Cancer Introduction – Flashcards

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Cancer process
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Chronic disease of gene mutation breakdown of normal growth controls cell undifferentiation malignant neoplasms- demonstrate uncontrolled cell growth that follows no physiologic demand
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cell undifferentiation
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(can't tell difference b/w cancer/normal cell, becomes "spy" in world of cells)
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cont'd
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Cancer is a Chronic disease, need to be treated over time Born with certain gene, and can have mutations based on certain lifestyles
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Cancer Epidemiology who does it effect?
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2st most common cause of death overall Recent decrease in male death rates Risk increases with age in most cancers (long-term exposure, and immune system isn't as strong) Rate and mortality higher in African American, but 2008 decrease due to smoking
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in overall death rates, survival rates due to: 1o prevention
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early detection through screening more effective treatment
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prevent 2o disease and recurrence
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mortality from other causes--ie, heart
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Genetic Influences Heredity—predisposition
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Genes we are born with are different from the genes we have now Pass down through family Break, gas pedals
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Somatic--acquired
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Initiation, progression, metastasis -cancer happens in phases over a long-period of time (takes a long-time to develop)
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process?
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Series of mutations changing normal genotype to cancer genotype then cancer phenotype ( that's when it starts to present itself as cancer)
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Immunologic—altered defense
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Immune system can't kill off cancer cells Aging (immune system gets weaker as people age) Immunosuppression (meds/conditions that suppress IS)
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Genetic mechanisms/mutations -DNA -proto-oncogene -supressor gene
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DNA repair mechanisms don't work Proto-oncogeneoncogene (gas pedal) Supressor genes (break pedals—2-hits required)
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Genomics
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Hereditary mutations? Acquired mutations? Much unknown Research area
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pharmacogenetics -
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if have a hereditary mutating, have the genotype is there a medication that can prevent it from mutating and becoming a phenotype
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We are in a constant state of gene mutation So they why don't we get cancer all the time?
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b/c we have mechanisms in body to kill off cell in mutates (points in cell cycle)
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G0- We've mapped the genome so have a better understanding of hereditary mutations/ and somatic Still a lot that we don't know
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is when cell is not in division (doing its job, heart cell) If cells die need to replace themselves so flip into mutation
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G1 and G2
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G1 and G2 are resting states, check-off times to see if everything well
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Red-lines -
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times for apoptosis, if DNA not ok or mutation cell thrown into cellular death (normal process)
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S phase
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when organelles/DNA duplicate
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DNA repair mechanisms
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So when DNA repair mechanisms don't work that's when cancer wins, can stop the apoptosis
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Suppressor genes-
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which will prevent cancer form happening BRAC1/2, if they don't work get cancer So need both "brakes" to go out, two mutation is the gene to get cancer
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Proto-oncogenes
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Proto-oncogenes are born with them- if triggered by something go from dormant proto to bad guy oncogene (causes the cancer of cell) -only need one gene
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Initiation—initial mutation
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irreversible alteration of cell's genetic structure (apoptosis stops it) caused by carcinogens (being exposed to just one carcinogen doesn't mean you will get cancer but exposed to many over time may prevent apoptosis from working)
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Promotion
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—continued mutation and growth (b/c apoptosis hasn't worked) reversible proliferation of altered, initiated cells caused by promoting factors (things that help the cancer grow) So if get rid of promoting factors the immune system will be able to kill off the cell
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Progression—
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-continued mutation and spread (point where precancerous cells become cancer cells, diagnosed with cancer) increased growth and invasiveness Metastasis (when cancer spreads throughout body)
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Chemical
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asbestos, cigarette smoke, drugs (e.g., immunosuppressive agents, DES, anabolic steroids (get leukemia), dietary (e.g., nitrites(processed cold cuts, bacon, any smoked food), ETOH Vaginal, AML, Non-Hodgkin's lymphoma, multiple myeloma, lung
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Physical
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radiation (ionizing—α/radon,inhalation; γ/external; ultraviolet), foreign bodies (e.g., cigarette/pipe smoke), chronic irritation (e.g., UC, Crohn's, GERD) Leukemia, lymphoma, thyroid, bone, lung
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Viral Familial—
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viruses--HIV, Epstein-Barr, HPV mutation passed down in families
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Ionizing radiation
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is associated with cancer (Radon) internal alpha radiation that I inhaled or that you are physically exposed to (important to have house radon tested)
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Promotion-
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Promotion- so got gene mutation this would stop apoptosis, affect the oncogene and environment of cell Basically stop the good guys and help the bad guys
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Promoting Factors all preventable
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stress obesity dietary fat smoking alcohol
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Genetic impact: Time-dependent
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affect oncogenes and/or supressor genes affect DNA repair—enzymes for metabolism or apoptosis Time-dependent—multiple hits
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Progression-->Metastasis
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Pathogenesis—continued breakdown of normal cell checkpoints/characteristics
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"angiogenesis"-- lack of "contact inhibition" "adherence"--
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angiogenesis"--circulation for growth lack of "contact inhibition" "adherence"--group together
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"diapedesis"-- Invasion—
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"diapedesis"--cross into tissue Invasion—secretion of destructive enzymes spread through CV and lymphatic systems angiogenesis
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How Cancer works:
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Have mutated cells that band together and create separate circulation apart form rest of cells around it and that celled ANGIOGENESIS Then b/c is has that separate circulation the ABC don't see it, hides in plain site-so keeps growing so it loses CONTACT INHIBITION, cancer doesn't stop growing and takes over the area -They band together and ADHERE to each other, DIAPEDSIS theres little fingers (Cancer cells) on outside periphery of the tumor will slowly start taking over good cells (will eat all the food for the good people for themselve, starve good guys) -they go around secreting destructive enzymes and killing the good people (INVASION), once big enough a small group will break off and spread through lymph or cardiovadic system (METASTOSIS) and starts ANGIOGENSIS AGAIN!
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Benign- The name of cancer is contingent on originating tissue
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- not cancer, overgrowth of cells, has own characteristics, but doesn't metastasis, -omas
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Malignant cells
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- do metastisis, carcinoma or sarcoma
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Originating anatomical site, Tissue type Carcinomas-- Sarcomas-- Adenocarcinomas-- Lymphoma—
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--epithelial tissues --connective tissues -glandular tissues (cancer) —lymphoid tissue (cancer, breaks rule)
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Leukemia— Multiple myeloma— Neuroblastoma— Meningeal sarcoma—
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—blood forming tissues, WBC(cancer) —plasma (cancer) —nerve cells —meninges
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Stage
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Stage- the degree of metastosis, how far the cancer spread (Stage 0-IV ,local, regional, extensive, widely spread) The higher the # the more it spread
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Grade-
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is what the cell looks like, compare those cells to what the normal cells look like to original tissue from that area If lower grade then cells still look a lot alike, grade 4 cells look really different hard to sometimes hard to tell where cancer is from
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Unknown primary
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- means don't know what originating tissue, and this is dependent on treatment regiment to know place Ex: woman has Grade 4 cancer in abdomen, don't know if colon or ovarian cancer, since cancer crosses over both of tissues
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T, N, M
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T (size of tumor) N (nodal involvement, gives idea of spread) M (degree of metastisis),(1-4, +/-, X/0/1)
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Primary Prevention Strategies
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Stop Smoking/low alcohol/Sunscreen Exercise--moderate 30-60 min, 5 days/wk (25%) Maintain a healthy weight (35% obese) since adipose tissue hold estrogen linked to many cancers Nutrition—Repair/prevent damage (research!) 5 servings of fruit/veges a day a (colorful!) (24%) Low saturated fats High fiber (works at cellular level of colon) low salt-cured, smoked, nitrate-cured foods, processed & red meats Pharmacogenetics—research area!!! 1/3 Cancer deaths are related to activity/nutrition
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Secondary Prevention
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SCREENING, need to target the people who are at risk and screen them NANDA Deficient Knowledge (risk?) Altered Health Maintenance (need behavior change?) NOC Health Seeking Behavior Knowledge: Health Behavior NIC Health Screening/genomic screening Health Education Referral/Health System Guidance Diagnostic Testing
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CAUTION: need to know!
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Change in bowel or bladder habits (colon, bladder) A sore that does not heal (since don't have WBC to fight infection,leukemia) Unusual bleeding or discharge from any body orifice (vaginal, nipple) Thickening or a lump in the breast or elsewhere Indigestion or difficulty in swallowing (esophageal, stomach) Obvious change in a wart or mole (skin) Nagging cough or hoarseness (lung, laryngeal (hoarseness would affect speech since in larynx near vocal cords), if doesn't go away within 1wk/dry cough
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ACS Screening Guidelines NEED TO KNOW!
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Breast Cervix Endometrial
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Breast—BSE monthly, annual mamogram >40 Cervix= 18 yo, when become sexually active Endometrial—report spotting, inbetween periods
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Colon Prostate Physical check-up
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Colon50, fecal occult blood, sigmoid Prostate=50 yo, annual DRE, PSA (is a recommendation to get screened not a requirement) Physical check-up—periodic, MD determined based on risk factors
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how to diagnose cancer?
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Only way to diagnose cancer is BIOPSY, look at tissue under microscope -all tests sued to identify if have mass, where is it, and whats the nature of the mass
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Diagnostic Testing : Tumor markers— Genetic Profiling
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blood tests, look for tumor-made substances (antigens unique to cancer cells)
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MRI/CT/Fluoroscopy
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MRI/CT/Fluoroscopy (dye taken up) /Ultrasound/Nuclear medicine imaging (dye that sticks to antigens outside of tumor)—images
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PET Scan
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--marks biological activity, used to detect at early phase or measure response to treatment (do scan before/and after treatment to see if decrease in biological activity which would be good (doesn't measure outline of tumor but biological activity of it)
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PET fusion
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--outlines tumor and indicates biological activity
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Radioimmunoconjugates
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--monoclonial antibiodies attach to tumor for visualization (we can add to the good guys to affect the cancer treatment)
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Endoscopy
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Endoscopy--direct visualization (most invasive, surgery/biopsy ex:colonoscopy)
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what is physical care based on?
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on treatment plan on type of cancer
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Psychological Care
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NANDA Ineffective Coping Fear/Anxiety/Death Anxiety Grieving NOC Coping Anxiety Level NIC Coping Enhancement Family Support
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Pain (Acute and/or Chronic)2nd most common fear in Cancer Patients
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NOC Pain Level (tolerance, dependence, addiction) Psychological Response to Pain Disruptive Effects of Pain NIC Pain Management (atc and breakthrough) Non-pharm—affects modulators Relaxation Therapy, Imagery
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pain level
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Always treat the pain, and may need a lot of more medication (morphine) -need to make sure don't get constipation Dependence-is a physical need
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Pain management
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Have atc (around the clock) could be on drip, so constant blood supply of opoid If pt anticipates an activity that will cause more pain will take additional meds for the "breakthrough" pain
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PhysicalProcess: Nocioceptive
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Opoids work egenrally at transmission and perception
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Individualize plan
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People can be born with more pain receptors, so means not everyone can have the same dose of meds
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NIC: Pain Management
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Chronic pain protocol—WHO tx plan Tissue damage Ceilings—7 days tolerance—reassess, ∆ dose/meds Reach very high doses combination plan -atc AND breakthrough! GIconstipation Collaboration (patient and HCP) Non-Pharmacological therapy potentiating modulators/ inhibitory modulators
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goal
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Prevention and Control rather than Treatment
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WHO Treatment Plan
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Step 1: Nonopioids-mild pain NSAIDs, Acetaminophen, adjuvants Step 2: Opioids-mild/moderate pain Codeine, Vicodin, Tylenol #3 Step 3: Opioids-moderate/severe pain Morphine, Dilaudid, Demerol, Duragesic patches, Fentanyl
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Social Care
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NANDA Ineffective Role Performance Caregiver Role Strain Social Isolation NOC Role Performance Psychosocial Adjustment: Life Change Caregiver Lifestyle Disruption NIC Role Enhancement Support System Enhancement/Caregiver Support Family Involvement Promotion
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Spiritual Care
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NANDA Grieving/Anticipatory Grieving Spiritual Distress/Hopelessness Decisional Conflict NOC Grief Resolution Spiritual Well-being/Hope Decision Making NIC Grief Work Facilitation Spiritual Support/Hope Instillation Decision Making Support/Patient Rights Protection
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Initiation
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intiators (carcinogens) escape the normal enzymatic mechanisms and alter genetic structure of DNA
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promotion
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repeated exposure to carcinogen
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pro-oncogene suppressor genes
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just as pro-oncogene "turns on" cellular growth supressor genes "turn off" or regulate uneeded cellular proliferation
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TP53
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-tumor suppressor gene, determiens if cell lives or dies mutation of this decreases apoptosis signals and increases the incidence of cancer cells, BAD
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prophylatic surgery
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involves removing non-vital tissues/organs that are at increased risk of developing cancer
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two types of ionizing radiation electromagnetic: particulate
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x-rays, gamma beta, protons, neutrons, alpha particles
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both lead to
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tissue disruption
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teletherapy= external ebam radation why given over period of weeks?
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allows healthy tissues to prepair, achieve greater cell kill -also allows for periphery of tumor to be reoxygenated, which increases radiosensitivity
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chemotherapeutic agents
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affect the S phase by interfering with DNA/RNA synthesis
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septic shock S/S
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altered mental status change in temp cool/clammy skin dec. urine output hypotension, tachycardia
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since cancer causes thrombocytopenia watch for
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bleeding hemmorhage count of less than 100,000
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