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neoplastic disruptions


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neoplastic disruptions

  1. 1. Alteration in cell function and differentiation: Neoplastic Disruptions
  2. 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. 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. 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 720,280 291,270Data from the ACS. Cancer facts and figures 2006.
  5. 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. 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. 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. 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. 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. 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. 11. Cancer DefinitionsOncology: The study of tumors and their treatmentCancer: from the latin "crab-like"Tumor: Swelling that can be caused by a number ofconditions, usually marked by the suffix -omaCarcinoma: malignant tumor of epithelial tissueAdenocarcinoma: malignant tumor of glandular epithelialtissueSarcoma: Malignant tumor of mesenchymal origin
  12. 12. Host defense mechanisms againstcancer:Tumor Antigens o Tumor-Associated Antigens (TAA) o Tumor-Specific Antigens (TSA)Host defense mechanisms againstcancer:Tumor AntigensClick to add content
  13. 13. Host defense mechanisms againstcancer:Tumor Antigens altered cell surface antigens as aCancer cells may displayresult 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
  14. 14. Host defense mechanisms againstcancer:Tumor Antigens
  15. 15. Host defense mechanisms againstcancer:Howare many theories how cancerthe immune There cancer cells evade cells are able to evadesystem.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
  16. 16. Blocking Antibodies on TAAs
  17. 17. Cell Life Cycle andMetabolic Activity FIG. 16-1
  18. 18. Cell life cycle:  the alternation betweenmitosis 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
  19. 19. Cell life cycle:  the alternation betweenmitosis and interphaseM 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
  20. 20. Cell life cycle:  the alternation betweenmitosis 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-enterthe 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.
  21. 21. Cell proliferationThis is a highly regulated process by which cells divide andreproduce. Feedback regulation of this process occurs innormal 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
  22. 22. 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."
  23. 23. Cellular differentiation in cancer cellsA mature, differentiated cell in a human is capable offunctioning only as the tissue/organ it has developed into can.The purpose of differentiation is to provide for organizationthroughout the tissues/organs/human system. Normal cellsdifferentiate 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).
  24. 24. Cellular metabolism in cancer cellsNormal cells depend on aerobic metabolism for 90% of theirenergy needs. Only cells without mitochondria use anaerobicmetabolism 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)
  25. 25. Characteristics of benign and malignantneoplasmsTumor: Swelling that can be caused by a number ofconditions including inflammation and trauma.Neoplasia: These are clusters of cells that can be benign ormalignantBenign Neoplasm: contain well differentiated cells that areclustered together in a single mass.Malignant Neoplasm: less well differentiated toundifferentiated and have the ability to break loose, enter thecirculatory or lymphatic systems and form secondarymalignant tumors at other sites.
  26. 26. 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 bytheir cell characteristics, rate of growth, manner of growth,capacity to metastasize and spread to other parts of the bodyand potential for causing death.
  27. 27. Examples of non-neoplastic growthpatterns
  28. 28. Comparison of benign and malignantneoplasms
  29. 29. Comparison of benign and malignantneoplasms
  30. 30. CarcinogenesisStrictly interpreted, this is the development of cancer inotherwise 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
  31. 31. Terms important in carcinogenesisOncogene: 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
  32. 32. Terms important in carcinogenesisTumor 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.
  33. 33. 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.
  34. 34. Carcinogenesis:  InitiationThis is a mutation in the cells 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
  35. 35. 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 ofmalignant change and a promoter of cancer development.
  36. 36. Carcinogenesis:  ProgressionThis 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
  37. 37. Process of Cancer Development
  38. 38. Process of metastatic spread FIG. 16-5
  39. 39. What do Metastases look like? FIG. 16-4
  40. 40. What about the Oncofetal Antigens?Oncofetal antigens are tumor antigens that are found on the surfacesand 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, pts with ulcerative colitis and cirrhosis of the liver o Alpha-Fetoprotein (AFP): fetal liver cells and liver cancer o CA-125: Ovarian cancer
  41. 41. Risk factors that predispose for cancerdevelopment1. Heredity2. Hormones3. Immunologic mechanisms4. Chemical Carcinogens5. Radiation6. Oncogenic viruses
  42. 42. Risk factors that predispose for cancerdevelopmentHeredity: Hormones:• Cancer related genes • Hormones can have been identified that overstimulate the increase an individuals 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
  43. 43. Risk factors that predispose for cancerdevelopmentImmunologic 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 kaposis fats and nitrates sarcoma • some of these compounds are either initiators or promotors, cigarette smoke is both
  44. 44. Risk factors that predispose for cancerdevelopmentRadiation: 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
  45. 45. Risk factors that predispose for cancerdevelopmentAge:• 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
  46. 46. Prevention and the early detection ofcancerPreventative 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
  47. 47. Warning signs of cancer development
  48. 48. Screening Guidelines for the Early Detectionof 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.
  49. 49. Screening Guidelines for the Early Detectionof 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.
  50. 50. Screening Guidelines for the Early Detectionof Prostate Cancer, American Cancer SocietyThe prostate-specific antigen (PSA) test and the digital rectal examination(DRE) should be offered annually, beginning at age 50, to men who have alife expectancy of at least 10 years.Men at high risk (African-American men and men with a strong familyhistory of one or more first-degree relatives diagnosed with prostate cancerat an early age) should begin testing at age 45.For men at average risk and high risk, information should be providedabout what is known and what is uncertain about the benefits andlimitations of early detection and treatment of prostate cancer so that theycan make an informed decision about testing.
  51. 51. Screening Guidelines for the Early Detection ofColorectal Cancer and Adenomas, American CancerSociety 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
  52. 52. Other Diagnostic tests if cancer issuspected or diagnosed (will depend onprimary site)examination of cells that are sloughed into the1. Cytology studies:various body secretions or scraped from organ cavities (i.e. papsmear)....suspicious findings may necessitate an actual biopsy2. Chest Xray/Mammogram: looking for radiological evidence of aprimary or a metastatic cancer site (not very sensitive, you need apretty big lesion to see it on chest xray)3. CBC: evaluate the blood for anemia, alterations in WBCs,thrombocytopenia or thrombocytosis4. Blood tests for tumor markers/antigens: CEA, AFP, CA19-9, CA-125, CA15-3, CA27-3, PSA
  53. 53. Other diagnostic tests if cancer issuspected or diagnosed (will depend onthe primary site)5. Biopsy: refers to the process of obtaining tissue for histologic examand susequent diagnosis of the disease • Needle Biopsy • Incisional • Excisional6. CT Scan: Multiple xrays are done, usually from the neck to groin toget a picture of the internal organs and look for metastatic disease(often part of routine staging of cancer7. PET Scan: This is a specialized test looked at the metabolic rate oftissues. A radioactively labeled sugar solution is ingested and thescanner looks for areas of the body that take up the sugar...good incancer because of the elevated glucose needs of cancerous cells
  54. 54. Other diagnostic tests if cancer issuspected or diagnosed (will depend onthe primary site)8. Sigmoidoscopy/Colonoscopy: Visualize and removepolyps, precancerous lesions and cancerous lesions from thecolon.9. Bone Scan: Radioisotopes are injected and looks forincreased uptake in the bone (hot spots) which indicatemetastatic disease in the bones10. Bone Marrow Study: evaluate the progenitor cells, lookfor genetic abnormalities (most often used in hematologicmalignancies, but a metastatic cancer to the bone marrow canalso be evaluated).
  55. 55. Ways of classifying cancer...1. Anatomic Site2. Histological Analysis (grading)3. Extent of Disease (Staging)
  56. 56. Ways of classifying cancer:  AnatomicsiteThe tumor is identified by the tissue of origin, the anatomicsite, 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
  57. 57. Ways of classifying cancer:  HistologicalanalysisThis is a microscopic analysis of the tumor, looking at theappearance of cells and the degree of differentiation. Brokendown 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
  58. 58. Ways of classifying cancer:  Extent ofdiseaseThis is describing the extent of the disease in the body. Theycan be broken up into the American Joint Committee onCancer (AJCC) and Tumor/Node/Metastases (TNM) staging.Both these staging systems are more amenable to solid tumorevaluation (not leukemias/lymphomas).stage 0: cancer in situstage I: tumor limited to the tissue of origin; localized tumorgrowthstage II: limited local spreadstage III: extensive local and regional spreadstage IV: metastasis
  59. 59. Ways of classifying cancer :  Extent ofdisease
  60. 60. Major treatment options in cancer1. Surgery2. Radiation3. Chemotherapy4. Hormonal therapy5. Biotherapy6. Targeted therapy7. Bone Marrow and peripheral blood stem cell transplantation
  61. 61. How do you choose an option for cancertreatment?Treatment option choices are dictated by the goals of therapy.• Cure• Control• Palliation
  62. 62. Surgery1. 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)
  63. 63. Complications of surgery and nursingcare• 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 Anxiety o Body image disturbance• Attention to the other risk factors that accompany a patient with cancer
  64. 64. 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 divideIndicated as primary therapy for cancer if the tumor is inan area that is difficult to reach surgically or wheresurgery 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
  65. 65. 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)
  66. 66. Nursing Management of RadiationTherapy 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
  67. 67. Nursing Management of RadiationTherapy 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.
  68. 68. Nursing Management of RadiationTherapy 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
  69. 69. Skin Complications with RadiationTherapy
  70. 70. Skin Complications with RadiationTherapy
  71. 71. Nursing Management of RadiationTherapy 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
  72. 72. ChemotherapyThis is indicated in the treatment of hematologic and solidtumor malignancies. Can be the primary therapy or usedadjunct to another therapy (surgery or radiation).Chemotherapy works in different ways, but primarily bydisrupting the production of essential enzymes, inhibits RNA,DNA, and protein synthesis, and can prevent cell mitosis.Most effective against rapidly dividing cells.
  73. 73. Goals of ChemotherapyThe goal of chemotherapy is to eliminate or reduce the numberof malignant cells in the primary tumor and/or the metastatictumor site. The response of malignant cells to chemotherapyis 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
  74. 74. Chemotherapy ClassificationsCell 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
  75. 75. Chemotherapy ExamplesCell 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 arent 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
  76. 76. Methods of ChemotherapyAdministration
  77. 77. Extravasations of ChemotherapyChemotherapy drugs can have direct affects on the tissue itsexposed to upon administration. One of the major routes ofadministration for chemotherapy is the IV route. Since mostchemotherapy drugs are either irritants or vesicants, a majorrisk 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 functionAll vesicant chemotherapy should be administered usinga central venous access device (CVAD)
  78. 78. Why?
  79. 79. 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
  80. 80. Examples of CVADs
  81. 81. Examples of CVADs
  82. 82. Toxicities/Side Effects fromChemotherapyChemotherapy does not distinguish between normal cells andcancer cells so toxicity to normal tissues is expected.Acute Toxicity: Nausea, vomiting, allergic reactions,dysrhythmias, cold sensitivityDelayed Toxicity: mucositis, diarrhea, stomatitis, alopecia,neutropenia, anemia, pancytopeniaChronic Toxicity: damage to organ systems such as theheart, liver, kidneys, lungs, nervous system, and bone marrow. Of all of the above, the most life threatening is the neutropenia/pancytopenia
  83. 83. Nursing Management andConsiderations• 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 others 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.
  84. 84. Hormonal TherapySome tumors are very hormone dependent, and can grow atan increased rate in the presence of certain hormones (egbreast, 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
  85. 85. 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
  86. 86. Biotherapy/Targeted Therapy:This consists of agents that modify the relationship betweenthe biologic response of the host to the tumor cells. Includesimmunotherapy, monoclonal antibodies, antiangiogenic agentsand 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 cancers ability to metastasize or differentiate.
  87. 87. 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 DNA o stimulates the expression of TAAs 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
  88. 88. ImmunotherapyInterleukin 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
  89. 89. Monoclonal AntibodiesThese are antibodies or immunoglobulins that are produced tobind antigens that are overexpressed on cancer cells. Thisblocks the "downstream activity" of these receptors instimulating 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)
  90. 90. Sites of Action of TargetedTherapy FIG. 16-21
  91. 91. Targeted Therapies (which can beinterchanged often with monoclonalantibodies)Interferes with cancer growth by targeting specific cellularreceptors and pathways that are important in tumor growth.They have a very different side effect profile than chemo andare often successful at improving the outcome ofchemotherapy 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.
  92. 92. Bone marrow and peripheral bloodstem cell transplantationLife saving treatment option for malignant and non-malignantconditions. Involves giving high dose chemotherapy with thegoal of clearing all the malignant cells and then "rescuing" thepatient with new hematopoietic stem cells that can repopulatethe 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)
  93. 93. Harvesting of Peripheral Blood for StemCell• 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.
  94. 94. Stem Cell Transplant
  95. 95. 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 patients 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.
  96. 96. Whats 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
  97. 97. Thank you for your attention Good luck studying!!! See you on Tues, Dec. 6th in the Little theater at 7am