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HLSC 222 Pathophysiology 🧫 > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q

What is the leading cause of suffering and death in the developed world?

A

Cancer

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2
Q

What is cancer?

A

Collection of more than 100 different diseases, each caused by a specific
and often age-related accumulation of genetic and epigenetic alterations.

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3
Q

What 3 things interact to modify the risk of developing cancer?

A
  1. Environment
  2. Heredity
  3. Behaviour
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4
Q

What does Epignetic mean?

A

Study of how behaviors and environment cause changes that affect gene function

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5
Q

Are all tumours or neoplasms cancer?

A

No, they can be benign or malignant

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6
Q

What cells do benign tumours have?

A

Well-differentiated cells and is encapsulated

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7
Q

What do benign tumours have that is well-organised?

A

Stroma
e.g Connective tissue

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8
Q

What kind of tissue structure do benign tumours retain?

A

Normal tissue structure

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9
Q

Where don’t benign tumours invade beyond?

A

The capsule

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10
Q

Are benign tumours dangerous?

A

Yes
e.g Benign meningioma at base of skull can compress local brain tissue

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11
Q

What are well-differentiated tumours?

A

Cells and tissue structures that are like normal tissues and tend to grow and spread slowly

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12
Q

What are poorly differentiated/undifferentiated tumours?

A

Made up of cells that look very abnormal and often grow and spread quickly

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13
Q

What do malignant tumours progress to?

A

Cancer

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14
Q

What kind of organisation do malignant tumours have?

A

Abnormal

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15
Q

Malignant tumours growth rates?

A

Rapid growth rates

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16
Q

What is the hallmark of cancer?

A

Anaplasia

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17
Q

What is anaplasia?

A

Loss of cellular differentiation, undifferentiated cells

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18
Q

What do malignant tumours exhibit?

A

Pleomorphism

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19
Q

What does it mean if a tumour is pleomorphic?

A

Variability in size and shape

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20
Q

What kind of stroma do malignant tumours have?

A

Large stroma that is disorganised with an abnormal structure

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21
Q

What is the most deadly characteristic that malignant tumours have?

A

Metastasis

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22
Q

What is Metastasis?

A

Ability to spread far beyond tissue of origin

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23
Q

What are some types of malignant tumours?

A

Carcinomas
Adenocarcinomas

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24
Q

What are carcinomas?

A

Cancers arising from epithelial tissue

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25
Q

What are adenocarcinomas?

A

Cancers arising from ductal or glandular structures

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26
Q

Are malignant tumours encapsulated?

A

NO

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27
Q

What does Situ mean?

A

In natural or original place

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28
Q

What are Carcinoma in situ CIS?

A

Preinvasive epithelial tumours of glandular or squamous cells origin

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29
Q

How do carcinoma in situ cancers develop?

A

Incrementally as they accumulate specific genie lesions (mutations)

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30
Q

Why are CIS not considered malignant?

A

CIS have not broken through basement membrane or invaded surrounding stroma

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31
Q

What are the three fates of CIS?

A
  1. Remain stable for a long time
  2. Progress to invasive/metastatic cancers
  3. Regress and disappear
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32
Q

What cancer predominantly a disease of?

A

Aging

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33
Q

What is required before cancer can develop?

A

Multiple mutations

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34
Q

What is a mutation?

A

Cell acquires characteristics that provide advantage over neighboring cells

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35
Q

What are some common advantages gained from mutations?

A

Increased growth rate and/or decreased apoptosis

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36
Q

What is the result of common advantages caused by mutations?

A
  • Decreased need for growth factors to
    multiply
  • Lack contact inhibition
  • Anchorage independence to disseminate through body (metastasis)
  • Immortality: no apoptosis
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37
Q

What are the two fundamental cancer concepts?

A
  1. Cancer is a genetic disease arising from multiple mutations
  2. Tumour microenvironment is a mixture of cells (cancerous and benign) as well as their secretions.
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38
Q

What are the 3 stages of Cancer?

A
  1. Tumour initiation
  2. Tumour promotion
  3. Tumour progression
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39
Q

What is tumour initiation stage?

A

-Producing initial cancer cell
-First stage of cancer development
-Dependent on specific mutations

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40
Q

What is tumour promotion stage?

A

-Population of cancer cells expands with diversity of phenotypes
-Additional mutations

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41
Q

What is tumour progression stage?

A

-Spread of tumour to adjacent (invasion) and distal sites (metastasis)
-Governed by more mutations and changing microenvironments

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42
Q

What are the 2 divisions of mutations?

A

Small-scale changes
Large-scale changes

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43
Q

What are small-scale changes called?

A

Point mutations

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44
Q

What are large-scale changes called?

A

Translocations

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45
Q

What are point mutations?

A

Alteration of one or a few nucleotide base pairs
-can have profound effects on activity of resultant proteins.

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46
Q

What are the types of point mutations?

A

Substitution
Insertion
Deletion

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47
Q

What are driver mutations?

A

Mutations that drive the progression of cancer

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48
Q

What are passenger mutations?

A

Mutations that don’t contribute to malignant phenotype. Some are just random events and referred to as “passenger mutations”

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49
Q

What are the 2 kinds of large scale mutations?

A
  1. Chromosome translocation
  2. Gene amplification
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50
Q

What is chromosome translocation?

A

-Large changes in chromosome structure.
-Section of one chromosome is translocated to another chromosome.

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51
Q

What is Gene amplification?

A

Instead of normal two copies of gene, tens or even hundreds of copies are present.
-Example: gene expression of HER2 proteins

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52
Q

What is the clonal proliferation model?

A

selective advantage cancer cell has over neighboring cells
-it can replicate faster than nonmutant neighbors.

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53
Q

What mechanisms of cancer cells continue the accumulation mutations?

A

Increasingly rapid cell division and impaired DNA repair

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54
Q

The continuing accumulation of mutations progress to?

A

To most aggressive metastatic lesion

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55
Q

What is transformation (mutations)?

A

Process by which a normal cell becomes a cancer cell

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56
Q

What directs transformation?

A

Progressive accumulation of genetic changes that alter basic nature of cell and drive it to be malignant

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57
Q

What can each cancer cell develop?

A

Its own set of mutations

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58
Q

What is the result of cancer cells developing mutations?

A

Genomically heterogeneous mixture of cells

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59
Q

What increases the cell’s malignant potential?

A

Subsets accumulating more and more mutations

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60
Q

What happens to cancer cells that do not accumulate a set of mutations?

A

Lose to competition and die.

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61
Q

What is cancer development similar to?

A

Wound healing

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62
Q

What about cancer development and would healing are similar?

A

The initial pro inflammatory response

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63
Q

What does initial cancer cell proliferation trigger?

A

A typical pro inflammatory response by itself and adjacent nonmalignant cells

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64
Q

What do mediators recruit during the initial pro inflammatory response?

A

-Inflammatory or immune cells
-Cells associated with tissue repair

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65
Q

What kind of inflammatory or immune cells do mediators recruit?

A

T cells
B cells
Macrophages

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66
Q

What cells associated with tissue repair do mediators recruit?

A

Fibrolasts
Adipocytes
Mesenchymal stem cells
Endothelial cells

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67
Q

What do recruited cells form during abnormal wound healing?

A

A stroma (tumour microenvironment)

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68
Q

What does the Stroma do during abnormal wound healing?

A

Surrounds and infiltrates tumour

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69
Q

What percentage of tumour mass is made up of stroma cells?

A

90%

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70
Q

What is stroma growth affected by?

A

a. Rapid cancer cell proliferation
b. Various cell additions

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71
Q

What affects both stroll and cancer cell populations?

A

Paracrine signalling

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72
Q

What is the effect of paracrine signalling on cancer cells during abnormal wound healing?

A

Cancer cells increase proliferation
Become more heterogenous/diverse

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73
Q

During the process of abnormal wound healing what happens to most cancer cells?

A

They die

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74
Q

What happens to the surviving cancer cells during abnormal wound healing?

A

They are more aggressive and take on a metastatic phenotype

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75
Q

What mechanism is used to give cancer cells the ability of uncontrolled growth?

A

Sustained proliferation signals

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76
Q

What controls sustained proliferation signals?

A

Pro-oncogene

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77
Q

What is the result of oncogenes on the sustained proliferation signalling mechanism?

A

Body’s mechanism to stop uncontrolled growth is blocked

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78
Q

What is the first hall mark of cancer?

A

Uncontrolled cellular proliferation

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79
Q

How do normal cells enter proliferative phases?

A

In response to growth factors

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80
Q

How do growth factors control cellular growth?

A

Generally bind to specific receptors on cell surface and activate intracellular signalling pathways affecting DNA synthesis and cellular growth

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81
Q

What are Proto-oncogenes?

A

normal genes that direct protein synthesis and cellular growth

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82
Q

What are Oncogenes?

A

Mutated proto-oncogenes cells

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83
Q

What are oncogenes independent from?

A

Normal regulatory mechanisms

84
Q

What do mutations produce?

A

Oncogenes

85
Q

What do oncogenes allow?

A

Uncontrolled growth

86
Q

In addition to oncogenes, what else contributes to uncontrolled growth?

A

Stroma cells that produce their own growth factors

87
Q

What growth receptors are activated by cancer oncogenes?

A

RAS, P13K, MYC, and D-cyclins

88
Q

What kind of mutations can cause excessive production of oncogenes?

A

Translocations

89
Q

What is an example of translocation changing normal chromosomes to cancer?

A

Burkitt Lymphoma
-Abnormal B lymphocytes

90
Q

What mechanism allows cancer cells to stop tumour suppressor genes?

A

Evading growth suppressor

91
Q

What is required for the evading growth suppressor mechanism to function?

A

Two mutations

92
Q

What is the result of the evading growth suppressor?

A

Tumour suppressor genes are inactivated

93
Q

How does the evading growth suppressor inactivate the tumour suppressor genes?

A

Via mutations

94
Q

What do NORMAL tumour-suppressor genes do?

A
  1. Inhibit ptoliferation
  2. Stop cell division of damaged cells
  3. Prevent mutations
95
Q

What is the other name for tumour-suppressor genes?

A

Anti-oncogenes

96
Q

What must be inactivated for cancer proliferation to occur?

A

Tumour suppressing genes

97
Q

What is the classic tumour suppressor gene?

A

Tumour-protein P53

98
Q

What is P53 referred to as?

A

Guardian of the Genome

99
Q

What is the function of P53?

A

-Monitors cellular stress and activates caretaker genes to repair genetic damage
-Controls apoptosis

100
Q

The inactivation of P53 requires what?

A

2 mutations

101
Q

If P53 undergoes a single mutation what happens?

A

Increased cancer risk in OFFSPRING

102
Q

What does cancer activate to allow it to divide as many times as it wants?

A

Activates telomeres

103
Q

Are most body cells immortal?

A

No, most can only divide a limited number of times
aka Hayflick Limit

104
Q

What are telomeres?

A

Protective caps on each chromosome

105
Q

What happens to telomeres when most cells proliferate?

A

Telomere caps shorten with each cell division and become smaller and smaller

106
Q

What happens when the telomeres run out?

A

The cell can’t divide anymore and dies via apoptosis

107
Q

What enzyme is maintains telomeres?

A

Telomerase

108
Q

What does telomerase prevent?

A

Prevents telomeres from decreasing in number with cell division

109
Q

Where is telomerase usually active?

A

Only in ovaries, testes (germ cells) and stem cells

110
Q

What do cancer cells activate to be immortal?

A

Activate telomerase (for unlimited telomeres —> causes unlimited proliferation)

111
Q

How do cancer cells create their own blood supply?

A

Angiogenesis

112
Q

What does Angiogenesis increase the risk of?

A

Haemorrhage

113
Q

What is angiogenesis?

A

Production of new blood vessels

114
Q

What is the result of cancer cells activating angiogenesis?

A

Cancer has access to systemic blood system

115
Q

What do advaced cancers secrete?

A

Angiogenic factors

116
Q

What growth factors are involved in Angiogenesis?

A

Vascular endothelial GF
Platelet-derived GF
Basic Fibroblast GF

117
Q

Are vessels formed within tumours the same as healthy vessels?

A

No they are different

118
Q

How are tumour vessels different from healthy vessels?

A

Tumour vessels perform irregular branching from existing capillaries
Healthy vessels perform regular branching

119
Q

Why are tumour vessels more prone to haemorrhage?

A

They are more porous because cell contact between endothelial cells is less tight

120
Q

How do tumour vessels contribute to metastasis?

A

The vessels allow passage of tumour cells into the vascular system

121
Q

How do cancer cells get more building blocks to build more cells?

A

Programming Energy Metabolism

122
Q

What risk is associated with programming energy metabolism?

A

Increased risk of hemorrhage

123
Q

What is the result of programming energy metabolism?

A

Rapid cellular growth

124
Q

What method of metabolism do cancer cells use?

A

Even in adequate oxygen only use Glycolysis
-Aerobic glycolysis

125
Q

What is the name of the effect of cancer cells only using glycolysis?

A

Warburg effect

126
Q

How do cancer cells benefit from the Warburg effect?

A

Allows continual production of lactate

127
Q

What is the purpose of lactate?

A

Produces building blocks needed or rapid cell growth

128
Q

Production of what uses lactate?

A

-Lipids
-Nucleosides
-Amino acids
plus other molecular building blocks

129
Q

What do cancer cells resist?

A

Apoptosis

130
Q

What are the 2 pathways that control apoptosis?

A
  1. Intrinsic
  2. Extrinsic
131
Q

What does the Intrinsic pathway monitor?

A

Cellular stress

132
Q

What 2 groups can the intrinsic pathway activate?

A

BAX and BAK group

133
Q

What activates BAX?

A

If the cell can recover

134
Q

What activates BAK?

A

If the cell must be destroyed

135
Q

What do BAX and BAK groups regulate?

A

The mitochondrial release of pro-apoptotic molecules

136
Q

What is the pro-apoptotic molecule?

A

Cytochrome c

137
Q

What triggers the extrinsic pathway?

A

Death or BAK receptor is activated

138
Q

What happens when both pathways are activated?

A

Cytotoxic T-cells and Natural Killer cells induce apoptosis

139
Q

How do Cancer cells resist apoptosis?

A

The apoptotic pathways are dysregulated and cancer cells do not undergo programmed apoptosis

140
Q

How do cancer cells develop the ability to metastasise?

A

EMT

141
Q

What is EMT?

A

epithelial-mesenchymal transition

142
Q

What is Metastasis?

A

Spread of cancer cells from site of original tumour to distant tissues and organs through body.

143
Q

What is the major cause of death from cancer?

A

Metastasis

144
Q

Example of Metastasis affecting the survival rate of cancer?

A

-localized low-stage breast cancer 5-year survival rate =
greater than 90%

-metastasized breast cancer survival rate = 30% after 5 years

145
Q

Can non-metastasised cancer be cured?

A

Often can be cured with surgery, chemo and radiation

146
Q

Can metastasised cancer be cured?

A

It is less curable, often the therapies that work on not metastasised cancer are ineffective against metastasised cancer

147
Q

Where do Carcinomas originate from?

A

Highly differentiated epithelial cells

148
Q

What must cancer cells dissociate from to metastasise?

A

Dissociate from extra cellular matrix ECM

149
Q

What prevents dissociation from the ECM in initial carcinomas?

A

They still retain epithelial-like characteristics

150
Q

How do carcinomas dissociate from the ECM?

A

With a programmed transition from a partially epithelial-like carcinoma to a more undifferentiated mesenchymal-like carcinoma aka initiation of EMT

151
Q

Where does EMT normally occur?

A

Embryonic development
Wound healing

152
Q

What happens to normal cells when dissociated from their ECM?

A

Undergo Anoikis

153
Q

What is Anoikis?

A

Induction of apoptosis when cell loses ECM attachment

154
Q

Do cancer cells undergo Anoikis?

A

NO they don’t. Cancer cells avoid Anoikis so they can enter circulation and spread/metastasize

155
Q

What are the 3 steps to Epithelial-mesenchymal Transition (EMT)?

A
  1. Intravasation
  2. Extravasation
  3. Survival in circulation
156
Q

What is Intravasation?

A

Entry of tumour cells into circulation

157
Q

How is Intravasation completed?

A

Often via leaky angiogenesis vessels cancer has created

158
Q

What pathways spread tumour cells?

A

Vascular and lymphatic pathways

159
Q

What is Extravasation?

A

Exit of tumour cells from circulation to host tissue

160
Q

How do tumors survive in circulation?

A

Platelets coat the tumour and provide protection
-Cancer clot

161
Q

What are cancer cells that establish a tumour in a new location called?

A

Tumour-initiating cells (TICs)
or Cancer stem cells

162
Q

What is Dormancy?

A

A stable non-proliferating state that is reversible

163
Q

Does metastasis guarantee proliferation?

A

No

164
Q

When do 2/3 of breast cancer deaths occur?

A

After a 5 year disease free interval

165
Q

What do deceased individuals with no history of cancer have?

A

Dormant cancer cells

166
Q

What viruses are associated with cancer?

A

Human Papillomavirus HPV
Epstein-Barr virus EBV
Hepatitis B and C

167
Q

How do Cancer cells avoid immune detection?

A

Using 3 mechanisms
1. Failure to produce tumour antigen
2. Mutation in MHC genes needed for antigen presenting
3. Production of immunosuppressive proteins
or expression of inhibitory cell surface proteins

168
Q

Can a normal immune system protect against cancer?

A

Yes

169
Q

Are those with immunosuppression more likely to foster cancer?

A

Yes

170
Q

How many times more likely are immunosupressed people to get Non-hodgkin’s lymphoma?

A

10x

171
Q

How many times more likely are immunosupressed people to get Kaposi sarcoma?

A

1000x

172
Q

Why does immunosuppression foster cancer?

A

The release of immunosuppressive factors into tumour microenvironment increases resistance of tumour to chemo and radiation

173
Q

Depending on the tumour microenvironment, there are different what?

A

Phenotypes of macrophages

174
Q

What are the types of macrophages?

A

M1
M2
TAM

175
Q

What are M1?

A

Classic macrophages

176
Q

What do M1 respond to?

A

Inflammatory stage

177
Q

What do M1 do?

A

Phagocytosis

178
Q

What are M2?

A

Macrophages used during healing

179
Q

What do M2’s do?

A

Produce anti-inflammatory mediators to suppress inflammation

180
Q

What are TAMs?

A

Tumor-associated macrophages

181
Q

What macrophage type do TAMs preform like?

A

M2

182
Q

What do TAMs do?

A

-Block T cells and NK cells
-Produce cytokines to help tumour grow and spread

183
Q

How are cancers staged?

A

Based on presence of metastasis

184
Q

What is Stage I?

A

No metastasis

185
Q

What is Stage II?

A

Local invasion

186
Q

What is Stage III?

A

Spread to regional structures

187
Q

What Stage IV?

A

Distant metastasis

188
Q

What are some treatments for cancer?

A

a. Surgery
b. Radiation
c. Chemotherapy

189
Q

What are some ways surgery is used for cancer treatment?

A

Prevent cancer
Biopsy
Lymphnode sampling
Palliative surgery (relieve pain)

190
Q

How does radiation treat cancer?

A

Ionising radiation damages cancer cell’s DNA

191
Q

What are the goals of radiation treatment?

A

Eradicate cancer without excessive toxicity
Avoid damage to normal structures

192
Q

What does chemotherapy take advantage of?

A

Specific vulnerabilities in target cancer cells

193
Q

How is chemotherapy given?

A

In combinations designed to attack a cancer’s different weaknesses at the same time

194
Q

What are Paraneoplastic syndromes?

A

Group of rare disorders that are triggered by an abnormal immune system response to a cancerous tumor.

195
Q

What causes Paraneoplastic syndromes?

A

Caused by biological substances released by tumour

196
Q

What may be the earliest symptom of unknown cancer?

A

paraneoplastic syndromes

197
Q

How much pain is associated with early stages of malignancy?

A

Little to no pain

198
Q

What influences pain in the manifestation of cancer?

A

Fear, anxiety, sleep loss, fatigue and overall physical deterioration

199
Q

What is Cachexia syndrome?

A

Weakness and wasting of body due to severe chronic illness

200
Q

Cachexia is the most severe form of what?

A

malnutrition

201
Q

What are signs/symtoms of Cachexia?

A

anorexia, early satiety, weight loss, anemia, asthenia, taste alterations, and altered protein, lipid, and carbohydrate metabolism

202
Q

Direct tumour invasion of bone marrow causes what?

A
  1. leukopenia
  2. Thrombocytopenia
203
Q

What is Leukopenia?

A

Reduces WBC in blood

204
Q

What is Thrombocytopenia?

A

Blood platelet count too low

205
Q

When does risk of infection increase?

A

When absolute neutrophil and lymphocyte counts fall

206
Q

What is Asthenia?

A

Weakness, lack of energy and strength

HLSC 222 Pathophysiology 🧫 (16 decks)

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