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Pathophysiology SU BSN > Exam 1 - Ch. 12 > Flashcards

Exam 1 - Ch. 12 Flashcards

1
Q

Cancer

A

Is not a tumor

Is an abnormal growth resulting from uncontrolled
proliferation; it serves no physiologic function.

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2
Q

Benign tumors

A

Non-cancerous

Are named according to the tissues from which they
arise and include the suffix, -oma

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3
Q

Malignant tumors

A

Cancerous tumors

Are named according to the tissues from which they arise

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4
Q

Carcinoma in situ (CIS)

A

Are preinvasive epithelial malignant tumors of glandular
or squamous origin

Have not broken through the basement membrane or
invaded the surrounding stroma

Are not malignant

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5
Q

Point mutations

A

Small scale changes

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6
Q

Driver mutations

A

“Drive” progression of cancer

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7
Q

Passenger mutations

A

Random events

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8
Q

Gene amplification

A

Repeated duplication of chromosome → 10s or 100s of gene copies

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9
Q

Chromosome translocation

A

Large changes in chromosome structure

Piece of one chromosome is translocated to another chromosome

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10
Q

Oncogene

A

Mutant gene that would normally direct protein synthesis and cellular growth - contributes to the development of a cancer

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11
Q

Clonal proliferation (expansion)

A

Cancer cell progeny can accumulate faster than nonmutant neighbors. It acquires selective advantage over its neighbors

→↑ growth rate or ↓ apoptosis

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12
Q

Malignant transformation

A

Is the process during which a normal cell becomes a cancer cell

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13
Q

T OR F: Cancer cells are heterogeneous

A

TRUE

Cancer heterogeneity: due to proliferation and mutation

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14
Q

Proto-oncogenes

A

Normal nonmutant genes that code for cellular growth

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15
Q

Tumor-suppressor genes

A

Encode proteins that normally negatively regulate proliferation

anti-oncogenes

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16
Q

Activation of proto-oncogenes

A

hyperactivity of oncogenes

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17
Q

Mutation

A

loss or inactivity of tumor-suppressor genes

overexpression of products that prevent apoptosis, thus allowing continued growth of tumors

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18
Q

Growth factor signaling in cancer - Receptors

A

RAS
PI3K
MYC
D cyclins

Are oncoproteins that are activated by mutations in various cancers

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19
Q

retinoblastomaprotein(Rb)

A

RB is mutated in childhood retinoblastoma, and in many lung, breast, and bone cancers.

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20
Q

Mutation in the TP53 gene (tumor-suppressor gene)

A

“P53 protein is the guardian of the genome”
It monitors intracellular signals related to stress and
activates caretaker genes.
Mutation → Suppression of normal apoptosis.

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21
Q

Caretaker genes

A

Maintain genomic integrity.
• Encode proteins that are involved in DNA repair:
• errors in DNA replication
• mutations caused by UVR or ionizing radiation
mutations caused by chemicals and drugs.

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22
Q

Genomic Instability

A
  1. Loss of function of caretaker genes.
  2. Epigenetic silencing or modulation of gene function.
  3. Gene expression networks can be regulated by changes in miRNAs (miRs) and ncRNAs.
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23
Q

Oncomirs

A

miRs that stimulate cancer development and progression. miRs ↓ the stability and expression of other genes by pairing with mRNA.

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24
Q

BRCA1 and BRCA2

A

tumor-suppressors and caretaker genes that repair double-stranded DNA breaks

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25
Q

Causes↑↑ risk of breast cancer in both women and men, and ovarian or prostate cancers

A

Inherited mutations in BRCA1 and BRCA2

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26
Q

Chromosome instability (CIN) ↑ in malignant cells may be due to

A

malfunctions in the cellular machinery that regulates chromosomal segregation at mitosis.

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27
Q

Telomeres

A

protective caps on each chromosome that are held in place by a telomerase

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28
Q

T OR F: Cancer cells can activate telomeres

A

TRUE

→continued division

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29
Q

Cancer Metabolism

A

Cancer cells perform glycolysis

Allows lactate and its metabolites to be used for the more efficient production of lipids and other molecular building blocks needed for rapid cell growth

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30
Q

Warburg effect

A

is the use of glycolysis under normal oxygen conditions

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31
Q

Reverse Warburg effect

A

cancer cells generate large amounts of ATP→
oxidative stress → manipulate and destroy “cancer associated fibroblasts” → secrete metabolites and components → grow cancer cells

How well did you know this?
1
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2
3
4
5
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32
Q

Chronic inflammation

A

an important factor in the development of cancer.

Active inflammation predisposes a person to cancer.

By stimulating a wound-healing response that includes proliferation and new blood vessel growth

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

Examples of inflammation as a cause for cancer

A

Those with ulcerative colitis for 10 years or more have up to a 30-fold ↑ in developing colon cancer.

Hepatitis B (HBV) or hepatitis C (HCV) ↑ the risk of liver cancer.

H. pylori ↑ the risk of stomach cancer.

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34
Q

tumor-associated macrophage (TAM)

A

the key cell that promotes tumor survival

  • Blocks cytotoxic T cell and NK cell functions.
  • Produces cytokines that help tumor growth and spread.
  • Secretes angiogenesis factors.
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35
Q

Tumor associated antigens

A

oncogenes, antigens from oncogenic viruses, oncofetal antigens, and altered glycoproteins and glycolipids

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36
Q

Active immunotherapy

A

Immunization with tumor antigens to elicit or enhance the immune response against a particular cancer

How well did you know this?
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37
Q

Passive immunotherapy

A

Injecting the patient diagnosed with cancer with antibodies or lymphocytes directed against the tumor-ssociated antigens

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38
Q

Cancer invasion

A

Local spread

• Is a prerequisite for metastasis and the first step in the metastatic process.

Cancer often spreads first to regional lymph nodes through the lymphatic system

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39
Q

Metastasis

A

the spread of cancer cells from the site of the

original tumor to distant tissues and organs through the body.

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40
Q

Metastasis process

A

Cancer cells secrete protease→ digest the extracellular matrix and basement membranes → create pathways through which cells can move.

• Metastatic cells must be able to withstand the physiologic stresses of travel in the blood and lymphatic circulation.

How well did you know this?
1
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2
3
4
5
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41
Q

Epithelial-mesenchymal transition (EMT)

A

a process by which epithelial cells lose their cell polarity and cell–cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell type

How well did you know this?
1
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42
Q

Paraneoplastic syndromes

A

Symptom complexes are triggered by a cancer but are not caused by direct local effects of the tumor mass.

How well did you know this?
1
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2
3
4
5
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43
Q

Cachexia

A

the most severe form of malnutrition.

→ protein-calorie malnutrition and progressive wasting.

How well did you know this?
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2
3
4
5
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44
Q

Diagnosing and staging of cancer involves

A

The size of the tumor, the degree to which it has invaded, and the extent of the spread.

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45
Q

Stage 1

A

Is confined to its organ of origin

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46
Q

Stage 2

A

Is locally invasive

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47
Q

Stage 3

A

Has advanced to regional structures.

48
Q

Stage 4

A

Has spread to distant sites.

49
Q

Tumor Markers

A

• Are substances produced by benign or malignant cells.

  • Hormones • Enzymes • Genes
  • Antigens
  • Antibodies
50
Q

Tumor markers are used to

A

screen and identify individuals at high risk for cancer.

diagnose specific types of tumors.

follow the clinical course of cancer.

51
Q

Palliative Surgery

A

indicated for the relief of symptoms

52
Q

Prophylactic surgery

A

selected high-risk diseases:
• Mutations of the APC gene have close to a 100% lifetime risk of colon cancer: Colectomy.
• Women with BRCA1/2 mutations have a significantly ↑ risk of breast and ovarian cancer: Prophylactic mastectomy or bilateral salpingo-oophorectomy or both.

53
Q

Radiation Therapy

A

Is used to kill cancer cells while minimizing the damage to normal structures.

54
Q

Ionizing radiation

A

Damages cells by imparting enough ionizing radiation to cause molecular damage to the DNA.

Causes irreversible damage to normal cells.

Lifetime radiation dose

55
Q

Brachytherapy

A

Radiation therapy where Seeds are implanted

56
Q

Induction chemotherapy

A

Causes shrinkage or the disappearance of

tumors

57
Q

Adjuvant chemotherapy

A

Is administered after the surgical excision with

a goal of eliminating micrometastases

58
Q

Neoadjuvant chemotherapy

A

Is administered before localized (surgical or radiation) treatment.

59
Q

Ch. 12 reverse

Is not a tumor

Is an abnormal growth resulting from uncontrolled
proliferation; it serves no physiologic function.

A

Cancer

60
Q

Ch. 12 reverse

Non-cancerous

Are named according to the tissues from which they
arise and include the suffix, -oma

A

Benign tumors

61
Q

Ch. 12 reverse

Cancerous tumors

Are named according to the tissues from which they arise

A

Malignant tumors

62
Q

Ch. 12 reverse

Are preinvasive epithelial malignant tumors of glandular
or squamous origin

Have not broken through the basement membrane or
invaded the surrounding stroma

Are not malignant

A

Carcinoma in situ (CIS)

63
Q

Ch. 12 reverse

Small scale changes

A

Point mutations

64
Q

Ch. 12 reverse

“Drive” progression of cancer

A

Driver mutations

65
Q

Ch. 12 reverse

Random events

A

Passenger mutations

66
Q

Ch. 12 reverse

Repeated duplication of chromosome → 10s or 100s of gene copies

A

Gene amplification

67
Q

Ch. 12 reverse

Large changes in chromosome structure

Piece of one chromosome is translocated to another chromosome

A

Chromosome translocation

68
Q

Ch. 12 reverse

Mutant gene that would normally direct protein synthesis and cellular growth - contributes to the development of a cancer

A

Oncogene

69
Q

Ch. 12 reverse

Cancer cell progeny can accumulate faster than nonmutant neighbors. It acquires selective advantage over its neighbors

→↑ growth rate or ↓ apoptosis

A

Clonal proliferation (expansion)

70
Q

Ch. 12 reverse

Is the process during which a normal cell becomes a cancer cell

A

Malignant transformation

71
Q

Ch. 12 reverse

TRUE

Cancer heterogeneity: due to proliferation and mutation

A

T OR F: Cancer cells are heterogeneous

72
Q

Ch. 12 reverse

Normal nonmutant genes that code for cellular growth

A

Proto-oncogenes

73
Q

Ch. 12 reverse

Encode proteins that normally negatively regulate proliferation

anti-oncogenes

A

Tumor-suppressor genes

74
Q

Ch. 12 reverse

hyperactivity of oncogenes

A

Activation of proto-oncogenes

75
Q

Ch. 12 reverse

loss or inactivity of tumor-suppressor genes

overexpression of products that prevent apoptosis, thus allowing continued growth of tumors

A

Mutation

76
Q

Ch. 12 reverse

RAS
PI3K
MYC
D cyclins

Are oncoproteins that are activated by mutations in various cancers

A

Growth factor signaling in cancer - Receptors

77
Q

Ch. 12 reverse

RB is mutated in childhood retinoblastoma, and in many lung, breast, and bone cancers.

A

retinoblastomaprotein(Rb)

78
Q

Ch. 12 reverse

“P53 protein is the guardian of the genome”
It monitors intracellular signals related to stress and
activates caretaker genes.
Mutation → Suppression of normal apoptosis.

A

Mutation in the TP53 gene (tumor-suppressor gene)

79
Q

Ch. 12 reverse

Maintain genomic integrity.
• Encode proteins that are involved in DNA repair:
• errors in DNA replication
• mutations caused by UVR or ionizing radiation
mutations caused by chemicals and drugs.

A

Caretaker genes

80
Q

Ch. 12 reverse

  1. Loss of function of caretaker genes.
  2. Epigenetic silencing or modulation of gene function.
  3. Gene expression networks can be regulated by changes in miRNAs (miRs) and ncRNAs.
A

Genomic Instability

81
Q

Ch. 12 reverse

miRs that stimulate cancer development and progression. miRs ↓ the stability and expression of other genes by pairing with mRNA.

A

Oncomirs

82
Q

Ch. 12 reverse

tumor-suppressors and caretaker genes that repair double-stranded DNA breaks

A

BRCA1 and BRCA2

83
Q

Ch. 12 reverse

Inherited mutations in BRCA1 and BRCA2

A

Causes↑↑ risk of breast cancer in both women and men, and ovarian or prostate cancers

84
Q

Ch. 12 reverse

May be due to malfunctions in the cellular machinery that regulates chromosomal segregation at mitosis.

A

Chromosome instability (CIN) ↑ in malignant cells

85
Q

Ch. 12 reverse

protective caps on each chromosome that are held in place by a telomerase

A

Telomeres

86
Q

Ch. 12 reverse

TRUE

→continued division

A

T OR F: Cancer cells can activate telomeres

87
Q

Ch. 12 reverse

Cancer cells perform glycolysis

Allows lactate and its metabolites to be used for the more efficient production of lipids and other molecular building blocks needed for rapid cell growth

A

Cancer Metabolism

88
Q

Ch. 12 reverse

is the use of glycolysis under normal oxygen conditions

A

Warburg effect

89
Q

Ch. 12 reverse

cancer cells generate large amounts of ATP→
oxidative stress → manipulate and destroy “cancer associated fibroblasts” → secrete metabolites and components → grow cancer cells

A

Reverse Warburg effect

90
Q

Ch. 12 reverse

an important factor in the development of cancer.

Active inflammation predisposes a person to cancer.

By stimulating a wound-healing response that includes proliferation and new blood vessel growth

A

Chronic inflammation

91
Q

Ch. 12 reverse

Those with ulcerative colitis for 10 years or more have up to a 30-fold ↑ in developing colon cancer.

Hepatitis B (HBV) or hepatitis C (HCV) ↑ the risk of liver cancer.

H. pylori ↑ the risk of stomach cancer.

A

Examples of inflammation as a cause for cancer

92
Q

Ch. 12 reverse

the key cell that promotes tumor survival

  • Blocks cytotoxic T cell and NK cell functions.
  • Produces cytokines that help tumor growth and spread.
  • Secretes angiogenesis factors.
A

tumor-associated macrophage (TAM)

93
Q

Ch. 12 reverse

oncogenes, antigens from oncogenic viruses, oncofetal antigens, and altered glycoproteins and glycolipids

A

Tumor associated antigens

94
Q

Ch. 12 reverse

Immunization with tumor antigens to elicit or enhance the immune response against a particular cancer

A

Active immunotherapy

95
Q

Ch. 12 reverse

Injecting the patient diagnosed with cancer with antibodies or lymphocytes directed against the tumor-ssociated antigens

A

Passive immunotherapy

96
Q

Ch. 12 reverse

Local spread

• Is a prerequisite for metastasis and the first step in the metastatic process.

Cancer often spreads first to regional lymph nodes through the lymphatic system

A

Cancer invasion

97
Q

Ch. 12 reverse

the spread of cancer cells from the site of the

original tumor to distant tissues and organs through the body.

A

Metastasis

98
Q

Ch. 12 reverse

Cancer cells secrete protease→ digest the extracellular matrix and basement membranes → create pathways through which cells can move.

• Metastatic cells must be able to withstand the physiologic stresses of travel in the blood and lymphatic circulation.

A

Metastasis process

99
Q

Ch. 12 reverse

a process by which epithelial cells lose their cell polarity and cell–cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell type

A

Epithelial-mesenchymal transition (EMT)

100
Q

Ch. 12 reverse

Symptom complexes are triggered by a cancer but are not caused by direct local effects of the tumor mass.

A

Paraneoplastic syndromes

101
Q

Ch. 12 reverse

the most severe form of malnutrition.

→ protein-calorie malnutrition and progressive wasting.

A

Cachexia

102
Q

Ch. 12 reverse

Involves the size of the tumor, the degree to which it has invaded, and the extent of the spread.

A

Diagnosing and staging of cancer

103
Q

Ch. 12 reverse

Is confined to its organ of origin

A

Stage 1

104
Q

Ch. 12 reverse

Is locally invasive

A

Stage 2

105
Q

Ch. 12 reverse

Has advanced to regional structures.

A

Stage 3

106
Q

Ch. 12 reverse

Has spread to distant sites.

A

Stage 4

107
Q

Ch. 12 reverse

• Are substances produced by benign or malignant cells.

  • Hormones • Enzymes • Genes
  • Antigens
  • Antibodies
A

Tumor Markers

108
Q

Ch. 12 reverse

used to screen and identify individuals at high risk for cancer.

diagnose specific types of tumors.

follow the clinical course of cancer.

A

Tumor markers are

109
Q

Ch. 12 reverse

indicated for the relief of symptoms

A

Palliative Surgery

110
Q

Ch. 12 reverse

selected high-risk diseases:
• Mutations of the APC gene have close to a 100% lifetime risk of colon cancer: Colectomy.
• Women with BRCA1/2 mutations have a significantly ↑ risk of breast and ovarian cancer: Prophylactic mastectomy or bilateral salpingo-oophorectomy or both.

A

Prophylactic surgery

111
Q

Ch. 12 reverse

Is used to kill cancer cells while minimizing the damage to normal structures.

A

Radiation Therapy

112
Q

Ch. 12 reverse

Damages cells by imparting enough ionizing radiation to cause molecular damage to the DNA.

Causes irreversible damage to normal cells.

Lifetime radiation dose

A

Ionizing radiation

113
Q

Ch. 12 reverse

Radiation therapy where Seeds are implanted

A

Brachytherapy

114
Q

Ch. 12 reverse

Causes shrinkage or the disappearance of

tumors

A

Induction chemotherapy

115
Q

Ch. 12 reverse

Is administered after the surgical excision with

a goal of eliminating micrometastases

A

Adjuvant chemotherapy

116
Q

Ch. 12 reverse

Is administered before localized (surgical or radiation) treatment.

A

Neoadjuvant chemotherapy

Pathophysiology SU BSN (8 decks)

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