2. Objectives
• Compare the characteristics of abnormal cell growth and
reproduction processes to normal cell growth and
reproduction.
• Describe the process of carcinogenesis, major risk factors
and preventative measures.
• Discuss the general premise of the concept of prevention
and early detection of cancer.
• Describe the ways a cancer can be classified.
• List the major treatment options for cancer and discuss
each according to: indication for method, common
complications, and medical/nursing management related to
each method.
3. Epidemiology of Cancer
• Second leading cause of death in the United States (What
is the first?)
• Leading cause of death from disease in children aged 1 to
14 years old (leading cause of death is accidents in this age
cohort)
• over 1.2 million cases in 2006, with over 570,000 deaths
• Approximately 62% of individuals diagnosed will be alive at
5 years
• Most common in men is prostate cancer, and in women
breast cancer
• Most common cause of cancer death in both men and
women is lung cancer
• 10 million adults are cancer survivors
4. Cancer Incidence and Mortality
2006 ACS Projections
Cases Deaths Cases Deaths
Prostate 234,460 27,350 Breast 212,920 40,970
Lung & bronchus 92,700 90,330 Lung & bronchus 81,770 72,130
Colon & rectum 72,800 27,870 Colon & rectum 75,810 27,300
Urinary bladder 44,690 8,990 Uterine corpus 41,200 7,350
Lymphomas 34,870 10,770 Lymphomas 31,800 9,560
Melanoma 34,260 5,020 Melanoma 27,930 2,890
Kidney & 24,650 8,130 Ovary 20,180 15,310
renal pelvis Pancreas 16,580 16,210
Leukemia 20,000 12,470 Urinary bladder 16,730 4,070
Pancreas 17,150 16,090
All sites 679,510 273,560
All sites 720,280 291,270
Data from the ACS. Cancer facts and figures 2006.
5. Change in the US Death Rates* by Cause,
1950 & 2005
Rate Per 100,000
1950
2005
Heart Cerebrovascular Influenza & Cancer
Diseases Diseases Pneumonia
* Age-adjusted to 2000 US standard population.
Sources: 1950 Mortality Data - CDC/NCHS, NVSS, Mortality Revised.
2005 Mortality Data: US Mortality Data 2005, NCHS, Centers for Disease Control and Prevention, 2008.
6. Cancer Death Rates* Among Men, US,1930-2004
Rate Per 100,000
Lung & bronchus
Stomach Prostate
Colon & rectum
Pancreas
Leukemia
Liver
*Age-adjusted to the 2000 US standard population.
Source: US Mortality Data 1960-2004, US Mortality Volumes 1930-1959,
National Center for Health Statistics, Centers for Disease Control and Prevention, 2006.
7. Cancer Death Rates* Among Women, US,1930-2004
Rate Per 100,000
Lung & bronchus
Uterus
Breast
Colon & rectum
Stomach
Ovary
Pancreas
*Age-adjusted to the 2000 US standard population.
Source: US Mortality Data 1960-2004, US Mortality Volumes 1930-1959,
National Center for Health Statistics, Centers for Disease Control and Prevention, 2006.
8. Cancer Death Rates* by Sex and Race, US, 1975-2004
Rate Per 100,000
African American men
White men
African American women
White women
*Age-adjusted to the 2000 US standard population.
Source: Surveillance, Epidemiology, and End Results Program, 1975-2004, Division of Cancer Control and
Population Sciences, National Cancer Institute, 2007.
9. Cancer Incidence Rates* Among Men, US, 1975-2004
Rate Per 100,000
Prostate
Lung & bronchus
Colon and rectum
Urinary bladder
Non-Hodgkin lymphoma
Melanoma of the skin
*Age-adjusted to the 2000 US standard population and adjusted for delays in reporting.
Source: Surveillance, Epidemiology, and End Results Program, Delay-adjusted Incidence database:
SEER Incidence Delay-adjusted Rates, 9 Registries, 1975-2004, National Cancer Institute, 2007.
10. Cancer Incidence Rates* Among Women, US, 1975-2004
Rate Per 100,000
Breast
Lung & bronchus
Colon and rectum
Uterine Corpus
Ovary
Non-Hodgkin lymphoma
*Age-adjusted to the 2000 US standard population and adjusted for delays in reporting.
Source: Surveillance, Epidemiology, and End Results Program, Delay-adjusted Incidence database:
SEER Incidence Delay-adjusted Rates, 9 Registries, 1975-2004, National Cancer Institute, 2007.
11. Cancer Definitions
Oncology: The study of tumors and their treatment
Cancer: from the latin "crab-like"
Tumor: Swelling that can be caused by a number of
conditions, usually marked by the suffix -oma
Carcinoma: malignant tumor of epithelial tissue
Adenocarcinoma: malignant tumor of glandular epithelial
tissue
Sarcoma: Malignant tumor of mesenchymal origin
13. Host defense mechanisms against
cancer:
Tumor Antigens
o Tumor-Associated Antigens (TAA)
o Tumor-Specific Antigens (TSA)
Host defense mechanisms against
cancer:
Tumor Antigens
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14. Host defense mechanisms against
cancer:
Tumor Antigens altered cell surface antigens as a
Cancer cells may display
result of their malignant transformation.
• Through immunogenic survellience our immune system
recognizes and destroys the cells that exhibit these non-self
tumor antigens
o Mainly mediated by T-cells (both CD4+ and CD8+ cells)
o Anti-tumor antibodies can be found in patients with
cancer suggesting a role for B-cells in cancer
surveillance (humoral immunity)
o Macrophages and dendritic cells function as APCs to the
Immune System and also directly phagocytize CA cells
o NK cells engage in actual killing/lysis of the tumor cells
16. Host defense mechanisms against
cancer:
Howare many theories how cancerthe immune
There cancer cells evade cells are able to evade
system.
the immune system.
• Suppression of factors that stimulate T-cells to react to CA
cells
• Weak surface antigens allowing CA cells to "sneak through"
immune surveillance
• Development of tolerance to some tumor antigens
• Suppression of the immune response by products secreted
by CA cells
• Induction of Suppressor T-cells by the tumor
• Blocking antibodies that bind to Tumor Associated
Antigens, thus preventing recognition by T-cells
19. Cell life cycle: the alternation between
mitosis and interphase.
S phase: G2 phase:
• Synthesis phase • G=gap
• synthesis of DNA and • RNA and protein synthesis
proteins for new occur
chromosomes • period between the
• Get two separate sets of completion of DNA
chromosomes synthesis and the next
phase which is the M
phase
20. Cell life cycle: the alternation between
mitosis and interphase
M phase: G1 phase:
• Mitosis phase • G=gap
• Nuclear and cytoplasmic • period between the M
division occurs producing phase and the start of
two daughter cells DNA synthesis
• phases of mitosis include • energy is generated and
prophase, metaphase, extra membranes and
anaphase and telophase cytoplasm are made
21. Cell life cycle: the alternation between
mitosis and interphase
G0 phase:
• Not really part of the cell cycle
• the cell is reproductively resting
• cell is functional but not dividing
• most cells spend their time in G0
o eg. hepatocytes (liver cells) do not divide unless some
injury to the liver has occured.
There are some permanent cells that are unable to re-enter
the cell cycle (Neuron cells)
• Stable cells can re-enter the cell cycle if stimulated by
extracellular nutrients, growth factors, hormones, and other
signals such as blood loss or tissue injury.
22. Cell proliferation
This is a highly regulated process by which cells divide and
reproduce. Feedback regulation of this process occurs in
normal cells and tissues.
• Normal cells will also stop dividing based on "contact
inhibition."
• Normal cells keep an equal balance between cellular
proliferation and cellular degeneration or death
• Rate of proliferation differs in different cells and tissues
o Bone marrow, epithelial cells of the GI tract, and hair
follicles have a rapid rate of cellular proliferation
o Myocardium and cartilage either have no or slow rates of
cellular proliferation
23. Cellular proliferation in cancer cells
1. They divide nearly continuously with little time spent in the
G0 phase, with some cells dividing haphazardly generating
more than 2 daughter cells with one division.
2. They have a short "generation time" which is the period of
time necessary for the cell to enter and complete one round
of cell division by mitosis.
3. They can have a rapid growth rate and "doubling time."
4. They have a high proportion of cells within the tumor
population that are in the proliferative pool undergoing cell
division.
5. They have a loss of "contact inhibition."
24. Cellular differentiation in cancer cells
A mature, differentiated cell in a human is capable of
functioning only as the tissue/organ it has developed into can.
The purpose of differentiation is to provide for organization
throughout the tissues/organs/human system. Normal cells
differentiate in an orderly, stable process.
• CA cells (neoplastic cells) lack this differentiation, and do
not resemble or function like their parent cells
• This differentiation is thought to be controlled by genes
(protooncogenes and oncogenes which will be discussed
later).
25. Cellular metabolism in cancer cells
Normal cells depend on aerobic metabolism for 90% of their
energy needs. Only cells without mitochondria use anaerobic
metabolism for their primary energy needs.
• Neoplastic (CA) cells depend more on anaerobic
metabolism
• CA cells use higher levels of glucose
• CA cells are engage in high levels of protein catabolism in
order to get energy (rob normal cells of protein)
26. Characteristics of benign and malignant
neoplasms
Tumor: Swelling that can be caused by a number of
conditions including inflammation and trauma.
Neoplasia: These are clusters of cells that can be benign or
malignant
Benign Neoplasm: contain well differentiated cells that are
clustered together in a single mass.
Malignant Neoplasm: less well differentiated to
undifferentiated and have the ability to break loose, enter the
circulatory or lymphatic systems and form secondary
malignant tumors at other sites.
27. Non-neoplastic growth patterns
• Hyperplasia: Increase in the number of cells in a tissue or
an organ
• Metaplasia: Conversion of one cell type to another
• Dysplasia: Alteration in the size, shape and organization
of cells. Dysplastic cells can become or precede
neoplastic/cancerous changes.
Benign and malignant neoplasms are usually differentiated by
their cell characteristics, rate of growth, manner of growth,
capacity to metastasize and spread to other parts of the body
and potential for causing death.
31. Carcinogenesis
Strictly interpreted, this is the development of cancer in
otherwise normal tissue.
• The natural development of cancer is usually an orderly
process that comprises several stages and occurs over a
period of time.
• Includes initiation, promotion and progression
32. Terms important in carcinogenesis
Oncogene: Proto-Oncogene:
• These are genes that can • These are genes that
promote the growth of cancer regulate normal cellular
cells processes (very important)
• these genes are usually • promote normal embryonic
derived from mutations of cellular development
normal genes • Once growth and
• Can interfere with the cells' development ceases, they
normal functions and protein genes are usually "turned off"
expression • Can be "turned on" by
viruses, chemicals, or any
carcinogen
33. Terms important in carcinogenesis
Tumor Suppressor Genes: Mutations in proto-oncogenes
• They normally function to and tumor suppressor genes
regulate growth can occur in embryonic
• Mutations to this part of development, and this usually
the genome can cause the leads to an earlier
cell to engage in development of cancer, and a
unregulated growth more significant presentation
o p53 gene in many of the cancer
cancers
o BRCA-1, BRCA-2 Mutations in these genes can
o APC gene also be induced by exposure
• Can be inherited to carcinogens.
34. CRC Development:
Adenoma-to-Carcinoma Sequence
First somatic APC Second APC K-ras Further changes
mutation or loss mutation or loss mutation DCC loss TP53 loss eg, NM23 loss
Normal
mucosa
Hyperproliferative Adenoma, increasing
epithelium in size, and dysplasia Carcinoma
Germline APC
mutation (FAP)
Adapted from Bishop and Hall. Eur J Cancer. 1994;30A:1946-1956, with permission.
35. Carcinogenesis: Initiation
This is a mutation in the cell's genetic structure
• Can be inherited
• Can be induced after exposure to a carcinogen (chemical,
radiation, or viral agent)
o the altered cell becomes a clone
• This is an irreversible process, but:
o the DNA may repair itself
o most deranged cell can undergo apoptosis
o cells with altered antigens are subject to immune
surveillance
o or the DNA alteration may not become functionally
significant
• Often, for the DNA alteration to be significant, more than
one episode of genetic damage must occur
37. Carcinogenesis: Promotion
• During this stage, the environment has to promote or favor
the development of the "initiated" or altered cell
• There is a period of latency from 1 to 40 years, between the
initial genetic alteration and the actual clinical evidence of
cancer
• An important distinction between initiation and promotion is
that the action of promoters is reversible.
o important promoters include: dietary fat, smoking,
obesity, and alcohol consumption
****Cigarette smoke can act as both an initiator of
malignant change and a promoter of cancer development.
38. Carcinogenesis: Progression
This is the final stage in the natural history of cancer.
• Increased growth of the tumor (Significant)
• Increased invasiveness of the tumor
• Spread of the cancer to a distant site
o Metastasis: the cancer has spread from the primary site
(where the cancer developed) to another organ or part of
the body
Most frequent sites: lungs, brain, bone, liver, and
adrenal glands
often determined or limited by angiogenesis
get hematogenous metastases and lymphatic
metastases
42. What about the Oncofetal Antigens?
Oncofetal antigens are tumor antigens that are found on the surfaces
and inside of cancer cells, as well as fetal cells.
• Appearance in cancer cells is thought to be reflective of that cell
regaining its embryonic capability to differentiate into various types
of cells
o Carcinoembryonic antigen (CEA): normally found in fetal gut,
liver, and pancreas cells and disappears during the last 3
months of fetal life. This antigen is overexpressed in colon
cancer and also elevated in cigarette smokers, pt's with
ulcerative colitis and cirrhosis of the liver
o Alpha-Fetoprotein (AFP): fetal liver cells and liver cancer
o CA-125: Ovarian cancer
43. Risk factors that predispose for cancer
development
1. Heredity
2. Hormones
3. Immunologic mechanisms
4. Chemical Carcinogens
5. Radiation
6. Oncogenic viruses
44. Risk factors that predispose for cancer
development
Heredity: Hormones:
• Cancer related genes • Hormones can
have been identified that overstimulate the
increase an individual's proliferation of certain
susceptibility to the cells overtime
development of certain o Prostate cancer is
cancers thought to develop in
o BRCA-1/BRCA-2: 40- elder males because of
80% lifetime risk of lifetime exposure to
breast cancer androgens
o Accounts for approx. o DES babies had higher
10% of cancers rates of Uterine cancer
45. Risk factors that predispose for cancer
development
Immunologic Mechanisms: Chemical Carcinogens:
• Mutant cells are constantly • These include chemicals
formed, but are destroyed like cigarette smoke and
by immune cells through asbestos, drugs like
immuno-surveillance hormones,
• people with depressed immunosuppressive
immune systems have agents, cytotoxic drugs,
higher rates of cancer and dietary factors like
o AIDS related kaposi's fats and nitrates
sarcoma • some of these compounds
are either initiators or
promotors, cigarette
smoke is both
46. Risk factors that predispose for cancer
development
Radiation: Oncogenic Viruses:
• When cells are exposed to • Some viruses can infect a
radiation, there is damage cell and inject their genetic
to one or both strands of material into the host
DNA DNA...this can either
• This can be exposure to disrupt a tumor
ionizing radiation or suppressor gene or add
exposure to UV radiation an oncogene to the DNA
• Melanoma is a cancer causing malignant
with significant transformation
increases in incidence o Hep B/C and HCC
• Hiroshima survivors o HPV and Cervical
Cancer
47. Risk factors that predispose for cancer
development
Age:
• Advanced age is the single most significant risk factor
o 50% of cancers occur in those >65 years of age
o the symptoms of cancer are often perceived or
written off as "age related changes"
o Can be more vulnerable to complications from
cancer treatment
48. Prevention and the early detection of
cancer
Preventative Measures:
• Patient education is one of the most important nursing
interventions that can be utilized in the prevention and
progression of cancer. Patients should be educated in the
following:
o Risk factors: what are they (sun exposure, smoking,
diet, exposure to chemicals, radiation) and how to avoid
exposures
o Health Promotion behaviors: quit smoking, low fat, high
fiber, low nitrate diet, exercise, routine screening exams
51. Screening Guidelines for the Early Detection
of Breast Cancer, American Cancer Society
• Yearly mammograms are recommended starting at age 40.
• A clinical breast exam should be part of a periodic health exam, about
every 3 years for women in their 20s and 30s, and every year for
women 40 and older.
• Women should know how their breasts normally feel and report any
breast changes promptly to their health care providers. Monthly breast
self-exam is an option for women starting in their 20s.
• Screening MRI is recommended for women with an approximately
20%-25% or greater lifetime risk of breast cancer, including women
with a strong family history of breast or ovarian cancer and women
who were treated for Hodgkin disease.
52. Screening Guidelines for the Early Detection
of Cervical Cancer, American Cancer Society
• Screening should begin approximately three years after a women
begins having vaginal intercourse, but no later than 21 years of age.
• Screening should be done every year with regular Pap tests or every
two years using liquid-based tests.
• At or after age 30, women who have had three normal test results in a
row may get screened every 2-3 years. However, doctors may
suggest a woman get screened more frequently if she has certain risk
factors, such as HIV infection or a weakened immune system.
• Women 70 and older who have had three or more consecutive Pap
tests in the last ten years may choose to stop cervical cancer
screening.
• Screening after a total hysterectomy (with removal of the cervix) is not
necessary unless the surgery was done as a treatment for cervical
cancer.
53. Screening Guidelines for the Early Detection
of Prostate Cancer, American Cancer Society
The prostate-specific antigen (PSA) test and the digital rectal examination
(DRE) should be offered annually, beginning at age 50, to men who have a
life expectancy of at least 10 years.
Men at high risk (African-American men and men with a strong family
history of one or more first-degree relatives diagnosed with prostate cancer
at an early age) should begin testing at age 45.
For men at average risk and high risk, information should be provided
about what is known and what is uncertain about the benefits and
limitations of early detection and treatment of prostate cancer so that they
can make an informed decision about testing.
54. Screening Guidelines for the Early Detection of
Colorectal Cancer and Adenomas, American Cancer
Society 2008
Beginning at age 50, men and women should follow one of the
following examination schedules:
• A flexible sigmoidoscopy (FSIG) every five years
• A colonoscopy every ten years
• A double-contrast barium enema every five years
• A Computerized Tomographic (CT) colonography every five years
• A guaiac-based fecal occult blood test (FOBT) or a fecal
immunochemical test (FIT) every year
• A stool DNA test (interval uncertain)
People who are at moderate or high risk for colorectal cancer should talk with
a doctor about a different testing schedule
55. Other Diagnostic tests if cancer is
suspected or diagnosed (will depend on
primary site)examination of cells that are sloughed into the
1. Cytology studies:
various body secretions or scraped from organ cavities (i.e. pap
smear)....suspicious findings may necessitate an actual biopsy
2. Chest Xray/Mammogram: looking for radiological evidence of a
primary or a metastatic cancer site (not very sensitive, you need a
pretty big lesion to see it on chest xray)
3. CBC: evaluate the blood for anemia, alterations in WBCs,
thrombocytopenia or thrombocytosis
4. Blood tests for tumor markers/antigens: CEA, AFP, CA19-9, CA-
125, CA15-3, CA27-3, PSA
56. Other diagnostic tests if cancer is
suspected or diagnosed (will depend on
the primary site)
5. Biopsy: refers to the process of obtaining tissue for histologic exam
and susequent diagnosis of the disease
• Needle Biopsy
• Incisional
• Excisional
6. CT Scan: Multiple xrays are done, usually from the neck to groin to
get a picture of the internal organs and look for metastatic disease
(often part of routine staging of cancer
7. PET Scan: This is a specialized test looked at the metabolic rate of
tissues. A radioactively labeled sugar solution is ingested and the
scanner looks for areas of the body that take up the sugar...good in
cancer because of the elevated glucose needs of cancerous cells
57. Other diagnostic tests if cancer is
suspected or diagnosed (will depend on
the primary site)
8. Sigmoidoscopy/Colonoscopy: Visualize and remove
polyps, precancerous lesions and cancerous lesions from the
colon.
9. Bone Scan: Radioisotopes are injected and looks for
increased uptake in the bone (hot spots) which indicate
metastatic disease in the bones
10. Bone Marrow Study: evaluate the progenitor cells, look
for genetic abnormalities (most often used in hematologic
malignancies, but a metastatic cancer to the bone marrow can
also be evaluated).
58. Ways of classifying cancer...
1. Anatomic Site
2. Histological Analysis (grading)
3. Extent of Disease (Staging)
59. Ways of classifying cancer: Anatomic
site
The tumor is identified by the tissue of origin, the anatomic
site, and the behavior of the tumor.
• Tissue of origin (embryonic):
o Carcinomas originate from the embryonal ectoderm (skin
and glands) and endoderm (mucous membranes of the
resp. tract, GI tract, GU tract)
o Sarcomas originate from embryonal mesoderm
(connective tissue)
o Lymphomas/Leukemias originate from the hematopoietic
system
• Location of primary tumor: Breast cancer in breast tissue,
prostate cancer in prostate tissue
• Behavior: Benign or Malignant
60. Ways of classifying cancer: Histological
analysis
This is a microscopic analysis of the tumor, looking at the
appearance of cells and the degree of differentiation. Broken
down into 4 grades based on the differentiation.
• Grade I: Cells differ slightly from normal cells (mild
dysplasia) and are well differentiated.
• Grade II: Cells are more abnormal (moderate dysplasia)
and moderately differentiated.
• Grade III: Cells are very abnormal (severe dysplasia) and
poorly differentiated.
• Grade IV: Cells are immature and primitive (anaplasia) and
undifferentiated; cell of origin is difficult to determine
61. Ways of classifying cancer: Extent of
disease
This is describing the extent of the disease in the body. They
can be broken up into the American Joint Committee on
Cancer (AJCC) and Tumor/Node/Metastases (TNM) staging.
Both these staging systems are more amenable to solid tumor
evaluation (not leukemias/lymphomas).
stage 0: cancer in situ
stage I: tumor limited to the tissue of origin; localized tumor
growth
stage II: limited local spread
stage III: extensive local and regional spread
stage IV: metastasis
63. Major treatment options in cancer
1. Surgery
2. Radiation
3. Chemotherapy
4. Hormonal therapy
5. Biotherapy
6. Targeted therapy
7. Bone Marrow and peripheral blood stem cell transplantation
64. How do you choose an option for cancer
treatment?
Treatment option choices are dictated by the goals of therapy.
• Cure
• Control
• Palliation
65. Surgery
1. Indicated if the cancer is confined and well-encapsulated,
where surgery alone can "cure" the cancer.
2. "Debulk" the tumor so other treatments can be more
effective.
3. Prophlaxis, prevent the development of cancer
4. Diagnose or stage a tumor
5. Palliate the symptoms from a cancer
6. Reconstruction from previous cancer surgery
7. Determine if therapy if effective (very rarely the primary goal
of surgery, but may be secondary)
66. Complications of surgery and nursing
care
• Loss of body part/function
• Disfigurement
• Increased risk for infection if immune suppressed
• Increased risk for bleeding if thrombocytopenic
• Increased risk for wound healing if the patient is on
antiangiogenic therapy
Nursing Care
• Routine pre- and post-op care
• Additional psycho-social needs of cancer patients
o Anxiety
o Body image disturbance
• Attention to the other risk factors that accompany a patient
with cancer
67. Radiation Therapy
Ionizing radiation is used for most treatments:
• acts at the cellular level to damage or alter the cells
• breaks chemical bonds, disrupts DNA and interferes with
cell activity and mitosis
• Affects the cell cycle in the following order: M-phase, G2-
phase, G1-phase, and S-phases
• Cells damaged by radiation either die or are unable to
divide
Indicated as primary therapy for cancer if the tumor is in
an area that is difficult to reach surgically or where
surgery could be significantly disfiguring (H&N CA)
• Some tumors are more radiosensitive than others
• Can shrink the tumor for potential surgery
• Can palliate complications from cancer
68. How is radiation therapy delivered?
• External Radiation:
o teletherapy: this form of therapy is external to the patient
and distant from the tumor.
• Internal Radiation:
o This is known as brachytherapy, and the radiation source
is placed in close contact with the tumor
Sealed: radiation is contained within some sort of
device like a needle or seed device which may be
placed near the tumor site temporarily or permanently
Unsealed: radiation is not contained in a device so
the radiation is not confined to one area of the body
(po, IV, or instilled into a body cavity)
69. Nursing Management of Radiation
Therapy Patients
Safety Precautions:
• Needed when caring for patients undergoing
brachytherapy. Remember, the patient is not radioactive
but the implant is.
• Handling of secretions and excretions must be done
wearing gloves if the patient has received an unsealed
radioactive source (the source is now systemic once in the
body).
• The patient who has sealed radiation implants emits
radiation while the implant is in place but his/her body
secretions are not radioactive
• Remember that the patient who receives external radiation
is not radioactive at any time
71. Nursing Management of Radiation
Therapy Patients
• Providing patient teaching based on the type of radiation
they are to receive...teletherapy or brachytherapy
o teletherapy: teach regarding the machinery, any braces
or adaptive devices that will be used, what will be
expected (positioning during therapy, side effects)
o brachytherapy: teach regarding how this is different from
teletherapy, what sort of care they will undergo, limiting
of visitors, and the distance visitors need to keep during
the therapy.
72. Nursing Management of Radiation
Therapy Patients
• Skin preparation prior to therapy: with teletherapy, the skin
is marked by the radiation therapist to identify the exact
area where the radiation should be delivered. The patient
should be instructed not to wash these markings off.
• Prevent skin breakdown...teach the patient to avoid
scratching...dry itchy skin is a common complication of
teletherapy. Usually recommend aloe vera and very simple
emoillients (no petroleum products, cause increased
breakdown)
• Promote healing of skin after therapy: cleanse thoroughly if
skin is broken, observe for s/s of infection and treat
promptly if infection occurs, optimize nutrition to promote
healing
75. Nursing Management of Radiation
Therapy Patients
• Minimize GI upset
o Mouth XRT causes dry mouth and stomatitis
Biotene mouthwash and gel
warm water/baking soda rinse
assess for and treat oral candidiasis quickly
for taste alterations, encourage moist, bland food
o Esophageal/Upper abdominal XRT causes
N/V/Esophagitis
antiemetics: teach about the medication, frequency
bland diet
Proton Pump Inhibitors
o Rectal/lower abdominal radiation causes diarrhea
teach about the use of immodium/Lomitil
Low residue diet
76. Chemotherapy
This is indicated in the treatment of hematologic and solid
tumor malignancies. Can be the primary therapy or used
adjunct to another therapy (surgery or radiation).
Chemotherapy works in different ways, but primarily by
disrupting the production of essential enzymes, inhibits RNA,
DNA, and protein synthesis, and can prevent cell mitosis.
Most effective against rapidly dividing cells.
77. Goals of Chemotherapy
The goal of chemotherapy is to eliminate or reduce the number
of malignant cells in the primary tumor and/or the metastatic
tumor site. The response of malignant cells to chemotherapy
is determined by:
1. Mitotic rate of the tissue from which the tumor arises.
2. Size of the tumor
3. Age of the tumor
4. Location of the tumor
5. Presence of resistant tumor cells
78. Chemotherapy Classifications
Cell Cycle Specific: Cell Cycle Nonspecific:
• these drugs are effective • Effective on both dividing and
during specific phases of the resting cells (G0 phase).
cell cycle (G1, S, G2, M) • Damage the cell at some
relating to cellular point in the cycle but death
proliferation/replication. does not occur until the cell
• Effective only during one attempts to divide
specific phase and are often • Very dose dependent
given over a prolonged period
to ensure that the majority of
cells reach the phase the drug
acts on.
• Very time dependent
Cell Cycle specific and Cell Cycle Non-
specific are often given together to
enhance death of tumor cells
79. Chemotherapy Examples
Cell Cycle Specific: Cell Cycle Non-specific:
• Antimetabolites: mimic • Alkalating Agents: first
naturally occuring substances chemotherapies used,
thus interfering with enzyme Damage DNA by breaking the
function or DNA synthesis double-stranded helix
o capecitabine (Xeloda) • Antitumor antibiotics: bind
o methotrexate (Trexall) directly to the DNA, inhibiting
• Mitotic Inhibitors: Some act DNA replication and
by stabilizing microtubules so interfering with transcription
they aren't able to align the • Hormone therapy: interferes
chromosomes to divide with the action of a hormone,
• Topsimerase Inhibitors: or with the enzymes that
Inhibit the enzyme produce hormones
topsimerase that function to
make breaks in DNA for
replication
81. Extravasations of Chemotherapy
Chemotherapy drugs can have direct affects on the tissue it's
exposed to upon administration. One of the major routes of
administration for chemotherapy is the IV route. Since most
chemotherapy drugs are either irritants or vesicants, a major
risk of peripheral IV chemotherapy is Extravasation.
• This is the infiltration of drugs into the tissues surrounding
the infusion site
o Can cause local tissue damage
o Can lead to permanent damage and loss of function
All vesicant chemotherapy should be administered using
a central venous access device (CVAD)
83. If extravasation occurs...
• Stop the infusion immediately, notify the MD
• Remove the IV infusion tubing and try and aspirate any
remaining drug in the catheter with a new syringe
• Inject the prescribed antidote, if one exists, in the infusion
needle or in a pincushion fashion in the skin around the
extravasation (the MD will direct the route/order)
• Topical corticosteroids may be applied if ordered
• Elevate the site
• Cold Compresses for 1st 24/48 hours unless an alkaloid or
oxaliplatin has been infiltrated (use heat with alkaloids or
oxaliplatin)
• Document the extravasation
• Observe the site at designated intervals
86. Toxicities/Side Effects from
Chemotherapy
Chemotherapy does not distinguish between normal cells and
cancer cells so toxicity to normal tissues is expected.
Acute Toxicity: Nausea, vomiting, allergic reactions,
dysrhythmias, cold sensitivity
Delayed Toxicity: mucositis, diarrhea, stomatitis, alopecia,
neutropenia, anemia, pancytopenia
Chronic Toxicity: damage to organ systems such as the
heart, liver, kidneys, lungs, nervous system, and bone marrow.
Of all of the above, the most life threatening is the
neutropenia/pancytopenia
87. Nursing Management and
Considerations
• Knowledge of safe administration and disposal of chemo
agents. Each hospital will have protocols for both
administration and disposal of the chemo agents.
• Know how to differentiate between tolerable side effects
and toxic effects (nausea and vomiting vs. pulmonary
fibrosis or cardiotoxicity) and how to deal with affects as
they occur.
• Lab Results need to be considered and followed prior to,
during and post chemotherapy administration (CBC and
other's per the chemo toxicity)
• Patient education is important during administration re: drug
action, how to deal with side effects. Remember that
information can decrease anxiety.
88. Hormonal Therapy
Some tumors are very hormone dependent, and can grow at
an increased rate in the presence of certain hormones (eg
breast, uterine, prostate cancers)
• Altering the level of hormone available can decrease or
stop the growth of a particular tumor.
o tamoxifen for breast cancer: blocks the estrogen
receptors on breast cancer cells
o letrozole for breast cancer: inhibits the enzyme that
converts androgen to estrogen
o Lupon for prostate: inhibits the production of
testosterone by the testicles
o Extreme hormone manipulation: orchiectomy/
oophorectomy
89. Side Effects of Hormone Therapy
• Hypercoagulability: more prone to DVTs/PEs
• Selective Estrogen Receptor Modulators: increased risk of
uterine cancer
• Weight gain
• Lupron: emotional lability, gynecomastia
90. Biotherapy/Targeted Therapy:
This consists of agents that modify the relationship between
the biologic response of the host to the tumor cells. Includes
immunotherapy, monoclonal antibodies, antiangiogenic agents
and tyrosine kinase inhibitors. Work 3 ways:
1. Have direct anti-tumor effects
2. They restore, augment, or modulate host immune system
mechanisms
3. They have other effects, like inhibiting the cancer's ability to
metastasize or differentiate.
91. Immunotherapy
Interferon:
• Naturally occuring protein that is produced by WBCs and
other body cells in response to a variety of stimuli including
viral infections
• Exposure of cells to interferon causes production of antiviral
proteins which then help to protect the neighboring cells
from attack by viruses.
• Other functions of interferon are:
o inhibition of viral DNA
o stimulates the expression of TAA's on the cell surface so
that the chance of an immune response against the
cancer is increased.
• Cannot be administered orally because of the protein
nature
• Significant side effects include depression and
Significant Fatigue
92. Immunotherapy
Interleukin 2:
• Approved for use in Renal cell cancer and melanoma
• Help the immune system cells recognize and destroy
abnormal cells
• IL-2 is produced by the helper T-lymphocytes and
stimulates the proliferation of other T-lymphocytes,
activates NK cells, stimulates the release of other cytokines
like gamma interferon, TNF, IL-1 and IL-6
• Side effects area also significant, IL-2 is given IV as an
inpatient. Causes "Shake and Bake" syndrome with
high fevers and rigors. Also can cause damage the
kidneys and a careful balance of hydration and
diuretics is needed....VERY SPECIALIZED NURSING
CARE
93. Monoclonal Antibodies
These are antibodies or immunoglobulins that are produced to
bind antigens that are overexpressed on cancer cells. This
blocks the "downstream activity" of these receptors in
stimulating the growth of these tumor cells
• Herceptin binds the Her2Neu molecule that is
overexpressed in some breast cancer tumors
• Cetuximab binds the EGFR receptor that is overproduced in
many cells, but is FDA approved for use in colon and head
and neck cancer
• Tarceva (erlotenib) is an oral agent that binds the EGFR
receptor and is approved in pancreatic cancer. (big side
effect is a significant dose limiting rash for erlotenib and
cetuximab)
95. Targeted Therapies (which can be
interchanged often with monoclonal
antibodies)
Interferes with cancer growth by targeting specific cellular
receptors and pathways that are important in tumor growth.
They have a very different side effect profile than chemo and
are often successful at improving the outcome of
chemotherapy without increasing the toxicity.
• Antiangiogenic therapies: block the circulating vascular
endothelial growth factor, leading to decreased blood
vessel formation to tumors/metastases
• Tyrosine Kinase Inihibitors: block the phosphorylation of
proteins in the cell leading to decreased growth.
96. Bone marrow and peripheral blood
stem cell transplantation
Life saving treatment option for malignant and non-malignant
conditions. Involves giving high dose chemotherapy with the
goal of clearing all the malignant cells and then "rescuing" the
patient with new hematopoietic stem cells that can repopulate
the bone marrow.
• Can be a donor that is HLA matched (preferably 6/6 match)
(Matched Unrelated Donor)
• Can be a syngenic donor (identical twin)
• Can be cord blood (only a small recipient) (again, Matched
Unrelated)
• Can be from your own stem cells harvested ahead of the
procedure (Auto)
97. Harvesting of Peripheral Blood for Stem
Cell
• Donor is given Colony stimulating factors that boost the
release of stem cells into the peripheral circulation
• May also be given chemotherapy to stimulate the release of
the stem cells
• Donor is then hooked up to a pheresis machine that takes
the blood out of one vein, filters out the stem cells, and
returns the blood back to the donor through another vein
• Those stem cells are collected over a week period and then
infused (IV) into the patient once they are completed with
their chemotherapy conditioning.
99. Complications of Stem Cell Transplants
• The biggest complication of stem cell transplants is the risk
of infection.
o patients are usually on protective isolation
o may have standing orders if a fever occurs
o +/- neutropenic diet (no raw fruits of vegetables, no
uncooked or undercooked meat)
• Graft vs. Host Disease is an often chronic complication: the
patient's new bone marrow if from an unrelated donor may
mount an immune response against the host (t-cell
mediated)
o instruct on the importance of adherence to the
immunosuppressive regimen.
100. What's upcoming in cancer care?
• Genetic profiling of individual tumors to determine the
effectiveness of potential chemotherapy drugs.
o ERCC1 in lung cancer for Irinotecan and platnim activity
o DPD in colon cancer to determine the responsiveness of
the tumor to fluropyrimidines
• More aggressive surgical and chemotherapy management
of metastatic disease rendering patients disease free who
were previously uncurable
• More targeted treatment and radiation, making cancer more
of a chronic disease
• Further advancements in the knowledge of prevention
leading to a lower incidence of cancer
101. Thank you for your attention
Good luck studying!!!
See you on Tues, Dec. 6th in the
Little theater at 7am