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NURS361 - Pathophysiology II > Module 4 - Neoplasia > Flashcards

Module 4 - Neoplasia Flashcards

1
Q

Neoplasia

A

Cancer

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2
Q

Cell Cycle

A

Orderly sequence of events (usually) during which duplicated chromosomes align appropriately and results in cell proliferation

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3
Q

Body tissues are divided into three types based on ability to undergo regeneration, what are the 3 types?

A
  1. Continuously dividing/Labile
  2. Stable
  3. Permanent Tissue
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4
Q

Labile Tissue

A

Continuously dividing tissue that can regenerate easily and do so constantly

ex: skin, cervix, epithelium of the GI tract, fallopian tubes, bone marrow

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5
Q

Stable Tissue

A

These cells stop dividing once growth ceases, but can undergo regeneration in response to a stimulus

ex: Solid organs, fibroblasts, endothelial cells

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6
Q

Permanent Tissue

A

These cells stop dividing once growth ceases, and have no further regeneration

When damaged, they are replaced with scar tissue, and this tissue lacks the cell’s functional characteristics

ex: Neural cells, cardiac cells, etc

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7
Q

Proliferation

A

Process of increasing cell numbers via mitotic division

It is the mechanisms for replacement when old cells die or additional cells are needed

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8
Q

What triggers proliferation?

A

Growth Factors (increase cell size and cell division)

Hormones

Cytokines

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9
Q

Growth cells stimulate proliferation usually, but they can also…

A

inhibit cell cycling or gene expression for other cells

ex: Erythropoietin, Granulocyte Colunate, Cytokines (All GH Examples)

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10
Q

Differentiation

A

Process by which the structure and function of a cell becomes more specialized

The new specialized cells get structural, microscopic, and functional characteristics of cells they replace.

Once the cell picks a line, they differentiate into mature cells of that line and stick to that line

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11
Q

Stem Cells

A

Undifferentiated cells that differentiate based on need in continuously dividing tissue

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12
Q

Examples of Differentiated Cells

A

Granulocytes

Agranulocytes

Platelets

Erythrocytes

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13
Q

Stem Cell division includes what 3 processes?

A

Self Renewal

Asymmetric Replication

Differentiation

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14
Q

Self Renewal

A

Process where stem cells undergo numerous mitotic divisions in an undifferentiated state

More stem cells are made

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15
Q

Asymmetric Replication

A

Stem cell divides and one daughter cell remains an undifferentiated stem cells, but the other daughter cell will become a progenitor cells that differentiates based on progenitor lines

This is how we maintain stem cells in the body while having cells that go on to differentiate

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16
Q

Apoptosis

A

Programmed cell death in multicellular organisms that keeps the number of total cells constant in death

Macrophages will recognize the “not you” cells and remove them as well as cell lyses

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17
Q

The rate of proliferation is = to the rate of ____ in health

A

Apoptosis

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18
Q

Hypertrophy

A

enlargement or overgrowth of an organ due to an increase in the size of the cells

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19
Q

Neoplasia

A

Unregulated/Dysregulation of cell differentiation and growth

Autonomous, Unregulated, and Lacks Physiologic Control

process of formation or presence of a new abnormal growth of tissue that is not under physiologic control

“Cancer”

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20
Q

Neoplasm

A

New Growth; Swelling that is caused by different etiologic factors (ex: Inflammation, trauma, etc)

A “Tumor” - Benign or Malignant

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21
Q

Neoplasm

A

New Growth; Swelling that is caused by different etiologic factors

A “Tumor” - Benign or Malignant

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22
Q

What about Neoplasia leads to the formations of Neoplasms?

A

Proliferation forms new growths, and cells do not die off (apoptosis) to keep the number of total cells constant –> therefore a neoplasm occurs

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23
Q

Benign Neoplasms are ___ Differentiated

A

Well Differentiated

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24
Q

What sort of factors determine if a tumor will be Benign or Malignant?

A

Characteristics of the cell (ex: Differentiation)

Local Invasion

Rate of Growth

Ability to Metastasize

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25
Q

What sort of factors determine if a tumor will be Benign or Malignant?

A

Characteristics of the cell (ex: Differentiation)

Local Invasion

Rate of Growth

Ability to Metastasize

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26
Q

Benign Tumors

A

Contain cells that look like normal tissue cells and may perform the normal function of that type of tissue (ex: secrete hormones which can lead to over secretion)

Grow slowly

Have a fibrous capsule

Do NOT infiltrate, invade, or metastasize

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27
Q

What about a benign tumor makes it easier to surgically remove?

A

It has a fibrous capsule

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28
Q

How can a benign tumor potentially damage nearby organs?

A

It could grow large and compress the organ thus damaging it

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29
Q

Malignant Tumors

A

Contain cells that do not look like normal adult cells and do not perform normal functions of that type of tissue

May secrete signals, enzymes, toxins, etc

Grow rapidly (rate depends on level of differentiation)

Can infiltrate, invade, and metastasize to distant sites via blood and lymph

No fibrous capsule

Can compress and/or destroy the surrounding tissues and organs - leads to injury and ischemia

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30
Q

Most common new male cancer? Most deadly male cancer? Most common new female cancer? Most deadly female cancer?

A

Most Common Male - Prostate
Most Deadly Male - Lung and Bronchus
Most Common Female - Breast
Most Deadly Female - Lung and Bronchus

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31
Q

Tumor Types

A

Solid

Hematologic Cancer

Cancer in Situ

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32
Q

Solid Tumors

A

Initially confined to specific tissue or organ but then detach and invade surrounding tissue, blood and lymph

Allows Metastasis to occur

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33
Q

Hematologic Cancer

A

Blood and lymph contain the cancer cells initially

These cancers are considered disseminated diseases from the beginning

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34
Q

Cancer in Situ

A

Cancer cells that are localized in the organ of origin

Considered preinvasive lesions, they can be surgically removed or treated MORE EASILY and have a smaller chance of recurrence

EX: Cervical cancer is so localized it is almost 100% curable

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35
Q

Anaplastic Cells

A

poorly differentiated or non differentiated tumor cells

they have numerous morphologic changes and vary in size and shape

these cells have a high proliferation rate, but do NOT resemble the tissue of origin

These are Malignant Tumor cells

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36
Q

Pleomorphism

A

cells that vary in size and shape

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37
Q

What is the basis for grading tumors?

A

It is based on how differentiated the cells are and the number of proliferating cells on a grade of I to IV

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38
Q

A Grade I tumor means…

A

the cells are well differentiated

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39
Q

A Grade IV tumor means…

A

the cells are Anaplasia/Anaplastic - poorly differentiated or not differentiated

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40
Q

Hypoplasia (Cells)

A

Fewer cells than what is deemed a normal amount

Usually benign

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41
Q

Hyperplasia (Cells)

A

Increased cell number.

Occurs due to a stimulus and is similar to the surrounding tissue and cells are the same relative to each other

ex: Callus formation on skin when exposed to pressure

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42
Q

Neoplasia (Cells)

A

Cells that are similar to hyperplasia, but there is NO stimulus that triggers this (it is loss of normal proliferation regulation) and the cells are all different from one another

Increased cell number

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43
Q

Dysplasia (Cells)

A

Cells with a change in normal shape, size or organization, usually d/t chronic irritation

ex: Cigarette smoke and inflammation

Changes are reversible if stimulus is removed, otherwise the cells eventually turn metaplastic

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44
Q

Metaplasia (Cells)

A

A change in the actual TYPE of cells

ex: Ciliated Columnar Epithelium of resp. surface turning into Stratified Squamous Epithelium after prolonged smoking

Changes are reversible if stimulus is removed, if not they will turn anaplastic

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45
Q

Anaplasia (Cells)

A

A reversal in differentiation (dedifferentiation) OR loss of structural and functional differentiation of normal cells

These cell changes are NOT reverisble

These cells are cancerous tumor cells

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46
Q

What is the hallmark of cancer

A

Genetic Instability

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47
Q

Genetic Instability

A

defined as the presence of a high frequency of mutations in cells that change the sequences of nucleic acid and arrangement of chromosomes

growth reg. genes and genes involved in the cell cycle are altered or arrested and lead to gross chromosomal abnormalities

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48
Q

What is the result of Genetic Instability

A

Aneuploidy

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49
Q

Aneuploidy

A

incorrect number of chromosomes

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50
Q

How do Cancer Cell growth properties differ from normal cells?

A
  1. They secrete growth factors and/or have receptors
  2. Lack cell density dependent or contact inhibition
  3. Anchorage independence (decreased anoikis; Shed into body fluids d/t loss of cohesiveness and adhesiveness)
  4. Faulty cell to cell communication
  5. They are immortal
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51
Q

What is Cell Density Dependence/Contact inhibition

A

in normal cells, the cells will cease to divide after cells become a certain density

ex: after a wound closes they will stop growing, but cancerous cells lack this and will continue

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52
Q

What does it mean if a cancer cell has anchorage independence?

A

They will grow when not anchored to the ECM, which is abnormal as normal cells need to be anchored or else they undergo anoikis

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53
Q

Anoikis

A

a version of apoptosis that occurs for normal cells when they detach from the ECM

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54
Q

How can faulty cell to cell communication lead to cancer?

A

If the cells signals for recognizing growth “short circuit” and do not signal inhibition they can lead to overgrowth and tumors

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55
Q

What does it mean that cancer cells are “Immortal”?

A

They can divide an infinite number of times unlike normal cells

They only end up having the functions of survival and proliferation though

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56
Q

What happens if a cell detaches in a normal cell versus a cancer cell?

A

Normal cell –> Cell shedding –> Cell is free from ECM –> Anoikis

Cancer cell –> cell shedding –> cell is free from ECM –> Metastasis

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57
Q

Mesenchymal Stem Cells (EMT)

A

Multipotent stem cells that can differentiate into different kinds of myocytes (muscles), adipocytes (fat), Osteoblasts (Bone cells), Chondrocytes (Cartilage cells) - and a lack of anoikis will lead to metastasis commonly with these cells if they shed

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58
Q

Normally, the number of cells produced is equal to …

A

the number of cells that die, such that the total number of cells in the body remains constant

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59
Q

In cancer, the cell cycle is ___ ___ than healthy cells

A

not shorter (d/t immortality, allowing for increased growth fraction)

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60
Q

What are some reasons cancer cells are so prolific?

A

Cells do not die on schedule

Cells respond to growth factors that keep the cancer cells actively dividing in the cell cycle

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61
Q

Growth Fraction

A

Ratio of dividing cells to resting cells

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62
Q

What is the growth fraction in healthy cells versus cancerous cells?

A

Healthy - equilibrium is established between cell birth and death

Cancer - growth factor increases since the cell cycle is far longer

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63
Q

Doubling Time

A

the length of time it takes a mass of cells in a tumor to double (for the tumor to double in size)

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64
Q

When does doubling time begin to decrease in cancerous cells?

A

Once blood supply and nutrients fail to support growth

So they divide slower

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65
Q

What does the tumor growth rate look like on a graph?

A

Tumor growth rate will be very fast initially but after a while they do not have the nutrients and blood supply needed so the doublings stabilize out and doubling slows down

It ends up looking like a massive and quick jump in number of cells from only a small increase in doublings, and eventually slows down considerably once nutrients are not enough

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66
Q

How many doublings are required, and how many cells that is, to detect a tumor on a scan?

A

30 doublings - 1 billion cells

This tumor would be about 1 centimeter in size (some scans can see smaller tumors - like MRI though)

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67
Q

At what amount of doublings and cell among can a tumor kill the host?

A

35 doublings - over 1 Trillion cancer cells

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68
Q

What is different about malignant cancer cells that make them able to shed and lead to metastatic spread?

A

Benign growth occurs via expansion in a capsule, but malignant cells invade other tissue d/t not having a capsule and seed in cavities thus leading to spread/metastasis

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69
Q

Where is the most common cavity for malignant spread/seeding?

A

Perineal Cavity

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70
Q

What allows malignant cells to invade and penetrate other surrounding tissue?

A

A lack of a capsule and having “legs” (similar to crab like projections) that allow penetration (and a lack of demarcated boundaries because of these)

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71
Q

Malignant cells ___ into body cavities

A

seed

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72
Q

Cells in a primary tumor develop the ability to do what?

A

escape, travel, and survive in the blood. They then are able to exit the blood and develop a secondary tumor

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73
Q

What are some pathways for malignant tumors?

A

Lymph Channels (Lymphatic Spread)

Blood Vessels (Hematogenous Spread)

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74
Q

Sentinel Node

A

Initial lymph node to which the tumor drains

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75
Q

What can metastatic/secondary tumors do relative to the primary tumor?

A

because of different patterns of metastasis (early or late) they can potentially be larger than the primary tumor

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76
Q

What are the two main subgroups of malignant tumors?

A

Carcinoma

Sarcoma

77
Q

Carcinoma

A

Derived from epithelium

Always Malignant

Common

Mostly lymphatic spread

May have a pre-malignant (or in situ phase)

Common in older patients

78
Q

Sarcoma

A

Derived from connective tissue

Always malignant

Less common than a carcinoma

Spread by blood

Not believed to have a pre malignant phase unlike carcinoma

More often seen in younger patients

79
Q

Describe how lymphatic spread occurs for a metastatic carcinoma?

A

Cancer cells spread –> Lodge in the first node to receive drainage from tumor (sentinel node) –> Cells either die from lack of nutrients or non-good growth environment, remain dormant, or become a discernible mass (assuming the immune system did not already attack it) –> cells then can move to other nodes and go through ducts to enter blood cells or enter vessels providing tumors with blood.

80
Q

Why is Hematogenous spread more difficult than lymphatic spread?

A

Hematologic spread is selective and has many steps

In circulation the tumor cells are vulnerable to destruction by host immune cells d/t recognition of the different MHC1

Thicker walled arterials and arteries are resistant to invasion so they must invade via capillaries or venules

81
Q

Hematogenous spread involves cancer invading what?

A

Capillaries and Venules

82
Q

In order to metastasize via hematogenous spread, what must occur?

A

Cancer cell must break loose and invade the ECM (enzymes give it access to a blood vessel) –> They must get through the blood vessel alive –> find a favorable site in the vessel to invade tissue –> Begin growth

83
Q

How might a cancer cell gain protection in the blood vessels?

A

they sometimes aggregate and adhere to circulating blood components (especially platelets) to form tumor emboli which can then allow them to exit circulation by binding to the endothelium to form secondary tumors

84
Q

In order for a metastatic/secondary tumor to grow after traveling the blood, it must have what?

A

Angiogenesis (new vessels formed for it)

Growth factors that promote proliferations

Have its own blood supply

85
Q

Only select cancer cell clones have the right what, to perform all steps of metastasis to form a secondary tumor?

A

Right combination of gene products

86
Q

Common Metastatic Sites for Secondary Tumors

A
  1. Portal vein from venous blood of GI, pancreas and spleen going to the liver
  2. Vena cava blood heading to the lungs
  3. Preferential spread of cancer based on type?

!SO, Live and lungs are common sites from hematogenous spread to have metastasis

87
Q

Prostate cancer tends to have metastasis to ___

A

bone

88
Q

Bronchogenic cancer tends to have metastasis to ___ and ___

A

adrenals and brain

89
Q

Neuroblastomas tend to have metastasis to ___ and ___

A

liver and bones

90
Q

In health, proto-oncogenes code for what?

A

Normal cell division proteins

ex: Growth factors, growth factor receptors, transcription factors, cell cycle proteins, apoptosis inhibitors

91
Q

When proto-oncogenes mutate into oncogenes, what can occur?

A

Overactivity and gene activation

They mutate from insertions, deletions and translocations into increased or activated oncogenes

This can lead to cancer

92
Q

ras Oncogene

A

transmits signals to the cell nucleus to increase proliferation (cancer levels)

93
Q

Philadelphia Chromosome oncogene

A

oncogene commonly seen after translocation in chronic myeloid leukemia

it is from translocation of a gene on chromosome 9 to 22

94
Q

HER-1/neu oncogene

A

Multiple copies of this gene occur leading to overexpression and increased cell proliferation

This oncogene is seen in 30% of breast cancer cases when the cancer is considered AGGRESSIVE and with a POOR PROGNOSIS

95
Q

Antioncogenes

A

in health, these tumor suppressor genes inhibit cell division

When inactivated, there will be unregulated growth leading to cancer

96
Q

How can an antioncogene become inactivated?

A

Through either inherited or acquired mutations

But most mutations are acquired

97
Q

p53 Tumor Suppressor Gene

A

Autosomal Recessive Antioncogene (named after its molecular weight) that usually senses DNA damage and initiates repair or apoptosis

When mutated in cancers like colon, lung, and breast occur

You are more likely to respond to chemotherapy if your P53 gene is intact and activated

98
Q

RB Tumor Suppressor Gene

A

Autosomal Dominant or Sporadic Antioncogene

Hereditary form occurs 40% of the time with the rest acquired

If both RB genes are inactivated, the development of a retinoblastoma (malignant eye tumor) occurs

If only one gene is inactivated, that person is a carrier

Sporadic version of RB gene is non-inherited and is a result in both mutations occurring in one of the genes and inheritance of inactivation from parent in the other gene

99
Q

Lynch Syndrome (r/t Tumor Suppressor Genes)

A

Autosomal Dominant

Inherited cancer d/t mutation - “Hereditary Polyposis Colorectal Cancer”

It is associated with a genetic predisposition to acquiring other types of cancer, so there is an increased risk for bowel, colon, uterine, and ovarian cancer in the person

There is no cure for this syndrome as it is genetic and no symptoms associated with it early on, but early detection of colon cancer is 90% curable

100
Q

BRCA 1 and BRCA 2 (Tumor Suppressor Genes)

A

Autosomal Dominant Antioncogenes

Inactivation of these genes leads to a higher risk for breast cancer

101
Q

What is the growth pathway for oncogenesis occurance?

A

Carcinogenic Agent + Normal Cell –> DNA damage –> Failure to repair DNA leads to activation of growth promoting oncogenesis, inactivation of antioncogenes, and alterations in genes that control apoptosis –> unregulated cell differentiation and growth occur as a result –> A malignant neoplasm occurs

Normal Cell

102
Q

What is the pathway for growth regulation?

A

Stimulation of normal cells by growth factors will lead to growth factor receptor activation and signaling of proteins that promote growth promoting signals to the nucleus –> Nucleus modulates gene transcription and progression through the cell cycle and many of the signaling proteins exert their effects through proteins called kinases which controls regulation and growth

103
Q

3 Stages of Carcinogenesis

A
  1. Initiation
  2. Promotion
  3. Progression
104
Q

Initiation

A

First carcinogenesis stage which leads to an initial mutation occurring

This occurs when cells are exposed to appropriate doses of carcinogenic agents like physical, chemical, or biological and mutations occur

These changes are irreversible in the genome, the cells most vulnerable are actively making DNA at the time of exposure, and if these cells become latent they can move onto promotion (even for a long latency time)

105
Q

Promotion

A

Second stage of carcinogenesis where mutated cells are stimulated to divide

They do so in an unregulated and accelerated manner

Can be reversible if the substance stimulating the cells to do this are removed

106
Q

Progression

A

Third stage of carcinogenesis where tumor cells compete with one another and develop more mutations, which make them more aggressive and spread

Cells quickly are gathering malignant phenotypic changes and cells can proliferate autonomously, invade, or metastasize in this phase

107
Q

What are some etiologic factors for Cancer?

A

Cellular Level Factors

External and Host Factors

commonly both are working together when cancer develops and progresses over time

108
Q

Examples of Cellular Level Etiologic Factors for Cancer

A

Genetic damage

Mutation

epigenetic factors that silence a gene or genes

Role of cancer stem cells

ECM, cytokines, growth factors, and other cell types

109
Q

Examples of External and Host Factors for Cancer?

A

Age

Heredity (Mendelian inheritance of genes)

Hormonal Factors (from tumors, mutated hormones, etc)

Obesity

Immunologic Mechanisms

Environmental agents: chemical carcinogens, radiation, microorganisms

110
Q

Why can hormone therapy be concerning when the patient has cancer?

A

The hormones could be closely related to what the tumor uses and could cause further proliferation - there is an unknown link between hormones and cancer

111
Q

How can obesity lead to cancer?

A

Insulin resistance, increase in estrogen/androgen hormones, and lower insulin levels all lead to inhibition of apoptosis and increases in chronic inflammation and malignant cell transformation rate

112
Q

Evidence supports the idea that the lower the immune response …

A

the greater the incidence of cancer

113
Q

Types of Chemical Carcinogens

A

Direct

Indirect

114
Q

Direct Reacting Agents

A

Inherently carcinogenic (ex: charcoal smoke on meats)

115
Q

Indirect Reacting Agents

A

Only actively carcinogenic after metabolic conversion (Ex: chemicals in red meat)

Includes Procarcinogens which are initiators

116
Q

Promoters

A

chemicals that alter gene expression, enhance the # of copies of cells made, and alter intracellular communication

They alone are NOT carcinogenic, but act in the presence of carcinogens like cigarette smoke

117
Q

The longer the dose and longer the exposure and difference in age…

A

the greater the risk of cancer from radiation(ex: sunlight)

118
Q

UV exposure is more dangerous for what age group?

A

In childhood, so protect from sunburns prior to age 4!

119
Q

Treatment radiation has lower risks associated with it unless.

A

it is done over and over - time and amount and length of exposure effects risk

120
Q

HPV and Cancer

A

An oncogenic virus in humans leading to cervical and anogenital cancer and genital warts

121
Q

H. Pylori and Cancer

A

This bacteria is associated with gastric cancer, but also we need it for the benefits in our normal flora

Growing opportunistically is when it is a problem

122
Q

Local Effects of Tumor Growth

A
  1. Compression of Adjacent Structures

2. Effusions

123
Q

What can compression of adjacent structures lead to?

A
  1. Hollow organs

2. Blood vessels bleeding and hemorrhaging

124
Q

What can cancer related effusions lead to?

A

Fluid build up and interference with normal functions

This may cause the effusion to need mandatory removal

ex: build up in the lungs makes it so they cannot expand and could lead to atelectasis so it might need centesis removal

125
Q

Cancer impact moves from ___ to ___ upon metastasis

A

local to systemic

126
Q

Initially cancer affects ___ ___ only

A

target organs only

127
Q

S/S of cancer can be ___ or ___, but this changes to the former when the cancer progresses regardless of type

A

systemic/widespread or local

128
Q

Systemic Manifestations of Cancer

A

Anemia

Anorexia and Cachexia

Fatigue and Sleep Disturbances

Ectopic hormones or factors secreted by tumor cells (paraneoplastic disorders)

129
Q

The systemic manifestations of cancer can be compounded onto through…

A

the use of chemo meds!

130
Q

How does Anemia occur/impact in relation to cancer?

A

Commonly occurs, especially with medicines destroying cells

Bone marrow function and side effects (Nausea, vomiting, anorexia) of the medicine lead to nutritional deficiencies and iron deficiencies leading to anemia

Also, inflammation from tumors decreases erythropoietin synthesis so RBC maturation occurs less

Need to check WBC/RBC count since hypoxia in advanced solid tumors occurs - so we must make sure chemo therapy is safe

131
Q

Cancer r/t Anemia can lead to what effects regarding treatment and prognosis?

A

reduces effectiveness of treatment and safety of treatments

contributes to the needs of blood transfusions

increases mortality

132
Q

Why does Anorexia/Cachexia occur in Cancer and what can it lead to?

A

It occurs because it becomes difficult to eat d/t nausea from tumors and meds and also your tastes change

This can lead to wasting syndrome, and cancer progression causes anabolic processes to not be maintained leading to the body digesting muscle and fat leading to wasting and causing dramatic weight loss and decrease in strength

133
Q

Wasting Syndrome

A

Wasting of muscles and fat from cancer d/t increased CNF leading to hypothalamus satiety center suppression and increased lipoprotein lipase (increases FA release to use in metabolism thus causing acidosis)

This cancer anorexia cachexia syndrome can be seen in most solid tumor cancers and is impacted by may factors like tumor necrosis, changes in food taste, inflammation, treatment, and especially cytokines in more aggressive cancer

134
Q

Why does Fatigue and Sleep Disturbances occur with Cancer?

A

Most common cancer side effects

Resting/Sleeping does not resolve fatigue like in normal people

Cancer impacts both the central and peripheral levels:

  1. Peripheral levels do not have enough ATP leading to acid build up and muscles not responding to central stimulation
  2. Central levels have fatigue starting in the CNS and resulting in difficulty leading to voluntary activities and movement
135
Q

Paraneoplastic Syndrome (Disorders)

A

A consequence of cancer in the body but not from the cells themselves, rather the ectopic hormones and factors they release

RARE

can occur in benign OR malignant tumors d/t hormone release

commonly one of the first manifestations of lung, breast, hematologic cancers

136
Q

Manifestations of Paraneoplastic Syndrome

A

Encephalitis

Ataxia

Neuropathy

Body Jerking

Irregular Eye Movements

Psychiatric Disturbances

137
Q

Is Paraneoplastic Syndrome a direct consequence of cancer cells?

A

NO

the cancer cells themselves do not cause this, rather the ectopic hormones and factors they release do

138
Q

Syndromes Related to Cancer (Paraneoplastic Syndromes/From Hormones/Hormone like protein production)

A

Endocrinologic Syndromes

Hematologic Syndromes

Paraneoplastic Neurologic Disorders

139
Q

Endocrinologic Syndromes

A

Primarily occur from Lung Cancer

  1. ADH - SIADH Syndrome
  2. ACTH - Cushing Syndrome
  3. PTH-related protein - Hypercalcemia (from bone cancer breaking bones down)
140
Q

The 2 most common cancer syndromes are?

A

SIADH

Cushing Syndrome

141
Q

Hematologic Syndromes

A

Primarily occur in pancreatic and lung cancers

  1. Venous Thrombosis
  2. Non Bacterial Thrombolytic Endocarditis

Cancer cells produce proteins that impact clotting !

142
Q

Paraneoplastic Neurologic Disorders

A

Primarily occur in lung cancer

Leads to encephalitis, ataxia, neuropathy, progressive numbness and weakness of the hands and feet, myoclonus, and myasthenia gravis and lambert-eaton syndrome

143
Q

Ataxia

A

loss of balance

144
Q

Myoclonus

A

body jerks and irregular rapid eye movements and psychiatric disturbances

145
Q

Myasthenia Gravis

A

Progressive muscle weakness that begins in the mouth and eyes

146
Q

Lambert-Eaton Syndrome

A

Opposite of myasthenia gravis

Progressive muscle weakness beginning in the limbs

147
Q

What is the origin of a paraneoplastic neurologic disorder?

A

It occurs from an altered immune response and production of onconeural antigens normally expressed in the nervous system - but they are made by cancer cells and are attacked by the nervous system for being ID’ed as foreign (self attack/autoimmune)

148
Q

When do Paraneoplastic Disorders commonly appear?

A

Early and commonly lead to clinical challenges

149
Q

What can paraneoplastic disorders mimic?

A

Metastatic Disease

150
Q

The effects of paraneoplastic disorders can compound with …

A

drug side effects

151
Q

Cancer Screening is ___ Prevention

A

Secondary

152
Q

Is there a screening method for every type of cancer?

A

no

153
Q

Methods of Cancer Screening

A

Observation (type dependent, i.e. skin)

Lab Tests

Procedures

154
Q

Effective Screening Tests are available for what types of cancer?

A

Breast

Cervical

Colon

Rectal

Prostate

Skin

155
Q

How do we make a Cancer Diagnosis

A

the location and type of cancer determines the diagnosis - So TUMOR MARKERS, antigens on tumor surfaces, as well as hormones and enzymes being overexpressed need to be screened, staged, detected,, etc to diagnose cancer

example of tumor markers: CEA, hCG, calcitonin, catecholamines, monoclonal immunoclobulin, PSA, CA-125 and 19-1, CD Antigens

156
Q

What are some methods to gather the information needed for a cancer diagnosis?

A
  1. Cytologic Studies (ex: Pap smear)
  2. Tissue Biopsy (ex: Fine needle aspiration)
  3. Immunohistochemistry (ex: look at estrogen receptors)
  4. Molecular Diagnostics like Microarray Technology/Gene Chips
157
Q

Cytologic Studies

A

ex: pap smear

tissue and cells are taken to look for cancer

158
Q

Tissue Biopsy

A

ex: fine needle aspiration

taking a tissue sample either via fine need, bronchoscopy, surgical incision, endoscopy, and cytoscopy to check for cancer

159
Q

Immunohistochemistry

A

Uses antibodies to ID surface markers on cells and identification of the markers (i.e. estogen receptors) can facilitate more specific and effective treatment.

160
Q

Molecular Diagnostics

A

Detects individual molecules by looking at DNA or RNA based assays to check for cancer

It can identify molecular targets to attack with drugs and tumor fragments that float in blood samples

161
Q

What type of testing is very relevant when cancer is hereditary or treatment is based on characteristics of the tissue/tumor?

A

Molecular Diagnostics

162
Q

With hereditary cancer, there is an increased risk for what things …

A

secondary malignancy

early onset

multiple neoplasms

a recognizable histological pattern

163
Q

Genetics does not have much play in what type of cancer?

A

Lung Cancer

BRAC2 gene has a higher risk for lung cancer despite lung cancer not being a hereditary cancer, so sometimes genes play a role in history lung cancer, but genetics does not often play much into lung cancer specifically

164
Q

Microarray Tech and Gene Chips

A

Gene chips are used to detect and quantify the expression of large numbers of genes at the same time, so we can see the extent that genes are turned off and in in tissues

This can ID tumors, make a prognosis, classify hereditary tumors, and check on response to therapy

165
Q

Cancer Grading

A

Microscopic examination of differentiation

Comes up with either I, II, III, or IV with differentiation and prognosis becoming poorer the higher the number

166
Q

Cancer Staging

A

Clinical, radiographic, surgical examination of extent and spread –> Treatment and Prognosis

System that can be used to decide the extent of cancer

Include TNM and AJC

167
Q

What is the most common Staging system used?

A

TNM

168
Q

TNM

A

Staging system that is based on tumor size, whether it is in lymph nodes, whether cancer has metastasized

The higher the stage the worse the prognosis

T1-4 = Tumor Size

NO-3 = Lymph node involvement

M0-1 = Metastasis

169
Q

What would a T4N3M1 Cancer mean

A

It is a size 4 tumor, in 3 lymph nodes, and has metastasized

170
Q

AJC

A

Staging method by American joint committee

Less commonly used than TMN but stages cancers from 0 to IV based on size of primary lesion and presence of nodal spread and metastasis

171
Q

Methods for Cancer Treatment

A

Surgery

Radiation Therapy

Chemotherapy

Hormone and Antihormone Therapy

Biotherapy

Targeted Therapy

172
Q

When is surgery used for cancer?

A

to make diagnosis, staging, do tumor removal, for relief of symptoms

most feasible when tumor is smaller, has well defined margins, and potentially a capsule (benign)

173
Q

Radiation therapy

A

Ionizing radiation hurts and kills cancer cells - with cancer cells more likely to be hurt than healthy cells

However, rays can damage bone marrow and GI tract mucosal lining so adverse effects can occur like infection, bleeding, anemia, nausea, and vomiting

Given in small doses to prevent effects

174
Q

Chemotherayp

A

Major systemic treatment for tumor and metastasis sites with multiple anti cancer chemicals given

Many side effects occur such as hair loss, bone marrow suppression, anorexia, and vomiting

Nurses must be chemo certified in order to give these drugs

175
Q

Hormone and Antihormone therapy for Cancer

A

given to deprived cells that stimulate division

Mostly for breast, prostate, and endometrial cancers

Can be of concern if hormones can exacerbate tumor effects/growth

176
Q

Biotherapy

A

Immunotherapy used to change the immune response (increase) and change tumor cell biology

177
Q

Targeted Therayp

A

agents attack malignant cells but not healthy cells

It can disrupt molecular signaling pathways and inhibit cancer angiogenesis leading to deprivation of needed nutrients and blood and therefore death

178
Q

What is often needed regarding treatment for cancer?

A

use of more than one type of therapy to allow a longer life expectancy (even in poor prognosis)

179
Q

With chemotherapy, a constant progression of cancer cells are killed with each treatment, so what would happen if the last treatment was not given?

A

the cancer would return even if it was in clinical remission

180
Q

Why may targeted treatment become ineffective if a person has liver cancer that returns following treatment?

A

Liver cancer is not usually hereditary and hepatocellular carcinomas commonly mutate a lot

Once genes are mutated, the targeted treatments are unable to target the cancer and the treatment has become ineffective since the cancer cells are not the same

181
Q

Do childhood cancers have any discrimination in different groups?

A

No discrimination, it affects every socioeconomic group and ethnic group

every 2 minutes a child is diagnosed with cancer (300,000 annually)

182
Q

A childhood cancer can be hereditary or acquired, but when they are hereditary what occurs?

A

Occur at a very young age

Have a higher frequency of multifocal lesions in a single organ or both organs if that organ is paired

183
Q

Childhood cancer is not usually linked to ___ or ___ factors

A

environment or lifestyle factors

184
Q

The most common childhood cancers are?

A

Leukemia!

Usually childhood cancers are hematologic, nervous, soft tissue, or bone cancers

185
Q

There are no what for childhood cancers?

A

no early warning signs or screening tests

186
Q

Cancer treatment in children can cause what years after treatment?

A

cardiovascular complications

impaired growth

fatigue

cognitive problems

187
Q

What is critical for children who are cancer survivors?

A

Regular follow ups since there is a risk for recurrence of that type of cancer

188
Q

Why does it matter if a lump is painful or not?

A

Cancer masses are non-painful (and often moveable) while cysts are more commonly painful - So this matters a lot on palpation!

NURS361 - Pathophysiology II (20 decks)

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