neoplastic disruptions
DESCRIPTION
TRANSCRIPT
Alteration in cell function and differentiation:
Neoplastic Disruptions
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.
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
Cancer Incidence and Mortality 2006 ACS Projections
Data from the ACS. Cancer facts and figures 2006.
Cases DeathsProstate 234,460 27,350Lung & bronchus 92,700 90,330Colon & rectum 72,800 27,870Urinary bladder 44,690 8,990Lymphomas 34,870 10,770Melanoma 34,260 5,020Kidney & 24,650 8,130renal pelvisLeukemia 20,000 12,470Pancreas 17,150 16,090
All sites 720,280 291,270
Cases DeathsBreast 212,920 40,970Lung & bronchus 81,770 72,130Colon & rectum 75,810 27,300Uterine corpus 41,200 7,350Lymphomas 31,800 9,560 Melanoma 27,930 2,890Ovary 20,180 15,310Pancreas 16,580 16,210Urinary bladder 16,730 4,070 All sites 679,510 273,560
Change in the US Death Rates* by Cause, 1950 & 2005
* 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.
HeartDiseases
CerebrovascularDiseases
Influenza &Pneumonia
Cancer
19502005
Rate Per 100,000
Cancer Death Rates* Among Men, US,1930-2004
*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.
Lung & bronchus
Colon & rectum
Stomach
Rate Per 100,000
Prostate
Pancreas
LiverLeukemia
Cancer Death Rates* Among Women, US,1930-2004
*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.
Lung & bronchus
Colon & rectum
Uterus
Stomach
Breast
Ovary
Pancreas
Rate Per 100,000
African American men
White men
African American women
White women
Rate Per 100,000
Cancer Death Rates* by Sex and Race, US, 1975-2004
*Age-adjusted to the 2000 US standard population.Source: Surveillance, Epidemiology, and End Results Program, 1975-2004, Division of Cancer Control andPopulation Sciences, National Cancer Institute, 2007.
Cancer Incidence Rates* Among Men, US, 1975-2004
Prostate
Lung & bronchus
Colon and rectum
Urinary bladder
Non-Hodgkin lymphoma
Rate Per 100,000
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.
Cancer Incidence Rates* Among Women, US, 1975-2004
*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.
Colon and rectum
Rate Per 100,000
Breast
Lung & bronchus
Uterine Corpus
Ovary
Non-Hodgkin lymphoma
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
Host defense mechanisms against cancer:Tumor Antigens
o Tumor-Associated Antigens (TAA)o Tumor-Specific Antigens (TSA)
Host defense mechanisms against cancer:Tumor AntigensClick to add content
Host defense mechanisms against cancer:Tumor AntigensCancer cells may display altered cell surface antigens as a result of their malignant transformation.
• Through immunogenic survellience our immune system recognizes and destroys the cells that exhibit these non-self tumor antigenso 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
Host defense mechanisms against cancer:Tumor Antigens
Host defense mechanisms against cancer:How cancer cells evade the immune system. There are many theories how cancer cells are able to evade 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
Blocking Antibodies on TAA's
Cell Life Cycle and Metabolic Activity
FIG. 16-1
Cell life cycle: the alternation between mitosis and interphase.S phase:• Synthesis phase• synthesis of DNA and
proteins for new chromosomes
• Get two separate sets of chromosomes
G2 phase:• G=gap• RNA and protein synthesis
occur• period between the
completion of DNA synthesis and the next phase which is the M phase
Cell life cycle: the alternation between mitosis and interphaseM phase:• Mitosis phase• Nuclear and cytoplasmic
division occurs producing two daughter cells
• phases of mitosis include prophase, metaphase, anaphase and telophase
G1 phase:• G=gap• period between the M
phase and the start of DNA synthesis
• energy is generated and extra membranes and cytoplasm are made
Cell life cycle: the alternation between mitosis and interphaseG0 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.
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
Cellular proliferation in cancer cells1. 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."
Cellular differentiation in cancer cellsA 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).
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)
Characteristics of benign and malignant neoplasmsTumor: 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.
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.
Examples of non-neoplastic growth patterns
Comparison of benign and malignant neoplasms
Comparison of benign and malignant neoplasms
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
Terms important in carcinogenesis
Oncogene:• These are genes that can
promote the growth of cancer cells
• these genes are usually derived from mutations of normal genes
• Can interfere with the cells' normal functions and protein expression
Proto-Oncogene:• These are genes that
regulate normal cellular processes (very important)
• promote normal embryonic cellular development
• Once growth and development ceases, they genes are usually "turned off"
• Can be "turned on" by viruses, chemicals, or any carcinogen
Terms important in carcinogenesis
Tumor Suppressor Genes: • They normally function to
regulate growth• Mutations to this part of
the genome can cause the cell to engage in unregulated growtho p53 gene in many
cancerso BRCA-1, BRCA-2o APC gene
• Can be inherited
Mutations in proto-oncogenes and tumor suppressor genes can occur in embryonic development, and this usually leads to an earlier development of cancer, and a more significant presentation of the cancer
Mutations in these genes can also be induced by exposure to carcinogens.
CRC Development:Adenoma-to-Carcinoma Sequence
Adapted from Bishop and Hall. Eur J Cancer. 1994;30A:1946-1956, with permission.
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
Hyperproliferativeepithelium
Adenoma, increasingin size, and dysplasia Carcinoma
Germline APCmutation (FAP)
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 apoptosiso cells with altered antigens are subject to immune
surveillanceo 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
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.
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
Process of Cancer Development
Process of metastatic spread
FIG. 16-5
What do Metastases look like?
FIG. 16-4
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 cellso 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 cancero CA-125: Ovarian cancer
Risk factors that predispose for cancer development1. Heredity2. Hormones3. Immunologic mechanisms4. Chemical Carcinogens5. Radiation6. Oncogenic viruses
Risk factors that predispose for cancer developmentHeredity:• Cancer related genes
have been identified that increase an individual's susceptibility to the development of certain cancerso BRCA-1/BRCA-2: 40-
80% lifetime risk of breast cancer
o Accounts for approx. 10% of cancers
Hormones: • Hormones can
overstimulate the proliferation of certain cells overtimeo Prostate cancer is
thought to develop in elder males because of lifetime exposure to androgens
o DES babies had higher rates of Uterine cancer
Risk factors that predispose for cancer developmentImmunologic Mechanisms:• Mutant cells are constantly
formed, but are destroyed by immune cells through immuno-surveillance
• people with depressed immune systems have higher rates of cancero AIDS related kaposi's
sarcoma
Chemical Carcinogens:• These include chemicals
like cigarette smoke and asbestos, drugs like hormones, immunosuppressive agents, cytotoxic drugs, and dietary factors like fats and nitrates
• some of these compounds are either initiators or promotors, cigarette smoke is both
Risk factors that predispose for cancer developmentRadiation:• When cells are exposed to
radiation, there is damage to one or both strands of DNA
• This can be exposure to ionizing radiation or exposure to UV radiation
• Melanoma is a cancer with significant increases in incidence
• Hiroshima survivors
Oncogenic Viruses:• Some viruses can infect a
cell and inject their genetic material into the host DNA...this can either disrupt a tumor suppressor gene or add an oncogene to the DNA causing malignant transformationo Hep B/C and HCCo HPV and Cervical
Cancer
Risk factors that predispose for cancer developmentAge:• Advanced age is the single most significant risk factor
o 50% of cancers occur in those >65 years of ageo the symptoms of cancer are often perceived or
written off as "age related changes"o Can be more vulnerable to complications from
cancer treatment
Prevention and the early detection of cancerPreventative 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
Warning signs of cancer development
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.
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.
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.
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
Other Diagnostic tests if cancer is suspected or diagnosed (will depend on primary site)1. Cytology studies: examination of cells that are sloughed into the 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
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
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).
Ways of classifying cancer...
1. Anatomic Site2. Histological Analysis (grading)3. Extent of Disease (Staging)
Ways of classifying cancer: Anatomic siteThe 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
Ways of classifying cancer: Histological analysisThis 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
Ways of classifying cancer: Extent of diseaseThis 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 situstage I: tumor limited to the tissue of origin; localized tumor growthstage II: limited local spreadstage III: extensive local and regional spreadstage IV: metastasis
Ways of classifying cancer : Extent of disease
Major treatment options in cancer
1. Surgery2. Radiation3. Chemotherapy4. Hormonal therapy5. Biotherapy6. Targeted therapy7. Bone Marrow and peripheral blood stem cell transplantation
How do you choose an option for cancer treatment?Treatment option choices are dictated by the goals of therapy.
• Cure• Control• Palliation
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 cancer4. Diagnose or stage a tumor5. Palliate the symptoms from a cancer6. Reconstruction from previous cancer surgery7. Determine if therapy if effective (very rarely the primary goal
of surgery, but may be secondary)
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 therapyNursing Care• Routine pre- and post-op care• Additional psycho-social needs of cancer patients
o Anxietyo Body image disturbance
• Attention to the other risk factors that accompany a patient with cancer
Radiation TherapyIonizing 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
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)
Nursing Management of Radiation Therapy PatientsSafety 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
Nursing Management of Radiation Therapy Patients• Providing patient teaching based on the type of radiation
they are to receive...teletherapy or brachytherapyo 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.
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
Skin Complications with Radiation Therapy
Skin Complications with Radiation Therapy
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
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.
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 tumor3. Age of the tumor4. Location of the tumor5. Presence of resistant tumor cells
Chemotherapy Classifications
Cell Cycle Specific:• these drugs are effective
during specific phases of the cell cycle (G1, S, G2, M) relating to cellular proliferation/replication.
• Effective only during one specific phase and are often given over a prolonged period to ensure that the majority of cells reach the phase the drug acts on.
• Very time dependent
Cell Cycle Nonspecific:• Effective on both dividing and
resting cells (G0 phase).• Damage the cell at some
point in the cycle but death does not occur until the cell attempts to divide
• Very dose dependent
Cell Cycle specific and Cell Cycle Non-specific are often given together to
enhance death of tumor cells
Chemotherapy Examples
Cell Cycle Specific:• Antimetabolites: mimic
naturally occuring substances thus interfering with enzyme function or DNA synthesiso capecitabine (Xeloda)o methotrexate (Trexall)
• Mitotic Inhibitors: Some act by stabilizing microtubules so they aren't able to align the chromosomes to divide
• Topsimerase Inhibitors: Inhibit the enzyme topsimerase that function to make breaks in DNA for replication
Cell Cycle Non-specific:• Alkalating Agents: first
chemotherapies used, Damage DNA by breaking the double-stranded helix
• Antitumor antibiotics: bind directly to the DNA, inhibiting DNA replication and interfering with transcription
• Hormone therapy: interferes with the action of a hormone, or with the enzymes that produce hormones
Methods of Chemotherapy Administration
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 siteo Can cause local tissue damageo Can lead to permanent damage and loss of function
All vesicant chemotherapy should be administered using a central venous access device (CVAD)
Why?
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
Examples of CVADs
Examples of CVADs
Toxicities/Side Effects from ChemotherapyChemotherapy 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
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.
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 cellso letrozole for breast cancer: inhibits the enzyme that
converts androgen to estrogeno Lupon for prostate: inhibits the production of
testosterone by the testicleso Extreme hormone manipulation: orchiectomy/
oophorectomy
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
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 effects2. They restore, augment, or modulate host immune system
mechanisms3. They have other effects, like inhibiting the cancer's ability to
metastasize or differentiate.
ImmunotherapyInterferon:• 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 DNAo 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
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
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)
Sites of Action of Targeted Therapy
FIG. 16-21
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.
Bone marrow and peripheral blood stem cell transplantationLife 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)
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.
Stem Cell Transplant
Complications of Stem Cell Transplants• The biggest complication of stem cell transplants is the risk
of infection.o patients are usually on protective isolationo may have standing orders if a fever occurso +/- 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.
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 activityo 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
Thank you for your attention
Good luck studying!!!See you on Tues, Dec. 6th in the
Little theater at 7am