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Med-Surg II (Cancer)
Problems of Protection (Ch. 23)
| Question | Answer |
|---|---|
| A normal feature of embryonic cells | Rapid and continuous cell division |
| The time it takes one embryonic cell to divide into two cells | Generation time |
| Generation time ranges from ____ to_____ hours | 2-8 hours |
| Reason embryonic cells do not respond to signals for apoptosis | Early embryonic cells have long telomeres that do not shorten with each cell division |
| Without specific shape or differentiation | Anaplasia |
| Anaplastic appearance | small and rounded |
| Early embryonic cells have an unlimited potential for maturation and have not committed to a specific cell type | Pluripotency |
| Occurs in early embryonic cells because they do not make fibronectin and are not tightly bound together | Loose adherence |
| Occurs in early embryonic cells because they are not tightly bound together and can move throughout the early embryo | Migration |
| Does not occur in early embryonic cells, even when all sides of these cells are in continuous contact with the surface of other cells | Contact inhibition |
| Found in early human embryonic cells; 23 pairs | Normal chromosomes |
| Early embryonic cells start changing into differentiated cells at about day 8; group of cells will eventually become only one specific organ or tissue | Commitment |
| Early embryonic genes are "turned off" | suppression |
| Specific genes that control writing of differentiated functions are "turned on" selectively in different cell types | Expressed |
| Cell growth or cell funtion is changed | abnormal cells |
| Normal cells growing in the wrong place or at the wrong time | Benign tumor cells |
| Examples of benign tumor cells | moles, uterine fibroid tumors, skin tags, endometriosis, and nasal polyps |
| Occurs in benign tumors; tissues not needed for normal function, growing too much or in the wrong place | Continuous or inappropriate cell growth |
| Occurs in benign tumors; look like tissues they come from, retaining characteristics of parent cells | Specific morphology |
| Continue to be performed by benign tumors | Specific differentiated functions |
| Occurs because benign cells continue to make fibronectin | Tight adherence |
| Benign tissues are surrounded with fibrous connective tissue, helping to hold the tissue together | Encapsulated |
| occurs with benign tissues because they remain tightly bound and do not invade other body tissues | Wandering (not migration) |
| Occurs in benign tumor cells even though their growth is not needed, but rate of growth is normal | Orderly growth |
| In orderly growth, benign tumors grow by this route and DO NOT INVADE other tissues | Hyperplastic expansion |
| Normally found in benign tumor cells; 23 pairs of chromosomes | Normal chromosomes |
| Occurs in many types of cancer cells because they re-enter the cell cycle for mitosis almost continuously | Rapid or continuous cell division |
| These type of cells do not respond to apoptosis and have an unlimited life span | malignant "cancer" cells |
| Enzyme that maintains telomeric DNA | Telomerase |
| A feature of cancer cells; lose specific appearance of their parent cells | Anaplasia |
| A feature of cancer cells; Nucleus occupies much of the space within the cancer cell | Large nuclear-to-cytoplasmic ratio |
| Lost partially or completely in cancer cells | Specific functions of cells |
| Typical for cancer cells because they do not make fibronectin and easily break off from tumor | Loose adherence |
| Occurs because cancer cells do not bind tightly together and have many enzymes on their cell surfaces; features allow cells to slip through blood vessels and tissues, spreading from main tumor site to many other body sites | Migration |
| The ability of a cancer cell to spread | metastasize |
| Does not occur in cancer cells, even when all sides of these cells are in continuous contact with the surfaces of other cells and allowing cell division to continue | Contact inhibition |
| Common in cancer cells; chromosomes are lost, gained, or broken; more than 23 pairs or fewer than 23 pairs; may have broken and rearranged chromosomes | Aneuploidy (abnormal chromosomes) |
| The use of strategies to prevent the actual occurrence of cancer | Primary prevention |
| The use of screening strategies to detect cancer early, at a time when cure or control is more likely | Secondary prevention |
| An effective primary prevention strategy; most effective when cause of cancer in known | Avoidance of known or potential carcinogens |
| Appears to have a positive influence in reducing cancer risk by changing behavior | Modifying associated factors |
| Modifying cancer risk behavior examples | 1) limit alcohol to 1oz/day, 2) include more fruit, veggies, and whole grains in diet, 3) limit number of sexual partners, 4) use safer sex practices to reduce exposure to viruses that can increase risk of cervical cancer |
| Reduces risk for a person who has a known high risk for developing a specific type of cancer | Removal of "at risk" tissues |
| Uses drugs, chemicals, natural nutrients, or other substances to disrupt one or more steps important to cancer development; agents may be able to reverse existing gene damage or halt the progression of the transformation process | Chemoprevention |
| Chemoprevention agents found effective in reducing risk of colon cancer | aspirin; celecoxib (Celebrex) |
| Chemoprevention agents found effective in reducing risk of breast cancer | vitamin D; tamoxifen |
| Chemoprevention agent found effective in reducing risk of prostate cancer | lycopene |
| Target populations for whom chemoprevention might be effective | 1) healthy ppl w/no known specific cancer risk; 2) ppl at > than normal risk bc of increased environmental exposure or decreased immune function, 3) ppl with precancerous lesions, 4) ppl with hx of cancer |
| A new method of primary cancer prevention; associated with virus prevention | vaccination |
| The only vaccine approved for cancer prevention | Gardasil |
| Prevents infection from several forms of HPV | Gardasil |
| Recommended screenings | 1) yearly mammo & clinical breast exam > 40 yrs; 2) colonoscopy at 50 y/o and then q10yr if normal; 3) yearly fecal occult for all ages; 4) yearly PSA and DRE for men > 50yrs |
| Gene mutation that increases risk for breast and ovarian cancer | BRCA1 gene |
| Gene mutation that increases risk for breast cancer only | BRCA2 gene |
| Gene mutations that increase risk for colon cancer | APC, MLH1, & MSH2 genes |
| Create when pt has a strong family hx of breast or colon cancer | 3-generation pedigree |
| Other names for cancer development | Carcinogenesis; Oncogenesis |
| The process of changing a normal cell into a cancer cell; | Malignant transformation |
| Malignant transformation occurs through these steps | Initiation, promotion, progression, and metastasis |
| The first step in carcinogeneiss;caused by damage to the genes | Initiation |
| Substances that change the activity of a cell's genes so that the cell becomes a cancer cell | Carcinogens |
| Forms of carcinogens | chemicals, physical agents, or viruses |
| The enhancement of growth of an initiated cell | Promotion |
| Substances that enhance growth of the initiated cancer cell | Promotors |
| Normal body components that can act as promoters and make altered cells divide more frequently | hormones and body proteins |
| The time between a cell's initiation and the development of an overt tumor, which can range from months to years | latency period |
| Exposure to promoters can shorten this period | latency |
| The continued change of a cancer, making it more malignant over time | Progression |
| A detectable tumor | 1-cm tumor that has at least 1 billion cells in it |
| Events that must occur for tumor to become a health problem | 1) Malignant transformation, 2) Tumor vascularization, 3) Blood vessel penetration, 4) Arrest and invasion |
| Tumor receives nutrition by this route during early stages (Less than 1 cm) | Diffusion |
| Produced by tumor; triggers capillaries and other blood vessels in area to grow new branches into the tumor ensuring the tumor's continued nourishment and growth | Tumor angiogenesis factor (TAF) |
| Benefits that allow tumor cell groups to live and divide no matter how the conditions around them change | Selection advantages |
| Original tumor; usually identified by tissue from which it arose (parent tissue) | Primary tumor |
| Occurs when cancer cells move from primary location by breaking off from original group and establishing remote colonies | Metastasis |
| The creation of additional tumors | Metastatic or secondary tumors |
| Secreted by cancer cells; open up areas of surrounding tissue and make large ores in blood vessels, allowing tumor cells to enter blood and circulate throughout body | Enzymes |
| Created as tumor increases in size and forces tumor cells to invade new territory | Pressure |
| Required for cancer cells to spread to distant organs and tissues | Penetration |
| Tumor cell release into the blood; most common cause of cancer spread | Bloodborne metastasis |
| Reason clumps of cells break off of primary tumor into blood vessels for transport | tumor cells are loosely held together |
| Occurs when conditions in remote site can support tumor cell growth and allows invasion of surrounding tissues, creating a secondary tumor | cells stop circulating (arrest) |
| Related to the number, structure, and location of lymph nodes and vessels; another way cancers metastasize | Lymphatic spread |
| Two major categories of cancer | Solid & Hematologic |
| Develop from specific tissues | Solid tumors |
| Arise from blood cell-forming tissues | Hematologic Cancers |
| Classifies cellular aspects of the cancer; needed because some cancers are "more malignant" than others, varying in aggressiveness and sensitivity to treatment | Grading |
| Classifies tumor by chromosome number and appearance (normal, abnormal) | Ploidy |
| Classifies clinical aspects of the cancer; determines exact location of cancer and its degree of metastasis at dx | Staging |
| Grade cannot be determined | G-x |
| Tumor cells are well differentiated and closely resemble normal cells from which they arose | G-1 |
| Tumor cells are moderately differentiated; they still retain some of the characteristics of normal cells but have more malignant characteristics | G-2 |
| Tumor cells are poorly differentiated, but tissue of origin can usually be established; few normal cell characteristics | G-3 |
| Tumor cells are poorly differentiated and retain no normal cell characteristics; determination or tissue origin is difficult/impossible | G-4 |
| Abnormal chromosome number and/or appearance | aneuploidy |
| Chromosome abnormality often present in chronic myelogenous leukemia cells | "Philadelphia" chromosome |
| Clinical Staging | Assesses pt's clinical manifestations and evaluates clinical signs for tumor size and possible spread |
| Surgical Staging | Assesses tumor size, number, sites, and spread by inspection at surgery |
| Pathologic Staging | The most definitive type; determines tumor size, number, sites, and spread by examination of tissues obtained at surgery |
| 2 types of specific staging systems | Duke's Staging of colon and rectal cancer; Clark's levels method of staging skin cancer |
| Developed the tumor, node, metastasis (TNM) system | The American Joint Committee on Cancer |
| Describes anatomic extent of cancers | Tumor, node, metastasis (TNM) system |
| The amount of time it takes for a tumor to double in size | Doubling time |
| The percentage of actively dividing cells within a tumor | Mitotic index |
| The number of doublings a tumor must undergo to reach the detectable size | 30 doublings |
| Slow growing tumor | mitotic index of less than 10% |
| Fast growing tumor | mitotic index of more than 85% |
| 3 interactions that influence cancer development | Exposure to carcinogens, genetic predisposition, and immune function |
| The main mechanism of carcinogenesis regardless of the specific cause | Oncogene activation |
| Damage suppressor genes, preventing them from controlling the expression of oncogenes | mutation of DNA |
| Occurs when oncogenes are over-expressed in a cell | Excessive amounts of cyclins are produced, upsetting the balance btw cell growth enhancement and cell growth limitation |
| The number of oncogenes that have been identified | 70 |
| Responsible for 80% of cancer in north america | external factors |
| Chemical, physical, or viral agents that can cause cancer | environmental carcinogens |
| Can occur from exposures to many known chemicals, drugs, and other products used in everyday life | chemical carcinogenesis |
| When taken together, they enhance each other's carcinogenic activity | co-carcinogens |
| The single most important source of preventable carcinogenesis; both initiates and promotes cancer | Tobacco |
| Causes cancer by the same mechanism as for chemical carcinogens; 2 types include radiation and chronic irritation | Physical carcinogenesis |
| 2 types of radiation that cause cancer | Ionizing; ultraviolet (UV) |
| Reason skin cancer is the most common type of cancer caused by UV exposure | UV rays do not penetrate deeply |
| Undergo frequent cell division and thus are at increased risk for spontaneous DNA mutation | Chronically irritated tissues |
| Occurs when viruses infect body cells and break the DNA strands | Viral carcinogenesis |
| Mutates normal cells' DNA and can either activate an oncogene or damage suppressor genes | Breaking the DNA and/or viral gene insertion |
| Viruses that cause cancer | Oncoviruses |
| Suspected dietary factors with cancer-promoting effects | low fiber intake, high intake of red meat, high animal fat intake, preservatives, contaminants, preparation methods, and additives (dyes, flavorings, sweeteners) |
| Protects body from foreign invaders and non-self cells | Immune function |
| The part of the immune system that protects against cancer | Cell-mediated immunity |
| Cells that provide important immune surveillance | Natural Killer (NK) and helper T-cells |
| The single-most important risk factor for cancer | Advancing age (>60yrs) |
| Available to confirm or rule out a person's genetic risk for a few specific cancers; performed on blood, expensive, often not covered by insurance; do NOT dx presence of cancer | Genetic testing for cancer predisposition |
| 2 main ethical issues associated with genetic testing for cancer predisposition | 1) who will have access to info, 2) whether or not to share results with family members |
| Reasons the American Cancer Society reports that cancer incidence and survival rates are often related to socioeconomic factors | availability of health care services or the belief that seeking early health care has a positive effect on outcome of cancer dx |
| Every normal cell has at least one special function it performs to contribute to whole-body function | Differentiated Function(s) |
| Occurs because normal cells make proteins that protrude from membranes, allowing cells to bind closely and tightly together | Tight Adherence |
| A protein that keeps most normal tissues bound tightly to each other | Fibronectin |
| Cells that do not bind together because they do not produce fibronectin | RBCs and WBCs |
| The feature that means normal cells do not wander throughout the body (except for blood cells) | nonmigratory |
| A strong feature of normal cells; they don't divide unless body conditions are optimal for cell division: need for more cells, adequate space, and sufficient nutrients and other resources | Orderly and well-regulated growth |
| Living cells that are actively carry out their functions by do not actively reproducing; reproductive resting state | G-0 |
| Makes one cell divide into 2 cells | mitotic cell division |
| Produce proteins that regulate the control cell cycle of mitosis | suppressor genes |
| Proteins that promote cells to enter and complete cell division; | cyclins |
| once activated, they first allow a cell to leave the G-0 state and enter the mitotic cycle | cyclins |
| Cyclins are produced | oncogenes |
| The cell is getting ready for division by taking on extra nutrients, making more energy, and growing extra membrane; cytoplasm increases | G1-phase |
| DNA doubles in content through DNA synthesis | S phase |
| Cell makes important proteins that will be used in actual cell division and in normal physiologic function after cell division an in normal physiologic function after cell division is complete | G2 Phase |
| The single cell splits apart into two cells (actual mitosis) | M-phase |
| The stopping of further rounds of cell division when the dividing cell is completely surrounded and touched by other cells | Contact inhibition |
| A feature of most normal human cells; 23 pairs of normal chromosomes | Euploidy |
| Harmless | Benign |
| Cancer | Malignant cell growth |
| 2 reasons for increase in cancer | 1) long life expectancy 2) increased exposure to substances that cause cancer |
| cell division | mitosis |
| Growth that causes tissue to increase in size by enlarging each cell | Hypertrophy |
| Growth that causes tissue to increase in size by increasing the number of cells | Hyperplasia |
| Any new or continued cell growth not needed for normal development or replacement of dead and damaged tissues; always abnormal even if it causes no harm | Neoplasia |
| Occurs because normal cells divide for only 2 reasons | Limited cell division |
| 2 reasons limited cell division occurs | 1) to develop normal tissue 2) to replace lost or damaged normal tissue |
| Programmed cell death | Apoptosis |
| Purpose of apoptosis | To ensure that each organ has adequate number of cells at the functional peak |
| The feature in which each normal cell type has a distinct and recognizable appearance, size, and shape | Specific morphology |
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