Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Cancer, McCance
Cpt 11,12
| Question | Answer |
|---|---|
| tumor | new growth, neoplasm. not all tumors or neoplasm are cancerous |
| cancer | malignant tumor, grow rapidly, not encapsulated, invade local structure/tissue, poorly differentiated, high mitotic index, can mets |
| benign neoplasm | can be life threatening depending on their location. slow growing, well-defined, well-differentiated, low mitotic index, do not metastasize |
| anaplasia | loss of cellular differentiation, loss of normal tissue structure result in cancer |
| adenocarcinoma | arise from or form ductal or gladular structures |
| sarcoma | cancer from connective tissue |
| lymphomas | cancer of lympatic tissue |
| leukemia | cancer of blood forming cells |
| CIS | carcinoma in situ, preinvasive epithelial tumors of glandular/squamous cell origin) NOT broke basement membrane!common in the cervix, skin, oral cavity, esophagus, bronchus. ex: ductal CIS of the mammary ducts. |
| transformation | (autonomy) process by which normal cells become cancerous |
| characteristics of transformed cancer cells | autonomous, immortal, anchorage independent, anaplasia, pleomorphism, defective differentiation |
| pleomorphic | variable size and shape of anaplastic cells |
| tumor cell markers | substances produced by cancer cells, found in/on tumor, or in blood, spinal fluid, or urine. Table 11-3, p. 368. hormones, enzymes, genes, antigens, antibodies |
| AFP | alpha fetoprotein, secreted from liver & germ cells ; tumor marker |
| neoplasia | abnormal / uncontrolled growth of cells which result in neoplasm |
| naming tumors | named according to the cell type from which they originate, -oma if benign. -carcinoma if cancer. Review table 11-2, p. 364 |
| carcinoma | cancer arising from epithelial cells |
| adult stem cell | 1)self renew, 2) multipotent-differentiate. asymmetrical division-divide into another stem cell and the other one is differentiates depending on need. |
| cancer stem cells | cells that propogate cancer/tumor growth; cancer grows back if stem cell isn't killed during treatment |
| mesenchymal stem cell | normal adult stem cell that theoretically can differentiate into all body cell types |
| advantage of TCM (tumor cell markers) | 1) screen/ identify high risk pt. 2) help in diagnosis 3) follow clinic cours of disease-should be < if tx effective. NOT used alone to dx. |
| disadvantage of TCM | can't be used soley for diagnosis b/c nonmalignant conditions can > TCM |
| > catecholamines | suggest pheochromocytoma (adrenal medullary tumor) |
| PSA | prostate specific antigen; prostate |
| epigenetics | heritable changes in gene expression |
| clonal proliferation | or clonal expansion; as a clone with a mutation grows, it may become an early stage tumor |
| stepwise accumulation | accumulation of more genetic hits; the more mutations a cell has-the bigger the neoplasm/cancer |
| causes of cancer cell growth | 1) secrete growth factor, 2)increase in growth factor receptors, 3) mutated to "on" position, 4) RAS, 5) mutated antigrowth signal, 6) disabled apoptosis |
| autocrine stimulation | cancer that secrete growth factor that stimulate their own growth |
| RAS | signaling protein; stimulate cell growth even when growth factors are missing |
| angiogenesis | advanced cancer that stimulate new blood vessels |
| angiogenic factors | vascular endothelial growth factor-VEGF, platelet-derived growth factor-PDGF, basic fibroblast growth factor-bFGF; recruit endothelial cells and intiate proliferation of existing blood vessel cells that allow sm ca cells to become lg ca. |
| Hayflick limit | non-immortal cells; limited # of times a cell can normally divide. |
| telomerase | normally only in germ cells , but cancer cells activate to restore shortened telomeres so that cells can continue to grow (immortality of ca cells.) |
| proto-oncogenes | normal, nonmutant state of a gene; regulate growth & development by encoding growth factors or growth factor receptors |
| oncogenes | mutant genes that encode protein that promote growth by overexpression, amplification, gain of function. Dominant-one hit activates- 1) point mutation, 2) amplification 3) translocation |
| tumor suppressor genes | recessive oncogene; encodes protein that inhibit proliferation and prevent or repair mutations. require loss of both alleles to be inactivated and mutation/cancer to form-recessive; 1)point mutation, 2)silenced or LOH |
| point mutation | small scale changes in DNA |
| RAS protein | normally a proto-oncogene-inactive RAS exchanges GDP for GTP and is activated-active RAS sends growth signals. normally turns off when GTP turns back into GDP. oncogenic RAS stays "on". common in ca; esp. pancreatic and colorectal |
| chromosome translocation | one piece of a chromosome translocated to another chromosome. |
| Burkitt lymphoma | ex of translocation. t(8;14) Aggressive ca of B lymphocytes. myc proto-oncogene (8) and Ig (14) translocate & myc oncogene causes ca of B cells b/c myc doesn't turn off |
| MYC protein | part of positive signal for cell differentiation |
| myc gene | chromosome 8; on in growing lymphocytes-off when they mature |
| Ig | B cell immunoglobulin; actice in maturing lymphocytes; |
| ex of translocation mutations | Burkitt lymphoma, t(8;14). CML, t(9;22) |
| gene amplification | over duplication of gene, more than 2 copies. N-mic oncogene-childhood neuroblastoma. erbB2-breast ca. Also contributes to drug-resistance genes, but erbB2 breast ca responds well to targeted drug therapy |
| Rb gene | retinoblastoma; strongly inhibits cell division cycle. |
| childhood retinoblastoma | caused by inactivated RB gene. |
| loss of heterozygosity | loss of a chromosome region in a tumor; unmasks inactivation mutations in recessive tumor suppressor genes. 2nd copy is not there? |
| silencing | epigenetic; inherited gene expression that causes DNA methylation that turns off whole sections of chromosome. doesn't require mutation of gene-it's inherited that way. changes in gene silencing contribute to ca: > methylation in tumor suppressor gene |
| genetics and cancer | genetic ca events occur in somatic cells-they are not inheritable; but can inherit the mutation that predispose to ca. (usually affect tumor-suppressor gene such as LOH or silencing. |
| inheritable cancer | retinoblastoma-Rb gene; Wilms tumor-kidney; neurofibromatosis; inheritable breast ca-BRCA-1; familial ademoma of colon ca-APC. all inactivated tumor suppressor genes |
| Chronic inflammation & ca | ulceritive colitis; hepatitis; chronic asthma. cytokines: TNF-a, IL-6, IL-10 enhance tumor growth, angiogenesis, mets & suppress anti-tumor immunity. chronic-no stop in wound healing process. tumors activate same factors=tumor growth/angiogenesis. |
| anti-tumor immunity | IL-12= NK cells, CTL (cytotoxic T lymphocytes), IL-12 & IL-23=cytotoxic cytokines( IFN, TRAIL, TGF-b) |
| ROS | reactivce oxygen species in chronic inflammation-promote mutation and block DNA repair |
| COX-2 | enzyme cyclooxygenase-2-generates prostaglandins during inflammation. assoc w/ colon ca. NSAIDS block COX-2 |
| TRAIL | TNF-related apoptosis inducing ligand. antitumor |
| TNF | tumor necrosis factor |
| Invasion | local spread; prereq for mets. 1)ca proliferation 2)protease digest connective tissue capsule 3) adhesion changes (cadherins, integrins) 4) increased motility of ca cells |
| METS promotion | deatach, & invasion by neoangiogensis and lymphangiogenesis; survival in circulation; attach & grow in new site. most ca cells can't cause mets; those that do have > heterogeneity |
| detachment of ca cells | proteases and protease activators-digest extracellular matrix & basement membrane-pathway for ca to move; MMP-matrix metalloproteinase, plasminogen activators; also many protease that block cancer |
| EMT | epithelial-mesenchymal transition; loss of E-cadherin so that ca cells can detach for easier migration |
| anoikis | form of apoptosis that occurs when cells seperate from extracellular matrix (ECM). but tumor cells can resist apoptosis |
| WHO staging cancer | Tumor, Nodes, Metastases |
| Carcinoma in situ staging | 1) organ confined 2)locally invasive 3) regional structure-lymph nodes 4) distant sites |
| paraneoplastic syndrome | symptoms triggered by cancer, but not caused by tumor; hormones released by the tumor, table 11-12, p. 389 may be earliest sx of ca and life-threatening |
| fatigue | most frequent reported symptom of ca and treatment. consequence of metabolc products, of cancer treatment and muscle loss from cytokines (TNF, IL-1) |
| cachexia | anorexia, early satiety, wt loss, anemia, asthenia (marked weakness), alt taste/ metabolism. servere form of malnutrition even with adqut diet. alt metabolism r/t cytokines: TNF-a, IL-6, IFN-y and tumor metabolites. hyperinsulinemia, IR, hyperglycemia. |
| anemia | hgb < 9; chronic bleeding, iron deficiency. lack of iron transfer from storage pool to blood precursors-> IL6, hepcidin. defect in erythropoietin |
| erythropoeitin | stimulate production of erythrocytes; reserved for significant ca-related anemia due to risk of blood clots. |
| leukopenia | < total WBC, invasion of tumor to bone marrow or toxic side effect of chemo |
| thrombocytopenia | < platelets-invasion of bone marrow, chemo S.E.; cause hemorrhage-need platelet transfusion, accompany DIC w/ acute promyelocytic leukemia |
| granulocytopenia | neutropenia-no neutrophils. radiation or chemo tx. lessen w/ recombinant human granulocyte colony-stimulating factor (rhG-CS, filgrastim) stimulates WBC to proliferate and differentiate faster < 500: > infection chances |
| stomatitis | oral ulcers; < cell turnover from chemo/radiation |
| serotonin 5-HTP antagonist | ondasetron (Zofran) PO, IM, IV; dolasetron (only po form) for nausea symptoms r/t treatment |
| reproductive affect of tx | affect gametes-< fertility, early menopause. alkylating chemotherapy agents-greatest risk. craniospinal irradiation: CNS tumors-affect hypothalamus-pituitary gland: gonad failure r/t no GRH, LH, FSH. |
| tobacco use r/t what type of ca | lower urinary tract, upper aerodigestive tract, liver, kidney, pancreas, cervix, uterus, myeloid leukemia. squamous and small cell adenocarcinoma. Lack evidence of breast, prostate & endometrial ca. |
| Diet and ca | < folate r/t development of colorectal ca, but after tumor folate causes growth. Diet affects mylenation changes in DNA. SFN can inhit histone modifications: sulforaphane found in cruciferous vegetables: broccoli/sprouts |
| Obesity and ca | insulin resistance, hyperinsulinemia, increase growth factors, increased steroids, hormones, cytokines. Adipose tissue releases fatty acids. insulin & IGF promote growth, and inhibit apoptosis. Colon, breast, prostate, pancreatic, endometrial ca. |
| insulin resistance | > fatty acids, resistin, TNF-y, < adiponectin |
| Alcohol and ca risk | oral cavity, pharynx, hypopharynx, larynx, esophagus, liver. possible breast and colorectal ca. > interaction with smoking. early 60's laryngeal ca. |
| atomic bomb exposure | thyroid, breast ca, as well as lung, stomach, colon, esophagus, urinary tract & acute leukemia: latent period of 20 yrs. ex of ionizing radiation, same as x-rays, radioisotopes. |
| UV radiation | sunlight CAUSES basal cell ca (p53)(head/neck; light complex, burn easily, high sun exposure), squamous cell ca(p16)(outdoor working men, head, neck, arms.) mutate TP53 gene, release TNF-a in epidermis-reduces immune, ROS |
| carcinoma | cancer of epithelial tissue (ex: squamous cell line major organs) |
| ACTH | hormone tumor marker-pituitary adenoma |
| PSA | antigen tumor marker-protate |
| CEA | carcinoembryonic antigen, GI, pancreas, lung, breast |
| b-HCG | germ cell tumor marker |
| catecholamines | tumor marker-adrenal medulla; pheochromocytoma |
| p-53 | most common mutation that causes resistance to apoptosis, UV light can mutate p53 |
| pain | none or little in beginning stages, but affect terminally ill. |
| infection | most significant cause of complication/death in individual w/ malignant disease. |
| irradiation | affect fertility. (prepubertal-most resistant). brain rad: affect hypothalamus/pituitary-cause gonad failure |
| HPV-16 | account for 50-60% of cervical ca |
Created by:
Sniffen group
Popular Physiology sets