Cancer Flashcards
1
Q
What is the goal of Healthy People 2020 in terms of CA:
A
To trduce the number of new CA cases as well as illness, disability, and death caused by CA
2
Q
What is the objective of Healthy People 2020 in relation to CA:
A
- Increase the proportion of CA survivors who report healthy quality of life
- Decrease incidence of invasive: colorectal, cervical, BRCA
3
Q
When should men see their MD for a PSA test:
A
>50 yo should take the prostate-specific antigen (PCA) to screen for prostate CA
4
Q
What are the statistics on the incidence and death rates from all CA:
A
Both have decreased statistically
5
Q
What ethnicity will you find the highest rate in CA incidence and mortality:
A
African American; Vietnamese have a highr incidence of cervical CA
6
Q
What gender is at an increased risk of CA incidence:
A
Men
7
Q
What CA are gender specific and what are the common CA:
A
prostate and breast CA; lung, gender specific CA, colon, pancreas
8
Q
What is the number one barrier to CA prevention:
A
- Poverty, not race, accounts for 10-15% lower survival rate from CA in cultural groups
- Lack of health insurance
- inability to pay fee-for-service
- Limited health care access
9
Q
What are the other barriers to CA prevention:
A
- Knowledge level of risk factors/screening/guidelines
- psychosocial: anxiet/embarrassment…
- Cultural beliefs: Asians belief that CA is Karma/God’s will
- Complimentary Alternative Medicine (CAM): herbal interaction
- Level of Acculturation
- Health Care provider’s enthusiasm for compliance
10
Q
What is the key to the reduction of CA mortality by reducing incidence of CA:
A
PREVENTION
11
Q
How is the prevention of CA accomplished:
A
- avoiding carcinogen/altering it’s metabolism
- Modification of lifestyle
- medical intervention: chemoprevention to tx precancerous lesions
12
Q
What type of prevention in the nsg role includes health promotion activites where teaching about the strong association between tobacco and CA and modifying CA risk factors: chronic EtOH…
A
Primary prevention
13
Q
What type of prevention in the nsg role includes health behaviors that promote early dx/tx that includes: Genetic testing, enhanced surveillance, screening:
A
Secondary prevention: screening is secondary d/t targeting specific organs r/t risk factors according to family PMHx
14
Q
What type of prevention in the nsg role includes rehabilitation after a disease/condition that already exists to minimize disability and disease progression for productive living:
A
tertiary prevention: Care givers have the hardest challange in teritary prevention
15
Q
What does the acronym, CAUTION, stand for pretaining to warning signs of CA:
A
- C: change in bowel/bladder habit
- A: a sore throat that does not heal
- U: unusal bleeding/discharge from
- T: Thickening/lumps in/on the body
- I:indigestion/difficulty swallowing
- O: obivious change on mole
- N: Naggy cough/hoarshness
16
Q
A new and abnormal formation of tissue, as a tumor or growth is defined as:
A
Neoplasm
17
Q
A transformation/formation of cells into CA cells/tumor as a result of chemicals/viral/or radioactive damage to genes is defined as:
A
carcinogenesis/oncogenesis
18
Q
Any substance/agent that produces CA or increases the risk of developing CA (AKA cancer promoters) is defined as:
A
carcinogen
19
Q
Predetermined, undifferentiated cells of human tissues are defined as:
A
stem cells
20
Q
Stem cells of a particular tissue will ultimately differentiate into what:
A
mature, functioning cells of that particular tissue into that tissue=hence the word predetermined
21
Q
What theory proposes that it is the loss of intracellular control of profileration (only growing when cells die or not growing beyond respected boundaries) occurs when there’s a mutation of stem cells:
A
Stem cell theory
22
Q
Where (or what is the target) do CA cells develop from:
A
stem cells
23
Q
The length of total cell cycle varies d/t what:
A
Length varies d/t the SPECIFIC type of cell
24
Q
What length of time in the cell-cycle can result in a higher cell kill when utilizing chemotherapy:
A
SHORTER CELL CYCLE TIME
25
What type of chemotherapy has a better chance of causing cells to reach the S phase in order to effectively kill CA cells:
_Combination chemotherapy _
26
A normal, orderly process that progresses from a state of immaturity to state of maturity is defined as:
cellular differentation
27
Normally, what type of functions do cells performed as cells dfferentiate and mature:
specific functions
28
A differentiated cell reverting to a previous undifferentiated state d/t genetic mutation is defined as:
CA cell de-differentiation
29
What are the two types of normal genes that can be affected by mutation:
1. proto-oncogene
2. tumor suppressor gene
30
This type of normal gene that can be affected by mutation is important for regulating normal cellular processes via promoting growth d/t a _genetic 'lock' keeping the cell in a mture state_ is defined as:
proto-oncogenes
31
How can a proto-oncogene be "unlocked:"
Carcinogen can unlock a proto-oncogene causing de-differentation d/t mutations
32
How do proto-oncogene become malgnant:
mutations d/t unlocking mechanism
33
This type of normal gene that can be affected by mutation supresses growth of tumor cells while regulating cell growth:
Tumor suppressor gene
34
What can cause a tumor suppressor gene to become inactive:
mutations that alter tumor suppressor gene redering them inactive: BRCA1 and BRCA2 are examples
35
Exposure to radiation can cause cellular damage by what type of release:
_Physical_ release of energy
36
What is the common radiation carcinogen used in dx studies or therapeutic resources:
Ionizing radiation
37
This carcinogen can cause damage to a cell where the celll can repair itselfand no mutation is seen; malignancy can occur if the carcinogen affects/damages wither the proto-oncogenes or tumor suppressor gene; children, fetuses, elderly are at higher risk of this type of carcinogen:
ionizing radiation
38
This type of radiation carcinogen is a complete carcenogen; comes from the sun/tanning:
ultraviolet radiation
39
What are some examples of complete carcenogens and what does it mean to be a complete carcinogen:
_tobacco_ and UVR are complete carcenogens in that they both initiate (irreversible) and promote (reversible) CA
40
What are the risks of getting UVR associated CA:
1. prolonged exposure
2. hereditary disease characterized by inefficient repair
3. skin pigmentation: the greater amount of melanin=greater protection from UVR
41
This type of carcinogen can be chemo (cytoxan or alkylating drugs can cause secondary leukemias), immunosuppressive drugs; tobacco; _BENZYENE AROMATIC HYDROCARBON_ compounds found in soot/coal tar; inorganic compounds like nickel _all of which alter DNA_:
Chemical carcinogens
42
This type of carcinogen infect the DNA resulting in proto-oncogene changes and cell mutation are defined as:
viral carcinogenes
43
Who is more susucepitble to viral carcinogens:
immunocomprimised, very young, and the elderly are more at risk for viral carcinogens
44
What type of CA do these viral carcinogens cause: Human papillomavirus, hepatitis B, epstein-Barr virus
1. Human papillomavirus: cervical CA
2. Hepatitis B: hepatocellular CA
3. Epstein-Barr virus: Burkit's lymphoma
45
This system is compose of lymphatic tissue, organs, and physiological processes that identify an antigen as abnormal or foreign, and prevents it from harming the body is defined as:
Immune system
46
A response that reconizes and destroys CA cells within the immune system is termed:
Immune surveillance
47
How does the immunologic surveillance work in recognizing CA cells:
the immunologic surveillance causes lymphocytes to respond _to cells that have been marked with a tumor associated antigens=TAAs_
48
In the immune system, how are cells marked as non-self:
Cells that are deemed an antigen or CA are marked by the TAAs (tumor-associated antigen)
49
What prevents transformed cells from developing into detectable tumors in relation to the immune system:
Immunologic surveillance
50
Once lymphocytes detect the TAAs on non-self cells, what cells come to destory the CA cell:
Cytoxic T cells, natural killer cells, B lymphocytes, monocytes, macrophages
51
This immunologic surveillance response cell plays a dominant role in resisting tumor growth, kills tumor cells, produces cytokines:
Cytotoxic T cells
52
This immunologic surveillance response cell directly _lysis_ tumor cells spontaneously w/o any prior sensitization:
natural killer cells
53
This immunologic surveillance response cell produces a specific antibodies that bind to tumor cells and can kill CA cells by complement fixation and lysis:
B lymphocyte
54
This immunologic surveillance response cell is a phagocytic white cells derived from stem cells; circulates in the blood stream for 24 hr, then moves into the tissues where they mature:
monocytes
55
This immunologic surveillance response cell is a mature monocyte; one of the first lines of defense in the flammatory process; phagocytes that engulf foreign antigens and cell debris; secretes cytokins and colony-stimulating factors:
macrophages
56
What are the constitutional factors that causes a failure of immune response r/t CA:
1. Age: immature/senescent immune system
2. Tumor burden: too little to stimulate a resonse or too much overwhelms the immune system
3. CA cells: supress immune activity;sheid itself from recognition; resemble normal cells to escape detection
57
CA cells that resemble normal cells to escape detection from the immune system is defined as:
immunological surveillance escape
58
What are the **_latrogenic_** factors that causes a failure of immune response r/t CA cells:
immunosupressive drug therapy/radiation induced suppression
59
What is the genetic predisposition that causes a failure of the immne response in relation to CA:
certain CA may be inherited; mechanisms are unclear
60
In relation to the genetic link of CA, what is the **_multifactorial_** etiology that can produce a malgnancy:
genetic+environmental+personal factors--\> interact together to produce=malignancy
61
In relation to genetics, a malignant tumor will only arise after a series of what:
series of mutations have accumulated: 10% of CA have a strong genetic link
62
In relation to genetics, what is at the core of CA development:
genetic alterations
63
Is a single alteration of a genetic structure sufficient to result in CA:
NO, must be accumulated
64
What is the three stage theory of carcinogenesis:
Initiation, promotion, progression
65
In this stage of carcinogenesis, a carcinogen **_damages the DNA_** by changing a specific gene:
Initiation: this phase is irreversible
66
What may occur in the initiation process of carcinogenesis:
1. If cell undergoes repair, no initiation occurs
2. becomes permenantly mutated, but no CA unless exposed to threshold levels of promoters
3. Becomes mutated and produces a CA cell line if the initiator is a complete carcinogen
67
In this stage of carcinogenesis, the process by which carcinogens are subsequently introduced which **_results in changes:_**
Promotion: this stage can be reversible
68
What are the types of changes that occur during the promotion stage in CA development:
1. Reversible damage: to the proliferation mechanism of the cell
2. CA promoting factors inhibited: via antioxidants (CA-reversing agent); effective immune system; time/dose limit exposure to the promoter
3. Irreversible damage: to proliferation mechanism=CA cell transformation
69
In this stage of carcinogenesis, CA development is characterized by increase growth rate of tumor as well as invasiveness and metastasis:
Progression: metastasis occurs in this stage
70
The time between exposure to initiators and promoters and development of CA is variable that depends upon dosage or length of exposure to that promoter is defined and belongs to what stage in the CA development:
Time frame; promotion stage
71
When cells continue to divide, increase in bulk, pressure, secretion of enzymes resulting to local spread to surrounding structures is defined as and what stage of the CA development is it found:
Invasion; in the progression stage of CA development
72
The spread of a CA to another site that causes a production of secondary tumors to distant sites from origination is defined as and to what stage of the CA development does it belong to:
metastasis; progression stage
73
What are the routes of metastasis:
1. seedling thorughout: body cavity (peritoneal)
2. Dissenination: via the lymphatic system to organs/tissues
3. **_MOST COMMON FORM OF METASTASIS: via bld capillaries/veins_**
74
What are the most common sites of metastasis:
Bones, lungs, liver, CNS
75
What is the major cause of death from CA and when does it typically begin:
Metastasis; has typically begun to metastasize at time of detection
76
Examples of common screening tests for CA:
1. Pap, mammogram
2. colonoscopy
3. **_CEA: colorectal tumor marker_**; PSA: prostate
4. BRA1-2: genetic marker
5. **_Biopsy: removal of tissue sample_**
6. Bone marrow examination
77
The best and most effective Tx for CA is what in the Dx phase:
prevention
78
What part of the Dx phase can result in decreased morbidity/mortality:
early detection of CA and effective therapy
79
For the prevention and detection of CA, how many hrs of sleep should you strive for:
6-8 hrs/night
80
For the prevention and detection of CA, how much should you exercise:
\>30 min moderate activity x 5 days/week
81
For the prevention and detection of CA, what should your health examinaton include:
health Hx, risk factors, physical exam, specific dx studies
82
For the prevention and detection of CA, what age and how often should you be screened for a colonscopy:
beginning at 50 yo and every 10 yrs after
83
A histologic examination of a piece of tissue from a suspicious area by a pathologist and is the definitive means of Dx CA is defined as:
biopsy
84
Why is a biopsy preformed:
**_To determine if the tissue is benign or malignant_**
85
What are the types of biopsies:
1. FNA: fine needle aspiration
2. incisional: partial removal if excisional is not feasible
3. excisional: entire lesion/lymphnode/mass is removed: therapeutic and diagnostic
86
How long can a biopsy result occur:
72 hrs
87
This type of tumor grading is done through the appearance of cells and degree of differentation:
Histologic analysis classification
88
A pathologists is doing a histologic anaylsis classification on a tumor. He sees that the cells differ only slightly from normal cells and are well differentiated. What grade is this and what is the type of dysplasia:
Grade 1; mild dysplasia
89
A pathologists is doing a histologic anaylsis classification on a tumor. He sees that the cells are more abnormal and moderately differentiated. What is the grade and what type of dysplasia is it:
Grade 2; moderate dysplasia
90
A pathologists is doing a histologic anaylsis classification on a tumor. He sees that the cells are very abnormal and poorly differentiated. What grade is this and what type of dysplasia:
Grade 3; severe dysplasia
91
A pathologists is doing a histologic anaylsis classification on a tumor. He sees that the cells are immature and primitive and undifferentiated d/t the cells of origin are difficult to determine. What stage is this and what type od displasia:
grade 4; not dysplasia, **_ANAPLASIA_**
92
This type of staging is classifying the extent and spread of disease process is defined as:
Extent of disease classification/clinical staging: completed after Dx workup and helps determine Tx options
93
What stage is cancer in situ (in its place):
stage 0
94
What stage is a tumor that's limited to the tissue of origin/localized tumor growth:
stage 1
95
What stage is CA limited to local spread:
stage 2
96
What stage is extensive local and regional spread of CA:
stage 3
97
What stage is metastasis:
stage 4
98
What scan is used most often in the staging process of CA:
Positron emission tomography (PET scan)
99
This classification system is used to determined the anatomical extent of solid tumors according to: tumor size/invasiveness, lymph NODES, and metastasis:
TNM classification system
100
What is the TNM classification for the (**_T_**, has 4 parts):
* T0: no evidence of primary tumor
* Tis: CA in situ
* T1-4: ascending degrees of increase in size/involvement
* Tx: tumor cannot be found/measured
101
What is the TNM classification for **_(N)_**:
* N0: no evidence of CA in lymph NODES
* N1-4: Ascending degrees of nodal involvement
* Nx: regional NODES unable to assess clinically
102
What is the TNM classification for METASTASIS:
* M0: No evidence of metastasis
* M1-4: Ascending degrees of metastatic involvement
* Mx: cannot be determined
103
What are the goals of cancer treatment:
Cure, control, palliation
104
This specific goal of CA Tx includes the expectation after Tx is that the pt will be free of CA and will have a normal life span/permanent remission/5 yr landmark to be considered CA free:
CURE; The 5 yr landmark is not true for all CA, only some
105
This specific goal of CA tx includes: CA that are not usually cured/considered to be chronic; to limit the growth/spread of disease; includes maintenance therapy; pt is expected to have a period of symptom free time:
control
106
This specific goal of CA tx includes: relief/control of symptoms; maintenance of a satisfactory quality of life; life span is not expected to be extended and what is the main example:
Palliation; **_DEBULKING OF TUMOR_**
107
In the palliation goal of CA tx, surgical methods and debulking are used to provide supportive care that maximizes quality of life is also affected by distressing symtoms. What are the examples of pallitative Tx:
* debulking tumor
* Colostomy for bowel obstruction relief
* laminectomy: relief of spinal cord compression
* radiation tx: bone metastasis
