Med Surg 1 – Test 2 – Redo – Oncology Chapter 15 – Flashcards

Cancer is not a single disease with a single cause; rather, it is a group of distinct diseases with different causes, manifestations, treatments, and prognoses. The leading causes of cancer death in the United States in order of frequency and location are lung, prostate, and colorectal cancer in men and lung, breast, and colorectal cancer in women. Most cancer occurs in people older than 65 years. Overall, the incidence of cancer is higher in men than in women and higher in idustrialized nations. Although the overall rate of cancer deaths has declined, cancer death rates in African American men remain substantially higher than those among Causcasian men and twice those of Hispanic men.

Cancer is a disease process that begins when a cell is transformed by genetic mutations of the cellular DNA. Genetic mutations may result from inherited and/or acquired mutations that lead to abnormal cell behavior. The 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 other defense mechanisms of the body. The cells acquire a variety of capabilites that allow them to invade surrounding tissues and gain access to lymph and blood vessels, which carry the cells to other areas of the body.

Cancerous cells, described as malignant neoplasms, demonstrate uncontrolled cell growth that follows no physiologic demand (neoplasia).

Non-cancerous

Growth of new blood vessels that allows cancer cells to grow. This is a characteristic of Malignant cells.

Malignant cell membranes have been found to contain proteins called tumor-specific antigens and prostate-specific antigen, which develop over time as the cells become differentiated (mature). These proteins distinguish malignant cells from benign cells of the same tissue type. Many of the TSAs that have been identified have aided in assessing the extent of disease in a person and in tracking the course of illness during treatment or relapse.

Are large and irregularly shaped

(cell division) occurs more rapidly in malignant cells than normal cells. As the cells grow and divide, more glucose and oxygen are needed. If glucose and oxygen are unavailable, malignant cells use anaerobic metabolic channels for cell proliferation. Cancer cells utilize an increased amount of glucose even in the presence of oxygen, known as the Warburg effect. This increase in glucose uptake is the basis for positron emission tomography.

Malignant diseases have the ability to spread or transfer cancerous cells from one organ or body part to another by invasion and metastasis. Invasion, which refers to the growth of the primary tumor into the surrounding host tissues, occurs in several ways. Mechanical pressure exerted by rapidly proliferating neoplasms may force fingerlike projections of tumor cells into surrounding tissue and interstitial spaces. Malignant cells are less adherent and may break off from the primary tumor and invade adjacent structures. Malignant cells are thought to possess or produce specific destructive enzymes, such as collagenases, plasminogen activators, and lysosomal hydrolyses. These enzymes are thought to destroy surrounding tissue, including the structural tissues of the vascular basement membrane, facilitating invasion of malignant cells into blood and lymphatic vessels. The mechanical pressure of a rapidly growing tumor may enhance this process.

Cell - Well-differentiated cells resemble normal cells of the tissue from which the tumor originated. Mode of growth - Tumor grows by expansion and does not infiltrate the surrounding tissues; usually encapsulated. Rate of growth - Rate of growth is usually slow. Metastasis - Does not spread by metastasis. General effects - Is usually a localized phenomenon that does not cause generalized effects unless its location interferes with vital functions. Tissue destruction - Does not usually cause tissue damage unless its location interferes with blood flow. Ability to cause death - Does not usually cause death unless its location with vital functions.

Cell - Cells are undifferentiated and may bear little resemblance to the normal cells of the tissue from which they arose. Mode of growth - Grows at the periphery and overcomes contact inhibition to invade and infiltrate surrounding tissues. Rate of growth - Rate of growth is variable and depends on level of differentiation; the more anaplastic the tumor, the faster the growth. Metastasis - Gains access to the blood and lymphatic channels and metastasizes to other areas of the body. General effects - Often causes generalized effects, such as anemia, weakness, systemic inflammation, weight loss, and CACS. Tissue destruction - Often causes extensive tissue damage as the tumor outgrows its blood supply or encroaches on blood flow to the area; may also produce substances that cause cell damage. Ability to cause death - Usually causes death unless growth can be controlled

is the dissemination or spread of malignant cells from the primary tumor to distant sites by direct spread of tumor cells to body cavities or through lymphatic and blood circulation. Tumors growing in or penetrating body cavities may shed cells or emboli that travel within the body cavity and seed the surfaces of other organs. This occurs in ovarian cancer when malignant cells enter the peritoneal cavity and seed the peritoneal cavity or surfaces of abdominal organs such as the liver or pancreas. Patterns of metastasis can be partially explained by circulatory patterns and by the affinity for certain malignant cells to bind to molecules in specific body tissues. Patterns of metastasis associated with various types of cancer are often referred to as the natural history of the disease.

Lymph and blood are key mechanisms by which cancer cells spread. Lymphatic spread is the most common mechanism of metastasis. Tumor emboli enter the lymph channels by way of the interstitial fluid, which communicates with lymphatic fluid. Malignant cells aslo may penetrate lymphatic vessels by invasion. After entering the lymphatic circulation, malignant cells either lodge in the lymph nodes or pass between the lymphatic and venous circulations. Tumors arising in areas of the body with rapid and extensive lymphatic circulation are at high risk for metastasis in this manner through axillary, clavicular, and thoracic lymph channels. Hematogenous spread - the dissemination of malignant cells via the bloodstream, is directly realted to the vascularity of the tumor. Few malignant cells can survive the turbulence of arterial circulation, insufficient oxygenation, or destruction by the body's immune system. In addition, the structure of most arteries and arterioles is far too secure to permit malignant invasion. Those malignant cells that do survive are able to attach to endothelium and attract fibrin, platelets, and clotting factors to seal themselves from immune surveillance. The endothelium retracts, allowing the malignant cells to enter the basement membrane and secrete proteolytic enzymes. These enzymes degrade the extracellular matrix, allowing implantation.

is the growth of new blood vessels from the host tissue stimulated by the release of growth factors such as vascular endothelial growth factor. Rapid formation of new blood vessels helps malignant cells obtain the necessary nutrients and oxygen. However, the vessels formed in this deregulated process are morphologically abnormal and function inefficiently. It is also through this vascular network that tumor emboli can enter the systemic circulation and travel to distant sites. Large tumor emboli that become trapped in the microcirculation of distant sites may further metastasize to other sites. Therapies that target VEGF of its receptors are being used to treat many cancers effectively.

Malignant transformation, or carcinogenesis is thought to be at least a three-step process, involving initiation, promotion, and progression. Agents that initiate or promote cellular transformation are referred to as carcinogens. During initiation, carcinogens (substances that can cause cancer), such as chemicals, physical factors, and biologic agents, cause mutations in the cellular deoxribonucleic acid (DNA). Normally, these alterations are reveresed by DNA repair mechanisms or the changes initiate programmed cellular death (apoptosis) or cell senescence. Occasionally, cells escape these protective mechanisms, and permanent cellular mutations occur. These mutations usually are not significant to cells until the second step of carcinogenesis. During promotion, repeated exposure to promoting agents (co-carcinogens) causes proliferation and expansion of initiated cells with increased expression or manifestation of abnormal genetic information, even after long latency periods. Latency periods for the promotion of cellular mutations vary with the type of agent, the dosage of the promoter, and the innate characteristics and genetic stability of the target cell. The promotion phase generally leads to the formation of a preneoplastic or benign lesion. During progression, the altered cells exhibit increasingly malignant behavior. These cells acquire the ability to stimulate angiogenesis, to invade adjacent tissues, and to metastasize.

Factors implicated or known to induce carcinogenesis include viruses and bacteria, physical agents, chemicals, genetic or familial factors, diet, and hormones.

It is estimated that about 20% of all cancers worldwide are linked to viral and bacterial infections. Viruses are associated with cancer in one of two ways. After infecting individuals, DNA viruses insert a part of their own DNA near the infected cell genes causing cell division. The newly formed cells that now carry viral DNA lack normal controls on growth. Examples of these viruses that are known to cause cancer include HPV (cervical and head and neck cancers), hepatitis B (liver cancer), and Epstein-Barr virus (Burkitt lymphoma and nasopharyngeal cancer). There is 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 that continue to be investigated. Helicobacter pylori is one bacterium identified as a cause of cancer in humans. H.pylori has been associated with an increase incidence of gastric malignancy related to chronic superficial gastritis, with resultant atrophic and metaplastic changes to the gastric mucosa.

Physical factors associated with carcinogenesis include exposure to sunlight or radiation, chronic irritation or inflammation, and tobacco use. Excessive exposure to the ultraviolet rays of the sun, especially in fair-skinned people, increases the risk of skin cancers. Factors such as clothing styles, the use of sunscreen, occupation, recreational habits, and environmental variables, including humidity, altitude, and latitude, all play a role in the amount of exposure to ultraviolet light. Exposure to ionizing radiation can occur with repeated diagnostic x-ray procedures or with radiation therapy used to treat disease. 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 in the past have been associated with a higher incidence of leukemias, multiple myeloma, and cancers of the lung, bone, breast, thryroid, and other tissues. Background radiation from the natural decay processes that produce radon has also been associated with lung cancer, Ventilation is advised in homes with high levels of radon to allow the gas to disperse into the atmosphere.

Many cancers are thought to be related to environmental factors. Most hazardous chemicals produce their toxic effects by altering DNA structure in body sites distant from chemical exposure. Tobacco smoke, thought to be the single most lethal chemical carcinogen, accounts for at least 30% of cancer deaths in humans. Smoking is strongly associated with cancers of the lung, head and neck, esophagus, stomach, pancreas, cervix, kidney, and bladder and with acute myeloblastic leukemia. More than 4,000 individual chemicals have been identified in tobacco and tobacco smoke, including more than 60 chemicals that are known carcinogens. Tobacco may also act synergistically with other subtances, such as alcohol, asbestos, radiation, and viruses, to promote cancer development. Chewing tobacco is associated with cancers of the oral cavity, which primarily occur in men younger than 40 years. Passive smoke (second hand) has been linked to cancer. There is also evidence suggesting that passive smoke may be linked with childhood leukemia and cancers of the larynx, pharynx, brain, bladder, rectum, stomach, and breast. Many chemical substances found in the workplace are carcinogens or cocarcinogens. In the United States, carcinogens are classified by two federal agencies: the National Toxicology Program of the Department of Health and Human Services and the Environmental Protection Agency's Integrated Risk Information System. The Centers for Disease Control and Prevention established the National Institute for Occupational Safety and Health to provide occupational exposure limits and guidelines for protection of the workforce as regulated by the Occupational Safety and Health Act of 1970. The extensive list of suspected chemical substances continues to grow and includes aromatic amines and aniline dyes; pesticides and formaldehydes; arsenic, soot, and tars; asbestos; benzene; betel nut and lime; cadmium; chromium compounds; nickel and zinc ores; wood dust; beryllium compunds; and polyvinyl chloride.

Almost every cancer type has been shown to run in families. This may be owing to genetics, shared environments, cultural or lifestyle factors, or chance alone. Genetic factors play a role in cancer cell development. Abnormal chromosomal patterns and cancer have been associated with extra chromosomes, too few chromosomes, or translocated chromosomes. Specific cancers with underlying genetic abnormalites include Burkitt lymphoma, chronic myelogenous leukemia, meningiomas, acute leukemia, retinoblastomas, Wilms tumor, and skin cancers, inculding malignant melanoma. Additonally, there are syndromes that represent a cluster of cancers that are identified by a specific genetic alteration that is inherited across generations of a family. In these families, the associated genetic mutation is found in all cells and represents an inherited susceptibility to cancer for all family members who carry the mutation.

Dietary factors are also linked to environmental cancers. Dietary substances can be proactive (protective), carcinogenic, or cocarcinogenic. The risk of cancer increases with long-term ingestion of carcinogens or cocarcinogens or chronic 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 nitrate-containing foods, and red and processed meats. Alcohol increases the risk of cancers of the mouth, pharynx, larynx, esophagus, liver, colon, rectum, and breast. Alcohol intake should be limited to no more than two drinks per day for men and one drink per day for women. Greater consumption of vegetables and fruits is associated with a decreased risk of lung, esophageal, stomach, and colorectal cancers. Poor diet and obesity have been identified as contributing factors to the development of cancers of the breast, colon, endometrium, esophagus, and kidney. Obesity is also associated with 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. Recent epidemiologic studies have suggested an association between diabetes and cancer development. Although a scientific basis has yet to be identified, diabetes and cancer share common risk factors and incidence patterns.

Tumor growth may be promoted by disturbances in hormonal balance, either by the body's own hormone production or by administration of exogenous hormones. Cancers of the breast, prostate, and uterus are thought to depend on endogenous hormonal levels for growth. Diethylstilbestrol (DES) has long been recognized as a cause of vaginal carcinomas. Oral contraceptives and prolonged estrogen therapy are associated with an increased incidence of hepatpcellular, endometrial, and breast cancers but decrease the risk of ovarian cancer. The combination of estrogen and progesterone appears safer than estrogen alone in decreasing the risk of endometrial cancers; however, studies support discontinuing hormonal therapy containing both estrogen and progestin because increased risk of breast cancer, coronary artery disease, stroke, and blood clots. Hormonal changes related to the female reproductive cycle are also associated with cancer incidence. Early onset of menses before 12 and delayed onset of menopause after 55, nulliparity (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.

In humans, malignant cells are capable of developing on a regular basis. However, through surveillance, cells of the immune system can detect the development of transformed cells and destroy them before cell growth becomes uncontrolled. When the immune system fails to identify and stop the growth of transformed cells, cancer develops. Patients who are immunocompromised have an increased incidence of cancer. Renal transplant recipients who receive immunosuppressive therapy to prevent rejection of the transplanted organ have an increased incidence of lymphoma, Kaposi's sarcoma, and cancers of the skin and cervix. Patients with immunodeficiency diseases, such as acquired immunodeficiency syndrome (AIDS), have an increased incidence of Kaposi's sarcoma, non-Hodgkin's lymphoma, and cervical carcinoma. In addition, there is also an increase in the incidence of various non-AIDS-defining malignancies, including Hodgkin lymphoma; multiple myeloma; leukemia; melanoma; and cervical, brain, testicular, oral, lung, gastric, liver, renal, and anal cancers. Patients who were previously treated with alkylating chemotherapy agents, allogeneic hematopoietic stem cell transplantation involving total body irradiation, and certain types of chest radiation are at increased risk for secondary primary cancers related to treatment-associated immunosuppression. Autoimmune diseases, such as rheumatoid arthritis and Sjogren syndrome, are associated with increased development of cancer. Finally, age-related changes, such as declining organ function, increased incidence of chronic diseases, and diminished immunocompetence, may contribute to an increased incidence of cancer in older people.

Through the process of surveillance, an intact immune system usually has the ability to recognize and combat cancer through multiple, interacting cells and actions of the innate, humoral, and cellular components of the immune system. Tumor-associated antigens (TAAs) are found on the membranes of many cancer cells. TAAs are processed by antigen-presenting cells (macrophages and dentritic cells) that present antigens to both T- and B lymphocytes and are presented to T lymphocytes that recognize the antigen-bearing cells as foreign. Multiple TAAs have been identified--some are found in many types of cancer, some exist in the normal tissues of origin as well as the cancer cells, some exist in both normal and cancer cells but are overexpressed (exists in higher concentrations_ in cancer cells, and others are very specific to a limited number of cancer types. In response to recognizing TAAs as foreign, T-cell lymphocytes release several cytokines that elicit various immune system actions, including 1) proliferation of cytotoxic T lymphocytes capable of direct destruction of cancer cells, 2) induction of cancer cell apoptosis, and 3) recruitment of additional immune system cells (B-cell lymphocytes that produce antibodies, natural killer cells, and macrophages) that contribute to the destruction and degradation of cancer cells.

is concerned with reducing the risks of disease through health promotion and risk reduction strategies. It is estimated that almost 75% of all cancers in the United States are related to environmental and lifestyle factors. By acquiring knowledge and skills necessary to educate the community about cancer risks, nurses in all settings play a key role in cancer prevention. One way to reduce the risk of cancer is to help individuals avoid known carcinogens. Another strategy involves encouraging individuals to make dietary and lifestyle changes (smoking cessation, decreased caloric and alcohol intake, increased physical activity) that studies show influence the risk for cancer. Nurses use their education and counseling skills to provide patient education and support public education campaigns through organizations, such as the ACS, that guide indiviuals and families in taking steps to reduce cancer risks through health promotion and behaviors. Clinical trials that explore the use of medications for reducing the incidence of certain types of cancer are numerous. For example, large-scale breast cancer prevention studies supported by the National Cancer Institute indicated that chemoprvention with the medications tamoxifen or raloxifene can reduce the incidence of breast cancer by 50% in women at high risk for breast cancer. Daily aspirin has been reported to reduce colorectal cancers. Currently, the NCI lists more than 100 ongoing clinical trials exploring cancer prevention strategies.

involves screening and early detection activities that seek to identify early stage cancer in individuals who lack signs and symptoms suggestive of cancer. The goal is to decrease cancer morbidity and mortality associated with advanced stages of cancer and complex treatment approaches. Many organizations conduct cancer screening events that focus on cancers with the highest incidence rates of those that have improved survival rates if diagnosed early, such as breast or prostate cancer. These events offer education and appropriate assessments such as mammograms, digital rectal examinations, and PSA blood tests for minimal or no cost. Many screening and detection programs target people who do not regulary practice health-promoting behaviors or lack access to health care due to health insurance issues, financial or transportation limitations, competing priorities, or lack of knowledge. Nurses continue to develop evidence based approaches for community based screening and detection programs that reflect the cultural beliefs of the target population.

Radiology scans: MRI - Use of magnetic fields and radiofrequency signals to create sectioned images of various body structures. For neurologic, pelvic, abdominal, thoracic, breast cacers. CT - Computed tomography scan - Use of narrow-beam x-ray to scan successive layers of tissue for a cross sectional view. For neurologic, pelvic, skeletal, abdominal, thoracic cancers. PET - Through the use of a tracer, provides black and white or color-coded images of the biologic activity of a particular area, rather than its structure. Used in detection of cancer or its response to treatment. For lung, colon, liver, pancreatic, head and neck cancers; Hodgkin and non-Hodgkin lymphoma and melanoma. Labs: Electrolytes Liver Function Carcinoembryonic Antigen (CEA) Prostate-specific antigen (PSA) Alpha fetoprotein (AFP) Body fluid testing Biopsy: is performed to obtain a tissue sample for histologic analysis of cells suspected to be malignant. In most instances, the biopsy is taken from the actual tumor; however, in some situations, it is necessary to biopsy lymph nodes near the suspicious tumor. Many cancers can metastasize from the primary site to other areas of the body through lymphatic circulation. Knowing whether adjacent lymph nodes contain tumor cells helps health care providers plan the best therapeutic approach to combat tumor cells that have gone beyond the primary tumor site. The use of injectable dyes and nuclear medicine imaging can help identifying the sentinel lymph node or the initial lymph node to which the primary tumor and surrounding tissue drains. Sentinel lymph node biopsy is a minimally invasive surgical approach that in many instances has replaced more invasive lymph node dissections and the associated complications such as lymphedema and delayed healing. Three common types of Biopsys: Excisional biopsy is most frequently used for small, easily accessible tumors of the skin, breast, and upper or lower gastrointestinal and upper respiratory tracts. In many cases, the surgeon can remove the entire tumor as well as the surrounding marginal tissues. The removal of normal tissue beyond the tumor area decreases the possibility that residual microscopic malignant cells may lead to recurrence of the tumor. This approach not only provides the pathologist with the entire tissue specimen for determination of stage and grade but also decreases the change of seeding tumor cells. Incisional biopsy is performed if the tumor mass is too large to be removed. In this case, a wedge of tissue from the tumor is removed for analysis. The cells of the tissue wedge must be representative of the tumor mass so that the pathologist can provide an accurate diagnosis. If the specimen does not contain representative tissue and cells, negative biopsy results do not guarantee the absence of cancer. Needle biopsy is performed to sample suspicious masses that are easily and safely accessible, such as some masses in the breasts, thyroid, lung, liver, and kidney. Needle biopsies are most often performed on an outpatient basis. They are fast, relatively inexpensive, easy to perform, and usually require only local anesthesia.

CAUTION: Utilize the ACS 7 Warning Signals C- Change in bowel/bladder habits A- A sore that does not heal U- Unusual bleeding T- Thickening or lump in the breast I- Indigestion O- Obvious change in warts/moles N- Nagging cough and hoarseness

Presence of masses Anorexia Weight loss Frequent infection Skin problems Pain Swell/tenderness of lymph nodes Hair loss Fatigue Altered body function

Surgery: Prophylactic - involves removing nonvital tissues or organs that are at increased risk of developing cancer. Colectomy, mastectomy, and oophorectomy are examples. Palliative and Reconstructive surgerys are available as well. Radiation: skin problems, nausea, skin gets dry (lotion) Chemotherapy: hair loss, oral mucosa inflammation, nausea, vomting, no appetite Bone Marrow Transplantation

Impaired oral and skin integrity Altered nutrition Altered body image Fatigue Fluid and electrolyte imbalances Risk for infection Risk for bleeding