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General Pathology > Unit 5 > Flashcards

Unit 5 Flashcards

1
Q

What is the tumor structure of a which determines the biological nature (aggressiveness) of the tumor,are clonal, and basically are transformed cells or neoplastic?

A

Parenchyma

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2
Q

What is the tumor structure that is non- neoplastic, utilizes vessels and ecm as support and has a long term tumor survival?

A

Stroma (the more vascular a tissue is the more chances of stroma there are)

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3
Q

Which type of tumor exhibit “relatively innocent” features, is localized and reselectable, and posesses a favorable prognosis? Could cause : vascular compression and hormone production

A

Benign tumors

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4
Q

what is the name for a benign epithelial neoplasms producing or derived from glandular tissue?

A

adenoma

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5
Q

What is the name for a benign epithelial neoplasms that has Finger-like fronds?

A

Papilloma

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6
Q

what is the name for benign tumor of capillary endothelial cells?

A

hemangioma

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7
Q

what is the name for a benign tumor of adipose tissue?

A

Lipoma

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8
Q

What is the name for a benign smooth muscle tumors • “fibroid”?

A

leiomyoma

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9
Q

Malignant neoplasms that are composed of undiffer- entiated cells are said to be _______

A

anaplastic

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10
Q

These types of tumors are associated with cancer, they tend to be invasive and destructive, they have a tendency to metastasize, has parenchyma determining aggressiveness?

A

Malignant tumors

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11
Q

Malignant tumors are typically classified by

A

Embryonic tissue of origin

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12
Q

These tumors are typically derived from mesenchyme, associated with connective tissue and can develop at nearly any age?

A

Sarcomas

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13
Q

What is the 2nd most common cause of death in the US?

A

Cancer

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14
Q

This type of cancer has a higher incidence of cancer in males

A

Prostate

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15
Q

Most common type of cancer in females is

A

Breast cancer

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16
Q

This cancer is the cause of most death related to cancer

A

Lung and bronchus cancer

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17
Q

Cancer is basically a type of _____ growth

A

disregulated

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18
Q

What is neoplasia ?

A

new growth

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19
Q

Cancer is known to be a _____ ______ in which some sort of genetic material has been altered via mutations or epigenetics and is _____ to daughter cells

A

Genetic disorder; heritable

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20
Q

These characteristics Autonomous growth, independent of growth-inhibition, evasion of cell death & immune system, limitless replication, angiogenesis, invade/spread, abnormal metabolism are common with what?

A

neoplasia

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21
Q

It is important to note that neoplastic cells are _____ which means they are creating exact copies of themselves

A

clonal

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22
Q

What are the risks associated with cancer?

A

excessive alcohol, obesity, Toxins, irradiation, age, genetics

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23
Q

What is a parenchyma?

A

a cell that has undergone neoplasmic transformation, typically clonal and determine the aggressiveness of the tumor

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24
Q

What is a stroma?

A

Cells that support parenchyma, they are non neoplastic cells, necessary for long term tumor survival

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25
Q

What is a synonym to cancer?

A

Malignancy

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26
Q

Secondary site is a synonym for

A

metastasis

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27
Q

What is the rule of thumb for naming tumors?

A

Cell type + OMA

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28
Q

Where do carcinomas originate from?

A

Epithelial cells it is the MOST COMMON type of cancer 90%

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29
Q

What age range are carcinomas typically found in?

A

Mid to late adulthood

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30
Q

What is dysplasia?

A

Disorderly proliferation which means irregular growth but not neoplastic

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31
Q

In early neoplasia the carcinoma is _____ ___

A

in situ which means they have not penetrated the basement membrane

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32
Q

Invasive carcinoma are _____ and _____ aggressive

A

infiltrative and more aggressive which entails local destruction

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33
Q

multiple germ cell layers
• (Usually, described as 3)
• Bone, teeth, epithelia, muscle,
fat, & neurons

Are characteristics of which tumor?

A

Teratoma

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34
Q

MC benign tumor of the female breast • 2 tissue types
• Mixed tumor
• Only fibrous neoplasia

Are characteristics of which tumor?

A

Fibroadenoma

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35
Q

what is a benign tumor of tissue native to a particular site, well-differentiated

A

Hamartoma

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36
Q

What is a mass that projects from a mucosal surface (e.g. colon polyp)?

A

Polyp

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37
Q

What the criteria for Neoplasia?

A

Differentiation/anaplasia

Rate of growth

Local Invasiveness

Metastasis

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38
Q

Utilizing the criteria for neoplasia we are able to establish a _____

A

prognosis

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39
Q

What is differentiation?

A

How closely cells resemble their precursors

Normal: Well differentiated, slow mitosis

Benign: more well differentiated

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40
Q

What is anaplasia?

A

Loss of parenchymal differentiation

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41
Q

Cells that are poorly differentiated, are pleomorphic and have a high a rate of mitosis are said to be

A

Anaplastic

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42
Q

What is the difference in rate of growth between malignant and benign tumors?

A

Benign: Slow and controlled

Malignant: Fast and uncontrolled

  • correlation with differentiation

+ correlation with anaplasia

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43
Q

Which tumors are more likely to be invasive?

A

Malignant tumors which progress from local to distant invasion

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44
Q

In terms of invasiveness, this type of tumor is well localized, isolated and non invasive and capsulated

A

Benign tumor

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45
Q

What is the most reliable indicator of Cancer?

A

metastasis

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46
Q

Usually poor prognosis in cancer is attributed to _____ which causes tissue destruction and disturbs function

A

Metastasis

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47
Q

What are the types of dissemination ?

A

Seeding within body cavities, lymphatic spread, and hematogenous spread

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48
Q

How does seeding happen?

A

Invasion of cancer in natural body cavities and spreads to CNS or Ovaries

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49
Q

Which is the most common type of carcinoma spread?

A

Lymphatic spread

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50
Q

What is the most common type of SARCOMA spread?

A

Hematogenous spread

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51
Q

What is hematogenous spread?

A

Very rapid spread of cancer via the circulatory system and they stop at the 1st capillary bed which is usually in the liver

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52
Q

Most types of cancer are _____ and encompass 70-80% of all cancer diagnosis

A

sporadic many due to environmental factors which cause somatic mutations

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53
Q

Relocation might actually change the risks of cancer (T or F)

A

True

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54
Q

10% of all childhoold deaths (>15 years) are attributed to

A

Cancer (Leukemia, lymphomas

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55
Q

When a single mutant alelle is inherited and a specific phenotype marker such as neurofibromas and cafe au lait spots it is usually due to

A

Autosomal dominant CA syndromes

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56
Q

Altered NF1 genes cause

A

Neurofibromas and cafe au lait spots

57
Q

When there are two altered genes due to genomic instability and there are defective dna repair enzymes it is due to

A

Autosomal recessive syndrome of defective DNA

58
Q

An example of autosomal recessive syndrome of defective DNA would be

A

Xeroderma pigmentosa

59
Q

The most sporadic types of CA have a subtle familial association. This type of hereditary CA has no marker phenotypes

A

familial cancer of uncertain inheritance

60
Q

Why do preneoplastic lesions have an higher risk of cancer?

A

the cells in the lesions usuall are dysplastic or metaplastic

61
Q

An example of preneoplastic lesions in which white plaquing occurs in the buccal surface of mouth and could lead to squamous cell carcinoma?

A

leukoplakia

62
Q

what is carcinogenesis?

A

Creation of cancer

63
Q

The steps in the process of carcinogenesis are called

A

nonlethal genetic damage

64
Q

Genetic mutations that are usually ______ are found in a small subset of cells within the body (somatic cells) and are due to environmental factors such as irradiation and viral infection

A

Acquired

65
Q

Genetic mutation which involves all cells of the body and does not involve environmental factors

A

inherited

66
Q

What are the classes of regulatory genes?

A

proto oncogenes (later on oncogenes), TSGs, Apoptosis genes, and DNA repair genes

All of which incresase the growth and survival within the tumor cell

67
Q

Accumulation of mutations could lead to

A

Cancer

68
Q

What is a proto oncogene?

A

normal gene that regulates celullar growth

69
Q

What is an oncogene?

A

a mutated or overexpressed proto oncogen. It is anaplastic and contributes to cancer growth

70
Q

In order for an ocogene to gain function how many alelles need mutations?

A

1

71
Q

What is the karyotype?

A

number and appearance of chromosomes in the nucleus

72
Q

Damage to the karyotype could lead to

A

carcinogenesis by activating oncogenes and suprresing TSGs

73
Q

This type of structural abnormality is due to overexpression of proto-oncogenes and creation of a fusion gene (CML). It typically affects hematopoeitic cells

A

Balanced translocations

74
Q

A structural abnormality which is found in solid tissue cancers and impact TSGs

A

Deletion

75
Q

a structural abnormality in which overexpression of protooncogene leads to oncogene creation and is associated with breast cancer

A

overamplification

76
Q

What is micro RNA?

A

small non coding RNA molecules

77
Q

What is the function of micro RNA?

A

inhibiting gene expression and controlling growth and survival of cells. They also suppress translation

78
Q

When micro RNA is amplified it might lead to

A

Inhibition of TSGs

79
Q

Deletion of Micro RNA may lead to a

A

loss of oncogene inhibition

80
Q

What is epigenetics?

A

heritable changes of gene expression where there is no change in dna sequence. It is associated with silence genes (dna methylation/ histone modification)

81
Q

In tumor progression, when a clonal cell eventually starts unregulated production of clone cells and thus lead to production of subclonal cells because of the aggressiveness of the tumor. This could lead to ____

A

heterogeneity

82
Q

What are the hallmarks of cancer?

A

evading apoptosis, self sufficiency in growth signals, insensitivity to anti growth signals, tissue invasion and metastasis, limitless replicative potential, and sustained angiogenesis

83
Q

Mutations of a cell promote self sufficiency in which case it makes the cell not dependent on other cells for growth thus causing an _____ loop. CA cells can produce their own GFs and stimulate stromal GFs

A

autocrine

84
Q

HER2 mutations (overexpression of GF receptors) are usually involved with

A

breast cancer

85
Q

When a GF receives a signal and transmits across the cytosol to the nucleus it usually entails the use of a _____ which are also involved in the inhbition of apoptosis.

A

signal transducing molecule

86
Q

Mutations of STMs are common in tumors and could cause as much as ____ of all tumors

A

30%

87
Q

RAS and ABL mutations are the two most common types of mutations to _____

A

STMs

88
Q

STMs stimulate mitosis and initiation of transcription, thus if they are continuously stimulated they could lead to ____ of the cells

A

unregulated proliferation

89
Q

What is the restriction point in the cell cycle?

A

G1- S phase transition

90
Q

When CDKs are mutated what typically occurs?

A

unregulated proliferation of cells due to speeding through the restriction point of the cell cycle. ALL CANCERS DISABLE THIS RESTRICTION POINT

91
Q

TSGs encode inhibitory proteins and cause decreased proliferation, however if one is ______ to growth inhibition then cells can proliferate in an erratic manner

A

insensitive

92
Q

What do altered TSGs mimic?

A

oncogene stimulation

93
Q

Insensitivity of growth inhibition is typically recessive and requires ____ alleles to be inactivated

A

2

94
Q

What was the the first tumor suppressor gene to be discovered that is also expressed in every cell type examined?

A

RB GENE

95
Q

What is the importance of the RB Gene?

A

It regulates the G1/S checkpoint.

96
Q

Seeing as Cancer usually entails an unregulated growth and differentiation, the RB will usually be defective in many or most forms of cancer (T or F)

A

True

97
Q

What type of viruses might affect the RB gene?

A

HPV

98
Q

Which of the TSGs is one of the most commonly mutated genes in human cancers (70% ie Lung, breast, and colon cancer)?

A

TP53

99
Q

which gene thwarts neoplastic transformation by three interlocking mechanisms: activation of temporary cell cycle arrest (termed quiescence), induction of permanent cell cycle arrest (termed senescence), or triggering of pro- grammed cell death (termed apoptosis)?

A

TP53

100
Q

What are the stressors that might activate the P53 gene?

A

Anoxia, activation of oncogenes, and DNA damage

101
Q

When working with the P53 gene which may be considered the primor- dial response to DNA damage ?

A

Quiesence due to minor DNA damage

Increases the rate of dna repair

102
Q

What is the name for a permanent cellcycle arrest characterized by specific changes in morphology and gene expression that differentiate it from quiescence or revers-ible cell cycle arrest?

A

TP53 mediated senescence

103
Q

What is is the ultimate protective mechanism against neoplastic
transformation?

A

tp53-induced apoptosis

104
Q

In most cancers, there is a bi-allelic loss of the P53 gene (t or f)

A

true

105
Q

Less commonly, some patients inherit a mutant TP53 allele; the resulting disease is called ________

Patients with _______ have a 25-fold greater chance of developing a malignant tumor by age 50 com- pared with the general population

A

Li Fraumeni

106
Q

Cancers not only develop from unregulated growth it may also develop from a non functioning or mutation in apoptosis which helps CA cells survive instead of killing them. This increases the probability of _____ development

A

tumor

107
Q

It is known that both apoptotic pathways (Ext/Int) activate their respective caspases ( EXT -> 8 and INT ->9) however which caspase is stimulated by BOTH pathway?

A

Caspase 3 (executioner)

108
Q

most normal human cells have a capacity of 60 to 70 doublings. Thereafter, the cells lose the capacity to divide and enter _______ which is linked to telomere shortening

A

senesence

109
Q

If telomere shortening is pronounced, this might eventually lead to _______ _______ which is characterized by massive apoptosis

A

genomic instability

110
Q

t for tumors to grow indefinitely, as they often do, loss of growth restraints is not enough. Tumor cells also must develop ways to avoid both _____ and ______ therefore if a cell manages to activate telomerase then it might avoid death

A

senesence and mitotic catastrophe

111
Q

What is the Hayflick limit?

A

The finite number of divisions a cell can have

112
Q

Tumor growth without new blood vessels requires what diameter?

A

> 1-2mm

113
Q

What does sustained angiogenesis provide and remove?

A

nutrients and remove waste

114
Q

What is usually stimulated in neoplasia and is poorly organized (Leaky, dilated, tortuous)?

A

angiogenesis

115
Q

Pro angiogenic factors are usually stimulated by the tumors (t or F)

A

true

116
Q

Which system is utilized by the tumors in order to metastasize?

A

vascular

117
Q

What requires angiogenesis for growth support, has metabolic demands and has sequential spread?

A

Malignancy and metastasis

118
Q

What are the steps for the invasion mestastasis cascade?

A
  1. Invasion of ECM
  2. Vascular spread: dissemination & homing
  3. Micrometastases grow & invade
119
Q

Mutations develop because of __+_

A

genetic make up and environment

120
Q

What are the three DNA repair systems?

A
  1. Mismatch repair
  2. Nucleotide excision repair
  3. Homologous recombination repair
121
Q

which system of DNA repair works with genes to fix “spelling errors”?

A

mismatch

122
Q

When “spelling errors” accumulate they form a _______ phenotype which means the way the morphology of the cell will change

A

mutator

123
Q

The most common error which includes abnormal repeats of 1-6 nucleotides, is unstable, present in 15% of sporadic colorectal cancers, and is present in HNPCC

A

Microsatellite instability

124
Q

Which DNA repair mechanism Recognizes a segment of damaged DNA and removes it, then repairs the “gap” via DNA polymerase?

What is an example of it?

A

Nucleotide Excision repair

125
Q

Ultraviolet light could cause cancer (t or f)

A

True. excess exposure increases the chance of getting cancer dramatically

126
Q

Which DNA repair system involves DNA being exchanged between two homologous chromosomes to repair breaks in DNA?

A

Homologous recombination

127
Q

If one has Hypersensitivity to DNA-damaging agents then homologous recombination cant happen (t or F)

A

true

128
Q

Mutations in two genes, ____ and _____, account for 50% of cases of familial breast cancer.

A

brca 1 and 2

129
Q

inflammation, often thought of as a protective response against tumors, can paradoxically also enable malignancy (t or f)

A

true

130
Q

What are the two ways in which inflammation could stimulate tumor growth?

A

Persistent chronic inflammation in response to microbial infections or as part of an autoimmune reaction and When inflammation occurs in response to tumors

131
Q

Patients with GI tract infections, hepatitis B and C, and other autoimmune reactions are highly susceptible to Cancers due to the compensatory proliferation of
cells in an attempt to repair the damage. This regenera- tive process is aided and abetted by a plethora of growth factors, cytokines, chemokines, and other bioactive sub- stances produced by activated immune cells collected at the site. Persistent cell replication and reduced apoptosis under these conditions place the cells at risk of acquiring mutations in one or more of the genes involved in car- cinogenesis True or false

A

true

132
Q

In order for carcinogenesis to occur _____ genetic alterations are required however they need not follow an orderly sequence.

A

multiple

Breast and colon cancers have approximately 90 mutations

133
Q

Carcinogenesis results from the stepwise accumulation of several genetic alterations T or F

A

True

134
Q

. According to the scheme of Adenoma Carcinoma formation , inactivation of the ___ tumor suppressor gene occurs first, followed by activation of ____ and, ulti- mately, loss of a tumor suppressor gene on ____and loss of ____. The precise temporal sequence of mutations may be different in different tumors.

A

APC, RAS, 18q, TP53

135
Q

What are the 3 classes of carcinogenic agents ?

A

(1) chemicals, (2) radiant energy, and (3) microbial agents (mainly viruses such as HPV, EBV, Hep B, HEP C, KSHV but the one primary bacteria is Helicobacter pylori)

136
Q

What is a direct acting carcinogen?

A

carcinogens which require no metabolic conversion to become carcinogenic. They are in general weak carcino- gens but are important because some of them are cancer chemotherapy drugs

137
Q

What is an indirect acting carcinogen?

A

refers to chemicals that require metabolic conversion to an ultimate carcinogen. Exposure to Polycyclic Hydrocarbons can cause cancers because of these type of carcinogens but also another agent that might produce this would be Aflatoxin B1 which is produced by some strains of Aspergillus, a mold that grows on improperly stored grains and nuts

138
Q

Why is Aflatoxin B1 dangerous?

A

It carries a signature mutation which affects TP53

General Pathology (10 decks)

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