Q

Choristoma

A

NOT NEOPLASTIC; congenital growth of microscopically normal cells or tissues in an abnormal location

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37
Q

Hamartoma

A

NEOPLASTIC; excessive, focal overgrowth of cells and tissues native to the organ in which it occurs

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38
Q

Differentiation

A

degree to which the cellular constituents of a neoplasm resemble mature elements of the cell type

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39
Q

Differentiation of benign tumors

A

Highly differentiated

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40
Q

Differentiation of malignant tumors

A

tend to be less differentiated

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41
Q

Poorly differentiated tumors correlates with

A

advanced malignancy

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42
Q

Maturation

A

Directly related to differentiation; advancement of differentiation

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43
Q

Maturation of benign tumors

A

Very mature

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44
Q

Maturation of malignant tumors

A

tend to be less mature

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45
Q

Poorly maturated tumors correlate with

A

advanced malignancy

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46
Q

Dysplasia

A

Atypical nuclear and cytoplasmic changes which are considered PREmalignant

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47
Q

High grade dysplasia =

A

a lot of cellular atypia

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48
Q

Anaplasia

A

Atypical and aberrant changes within a cell or group of cells reflective of a MALIGNANT neoplastic changes

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49
Q

The greater the anaplasia

A

the more aggressive the tumor and the greater likelihood that the malignant cells become metastatic

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50
Q

Neoplastic rate of growth

A

When cellular replication and survival exceeds cellular loss

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51
Q

The greater the differentiation of a tumor, the _________ the growth

A

SLOWER; greater differentiation correlates with a slow growing tumor

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52
Q

In-situ carcinoma growth

A

Carcinomas begin to grow in the epithelium, but are confined by the basement membrane.

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53
Q

Why can’t you have in situ sarcomas?

A

Sarcomas derived from mesenchymal cells are not confined because there is no BM

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54
Q

What’s the difference between a high-grade dysplasia and in situ carcinoma?

A

Nothing, virtually impossible to tell

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55
Q

Encapsulated

A

Benign neoplasms: limited cohesive expansion

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56
Q

Unencapsulated

A

Malignant neoplasms: have the capacity for local infiltration and invasion leading to extensive tissue destruction

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57
Q

If an in situ carcinoma cell undergoes genetic alterations that allow it to invade the BM, it is now

A

a microinvasive carcinoma that has the ability to enter vessels if it comes into contact

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58
Q

Metastasis

A

tumor cells ability to leave their primary site or origin (primary neoplasm) and spread to a distant area of the body (separated in space) where they implant and replicate

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59
Q

Metastasis can occur via

A

direct seeding, lymphatic spread or hematogenous spread

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60
Q

Metastasis: lymphatic spread

A

tumor embolus is carried by lymph until it reaches a point where it lodges and begins to grow (generally at regional lymph nodes)

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61
Q

Lymphatic spread from breast cancer generally occurs at

A

axillary lymph nodes

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62
Q

Metastasis: Hematogenous spread

A

tumor embolus is carried by blood vessels, there are no gate keepers - wide-spread

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63
Q

Secondary Brain tumor indicates

A

Hematogenous spread, there is no lymph to brain

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64
Q

Metastasis: Direct seeding

A

the cancer is exposed to a cavity and cancer cells are carried in the fluid within the cavity and carried to another surface

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65
Q

Benign Neoplasm Characteristics

A

Encapsulated, well-differentiated, limited growth due to contact inhibition, freely moveable upon palpation due to capsule, no local invasion

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66
Q

Malignant Neoplasm Characteristics

A

Well-differentiated to undifferentiated, loss of maturity, loss of tissue and cellular organization, nuclear atypia, increased levels of mitoses, large nucleus, tumor giant cells, non-encapsulated, fixed position, often necrotic of hemorrhaging, local invasion, capacity to metastasize

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67
Q

Malignant tumor cell features

A

Large nucleus, abnormal increased mitoses, large, multi-nucleated cells, mitotic figures

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68
Q

Grading

A

Related to degree of differentiation of malignant neoplasm - phenotypic property

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69
Q

grade 1 neoplasms

A

well differentiated

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70
Q

Grade 4 neoplasms

A

poorly differentiated

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71
Q

High grade tumors have more

A

atypical cells and atypical mitotic figures, higher capacity to metastasize

72
Q

Low anaplastic potential

A

low-grade tumor

73
Q

Staging

A

classification of a tumor based on the extent of spread throughout the human body as determined by the UICC and AJC

74
Q

Staging considers

A

tumor size, the degree of regional lymph node involvement and the presence or absence of metastasis

75
Q

AJCC Staging

A

TNM (tumor size, number of nodes, metastasis)

76
Q

pT2N2 versus T2N2

A

‘p’ indicates pathologists staging based on the tissue biopsy; other indicates clinical staging based on diagnostics

77
Q

Incidence of cancer types is due to

A

environmental (geographical) and genetic determinants

78
Q

Cancer incidence in males

A

14% lung, 33% prostate, 11% colorectal

79
Q

Cancer incidence in females

A

33% breast, 12% lung, 11% colorectal

80
Q

Mortality from cancer in males

A

31% lung, 10% colorectal, 10% prostate

81
Q

Mortality from cancer in females

A

25% lung, breast 15%, 11% colorectal

82
Q

Autosomal dominant inherited cancer syndromes

A

means the person is born with a mutation in one gene and only needs to acquire 1 mutation in the other gene throughout life for cancer to develop (1 mutation = increased risk of cancer)

83
Q

Sporadic cancer

A

requires 2 mutations to occur throughout life, 1 in each chromosome, which is less likely to occur than if born with a mutation

84
Q

Familial Retinoblastoma

A

pt is heterozygous for Rb gene - when a mutation is acquired sporadically in the normal Rb gene chromosome (usually UV light), the patient becomes homozygous for mutant Rb gene, and retinoblastoma occurs

85
Q

Examples of Autosomal dominant inherited cancer syndromes

A

Retinoblastoma, MEN syndrome, Familial Adenomatous polyposis, hereditary nonpolyposis colon cancer, Li-Fraumeni Syndrome

86
Q

Li Fraumeni Syndrome

A

autosomal dominant p53 mutation, predisposes a person to a variety of cancer developments

87
Q

Autosomal Recessive Syndromes of Defective DNA Repair

A

pt is homozygous for the defective gene, inherits 2 copies of the mutated gene which puts them at increased risk for cancer

88
Q

Examples of Autosomal Recessive Syndromes

A

Xeroderma pigmentosum, Ataxia-telangiectasia, Fanconi anemia, HNPCC, Bloom Syndrome

89
Q

Familial Clustering

A

No clear defined transmission pattern, but som egene specificity; early age of onset, tumors in 2+ relatives

90
Q

Acquired Preneoplastic Disorders Include

A

Preceding inflammatory conditions, viral infection, chemical carcinogenesis, pre-existing benign neoplasm

91
Q

Growth-promoting proto-oncogenes

A

normal functional gene that regulates growth and differentiation, that when mutated is likely to lead to cancer due to its regulatory functions in a normal cell. Proto-oncogene -> mutation -> oncogene

92
Q

Oncogenes may alter

A

GFs, GFRs, signal transduction proteins, nuclear regulatory proteins, cell cycle regulators

93
Q

sis gene

A

oncogene that increases GF production

94
Q

erb-B2 gene

A

oncogene that increases GF receptors

95
Q

ras gene

A

oncogene that encodes for a mutated signal transducer protein (constitutively active)

96
Q

myc gene

A

oncogene coding for mutant TF (nuclear regulatory proteins); active w/o signal transduction

97
Q

Mutation examples

A

point mutation, chromosomal rearrangement, gene amplification

98
Q

Burkitt’s Lymphoma - c-myc mutation type

A

chromosomal rearrangement of 8 and 14

99
Q

n-myc mutation type

A

gene amplification

100
Q

anti-oncogenes

A

regulate nuclear transcription, cell cycle, signal transduction, stimulate cell surface suppressor molecules; normally act as BRAKES to cell cycle

101
Q

Growth inhibiting cancer suppressor genes (anti-oncogenes)

A

Normally suppress growth, but when mutated can no longer suppress growth

102
Q

Genes which regulate apoptosis

A

prevent or promote programmed cell death

103
Q

Multi-step carcinogenesis

A

requires a mutation that activates an oncogene AND suppresses an anti-oncogene, followed by clonal expansion and neoplasm formation

104
Q

Point mutation example

A

retinoblastoma

105
Q

Examples of anti-oncogenes

A

Rb, p53, BRCA1-2

106
Q

Clonal expansion characteristic

A

polyclonal cell population

107
Q

malignant cells have a high number of cells in G1-M phase

A

G1-M phase

108
Q

Malignant neoplasms have the ability to recruit

A

angiogenesis

109
Q

Angiogenesis - Proto-oncogenic regulation

A

Stimulate blood vessel growth.

110
Q

Angiogenesis - Tumor suppressor gene regulation

A

Normally inhibit blood vessel growth, unless mutated

111
Q

an invasive tumor that has gained the ability to breach basement membrane has likely undergone genetic alteration and now has the ability to bind

A

laminin of basement membrane

112
Q

monoclonal expansion –>

A

heterogeneity of the cell population overtime due to mutations in various daughter cells leading to sub-types of cells with various capabilities

113
Q

In situ transformation to invasive carcinoma

A

Cell must lose adhesion molecules to adjacent cells, obtain an active collagenase to break down ECM, tumor cells then bind to laminin receptors of BM

114
Q

Intravasation

A

attach and invade the BM of the vessel and migrate through the tight junctions of the endothelial cells

115
Q

Satellite nodules

A

earliest example of metastasis (intra-organ metastasis)

116
Q

Secondary tumor

A

arises in a distant location from primary

117
Q

Chemical initiator

A

causes a change in the cell which makes it susceptible to the development of a neoplasm. Initiation alone is insufficient for neoplasia to occur

118
Q

2 types of initiators

A

Direct acting agent and Indirect acting agents

119
Q

Indirect acting agents

A

Require in-vivo metabolic conversion into an active definitive carcinogen (metabolite or free radicals)

120
Q

v-onc

A

proto-oncogene mutation due to viral transduction

121
Q

c-onc

A

proto-oncogene mutation due to influences that alter their function in situ

122
Q

p53 is an example of

A

tumor suppressor (anti-oncogene)

123
Q

Rb is an example of

A

tumor suppressor (anti-oncogene)

124
Q

BRCA-1/2 is an example of

A

tumor suppressor (anti-oncogene)

125
Q

Direct acting initiator

A

Require no chemical transformation to induce their carcinogenic potential

126
Q

chemical initiators are

A

mutagenic at the molecular level inducing mutations in oncogenes

127
Q

Promoters

A

themselves are not mutagenic. Rather they stimulate activation and production of enzymes capable of inducing cell growth and proliferation.

128
Q

Examples of direct-acting initiators

A

alkylating agents, cyclophosphamide, chlorambucil, busulfan, melphalan, immunosuppressants

129
Q

direct-acting initiators are

A

weak carcinogens

130
Q

Examples of indirect-acting initiators

A

Polycyclic aromatic hydrocarbons, Aromatic amines/azo dyes, Aflatoxin B1 – Produced by Aspergillus flavus, Nitrosamines and amides

131
Q

Polycyclic aromatic hydrocarbons

A

indirect-acting initiator, potent carcinogen, can cause skin, colon, lung, bladder cancer, sarcoma

132
Q

Aromatic amines/azo dyes

A

indirect-acting initiator, activated by the cytochrome P-450 oxygenase activator systems, associated with HCC

133
Q

β-naphthylamine

A

indirect-acting initiator, present in aniline-dyes, associated with bladder cancer

134
Q

Aflatoxin B1

A

indirect-acting initiator, Produced by Aspergillus flavus, when Hep B infected person is exposed = increased risk of HCC

135
Q

Nitrosamines and amides

A

indirect-acting initiator, common food preservatives activated by gut bacteria, gastrointestinal carcinomas

136
Q

Exogenous promoters

A

Saccharin and cyclamates, Diethylstilbestrol (DES), Exogenous hormones

137
Q

Endogenous Promoters

A

Hormones, Bile salts/Dietary Fat

138
Q

UV exposure

A

causes pyrimidine dimers in DNA that overrides the body’s inherent Nucleotide Excision Repair (NER) mechanisms

139
Q

UV exposure primarily causes

A

cutaneous malignancies

140
Q

UV, electromagnetic, particulate, radon

A

Many can act directly by inducing DNA breaks or indirectly by generating free radicals

141
Q

Cytotoxic viruses

A

inject their DNA/RNA into a cell, this becomes incorporated into cells DNA and causes mutations/altered genes

142
Q

HPV

A

DNA oncogenic virus

143
Q

HPV Types 16 and 18 are associated with

A

invasive squamous cell carcinoma

144
Q

HPV Types 1, 2, 4, 7 are associated with

A

Benign squamous papillomas

145
Q

HPV Types 6 and 11 are associated with

A

Genital lesions with low malignant potential

146
Q

Epstein Barr virus (EBV)

A

DNA oncogenic virus

147
Q

EBV is associated with

A

Burkitt’s Lymphoma, B-cell lymphoma

148
Q

HBV virus

A

DNA oncogenic virus

149
Q

HBV is associated with

A

HCC esp in combo with Aflatoxin B1

150
Q

Kaposi virus

A

DNA oncogenic virus

151
Q

Kaposi virus KSHV is associated with

A

development of AIDS related Kaposi sarcoma

152
Q

Human T cell leukemia virus (HTLV-1)

A

RNA oncogenic virus

153
Q

Human T cell leukemia virus (HTLV-1) is associated with

A

T cell leukemia/lymphoma

154
Q

Hep C virus

A

RNA oncogenic virus

155
Q

Hep C virus is associated with

A

HCC

156
Q

Helicobacter pylori

A

gastric bacteria associated oncogenesis (gastric carcinoma, MALT lymphoma)

157
Q

MALT lymphoma caused by h/ pylori can be treated with

A

abx

158
Q

Local effects from tumor on host

A

Effects caused at site due to tumor growth

159
Q

Hormonal effects from tumor on host

A

tumors may possess the ability to secrete hormones or hormone-like factors

160
Q

Small cell cancer of the lung often secretes

A

ACTH causing Cushing’s Syndrome

161
Q

Cachexia

A

systemic effect due to tumor, causing increased TNF-alpha and cytokine release, resulting in increased basal metabolic rate, in addition to tumor cells increased need for nutrients

162
Q

Paraneoplastic syndrome

A

Constellation of physical findings that are in association to products of the tumor

163
Q

migratory thrombophlebitis

A

Malignancies associated with hypercoagulability

164
Q

Tumor lysis syndrome

A

group of metabolic complications that can occur after treatment of cancer: hyperkalemia, hyperphosphatemia, hyperuricemia and hyperuricosuria, hypocalcemia, and consequent acute uric acid nephropathy and acute renal failure

165
Q

Anti-tumor defenses include

A

CTL, NK, Macrophages, immunosurveillance, immunotherapy against tumor antigens

166
Q

Histology

A

staining and viewing tissue morphology and cells in relation to another

167
Q

Cytology

A

Cellular staining to look for characteristics of individual cells

168
Q

DNA probe

A

look for specific DNA sequences characteristic of cancer type

169
Q

Carcinoembryonic Antigen (CEA):

A

colon cancer

170
Q

Alpha-Fetoprotein (AFP):

A

HCC

171
Q

Beta Subunit Human Chorionic Gondotropin (β-HCG):

A

choriocarcinoma

172
Q

CA-125

A

ovarian cancer

173
Q

Flow cytometry

A

use to quantify B and T cells

174
Q

exfoliative cytology

A

scrape away epithelium and stain

175
Q

Fine needle aspiration

A

insertion of a needle into the neoplasm to collect fluid and cells

PATHOLOGY (18 decks)

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