ONCOLOGY

HEMALYMPHATIC SYSTEM Hema -blood circulation; blood vessels, capillaries, heart Lymphatic -Vital part of immune system for controlling infection -Lymphatic glands collecting waste product; lymph vessels LYMPH AND BLOOD are the key mechanism by which cancer cells spread Lymph is like a slow river Maam Ascue (Washes cells; correct foreign bodies/substances) INFLAMMED LYMP NODES Lymphatic Vessles ->Lymph Nodes (w/ lymphocytes *produces) *recognizes Antibodies Foreign Bodies/Substances *attack! *sending signals Immune system MODE: SPREAD OF TUMOR CELLS I. Lymphatic Spread(most common) -through lymphatic system *Tumor cells invading lymphatic vessels goes through lymphatic fluid II. Hematogenous Spread -via blood stream -directly related to the vascularity of the tumor III. Tumor Seeding -growth of tumor on adjacent sites ANGIOGENESIS -formation of new blood vessels 1. /Cancer humor cells/ produces VEGF (Vascular Endothelial Growth Factor) 2. /Cancer humor cells w/ blood vessel growth/ ?why need blood vessels? (tumor cells are always hungry) 3. /Tumor growth/ this time it can pass through the blood vessels IMMUNE SYSTEM Lymph nodes -groin, neck, chest, underarm, abdomen -lymph= 5 gallons inside our body Tonsils -filters bacteria in the mouth (dirtiest and most infectious) Spleen -filters dead RBC of blood Appendix -is stores good flora in the intestines Thymus -produces T-cells IMMUNE RESPONSE 1. /Normal Cells->Cancer cells/ releases /Tumor Specific Protein/ 2. Tumor specific protein is recognized by /antibodies/ 3. /antibodies/ alarming immune system resulting to release of 4. /T-cells, macrophage, cytotoxin cells, Helper T-cells/ DIFFERENTIATE CELL STRUCTURES NORMAL CELL STRUCTURE -large cytoplasm -single nucleus -single nucleolus -fine chromatin

CELL CYCLE Prophase Metaphase Anaphase Telophase

G1 S G3 G4

DNA and Protein synthesis Synthesis RNA and Protein Synthesis Division ; Apoptosis

ONCOLOGY: NURSING MANAGEMENT IN CANCER

CANCER -group of distinct disease with diff. causes, manifestations treatment and prognosis ONCOLOGY NURSING -the scope, responsibilities and goals of cancer nursing -support patients and families through a wide range of physical and emotional, social, cultural and spiritual crisis EPIDEMOLOGY OF CANCER -2nd leading cause of death in US (1st is CVA) -affects people of all ages (65 and up) -common in men and industrialized countries -3rd leading cause of death in RP CARCINOGENIC AGENTS -virues (Epstein-barr) -bacteria -physical factors -chemical factors

-Diet -Hormone -Genetic; Familial Factors

ROOTS WORDS: Neo- new Plasm- substance Statis- location Meta- change Toma Tumor Onco- Swelling/mass

Plasia- to shape Trophy- nourishment A- none/without Dys- bad/abnormal Carcin- cancer

PATHOPHYSIOLOGY 1. /abnormal cells/*transformed by genetic mutation of the cellular DNA; forms clones and proliferated anormally 2. /ignoring growth-regulating signals/*environment surrounding cells; cells acquire invasive characteristics and changes occur in surrounding tissues 3. /cells infiltrate tissues/*gaining access to lymph and blood vessels; carry cells to other areas of the body 4. /metastasis/ cancer spreas CANCER CELLS are MALIGNANT NEOPLASMS -uncontrolled cell growth that follows no physiologic demand -the degree of anaplasia determines the malignant potential Benigh Malignant Well differentiated undifferentiated Slow growth Erratic growth/uncontrolled Encapsulated Expansive and invasive Non-invasive Secretes abnormal proteins Does not metastasize metastasize CHARACTERISTICS of MALIGNANT CELLS -cell membrane altered-> affects fluid movement; in and out -> contains tumor specific antigens (CEA) Carcinoembryonic agents (PSA) Prostate specific antigen -> TSA distinguishes malignant/benign; measure extend of disease -> less FIBRONECTIN (cellular cemenent less cohesive; not adhere to adjacentcells -small chromatin -multiple nuclei (large and irregularly shaped) -Multiple and large nucleoli (houses RNA) -coarse chromatin -frequent mitosis (more glucose and O2 needed -> Metabolic anaerobic channels -> energy ) *cells less dependent of 02 INVASION AND METASTASIS -mechanical pressure exerted by rapid proliferating neoplasm -> finger like projection of tumor cells -less adherent and may break off and invade adjacent tissues -produces specific destructive enzymes: protenases, collagenases, plasminogen activators -destroys vascular basement membrane =INVASION MECHANISM OF METASTASIS 1. Lymphatic Spread Tumor emboli (*interstitial fluid) -> Lymphatic fluid -> Lymphatic Circulation (*lodge) -> Lymph nodes Malignant Cells(*invade) -> Lymphatic vessels BREAST CANCER-through axillary, clavicullar and thoracic lymph channels 2. Hematogenous Spread -xLess O2 XImmune System XTurbulence -attaches to endothelium (*allows invasion on basement membrance) -> attract fibrins -> platelets to cover CARCINOGENESIS (MALIGNANT TRANSFORMATION) 3 PROCESS: Initiation, Progression, Promotion Initiation -Initiators (carcinogens) escape normal enzymatic mechanism= alter genetic structure and DNA -reversd DNA repair mechanism apoptosis Promotion -repeated exposure to promoting agents causes mutant genetic informations Cellular Oncogenesis- Responsible for vital cellular functions of growth and differentiation Cellular Proto-oncogenes- on swatch = PROLIFERATION o Cellular Proto-oncogenes ON (Cellular Growth) o Cancer Supressor Genes OFF regulate unneeded cellular proliferation = malignant cells are allowed to reproduce Progression -increased malignant behaviors *CARCINOGENS!- initiate/promote cellular transformation

CANCER CELL STRUCTURE -small cytoplasm -multiple nucleus -multiple nucleolus -coarse chromatin

CELLULAR ABNORMALITIES Anaplasia -lack of differentiation of neoplastic cells Atrophy -decrease in size of cells, decrease size of affected tissues, wasting Dysplasia -bizarre cell growth resulting in cells that differ in size and shape Hypertrophy -increase in size of cells without division Hyperplasia -increase in number of cells, most often associated with rapid body growth Metaplasia -conversion of one cell to another cell Apoptosis -self-destruct

 ETIOLOGY VIRUSES AND BACTERIA -infections causes are suspected when specific cancers appear in clusters -incorporate themselves in genetic structures -EPSTEIN BARR VIRUS: Burkitts Lymphoma, Nasopharyngeal cancer, Hodgkin Lymphona and Non-Hodgkin -HSV2, Cytomegalo Virus: dysplasia, cervical cancer -Hepa B and C: Liver cancer -HIV: Kaposis Carcoma -Helicobacter Pylori: Gastric Malignancy PHYSCIAL AGENTS -radiation: leukemia, multiple myeloma, cancer lung, bone, thyroid and breast - chronic irritation/inflammation -tobacco -Excessive UV rays: on fair skin and blue/green eyes CHEMICAL AGENTS -75% are thought to be related to environment -Tobacco smoke 30% of cancer deaths: neck, lung, head, esophagus, pancreas, cervix, bladder -Synergestic effect: Tobacco + Alcohol, Asbastos, Uranium, Viruses -Amines, Aniline Dyes, Pesticides, Formaldehydes, Arsenic, Tars, Nickel, Zinc Ores GENETIC AND FAMILIAL FACTORS -genetics, harsh lifestyle and environment -too few chromosomes, extra chromososmes, translocated chromosomes -GENETIC: Burkitts Lymphoma, Chronic Myelogenous Leukemia, Meningiomas, Acute Leukemias, Retinoblastomas, Wilms Tumor -FAMILIAL: Retinoblastomas, Nephroblastomas, Phenochromocytomas, Ovarian Cancer DIETARY FACTORS -can be proactive, carcinogenics or cocarcinogenics long term ingestion -fats, alcohol, smoked meats, nitrate, nitrate content, salt cured -HIGH RISK: increased calorie intake, obesity -LOW RISK: high fiber food, cruciferous vegetables HORMONAL AGENTS -endogenous hormonal levels for growth: breast, prostate, uterus -Oral contraceptives + Prolonged hormonal replacement ( hepatocellular cancer, breast and endometrial) *decreased risk of Ovarian -hormonal Therapy (breast, CHD, stroke, blood clots ) TYPES Named according to embryonic cell origin Carscinoma- Ectodermal, endodermal, glandular epithelial Sarcoma- Mesodermal