Cancer Chapter 51 - Lecture notes 51 PDF

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CHAPTER 15 Management of Patients with Oncologic Disorders CANCER  large group of disorders with different causes, manifestations, treatments, and prognoses  Because cancer can involve any organ system and treatment approaches have the potential for multisystem effects, cancer nursing practice overlaps with numerous nursing specialties  Cancer nursing practice covers all age groups and is carried out in various settings, including acute care institutions, outpatient centers, physician offices, rehabilitation facilities, the home, and long-term care facilities  scope, responsibilities, and goals of cancer nursing, also called oncology nursing, are as diverse and complex as those of any nursing specialty  Nursing management of the patient with oncologic disorders care of pts throughout the cancer trajectory from prevention through end-of-life care  Precision medicine- possible due to recent development of biologic databases (human genome sequencing), technological advances that can identify unique characteristics of individual persons (genomics, cellular assay tests), and computer-driven systems that can mine and analyze datasets o immediate goal focus on preventing and curing cancers  Affects males/females  Ageless  Presentation varies- severe/acute/chronic  Clinical features o Type o Staging o Molecular characteristics Can affect any one o Lung, Breast, Colorectal, Prostate Epidemiology  cancer is the second leading cause of death in the United States  one in four deaths is caused by cancer. leading causes of cancer death in the U.S. in order of frequency and location are lung, prostate, and colorectal cancer in men and lung, breast, and colorectal cancer in women  occurs in older adults  all cancer diagnoses are in people 55 years of age or older  prevalence of cancer is higher in men than in women  despite the rate of cancer deaths being declined, AA continue to have the higher cancer rates compared to Caucasia men & 2x of Hispanic men  despite AA women have. flower risk of cancer overall than white women, they still have higher cases of of deaths from cancer overall to women in general or white women  racial dispraise is due to comorbid conditions such as CV disease & poverty in AA population than in others  Cancer incidence and death rates also vary by geography PATHOPHYSIOLOGY OF THE MALIGNANT PROCESS  disease process that begins when a cell is transformed by genetic mutations of the cellular deoxyribonucleic acid (DNA)  Genetic mutations may be inherited and/or acquired, leading to abnormal cell behavior  initial genetically altered cell forms a clone and begins to proliferate abnormally, evading normal intracellular and extracellular growth-regulating processes or signals as well as the immune system defense mechanisms of the body  Genetic mutations may lead to abnormalities in cell signaling transduction processes (signals from outside and within cells that turn cell activities either on or off) that can in turn lead to cancer development  cells acquire numerous capabilities that causes them to invade surrounding tissues and/or gain access to the lymph & blood vessels carrying the cells to other areas of the body which results in metastasis [spread of the cancer]  Cancer characteristics o Uncontrolled cell growth o Lack contact inhibition o Do not undergo apoptosis

o No anchorage dependence o Dysplasia- deranged cell growth o Neoplasia- uncontrolled cell proliferation o Anaplasia- cells lose regular structure (LOSES ITS FUNCTION) ex: skin cell Right picture: contact inhibition (cancer cells) get in there and proliferate and process no longer occurs Natural cell death: apoptosis Characteristics of Malignant Cells  Benign and malignant cells differ in many cellular growth characteristics like the method and rate of growth, ability to metastasize or spread, destruction of tissue, and ability to cause death  anaplasia [pattern of growth in which the cells do not have normal characteristics & are different in shape & organization with respect to their cells of origin] is related to an increased malignant potential BENIGN VS. MALIGNANT CELL CHARACTERISTICS [Know the difference between the cells **TABLE ACROSS Carcinogenic Agents/Factors of Malignant Cells Molecular Process  Malignant transformation/carcinogenesis o Three-step cellular process  Initiation: apoptosis  carcinogen such as chemicals, physical factors, or biological agents cause mutation in cellular DNA. These alterations are normally reversed by DNA repair mechanism/changes that cause apoptosis or cell senescence  Promotion: preneoplastic/benign lesions  repeated exposure to promoting agents (co-carcinogens) cause proliferation and expansion of imitated cells with increased expression or manifestations of abnormal genetic information, even after long latency periods – promotion phase leads to formation of preneoplastic or benign (non-cancerous) lesion 

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Progression: angiogenesis  altered cells exhibit increasingly malignant behavior – cells acquire ability to stimulate angiogenesis (growth of new blood vessels that allow cancer cells to grow), invade adjacent tissues, metastasize  Cellular oncogenes; responsible for vital functions (proliferation/differentiation)  Cellular proto-oncogenes: epidermal growth factor receptor (EGFR), transcription factors c-Myc, cell signaling proteins Kirsten ras (KRAS) act as on switches for cellular growth o Amplification of these genes or epidermal growth factor (EGF) lead to uncontrolled cell proliferation o mutations that increase oncogenes activity deregulate cell proliferation as well  in the gene for KRAS, genetic alterations have been associated with  pancreatic, lung, & colorectal cancer  Just as proto-oncogenes turn on cellular growth, cancer suppressors turn off or regulate unneeded cellular proliferation

Carcinogen agents that cause malignant transformation/substances that cause cancer

Even though cells can escape from these protective mechanisms [apoptosis], the mutations are not as important to the cells until the 2nd step of carcinogenesis Angiogenesis- develop own blood supply Cancer cells don’t want to die Cancer cells are able to proliferate and have their own blood supply Telemerase will release PROLIFERATIVE PATTERNS  numerous body tissues normally go thru periods of rapid/proliferative growth that must be differentiated from malignant growth activity the several pattern that cell growth exist are hyperplasia, dysplasia, & metaplasia  Cancer cells: malignant neoplasms – uncontrolled cell growth that follows no physiologic demand (neoplasia)  Both benign & malignant growths are classified & named by tissue of origin 

Etiology  causes indicated or known to cause carcinogenesis: viruses& bacteria, physical agents, chemicals, genetic or familial factors, lifestyle hormones. 1. Agents  Viruses, bacteria – infectious disease o DNA viruses infect part of own DNA near infected cell genes causing cell division – newly formed cells carry viral DNA lack normal control on growth  Exaples: human papillomavirus (HPV) - cervical and head and neck cancers, Hep B (HBV) - liver cancer, Epstein-Barr virus (EBV), - burkitt lymphoma and nasopharyngeal cancer  H. pylori – gastric cancer o little evidence to support the link of most bacteria to cancer, although chronic inflammatory reactions to bacteria and the production of carcinogenic metabolites are possible mechanisms o Helicobacter pylori is one bacterium identified as a significant cause of gastric cancer Classification of caner: Carcinoma: 80-90% of all cancers  Tissue of origin: epithelial (adenocardinoma) – glandular epithelium, – organs or glands capable of secretion o Ex: adenocarcinoma of breast, lung, prostate  squamous epithelium (squamous cell carcinoma) – covers/lines all external and internal body surfaces o Ex: squamous cell cancer of lung, skin, esophagus  Sarcoma: connective/supportive o Bone (osteosarcoma) most common form of cancer of bone  Example: osteosarcoma of femur, humerus o Cartilage (chondrosarcoma) - rare, arises from within bones  Ex: chondrosarcoma of femur, pelvis o Adipose (liposarcoma) - arises from deep soft tissue  Ex: liposarcoma of retroperitoneum, thigh o Smooth muscle (leiomyosarcoma) very rare  Ex: leiomyosarcoma of uterus, intestine, stomach o Skeletal muscle (rhabdpsarcoma) most common in young children  Ex: rhabdosarcoma of head and neck, limbs o Fibrous tissue (fibrosarcoma) often involves long/flat bones  Ex: fibrosarcoma of femur, tibia, mandible o Membranes lining body cavities (mesothelial sarcoma/mesothelioma) most often related to asbestos exposure  Ex: mesothelioma of pleura or peritoneum o Blood vessels: (angiosarcoma) with liver – involvement related to occupational exposure to vinyl chloride monomer  Ex: angiosarcoma of liver, heart  Myeloma o Plasma cells (N/A) - produced by B-cell lymphocytes; plasma cell produce antibodies  Lymphoma

Lymphocytes - (non-Hodgkin lymphoma): 2main classifications; may involve lymph nodes and/or body organs  Ex: b-cell lymphoma, T-cell lymphoma Leukemia o Hematopoietic cells in bone marrow – may involve various cell lines produced in bone marrow o WBC (myelogenous) - acute myelogenous leukemia  Lymphocytes: (lymphocytic) - acute lymphocytic leukemia o RBC – erythremia – involves overproduction of RBC and associated with increased levels of WBC/platelets; risk of additional bone marrow disease  Ex: polycythemia vera o

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Physical agents: Sunlight sunscreen [radiation] o being expose in the sun excessively especially in fair skinned folks increases the risk of skin cancers o exposure to sunlight, radiation, chronic irritation or inflammation, tobacco carcinogens, industrial chemicals and asbestos being exposed to ionizing radiation can occur w/repeated diagnostic x-ray procedures/radiation therapy used to tx disease chronic irritation/inflammation Improved x-ray equipment minimizes the risk of extensive radiation exposure Radiation therapy used in cancer treatment and exposure to radioactive materials at nuclear weapon manufacturing sites or nuclear power plants associated with a higher incidence of leukemia, multiple myeloma, and cancers of the lung, bone, breast, thyroid, and other tissues Background radiation from the natural decay processes that produce radon has also been associated with lung cancer it is advised to utilized ventilators at home in which high levels of trapped radon can disperse into the atmosphere Chemical agents a. numerous cancers are linked to environmental factors b. Tobacco c. Asbestos hazardous chemicals produce their toxic effects by altering DNA structure-occur in body sites distant from that of initial chemical exposure Tobacco smoke o single most lethal chemical carcinogen, accounts for about one third of cancer deaths Smoking is strongly associated with cancers of the lung, head and neck, esophagus, stomach, pancreas, cervix, kidney, and bladder and with acute myeloblastic leukemia Passive smoke (i.e., secondhand smoke) has been linked to lung cancer & may be linked with childhood leukemia and cancers of the larynx, pharynx, brain, bladder, rectum, stomach, and breast combustible forms of tobacco such as cigars, pipes, roll-your-own products, and water pipes (or hookah)- associated with increased cancer risk electronic cigarettes- great concern about potential negative health effects Smokeless tobacco products, such as chewing tobacco and snuff- associated with an increased risk of oral, pancreatic, and esophageal cancer chemical substances found in the workplace are carcinogens or co-carcinogens o aromatic amines and aniline dyes; pesticides and formaldehydes; arsenic, soot, and tars; asbestos; benzene; cadmium; chromium compounds; nickel and zinc ores; wood dust; beryllium compounds; and polyvinyl chloride o Betel nut and lime- chewed as stimulants in some cultures Genetics &familial Factors genetics, shared environments, cultural or lifestyle factors Genetic factors play a role in cancer cell development Cancer has been associated with extra chromosomes, too few chromosomes, or translocated chromosomes Cancers with these underlying genetic abnormalities include chronic myelogenous leukemia, meningiomas, acute leukemia, retinoblastomas, and Wilms tumor

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certain syndromes represent a cluster of cancers identified by a specific genetic alteration that is inherited across generations In these families, the associated genetic mutation is found in all cells (it is germline and somatic) and represents an inherited susceptibility to cancer for all family members who carry the mutation. cancers in adults display a pattern of cancers suggestive of a familial predisposition families with a hereditary cancer syndrome include cancer in two or more first-degree relatives (the parent, sibling, or child of an individual), onset of cancer in family members younger than 50 years, the same type of cancer in several family members, individual family members with more than one type of cancer, and a rare cancer in one or more family members evidence of an autosomal dominant inheritance pattern of cancers affecting several generations of a family advances in the recognition of inherited cancer susceptibility syndromes enabled the appropriate identification of families at risk for certain syndromes o Examples include hereditary breast and ovarian cancer syndrome (BRCA1 and BRCA2) and multiple endocrine neoplasia syndrome (MEN1 and MEN2)  nephroblastomas, pheochromocytomas, and colorectal, stomach, thyroid, renal, prostate, and lung cancers

Lifestyle Factors diet, obesity, and insufficient physical activity. second only to tobacco use as major risk factors associated with cancer development risk of cancer increases with long-term ingestion of carcinogens or co-carcinogens or the absence of protective substances in the diet  Dietary substances that appear to increase the risk of cancer include fats, alcohol, salt-cured or smoked meats, nitrate- and nitrite-containing foods, and red and processed meats  Heavy alcohol use increases the risk of cancers of the mouth, pharynx, larynx, esophagus, liver, colon, rectum, and breast  Poor diet and obesity- contributing factors to the development of cancers of the breast (in postmenopausal women), colon, endometrium, esophagus, and kidney o Obesity - increased risk for cancers of the pancreas, gallbladder, thyroid, ovary, and cervix, and for multiple myeloma, Hodgkin lymphoma, and an aggressive form of prostate cancer  sedentary lifestyles and lack of regular exercise to cancer development 5. Hormonal agents  tumor growth has been linked to disturbances in hormonal balance either by the endogenous [own body's] hormone production or by the administration of exogenous hormones.  cancers of the great, prostate, & uterus depend on endogenous hormonal levels of growth  prenatal exposure to diethylstilbestrol [synthetic form of female hormone estrogen] is a RISK AFCTOR for clear cell adenocarcinoma of the lower genital tract  Hormonal changes related to the female reproductive cycle- associated with cancer incidence  Early onset of menses before age 12 and delayed onset of menopause after age 55, null parity (never giving birth), and delayed childbirth after age 30 are all associated with an increased risk of breast cancer. Increased numbers of pregnancies are associated with a decreased incidence of breast, endometrial, and ovarian cancers.  Women who take estrogen after menopause appear to have an increased risk of ovarian cancer. Combination estrogen and progesterone therapy is linked to a higher risk of breast cancer  longer the combined therapy is used, the higher the risk. However, within 3 years of stopping the hormones, the risk returns to that of a woman who never used this therapy  Women who have taken hormonal therapy appear to have a lower risk of getting colorectal cancer, but when cancers are found it may be more advanced (more likely to have spread to lymph nodes or distant sites) than the cancers found in women not taking hormones Role of Immune System  transformed cells arise on a regular basis, but are recognized by surveillance cells of the immune system that destroy them before cell growth becomes uncontrolled (immune surveillance  immune system fails to identify and stop the growth of transformed cells, a tumor can develop and progress

Folks who have an increased incidence of cancer: immunocompromised pts & transplant recipients who received immunosuppressive therapy to prevent rejection of the transplanted organ  AIDS pts have an increased risk of Kaposi sarcoma & other cancers  folks treated for one cancer are at high risk for other [secondary] cancers 1. Normal immune response Intact immune system ability to recognize and combat cancer cells – innate, humoral, cellular components of immune system  Tumor associated antigens (TAA) found on membranes of many cancer cells  TAAs processed by antigen-presenting cells (APCS) - (macrophages, dendritic cells that present t and b lymphocytes) presented to T lymphocytes that recognize antigen-bearing cells as foreign o TAAs identified: found in many types of cancer, some exist in normal tissue of origin as well as cancer cells, some exist in both normal and cancer cells but overexpressed in cancer cells, some specific to cancer cell types o In response to recognizing TAAs as foreign o t lymphocytes release cytokines that elicit various immune system actions including:  1) proliferation of cytotoxic (cell killing T lymphocytes capable of direct destruction of cancer cells  2) induction of cancer cell apoptosis  3) recruitment of additional immune system cells (B-cell lymphocytes that produce antibodies, natural killer cells, macrophages) contribute to destruction and degradation of cancer cells 

2. Immune system evasion  If body fails to recognize TAAs on cancer cells or function of APCs is impaired, immune system is not stimulated: cancer cells been found to have altered cell membranes that interfere with APC binding and presentation to T lymphocytes  cancer cells release cytokines that inhibit APC’s and other cells in immune system, when tumors do not possess TAAs that label as foreign, immune response not alerted and tumor grows  Immunogenicity (immunologic appearance) of cancer cells can be alerted through genetic mutations allowing cells to evade immune cell recognition o Tumor antigens may combine with antibodies produced by immune system and hide themselves to normal immune defense mechanisms o tumor antigen-antibody complex creates message to decrease antibodies and other immune system complexes  Overexpression (abnormally high concentrations) of host suppressor T lymphocytes induced through the release of cytokines by malignant cells down regulates immune system  permitting uncontrolled cell growth  proliferation of T lymphocytes (promote immune response) impaired by cytokines produced by cancer cells  without helper T lymphocytes immune response is limited and cancer cells proliferate Influencing factors  environmental  Genetic/familial  Lifestyle  nutrition  Medications  Immune status  Advanced age Virus- HPV (cervical, head, and neck); Hep B (liver cancer) – liver inflammation and cells are destroyed Radiation exposure on a high level used in cancer treatments can lead to a higher incidence (leukemia or the breast) Tobacco (starting); vaping Hormonal agents: endogenous hormone production (breast, uterus) Lifestyle: obesity* Genetics: predisposition (1st degree relatives) PREVENTION

Primary prevention: reducing the risks of disease through health promotion and risk reduction strategies o Use of immunization to reduce the risk of cancer through prevention of infections associated with cancer o HPV vaccine recommended to prevent cervical, head, neck cancer o vaccine to prevent HBV infection reduce risk of Hep B and development of liver cancer o Risk factor modification, Immunization, Chemoprevention Risk factor modification: sunscreen smoking, smoking, immunizations (HPV, HEP vaccine Secondary preven...