Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Pathology > Exam 3 Part 2 > Flashcards

Exam 3 Part 2 Flashcards

1
Q

Scientific investigation into the “distribution an determinants of health-related states or events in specified populations”
Study of death or disease in groups of people (populations)

A

Epidemiology

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

Common cancer(s) in the US

A

Breast Cancer
Colorectal Cancer
Esophageal Cancer

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

Common cancer(s) in Africa

A

Liver Cancer

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

Common cancer(s) in Japan

A

Stomach Cancer

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

________ exposures appear to have a dominant role in the formation of many common cancers.

A

Environmental

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

_____ plays a major role in carcinogenesis, restricting it may increase life expectancy.

A

Diet

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

What are the environmental risk facts for cancer?

A 
Ultraviolet (UV) Light
Ionizing Radiation
Asbestos
Arsenic
Various Viral Infections
Chemical Agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What age group is most likely to suffer the highest rates of cancer-related deaths?

A

55-75

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

Cancers that develop in the absence of a family history of such a cancer and are thought to be primarily, the result of harmful environmental exposures and the resulting damage to individual’s genetic material.

A

Sporadic Cancer

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

_______ and inherited risk factors frequently interact to create an individuals unique cancer risk.

A

Environmental

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

Cellular ______ and ______ are characteristic preneoplastic lesions.

A

Metaplasia

Dysplasia

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

Removal of preneoplastic lesions ______ the cancer risk

A

Lowers

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

Bronchial epithelia resulting form habitual cigarette smoking is unable to be removed and is known as cellular _____

A

Dysplasia

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

Gastroesophageal reflux disease (GERD) known as Barrett’s Esophagus is unable to be removed and is known as cellular ______

A

Metaplasia

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

T/F. In most cases of preneoplastic lesions, they develop into cancer.

A

False (most cases do not develop into cancer)

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

The one exception of benign tumors having a high rate of malignant transformation (roughly 30%) is a(an)

A

Adenoma

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

Cancers develop following

A

Genetic alterations

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

When cellular growth becomes severely dysregulated, ______ forms.

A

Cancer

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

Gene alterations may be inherited down the _____ ____

A

Germ Line (germ line mutations)

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

Normal genes that promote cellular growth

A

Proto-Oncogenes

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

When _______ are altered (mutated or over-expressed), it promotes excessive cellular growth.

A

Proto-Oncogenes

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

When a proto-oncogene is altered it is then referred to as a

A

Cancer-Promoting Oncogene

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

___ allele(s) need to be altered to cause a proto-oncongene to change its phenotype and behave as an oncogene.

A

1

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

When a single allele alters a proto-oncogene which changes its phenotype, this is referred to as a ______ change of gene expression

A

Dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Normal genes that slow down cellular growth (defense mechanism)

A

Tumor Suppressor Genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If TSG’s become altered (mutated or over-expressed), they _____ the ability to slow down growth.

A

Lose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

___ allele(s) need to be altered to cause TSG’s to change its phenotype and lose normal ability to suppress tumor growth

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When two alleles alter TSG’s which changes its phenotype is referred to as a _______ change of gene expression

A

Recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Kill off cells that are detected as having genetic alterations.

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

If the body loses the ability to rid of dangerous cancer-promoting mutations, they will survive and contribute to

A

Carcinogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the two types of genetic alterations causing cancer?

A
  1. Mutations

2. Epigenetic Modifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

There are two types of mutations:

A
  1. Driver Mutations

2. Passenger Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Mutation that directly contributes to progression of a specific cancer. Acquired from an environmental carcinogen

A

Driver Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mutation more randomly throughout the genome, producing genetic variants (subclones)

A

Passenger Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

May give a tumor or selective advance against various forms of therapy

A

Subclones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Affect the entire body and may be inherited

A

Germline mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Affected somatic cells, more localized

A

Acquired Mutatiosn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

RB gene

A

Retinoblastoma

https://www.aao.org/detail/image.axd?id=ed79d903-78f5-47ab-9826-76e74da7023f&t=635858793952230000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

TP53 gene

A

Li-Fraumeni Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

APC Gene

A

Colorectal Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

NF1 Gene

A

Neurofibromatosis
http://api.ning.com/files/wBpujxu5Rsw1vKGYcx2muaZ4DZtwbI7mobRERp1YgoIYvXQwpCfbKlpIv3XPAxBWDF40boLeAd0nBEV3X0hvyAeot89wUV/Neurofibromatosis.jpg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

BRCA1 Gene

BRCA2 Gene

A

Breast Cancers and Ovarian Cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

May activate/deactivate proteins, but are most well-known for activating proto-oncogenes

A

Point Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

This single mutations is associated with dominant gain-of-function change in gene expression

A

Point Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Single point mutations are known to activate the ____ gene

A

RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

____ _______ may deactivate one of the TP53 genes

A

Point Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Occur on the level of the chromosome and included balanced translocations

A

Gene Rearrangements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

__ ___ cancers are frequently associated with very specific balanced translocations between two chromosomes

A

B cell (leukemia and lymphomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Chronic Myelongenous Leukemia (CML) involve a specific balanced translocation between genetic material on chromosome __ and ___, which is termed a Philadelphia chromosome

A

9 and 22

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Most cases of Burkitt Lymphoma have a balanced translocation between chromosome ___ and ____.

A

8 and 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Involve the loss of a section of genetic material

A

Genetic Deletions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Deletions may contribute to carcinogenesis by altering one (of the two) alleles that must be altered to deactivate a _____________

A

Tumor Suppressor Gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Segment of genetic material is multiplied many times, and may over-express a proto-oncogene and effectively activate an oncogene

A

Gene Amplifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Gene amplification that occurs in about 20% of all cases of breast cancer

A

HER2 Gene (HER2/neu)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Amplification of HER2 gene allows breast cancer cells to become much more sensitive to low levels of

A

Growth Factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Gene amplifications may also produce ______ ______, which are extrachromosomal DNA fragments that are evident within an involved cell.

A

Double Minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Reversible changes to gene expression

A

Epigenetic Modifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the two mechanisms of gene modification?

A

DNA Methylation

Histone Modification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

May contribute to carcinogenesis if TSG’s or DNA repair genes are deactivated

A

Epigenetic Modification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Multistep process that involves the accumulation of multiple genetic alterations, over time.

A

Carcinogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Over time, cancers evolve and become

A
  1. More aggressive

2. Less responsive to Therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Cancers accumulate greater gene alterations, which develop

A

Subclones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Even though cancers develop from a single transformed cell, in time these clonal cells will acquire _______ gene alterations.

A

Different

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

As _____ _______ occurs, cancer will develop greater invasive and malignant potential

A

Tumor Progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Unique characteristics that contribute to the dysregulated cellular growth of cancer cells

A

Hallmarks of Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Self-Sufficiency in Growth Signaling
Evasion of Immune Detection (Surveillance)
Insensitivity to Anti-Growth (inhibitory) Signaling
Cellular Immortality (limitless growth potential)
Altered Cellular Metabolism
Increased (sustained) Angiogenesis
Evasion of Apoptosis
Invasion and Metastasis

A

Hallmarks of Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Hallmarks of Cancer

A

Self-Sufficiency in Growth Signaling
Evasion of Immune Detection (Surveillance)
Insensitivity to Anti-Growth (inhibitory) Signaling
Cellular Immortality (limitless growth potential)
Altered Cellular Metabolism
Increased (sustained) Angiogenesis
Evasion of Apoptosis
Invasion and Metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Cancers may also involve tumor-promoting inflammation and genomic instability, which is referred to as

A

Enabling Hallmarks of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Evading growth suppression and evading anti-growth signals =

A

Tumor has become insensitive to normal inhibitory signals of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Group of genes that encode for inhibitory proteins that enact the function of limiting and controlling cellular growth

A

Tumor Suppressor Genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Their protein products “apply the brakes to cell proliferation”, servicing to suppress tumor growth

A

Tumor Suppressor Genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

The two-mutation loss-of-function change in TSG expression is known as the

A

Two-Hit Hypothesis (Knudson Hypothesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

TSG located on chromosome 13 and is an important mediator of the cell cycle

A

RB Gene (Retinoblastoma Gene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

First discovered in childhood eye cancer, but can be found in nearly all cells of the body

A

RB Gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

RB gene produces the ___ protein which regulates the G1-to-S phase of the cell cycle

A

Rb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Common oncovirus that deactivates the RB gene’s regulatory control of the cell cycle

A

Human Papillomavirus (HPV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

A virus that may cause cancer

A

Oncovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Classic TSG that produces protein product p53 and is known as the “Guardian of the Genome”

A

TP53 Gene (P53)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Three stimuli that activate a p53 response

A
  1. Cellular Anoxia
  2. Inappropriate pro-growth signaling (activation of oncogene)
  3. Genetic Damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

p53 will attempt to control harmful situations by initiating control mechansims:

A
  1. Quiescence
  2. Senescence
  3. Apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

p53 control mechanism that is a temporary pause affected cells cell cycle activity

A

Quiescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

p53 control mechanism that is a permanent arresting of affected cells cell cycle activity

A

Senescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

p53 control mechanisms that is a controlled/programmed cellular death

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

TP53 will regulate the cell cycle and attempt to fix genetic damage while a cell is in ______ via activation of DNA repair genes.

A

Quinescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

If DNA repair occurs, TP53 will release the affected cell back into normal cell cycle activity; if not, it will initiate _________ or ________.

A

Senescence

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

TP53 gene mutations are present in at least ____ of all human cancers

A

70%

87
Q

T{53 gene alterations are present in lethal cancers such as

A

Lung
Colorectal
Breast

88
Q

When the protein produce (p53) of TP53 is deactivated it is known as a

A

Functional Mutation

89
Q

When an altered TP53 gene is inherited this is known as

A

Li-Fraumeni Syndrome

90
Q

Involves affected individuals developing multiple primary tumors at a younger age

A

Li-Fraumeni Syndrome

91
Q

Li-Fraumeni Syndrome increases the risk of developing a cancer by about ___-fold

A

25

92
Q

Cancers of Li-Fraumeni Syndrome

A 
Sarcomas
Breast Cancers
Brain Tumors
Leukemias
Adrenal Cortex Adenocarcinomas
(SBLA)
93
Q

Cancer cells shirt their metabolism to a unique form of metabolism known as

A

Aerobic Glycolysis

94
Q

When cancer cells shift their metabolism to Aerobic Glycolysis

A

Warburg Effect

95
Q

T/F. Cancer cells do not shift their metabolism if there is a presence of adequate oxygen levels.

A

False

—Cancer cells shift to Aerobic Glycolysis EVEN in the presence of adequate oxygen levels—

96
Q

What are the normal periods of rapid growth that will utilize aerobic glycolysis

A

Embryogenesis

Immune Response

97
Q

Normal cells have a limited number of cellular divisions, known as its

A

Hayflick Limit

98
Q

T/F. Cancer cells do not have a Hayflick Limit

A

True

99
Q

When a normal cell’s telomeres become critically shortened following prolonged cellular growth, it initiates cellular

A

Senescence

100
Q

If a normal cell with shortening telomeres doesn’t enter cellular senescence the cell will enter

A

Non-Homologous End Joining

101
Q

Once the shortened telomere cell enters Non-Homologous End Joining this will result in the creation of

A

Dicentric Chromosomes (irregular chromosome with two centromeres)

102
Q

Dicentric Chromosomes will enter the cell cycle where they will be pulled apart (during Anaphase), and __________ chromosomal breaks are formed.

A

Double-Stranded

103
Q

Once double-stranded chromosomal breaks occur, this will produce mutations which will activate the enzyme

A

Telomerase

104
Q

Telomerase will ______ the telomeres of the haphazard chromosomes, giving immortality to these tumor cells

A

Lengthen

105
Q

Reactivation of telomerase is observed in about ____ of all cancers

A

90%

106
Q

A tumor must stimulate ______ in order to grow larger.

A

Angiogenesis

107
Q

Angiogenesis may allow sites of tumor metastasis to enter the _________ ________ and metastasize to distant sites.

A

Systemic Circulation

108
Q

What are the characteristics of new blood vessels formed form neoangiogenesis:

A
  1. Dilated
  2. Haphazardly Formed (Tortuous)
  3. Leaky
109
Q

Angiogensis is a common mechanism for

A

Edema

110
Q

Invasion and metastasis are classic features of more _______ cancers

A

Aggressive

111
Q

What are the steps of Invasion-Metastasis Cascade

A

Step 1: Invasion into the surrounding ECM
Step 2: Spreading into the Vasculature (intravasation)
Step 3: Spreading out of the circulation and invading a distant tissue (extravasation)

112
Q

Tumor cells must first loosen their surrounding intercellular connections, performed by cancer cells deactivating ________ genes.

A

E-Cadherin

113
Q

After E-Cadherin Genes are deactivated _____ enzymes degrade the local ECM

A

Proteolytic

114
Q

Once a carcinoma penetrates its surrounding ______ _____, it is no longer consdiered an “in situ” or Stage 0 Cancer.

A

Basement Membrane

115
Q

Once a carcinoma penetrates its surrounding basement membrane it is considered to be at least a Stage __ or _____ cancer.

A

1

“Invasive”

116
Q

Once a cancer cell has navigated into a _______ or ________ vessel it has the ability to spread throughout the body.

A

Lymphatic

Hematopoietic (blood)

117
Q

Cancer cells that are within circulation are referred to as

A

Cancer Embolus

118
Q

Cancer Embolus is vulnerable to the host’s immune destruction via

A

Natural Killer Cells
CD8+ T Cells
—Both kill detected cancer cells—

119
Q

If a cancer embolus avoids death by the immune system, it may travel to sites that will support survival, these sites are predicted by:

A
  1. Anatomical Location
  2. Vascular Drainage
  3. First Capillary Bed Encountered (in circulation)
120
Q

Sites that tend to be favorable for metastatic spread of cancer cells are equipped wtih:

A
  1. Area of Stasis
  2. Abundant Capillaries
  3. Physical protection/Protection from the Immune System
121
Q

Sites that fit the criteria of favorable sites for metastatic spread:

A
  1. Lungs
  2. Liver
  3. Bone Marrow
122
Q

T/F. Cancer is predicatable

A

False

—Cancer is unpredictable by its very nature—

123
Q

High frequency of mutations that occur in cancer cells

A

Genomic Instability

124
Q

The result of gene alterations to cancer genes, such as TSG’s or genes that control genetic repair.

A

Genomic Instability

125
Q

Three inherited DNA repair defects that result in unique cancer presentations:

A
  1. DNA Mismatch Repair
  2. Nucleotide Excision Repair
  3. Homologous Recombination
126
Q

Without fully functional _________, nucleotide mismatches go uncorrected

A

DNA Mismatch Repair

127
Q

Hereditary Nonpolyposis Colon Cancer (HNPCC or Lynch Syndrome) is the prototypical cancer syndrome that is associated with an inherited defect in

A

DNA Mismatch Repair

128
Q

Individuals with HNPCC inherit ___ altered allele(s) and acquire the second alteration from an environmental carcinogen.

A

1

129
Q

Xeroderma Pigmentosunm (XP) is the prototypical condition that develops following an altered

A

Nucleotide Excision Repair (NER)

130
Q

Repairs damage from Ultraviolet (UV) Light, specifically correcting the cross-linking of pyrimidine residues.

A

Nucleotide Excision Repair (NER)

131
Q

Children with XP are sometimes referred to as

A

“Moon Children”

132
Q

Familial breast cancer that is positive for the BRAC1 and 2 gene mutations are classically associated with altered

A

Homologous Recombination Repair

133
Q

Active in repairing damage associated with chromosomal breaks

A

Homologous Recombination Repair

134
Q

When an individual has abnormal homologous recombination, they are ____ sensitive to environmental carcinogens

A

More

135
Q

Individuals with BRAC1 or BRAC2 mutations have an increased risk of developing:

A 
Breast Cancer
Ovarian Cancer
Fallopian Tube Cancer
Prostate Cancer
Pancreatic Cancer
Stomach Cancer
Melanoma
136
Q

Known to assist in the reparative process that occurs at an area of inflammation

A

Growth Factors

137
Q

Various cells at the area of inflammation will release growth factors that promote _______ at the area of inflammation and repair.

A

Angiogenesis

138
Q

Sustained angiogenesis is a hallmark of tumor growth and is needed for tumors of growth beyond

A

1-2 mm in diameter

139
Q

Macrophages that are present at the site of inflammation will release proteases in

A

Local Invasion

140
Q

_____ may assist in a cancer’s ability to invade locally and metastasize to distant sites by breaking down the ECM that surrounds a mass of cancer cells

A

Proteases

141
Q

The three primary environmental carcinogens:

A
  1. Carcinogenic Chemicals
  2. Ionizing Radiation
  3. Microbial Infections
142
Q

Involve waves on the upper-end of the UV light spectrum, X-rays, and Gamma Rays

A

Ionizing Radiation

143
Q

Various elements in the environment may contain high levels of Ionizing Radiation:

A

Uranium
UV Light
Potassium (from a Banana)

144
Q

Most common forms of skin cancer:

A

Basal Cell Carcinoma

Squamous Cell Carinoma

145
Q

T/F. The most common forms of skin cancer are associated with intense UV exposure.

A

False
—The most common forms of skin caner (Basal and Squamous Cell Carcinoma) are associated with a total lifetime exposure to UV light—

146
Q

The most deadly form of skin cancer

A

Melanoma

147
Q

Melanoma is more likely to be associated with an

A

Intense UV exposure

148
Q

T/F. The risk of contracting skin cancer does not change if you have had multiple intense sunburns early in life.

A

False

—The risk of contracting skin cancer is amplified if you have had multiple intense sunburns early in life —

149
Q

Unprotected miners have about a ___-fold increased risk of developing lung cancer, due to their exposure to radioactive elements.

A

10

150
Q

Individuals surviving the atomic blasts at the end of WWII saw a spike in:

A 
Leukemia
Thyroid Cancer
Breast Cancer
Colorectal Caner
Lung Cancer
151
Q

How long was the latency period for most individuals exposed to the radiation from the atomic bombs?

A

7-year latency period

152
Q

Ionizing Radiation is known to cause

A

Chromosomal Breaks

153
Q

Microbial agents most likely to be associated with Carcinogenesis:

A 
HTLV-1
HPV
EBV
HBV and HCV
H. Pylori
154
Q

Oncogenic RNA virus that increases the risk of developing T Cell Leukemia or Lymphoma.

A

Human T-Cell Lymphotropic Virus Type 1 (HTLV-1)

155
Q

Where is HTLV-1 most commonl?

A

Japan, Caribbean, Africa and South America

156
Q

HTLV-1 tends to infect

A

CD4+ T Cells

157
Q

HTLV-1 can spread via

A

Sexual Contact
Direct contact with blood
Breastfeeding

158
Q

HTLV-1 injects its RNA genes, particularly ____ Genes, into infected cells.

A

Tax

159
Q

The Tax Gene will activate _____, which accelerates cellular growth.

A

Cyclins (Cyclin D)

160
Q

Name given to a group of viruses that are likely to produce warts

A

Human Papillomavirus (HPV)

161
Q

HPV’s producing warts

A

HPV-6 HPV-11

162
Q

Aggressive HPV’s that increase the risk of cancerous transformation

A

HPV-16 HPV-18

163
Q

HPV infections are most commonly associated with _______________ of the cervix or anogenital region.

A

Squamous Cell Carcinoma

164
Q

HPV infections cause _______ ______ in two classic TGS’s

A

Functional Mutations

165
Q

Responsible for causing infectious mononucleosis (“mono”) and the 1st virus detected to have an association with cancer.

A

Epstein-Barr Virus (EBV)

166
Q

Known to increase the risk of various B cell lymphomas, such as Burkitt Lymphoma

A

EBV

167
Q

_____ infections increase the risk of developing nasopharyngeal carcinomas

A

EBV

168
Q

Cause chronic inflammation in the liver (hepatitis)

A

Hepatitis B Vrius (HBV)

Hepatitis C Virus (HCV)

169
Q

70-85% of all cases of liver cancer worldwide, are the result of chronic

A

HBV or HCV infections

170
Q

Patients of hepatitis viral infection-related liver cancer are most likely to occur in areas of

A

Africa

Asia

171
Q

Bacterial infection that involve the distal stomach or proximal small intestine

A

Helicobacter Pylori (H. Pylori)

172
Q

Infections that involve gastric adenocarcinomas or mucosa associated lymphoid tymors (MALT Lymphomas).

A

H. Pylori

173
Q

H. Pylori causes chronic inflammation in the area of involvement, contributing to increased ______ exposure and ______ supply.

A

Reactive Oxygen Species

Growth Factor

174
Q

Impact of tumor growth depends upon:

A
  1. Location of the tumor
  2. Functional Activity
  3. Destruction Caused from growth/invasion
175
Q

Wasting away of body fat and lean muscle mass is known as

A

Cachexia

176
Q

When Cachexia occurs because of advanced cancer, it is known as

A

Cancer Cachexia

177
Q

Widespread cancer having a hypermetabolic state on the body

A

Cancer Cachexia

178
Q

____ is a cytokine that is commonly increased in the presence of advanced cancer or in states when cancer cachexia is present

A

Tumor Necreosis Factor (TNF)

179
Q

Present in about half of all patients with advanced (metastatic) cancer

A

Cancer Cachexia

180
Q

Collection of signs or symptoms that occur in someone with a neoplasia, most commonly an advanced cancer.

A

Paraneopalstic Syndrome

181
Q

Paraneoplastic syndromes are most likely to manifest following ________ ________ or ______ _____

A

Hormonal Abnormalities

Immune Dysregulation

182
Q

Paraneoplastic syndromes occur in up to ____ of all cases of cancer representing the earliest manifestation of an occult

A

15%

183
Q

Examples of Paraneoplastic Syndromes:

A 
Cushing Syndrome
Hypercalcemia
Polycythemia
Acanthosis Nigricans
Hypertrophic Osteoarthropathy
184
Q

What cancers are associated with Cushing Syndrome?

A

Lung Cancer (Small Cell Lung Cancer)

185
Q

What cancers are associated with Hypercalcemia?

A

Lung Cancer, Breast Cancer, Renal Cancer, or Leukemia/Lymphoma

186
Q

What cancers are associated with Polycythemia?

A

Renal Cancer, Liver Cancer

187
Q

What cancers are associated with Acanthosis Nigricans?

A

Stomach Cancer, Lung Cancer, Uterine Cancer

188
Q

What cancers are associated with Hypertrophic Osteoarthropathy?

A

Lung Cancer

189
Q

An endocrine disorder involving elevated glucocorticoid levels (Hypercortisolism).

A

Cushing Syndrome

190
Q

The most common reason for elevated glucocorticoids is receiving

A

Exogenous Glucocorticoid Medications (Steroids)

191
Q

When Hypercortisolism results from a pituitary adenoma

A

Cushing Disease

192
Q

Clinical features of Cushing Syndrome:

A 
Weight Gain (moon face, buffalo hump)
Purple Striae (stretch marks)
Hypertension
Muscle Atrophy/Weakness
Osteoporosis
Hirsutism
Menstrual Abnormalities 
Psychological Irregularities
193
Q

Quantifies the tumor’s level of cellular differentiation

A

Grading of Cancer

194
Q

The higher the grade, the more ______ the cells of the tumor are and the worse the cancer’s prognosis.

A

Anaplastic

195
Q

Method for quantifying the tumor’s extent of spread

A

Staging of Cancer

196
Q

The higher the stage, the greater the extent of _____ and worse the prognosis.

A

Spread

197
Q

T/F, Grading cancer has been shown to be of greater clinical value than staging cancer.

A

False

—Staging caner has been shown to be of greater clinical value than grading cancer—

198
Q

Information for establishing a cancer’s stage incorporates:

A
  1. Size of primary tumor
  2. Whether cancer has spread to the lymph nodes
  3. Presence of hematopoietic metastasis
  4. Information obtained during clinical examinations
  5. Imaging Studies
199
Q

The four histological (cellular) evaluations to examine a neoplasm:

A
  1. Excision
  2. Biopsy
  3. Fine-Needle Aspiration
  4. Cytological (Papanicolaou) Smear
200
Q

Partial removal of an organ or tissue from the body

A

Excision

201
Q

Removal of a smaller sample of cells

A

Biopsy

202
Q

Imaging procedure used to view an illuminated and magnified image of the cervix

A

Colposcopy

203
Q

Removal of cells via aspiration with a needle

A

Fine-Needle Aspiration

204
Q

Most likely to be used with superficial tumors and easily palpated

A

Fine-Needle Aspiration

205
Q

Examples of organs that can have fine-needle aspiration:

A
  1. Breast
  2. Thyroid
  3. Lymph Nodes
  4. Salivary Glands
  5. Liver
  6. Pancreas
206
Q

a.k.a. “Pap smear”, sampling of shed cells of the cervix

A

Cytological (Papanicolaou) Smear

207
Q

Examples of organs that can have cytological smears:

A
  1. Cervix
  2. Endometrium
  3. Meninges (CSF)
  4. Bronchi
  5. Urinary Bladder
  6. Prostate
  7. Stomach
208
Q

Body’s fluids may be sampled for biochemical abnormalities or irregular enzyme levels, which may indicate the presence of cancers, these types of techniques are known as

A

Tumor Markers

209
Q

Tumor markers are best used for _______ purposes.

A

Screening

210
Q

T/F. Tumor markers are diagnostic and can indicate the presence of cancer.

A

False

—Tumor markers are non-diagnostic and cannot indicate the presence of cancer, alone—

211
Q

Evaluates for a specific prostate enzyme

A

Prostate-Specific Antigen Test (PSA Test)

212
Q

PSA is secreted by the prostate gland and increased levels of PSA indicates _______ levels of prostate activity.

A

Elevated

213
Q

May increase activity levels of the prostate gland:

A
  1. Benign Prostatic Hyperplasia (BPH)
  2. Recent ejaculation
  3. Prostate Cancer
214
Q

PSA Tests may be useful when _______ for suspected prostate cancer.

A

Screening

General Pathology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions