Gen Path Exam 2 - Neoplasia Flashcards

(172 cards)

1
Q

New growth

A

Neoplasia

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2
Q

Loss of normal growth control; cells start doing their own thing, “transformed”

A

Neoplasia

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3
Q

Parasitic and autonomous qualities

A

Neoplasia

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4
Q

Study of neoplasms (tumors)

A

Oncology

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5
Q

What is the spectrum of neoplasia?

A

Benign -> locally aggressive -> intermediate malignant -> malignant

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6
Q

What are the 2 anatomic components of tumors?

A

Parenchyma
Stroma

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7
Q

Neoplastic cells; determines how a tumor is named

A

Parenchyma

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8
Q

Supporting CT and vasculature

A

Stroma

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9
Q

Degree of resemblance of tumor cells to parent cells

A

Differentiation

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10
Q

More resemblance between tumor cells and parent cells

A

Well differentiated (“low grade”)

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11
Q

Little resemblance between tumor cells and parent cells

A

Poorly differentiated (“high grade”)

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12
Q

Dedifferentiated or undifferentiated

A

Anaplasia

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13
Q

What does increased/abnormal DNA replication lead to (“poorly differentiated”)? (6)

A

Pleomorphism
Nuclear hyperchromatism
Increased nuclear/cytoplasmic ratio
Atypical nuclei
Numerous and atypical mitoses
Prominent nucleoli

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14
Q

A microscopic, potentially reversible, altered growth or maturation pattern

A

Dysplasia

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15
Q

In epithelial tissues (cervix, oral mucosa), it is precancerous and may progress to malignancy

A

Dysplasia

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16
Q

What is seen under the microscope in precancerous epithelial tissues undergoing dysplasia?

A

Disorderly:
Maturation
Pleomorphism
Mitotic activity

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17
Q

In bone lesions, it does NOT imply a precancerous state, just altered growth

A

Dysplasia

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18
Q

Dysplastic changes involving the full-
thickness of the epithelium

A

Carcinoma in-situ

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19
Q

Known as the most advanced stage of dysplasia

A

Carcinoma in-situ

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20
Q

Still a pre-invasive (precancerous) state, so
not cancer

A

Carcinoma in-situ

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21
Q

Clinical appearance, anatomic site, or
cell type (root word) + “oma”

A

Benign epithelial tumors

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22
Q

Named for appearance- finger-like epithelial
projections overlying cores of vascular fibrous CT

A

Papilloma

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23
Q

Arises from surface epithelium (Squamous-
skin, larynx, tongue; Transitional- bladder,
ureter, renal pelvis)

A

Papilloma

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24
Q

Benign tumor of glandular epithelium; can have many variants

A

Adenoma

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25
Characterized by adenomatous papillary processes that extend into cystic spaces, as in cystadenoma of the ovary
Papillary cystadenoma
26
Most often named by tissue of origin
Benign mesenchymal
27
Fibrous tissue (benign mesenchymal)
Fibroma
28
Cartilaginous (benign mesenchymal)
Chondroma
29
Smooth muscle (benign mesenchymal)
Leiomyoma
30
Skeletal muscle (benign mesenchymal)
Rhabdomyoma
31
Fat (benign mesenchymal)
Lipoma
32
Bone (benign mesenchymal)
Osteoma
33
Vessels (benign mesenchymal)
Angioma
34
Pleomorphic adenoma (salivary), fibroadenoma (breast)- only fibrous portion is neoplastic
Benign mixed tumors
35
Neoplasm with cells derived from more than 1 germ layer, totipotent cells
Teratoma
36
Disorganized tissue native to the site (non-neoplastic generally)
Hamartoma
37
Disorganized tissue at unexpected site (non-neoplastic)
Choristoma
38
A mass that projects above a mucosal surface
Polyp
39
What are the notable malignant -oma exceptions? (6)
Lymphoma Melanoma Mesothelioma Seminoma Glioblastoma Hepatoma
40
What are the notable non-neoplastic -oma exceptions?
Granuloma (group of macrophages) Hematoma (bruise)
41
Root word anatomically or cellularly + “Carcinoma"
Malignant epithelial
42
Synonym of malignant
Cancer
43
From squamous epithelium (skin, mouth, esophagus, vagina) or areas of squamous metaplasia (bronchi or cervix)
Squamous cell carcinoma
44
Marked by production of keratin
Squamous cell carcinoma
45
From urinary tract epithelium
Transitional cell carcinoma
46
Glandular origin; includes tumors of GI, mucosa, endometrium, pancreas
Adenocarcinoma
47
Often shows desmoplasia
Adenocarcinoma
48
The root word anatomically/cellularly + “Sarcoma
Malignant mesenchymal
49
Fibrous (malignant mesenchymal)
Fibrosarcoma
50
Cartilaginous (malignant mesenchymal)
Chondrosarcoma
51
Bone (malignant mesenchymal)
Osteosarcoma
52
Skeletal muscle (malignant mesenchymal)
Rhabdomyosarcoma
53
Smooth muscle (malignant mesenchymal)
Leiomyosarcoma
54
Fat (malignant mesenchymal)
Liposarcoma
55
Vessels (malignant mesenchymal)
Angiosarcoma
56
Burkitt lymphoma Hodgkin disease/lymphoma Wilm’s tumor
Eponyms
57
Which one is correctly matched? a. chondroma, non-neoplastic collection of tissue not native to the site b. angioma, malignant tumor of blood vessels c. pleomorphic adenoma, a high-grade malignancy of glandular epithelium d. rhabdomyoma, benign tumor of skeletal muscle
d. rhabdomyoma, benign tumor of skeletal muscle
58
Name some words often added to describe variants of a tumor's appearance under the microscope
Cystic, papillary, tubular, solid, etc
59
Benign or malignant? Clinical presentation: Non-cancerous Slow growing Local, does not spread, may cause local damage Surgically removable Survivable - good prognosis
Benign
60
Benign or malignant? Clinical presentation: Cancerous Rapid growth Invade and destroy adjacent tissue Metastasis = defining feature Can cause death - poor prognosis
Malignant
61
Benign or malignant? Microscopic: Well-differentiated Normal mitoses Encapsulation
Benign
62
Benign or malignant? Microscopic: Well to poorly differentiated (or anaplastic) Atypical mitoses Non-encapsulated
Malignant
63
Benign or malignant? Rate of growth is slow (months to years)
Benign
64
Benign or malignant? Rate of growth affected by hormones, blood supply, pressure constraints
Benign
65
Benign or malignant? Rate of growth is variable, may be rapid
Malignant
66
Benign or malignant? Rate of growth may outgrow blood supply, leading to necrosis
Malignant
67
Benign or malignant? Local invasion capsule at periphery
Benign
68
Benign or malignant? Local invasion beyond anatomic tissue boundaries
Malignant
69
Benign or malignant? Local invasion is destructive and no capsule
Malignant
70
Benign or malignant? Crosses over anatomical boundaries (ex: nose up to brain)
Malignant
71
What is the hallmark of malignancy?
Metastasis
72
What does the capacity of metastasis depend on?
Tumor type
73
What percentage of newly diagnosed malignant tumors have clinically evident metastases?
30% (early detection is important!)
74
More anaplastic, larger tumor = _______ likely to spread
more
75
In what ways does malignancy spread?
Seeding in body cavities Lymphatic spread Hematogenous (blood) spread Paths of least resistance
76
What type of malignancy spread? Ovarian cancer
Seeding in body cavities
77
What type of malignancy spread? Carcinomas
Lymphatic spread
78
What type of malignancy spread? Sarcomas
Hematogenous (blood) spread
79
What type of malignancy spread? Lung and liver are common vsecondary sites
Hematogenous (blood) spread
80
What type of malignancy spread? Neural spread
Path of least resistance
81
What type of malignancy spread? Batson's venous plexus - along vertebral column, potential spread to jaw
Path of least resistance
82
Cancer is a _________ disorder- mostly from acquired random mutations during regular ______ ___________ (Bad luck!) or from environmental exposure
genetic; cell division
83
Genetic changes are heritable with the accumulation of mutations leading to characteristic features of cancer; however, actual inherited cancers are ____________
infrequent
84
Cancer is a _____________ process. It does not just happen from one time of "bad luck"
multi-step
85
What are the steps of neoplasm formation?
Initiation Promotion Progression
86
What step of neoplasm formation? Carcinogen exposure causing genetic damage and single cell (“monoclonal”) growth
Initiation
87
What step of neoplasm formation? Additional genetic damage over time leads to heterogenous population of cells (visible clinically)
Promotion
88
What step of neoplasm formation? Evolution and selection of more aggressive tumors capable of metastasis that are less responsive to treatment
Progression
89
Name 3 carcinogens that can cause a neoplasm to form
Chemicals Radiant energy Microbial agents (ex: viruses like HPV, EBV)
90
What are the 4 major classes of cancer genes that control growth?
Proto-oncogenes Tumor suppressor genes Apoptosis regulation genes Tumor cell/host cell interaction genes
91
Which major class of cancer genes that control growth? Increase growth
Proto-oncogenes
92
Which major class of cancer genes that control growth? Stop cell growth and help in DNA repair
Tumor suppressor genes
93
What is the classic example of a tumor suppressor gene?
TP53 (aka p53)
94
Which major class of cancer genes that control growth? Determine cell death
Apoptosis regulation genes
95
Which major class of cancer genes that control growth? Cytotoxic T lymphocytes kill cells with unrepaired genetic damage
Tumor cell/host cell interaction genes
96
Name the 4 hallmarks of cancer highlighted in class
1. Self-sufficiency in growth signals (oncogenes) 2. Insensitivity to growth inhibition (tumor suppressor genes) 3. Evasion of apoptosis (apoptosis regulation genes) 4. Evasion of immune system (tumor cell/host interaction genes)
97
The immune system (cell-mediated) helps prevent what?
Tumor formation/progression
98
What is the evidence that the immune system helps prevent tumor formation and progression?
Increased frequency of cancer in immunocompromised (ex: congenital, transplant, AIDS)
99
Uses endogenous or synthetic substances to improve or restore immune system function to fight cancer
Immunotherapy
100
What is the target and indication of Rituximab?
Target = CD20 Indication = B-NHL
101
What is the target and indication of Herceptin?
Target = HER2/neu Indication = breast cancer
102
What is the target and indication of Certuximab?
Target = EGFR Indication = Head, neck, oral cancer
103
The majority of cancers are inherited. About 1/3 of newly diagnosed malignancies have already metastasized. a. Both statements are true b. Both statements are false c. The first statement is true, the second statement is false d. The first statement is false, the second statement is true
d. The first statement is false, the second statement is true
104
The branch of medicine which deals with the incidence, distribution, and possible control of diseases and other factors relating to health
Epidemiology
105
Studying who (Age, gender) gets a tumor, where they live (environmental risk factors) and their family (genetic factors, acquired predisposing conditions) helps identify etiology and pathogenesis
Epidemiology
106
What helps with the following? Preventing and reducing disease burden Improving tx Reducing cost Predicting needs for resource allocation
Epidemiology
107
Has the overall death rate increased or decreased?
Decreased (less smoking, earlier detection, better tx)
108
Has the overall incidence rate increased or decreased for women and men?
Increased for women Stable for men
109
Which state has the highest incidence of new cancer cases and deaths in the US?
KY
110
Name environmental exposures that are associated with increased cancer risk
Occupational Chronic sun exposure Smoking Alcohol Obesity Oncogenic viruses (HPV)
111
T/F: Older people are more likely to get cancer
True
112
What kind of cancers do children usually get?
Leukemia, lymphoma, sarcoma, CNS tumor
113
What should you closely follow for early cancer detection?
Precursor (precancer/premalignant) lesions
114
Risk for? Smoking induced squamous metaplasia Dysplasia of bronchial mucosa
Bronchogenic carcinoma
115
Risk for? Endometrial hyperplasia and dysplasia
Endometrial carcinoma
116
Risk for? Oral, vulvar, and penile leukoplakia
Squamous cell carcinoma
117
Risk for? Villous adenoma of colon
Colorectal carcinoma
118
Are benign tumors premalignant?
Generally no
119
Name the tumor effects on host
Location is crucial Hormone production Bleeding + infedction Intestinal complications
120
Symptoms not related to tumor spread or hormone production
Paraneoplastic syndromes
121
Affects 10-15% of cancer patients
Paraneoplastic syndromes
122
May indicate underlying neoplasm
Paraneoplastic syndromes
123
Can be lethal and can mimic metastatic disease
Paraneoplastic syndromes
124
Diverse and associated with many tumors
Paraneoplastic syndromes
125
Name the 4 Paraneoplastic syndromes
Cachexia Hypercalcemia Cushing syndrome Hypercoagulability
126
Which Paraneoplastic syndrome? Progressive loss of body fat and lead body mass with weakness, anorexia, and anemia
Cachexia
127
Which Paraneoplastic syndrome? High metabolic rate
Cachexia
128
Which Paraneoplastic syndrome? Caused by tumor and host cytokines, not due to tumor's nutritional demands
Cachexia
129
Which Paraneoplastic syndrome? Due to release of PTHrP, TGF-a (activates osteoclasts and active vitamin D)
Hypercalcemia
130
Which Paraneoplastic syndrome? Ectopic ACTH production
Cushing syndrome
131
Which Paraneoplastic syndrome? Venous thrombosis and nonbacterial thrombotic endocarditis
Hypercoagulability
132
Estimates aggressiveness based on cytologic differentiation
Grading
133
Goes from I - IV in order of increasing anaplasia
Grading
134
Which has greater clinical value, grading or staging?
Staging
135
Size of primary tumor and extent of regional and distant spread
Staging
136
TNM system
Staging
137
What does TNM system measure/stand for?
T = tumor size (1-4) N = regional nodal involvement (0-3) M = metastasis (0,1)
138
AJC system (0-IV)
Staging
139
What is required for a lab diagnosis of cancer?
Detailed clinical findings Adequate, representative, properly preserved biopsy
140
What do you put biopsied samples in?
Formalin
141
What are the sampling approaches?
Cytologic smear Biopsy
142
What are the 2 types of cytologic smears?
Direct scraping Fine needle aspiration
143
Which type of cytologic smear? Good for superficial fungal and herpes infections
Direct scraping
144
Which type of cytologic smear? Good for readily palpable lesions (breast, thyroid, lymph node, salivary gland)
Fine needle aspiration
145
Which sampling approach? Incisional (part of the tissue) or excisional (all abnormal tissue)
Biopsy
146
____________ assistance ensures accurate sampling for internal lesions. Name a few examples
Radiologic Ex: mammogram-guided, CT-guided, ultrasound-guided
147
Routine samples are _________ fixed and embedded in paraffin wax (FFPE) for routine H&E staining. This same tissue block can later be used for additional ______-based molecular tests (FISH, IHC, PCR etc.)
formalin; DNA
148
Useful to determine the cellular differentiation of poorly differentiated tumor cells
Immunohistochemistry
149
Useful in diagnosis of lymphomas to determine lineage (B or T cell) and differentiation stage and in treatment of B-cell lymphomas
Immunohistochemistry
150
Requires fresh tissue (no formalin!)
Flow cytometry
151
Helps classify leukemia and lymphoma
Flow cytometry
152
What are the serologic markers for tumors?
PSA Carcinoembryonic antigen (CEA) Alpha-fetoprotein
153
Which serologic marker for tumors? Low sensitivity and low specificity
PSA
154
Which serologic marker for tumors? Cancers of colon, pancreas, stomach, and breast
Carcinoembryonic antigen (CEA)
155
Which serologic marker for tumors? Hepatocellular carcinomas, yolk sac remnants
Alpha-fetoprotein
156
Which serologic marker for tumors? Not good for early detection, but GREAT for detecting reccurrences
PSA, CEA, and alpha-fetoprotein
157
Uses body fluids that contain tumor cells or their products for screening, detecting, and monitoring cancer
Liquid biopsy
158
Can detect monoclonality in lymphoid malignancies
PCR
159
Translocations and gene amplification
FISH/PCR
160
Which molecular technique? Tumors from different sites with similar mutations can be given similar drugs
Targeted therapy
161
Rapid sequencing on entire genome
Genomics
162
Can identify driver and passenger mutations that help target treatment
Genomics
163
Epigenetic modifications genome-wide
Epigenomics
164
Microarray quantifies all RNAs expressed
Transcriptomics
165
Measure all proteins simultaneously
Proteomics
166
Test all of the cell's metabolites
Metabolomics
167
T/F: RNA is easier to work with than DNA
FALSE, DNA is easier to work with
168
Currently developing methods to sequence several hundred _____ _________ to detect mutations in as few as 5% of tumor cells
key genes
169
Used to identify changes in DNA copy number
DNA arrays
170
In the future, may be used to predict drug efficacy
Epigenomics
171
In the future of cancer diagnostics, there will be a paradigm shift to classify tumors based on _____________ and associated therapeutic _________, rather than on morphology or cell origin
mutation; targets
172
Optimal diagnosis and management combines what?
Histopathology + molecular diagnostic techniques