Secondary preventions: Also called early detection >> good prognosis Detection of precancerous lesions Methods: inspect, palpate,

te, & use of tests/procedures Premalignant lesions can be removed Cancer can be treated earlier Screening programs Objectives: 1. Identify high-risk population 2. Breast cancer BSE 3. testicular cancer TSE 4. Prostate cancer PSA (prostate specific Ag); digital rectal exam 5. Colorectal cancer FOBT (fecal occult blood test) Recommendations for early detection t Cancer-related check up: Age 20-40 q 4 yrs; 40 q yr t Breast

40: annual mammogram & clinic breast exam & monthly BSE 20-39: clinic breast exam q 3 yrs & monthly BSE Personal or family history of breast, endometrial,ovarian cancer

50(M&F): follow 1 of the suggestions 1. FOBT q yr & flexible sigmoid copy q 5 yrs 2. colonoscopy q 10 yrs 3. Double-contrast barium enema q 5-10 yrs 4. Black 5. Age above 40 6. Family history 7. Personal history of ulcerative colitis, crohns ds for more than 10 years 8. High fat diet 9. Excess alcohol intake Prevention of colorectal cancer 1. High fiber, low fat diet 2. Avoid salt cured or nitrite cured foods 3. Avoid obesity 4. Annual occult exam above 50 yrs old 5. Digital rectal exam for 50 years and above 6. Sigmoidoscopy every 5-10 years 7. Total colon exam every 510 years

t Prostate (male) 50: annual PSA & digital rectal exam Earlier to high risk men Never married, no children, or Increasing age first child after age 30 African-american Early menarche and late population menopause Family history History of fibrocystic disease Exposure to cadmium, Triad of diabetes, obesity, fertilizers, rubber hypertension Sexual behavior Prevention of breast cancer Change in bladder habits t Monthly BSE age 18 and older Diet high in fat t P.E. yearly Excess alcohol intake t Yearly mammogram at after Prevention of prostate cancer age 40 Annual digital exam above t Avoid high-fat diet and obesity 40 years old Test for prostate specific antigen (PSA) and t Colon & Rectum (colorectal) transrectal ultrasound

t Uterus

Cervix: annual PAP smear & pelvic exam for all women who are or who have been sexually active or who are 18 PAP smear may be done less frequently after 3 successive satisfactory results Endometrium: endometrial tissue sample exam after menopause Skin Risk factors Light complexion, red hair with freckles Frequent exposure to sun or tanning parlors

Occupational exposure to chemicals, pesticides Frequent exposure to radiation Precancerous lesions Genetic predisposition Change in mole

Skin cancer Prevention Limit sun exposure between 10am to 3pm Cover exposed skin Apply spf 15 or more Be aware of meds that inc photosensitivity Cleanse skin after use of chemicals Wear protective clothing if exposed to chemicals Lung cancer Risk factors Habitual smoker Side stream smoker Exposure to environmental carcinogens Family history of cancer Prevention of lung cancer Do not smoke or stop smoking

Wear protective clothing and masks Medical check-up if high risk Testicular Cancer Risk factors Young, white males (15-40) History of cryptorchidism Testicular atrophy after mumps Personal history Trauma History of inguinal hernia Maternal history of ingestion of diethylbestrol during pregnancy Prevention of testicular cancer Testicular self examination monthly Orchiopexy before age 2 years Cervical cancer Risk factors Early sexual activity, multiple partners Genital infections (herpes) Dysplasia Multiple pregnancies Poor personal hygiene Prevention of Cervical cancer Barrier protection during coitus Lifestyle modification Annual pelvic exam and papanicolau smear at age 18 or earlier if sexually active Endometrial cancer Risk factors Increasing age Triad of diabetes, hypertension, obesity Nulliparity History of hormonal therapy Prevention of endometrial cancer Annual pelvic exam and pap test Endometrial biopsy at menopause

Nurses role in early detection Cancer risk assessment Case finding

 Counsel & direct patient to proper source of help Other topics for prevention & detection >>BSE, TSE, Dietary modification & weight control, Alcohol intake, smoking cessation, personal hygiene measures, skin-self exam, know the 7 warning signs of cancer, Importance of early detection. 3 approaches to CA prevention 1. Education 2. Regulation 3. Host modification Nurses role in the diagnosis of CA Explanation of the tests to be performed, sensations likely to be experienced, patients role in the test Encourages patient and family to express fears about test results Supports patient and family throughout the test period Reinforces and clarifies information

Cut down total fat intake Limit alcohol Limit salt-cured, smoked & nitrate-cured food PATHOPHYSIOLOGY TERMS: NEOPLASM - abnormal tissue that serve no purpose - benign or malignant CANCER - normal cells mutate into normal abnormal cells that take over tissue - Eventually harm & destroy host - Historically, it is a dreaded disease ONCOLOGY - deals with diagnosis, treatment & study of cancer (medical specialty) - Oncologist the specialist ONCOLOGY NURSE - received specialized training in cancer treatment modalities - can administer cancer medications, chemotherapy medications

Diagnosis of CA 1. Cystologic Exams PAP smear 2. Biopsy obtaining tissue for histologic Incidence & Prevalence exam; needle incision (large Cause of 25% of death/yr tumor), Excision (remove entire Females: 3 most common tumor) 3. Imaging conventional radiography exams, types of cancer are mammography, BREAST, LUNG & BROCHIAL lymphangiography, tomography Males: 3 most common types MRI ( CT scan), ultrasound of cancer are 4. Tumor markers substances synthesized PROSTATE, LUNG & & release by tumor cells BRONCHIAL Indicators of the presence of tumors Risk factors for cancer May be present in benign conditions 1. Heredity: 5-10% of cancer; documented with (GIT cancer-neuroblastoma) some breast & colon caners Used to diagnose, determine 2. Age: 70% of all cancer occur in persons >65 response to therapy & predict or due to longer exposure to carcinogen confirm relapse & assess prognosis 3. Lower socio-economic status: lack of knowledge, faulty diet, sanitation American CA Society Nutritional Guidelines 4. Stress: no known relationship with cancer; Maintain desirable diet type C personality; leads to greater wear Eat a varied diet & tear Eat more fibers, whole 5. Diet: picked, salted foods; fried foods; highgrains, cereals, bread, pasta fat, low fiber foods, charred food; hormones

implicated to development of cancer 6. Occupational risk: exposure to known carcinogens, radiation, high stress 7. Infections: (ex. papiloma virus); HPV r/t cervical cancer; HIV associated with cancer of skin (Kaposis sarcoma) 8. Tobacco use: bladder cancer, lung, oral & laryngeal, esophageal, gastric, pancreatic 9. Alcohol use: also tied with smoking; cancer of the tongue 10. Sun exposure: universal carcinogen; radiation; ex. skin ca 11. Obesity: sex hormones are synthesized by fats

Begins with exposure of normal cells to carcinogens Carcinogens are substances that can cause cancer Escape normal enzymatic mechanisms and alter the genetic structure of the cellular DNA. *Normally, alterations are reversed by DNA repair mechanisms, or the changes initiate programmed cellular death (apoptosis).

CARCINOGENS 1. Chemical Cigarette smoke, asbestos, nitrates, isopropyl oil Drugs Alkylating agents(very Nursing Role dangerous to administer because they Health promotion to lower the controllable treat & would also destroy normal risks cells), cychlophosphamide, nitrogen 1. Routine medical check up & mustard screenings Hormones estrogen, 2. Client awareness to act if symptoms of diethylstilbestrol cancer occur 2. Physical 3. Screening exam recommendations by Ionizing radiation causes American Cancer Society leukemia UV light squamous or basilar Characteristics of Malignant cells cell carcinoma (more dangerous, Growth is defective unresponsive) Loss of differentiation & normal restraints Foreign - asbestos on growth 3. Biological Ability to metastasize DNA/RNA virus Ex. Epstein- Bar Virus = Burkitts lymphoma THEORIES of CARCINOGENESIS HIV = Kaposis sarcoma Cellular Mutation Theory Hep B = hepatocellular Cancer Stages of the development of carcinogenesis HPV = cervical & hepatocellular cancer AInitiation stage when a carcinogen acts Complete carcinogens on a target capable of both initiating & promoting cell & cause changes the development of cancer Irreversible alterations in the cells Ex. cigarette smoke weak genetic structure carcinogen Carcinogens enter the cells nucleus & alter the DNA Without DNA repair, the cell replicates B Promotion stage producing 2 daughter cells with the Reversible & fast proliferation genetic alteration of cancer cells Carcinogen binds to DNA Probably the cancer have developed its own blood supply Cell division

proliferating cells drains from the Many cancers are diagnosed major lymphatics to the larger veins at this stage cancer cells penetrate the blood Cure may still be possible vessels (enter the circulations) & released into Promoting factors: the bloodstream >>cigarettes, alcohol, age, hormones, LYPMHATIC SPREAD coping potentials, fats (20% prone to ca), Good prognosis good when there are stress no palpable lymph nodes in the site of primary Lasts for many years tumor Promoting factors include cigarette smoking, alcohol abuse, and dietary Oncogens components that act repeatedly over Body cells have oncogenes time on the already transformed cell Genes that promote cell proliferation & Promoters enhance the structural can trigger cancer changes within the cell Proto-oncologenes = present in cells; swith on for cellular growth C Latency stage Cancer suppressor genes switch off Time elapse between genetic alteration & the actual clinical PROTOONCOGENES lock that keeps the evidence of cancer cell in its mature functioning state Comprise both the initiation When unlocked genetic mutation & stage & promotion stage alteration may occur Range from 1 - 4 yrs Abilities & properties of cells in the fetal development are again expressed Critical mass reached before The cell regain a fetal appearance & the disease becomes clinically evident function Ex. CEA & AFP 1 cm tumor palpable How was it cooked? RNA virus, immature 0.5cm smallest detectable cells reverted and released by diagnostic measurement p53 gene = regulates whether cells will the period of time ranging from 1 to repair or die after DNA damage 40 years that elapses between the initial genetic alteration and the actual Immune Response Failure evidence of cancer Oncogenes DProgression are remnants of embryonic cells that Increased growth rate with are not suppressed during fetal G/D invasiveness & metastasis checked by T-lymphocytes (immune system) -surveillance To major areas of metastasis cancer cells normally form >> brain, lungs, and bones due to continuously within the body lymph nodes tumor specific Igs produced by The uncontrolled growth of a malignant immune system to destroy cancer cells tumor capable of metastasis Tumor cells compete with normal cells Tumor-associated Ags (TAA) and tissue for blood supply produced by cells as a result of As tumor cells grow, they stimulate malignant transformation vascularization (Angiogenesis) these are detected by the IS & Rate of growth is referred to as doubling removed Cytotoxic T-cells resist tumor growth time- time required for tumor mass to NK cells can lyses tumor cell double. spontaneously even if they are not detected VASCULAR SPREAD

Macrophages Have a role in tumor immunity Can be activated by gamma-interferon & become lytic for tumor cells Secrete cytokines: A-interferon, augments the killing ability of NK cells TFN (tumor necrosis factor) causes necrosis of tumors Failure of the immune mechanism may predispose a person to certain cancers Some tumors arise in areas poorly served by the immune system like the CNS Some tumors do not stimulate antibody formation since they are similar to normal cells Control system may become overactive and suppress the immune system Cont. Tumor mass grows at a rate faster than the normal immunologic response can handle o 10 million cancer cells at a time can be detected o At least 1 cm in size can be detected by conventional diagnostic methods o Tumor of 1 cm diameter contains more than 1 billion malignant cells

*these antigens attach to the receptors on the lymphocytes & prevent recognition 4. Blocking factors prevent the attack of the TAA by T-lymphocytes *Ex. Antibody ma combined with TAA & prevents recognition by T-cells
Exposure

to known carcinogens 2 groups: A. Genotoxic directly altering the cellular DNA B. Promotional affecting the immune system *ARSENIC very toxic; Genotoxic; weakened mitochondria leading poor production of ATP *Lead poisoning slowly genes of cells they invade

Viruses Modify Drugs

& Sex hormones

A
Sex hormones affect cancers of the reproductive systems (estrogen in some breast cancer; testosterone in prostate

B
Glococorticoids & steroids alter immune Cytotoxic agents Immunosuppressive agents Estrogens Oral contraceptives Androgenic anabolic steroids Phenacetin containing analgesics

Escape mechanism from Immunologic surveillance 1. Sneaking through due to weak cell Chemical Agents surface antigen Industrial and chemical 2. Antigenic modulation ability to change or Ex. hydrocarbons in soot, smoke, arsenics lose antigenic determinant during or and pesticides after a response by the immune system contacts alterations of DNA *altered cells are quick to express transformation new set of antigen change displays Radon an inert gas that 3. Overwhelming antigen exposure flooding emanates from the ground and stone the body with tumor antigen building materials from the decay of *antigen attach to surface (may uranium. displays) differently failing to EMF exposure from household recognition appliances, electrical wiring, or living near electrical power lines

The nearer one is to the source (within 50m), the greater the exposure Cellular phones are being studied as a source Air pollution Depletion of ozone layer Nitrates as food additives Aflatoxin 13 from common molds on peanuts, soybeans, fruit, meats, cheeses Cyclamates used a sugar substitute Some hair dyes Smoking and tobacco use Smokers of 2 or more packs/day have lung cancer mortality rate 12 to 25 times greater than that of a nonsmoker Physical Agents Exposure to radiations Ex. Nuclear power Ionizing radiation Electromagnetic waves or material particles with sufficient energy to ionize atoms or molecules thereby alter their chemical behavior Results in the breakage of either a single or double strand of the DNA helix Sun exposure Ultraviolet radiation Depletion of ozone layer Light complexioned individuals are most susceptible Radon and electromagnetic field effects Connected with oral, esophageal, bladder cancer Smoking cessation after a habit of 30 years, incidence of lung cancer decreases Cont. Environmental tobacco smoke (ETS) exposes non-smoker to the same carcinogens as the smoker Nutrition High fat, high caloric diet asso with increased risk for colon, breast, prostate, pancreatic and endometrial cancers

Alcohol consumption and nutritional def may enhance carcinogenesis by increasing metabolic activity of specific tobacco carcinogens Sexual practices Higher incidence of uterine cervix carcinoma those who have first coitus at an early age, early first marriage, multiple sex partners Carcinoma of penis virtually unknown among circumcised men First child before age 20 have only 1/3 the risk of women older than 35 who deliver a first child Viruses Viruses are thought to incorporate themselves in the genetic structure of cells Cervical cancer may result from a virus (human papilloma virus) introduced during sexual intercourse Herpes like viruses (Epstein-barr) have been seen in Burkitts tumor and hodgskins ds cells. Hepatitis B and C viruses in Liver cancer. Helicobacter pylori in gastric malignancy Psychosocial factors Stressors such as life changes, loss of a sig other, personality variables have been suggested as etiologic factors Cancer prone personality suggested but unproven Minimal social support my be a risk factor NEOPLASMS: also called tumors - mass of new tissue that grows independently of surrounding organs Factors that affect tumor growth Cell cycle time- the rate of replication of proliferating cells Growth fraction proportion of total cell population actively proliferating Rate of cell loss from cell death and exfoliation of cells from tumor surface Tumor growth Metastasis Certain cancers have affinity for a particular tissue or organ

Lungs, brain, bone, and liver are common sites of metastasis Vascular, lymphatic spread Implantation - cells become embedded along serosal surfaces of body organs

TYPES of NEOPLASMS: A. Benign Localized growths respond to bodys homeostatic controls Encapsulated; harmless tumor that dont metastasize Contact inhibition Can be destructive Ability to compress organs & blood tissues B. Malignant Harmful tumor that metastasize Aggressive growth; Rapid cell division Not under bodys homeostatic control due to secretion of own calatonin Parathyrtoid releases calcitonin (-) neg. feedback Cut through surronding tissues causing bleeding, inflammatory, necrosis

Characteristics 1. spread of growth 2. mode of growth 3. capsule 4 cell characteristics

Benign Slow Enlarging & expnadng, always localized, never infiltrate Capsulated Well differentiated, mature cells, may secrete hormones

Malig rapid

Grows b infiltratin

CALATONIN serum level causing

ccucipoalsemia

5. recurrence Unusual 6. metastasis Never Malignant tumors: can metastasize A. Tumor cells travel through blood or lymph circulation 1. primary tumor: the original site of the malignancy 2. secondary tumor: areas of metastasis (lymph nodes, liver, lungs, bone, brain) 3. 50-60% of tumors have metastasized by the time primary tumor is identified 4.

Non cap Poorly different may sec hormone Common Common

Mechanism of metastasis: Intravascation through blood of lymph & into blood stream seed Survival of malignant cells in their blood stream Intravascation from the circulation & implantation in the new tissue soil Malignant neoplasms can reoccur after vary in differentiation

a.

highly differentiated are more like the originated tissue b. undifferentiation consist of immature cells with no resemblance to parent tissue &have no useful function -

malignant cells progress in deviation with

each generation & do not stop growing & die as do normal cells malignant cells are irreversible: like parasite that competes t nutrients & ha own blood supply Malignant cells promote their own survival by hormone production, cause vascular, and permeabilities angiogenesis; divert nutrition from host cells. EFFECTS OF CANCER 1. disturbed or loss of physiologic functioning, from pressure or obstruction - anorexia & necrosis of organs - loss of function: bowel/bladder obstruction - intracranial pressure - Interrupted vascular/venous blockage: Ascitis (disturbed liver functioning) - Portal hypertension (production of varices fragile 2. Hematologic alterations: impaired function of blood cells - abnormal WBC: impaired immunity - diminished RBCs & platelets :anemia & clotting disorders - GI tumors: impaired vitamin B12 & iron absorption - Tumor compete with bone marrow for purines & folate - Renal carcinoma may produce erythropoietin 3. infections: fistula development & tumors may become necrotic; erode skin surface - Ex. Kaposis Sarcoma when opened, leads to infection 4. hemorrhage: tumor erosion, bleeding, severe anemia

5. Anorexia- Cachexia syndrome: wasting unexplained rapid weight loss, anorexia hormones/malignant neoplasm releases cachictin contribute early satiety, smell & taste altered catabolite state T, T4 for hyperthyroidism caused 6. Paraneoplastic syndromes: ectopic (outside the normal source of hormones) parathyroid hormone (Hypercalcemia)

ORIGIN ECTO DERM ENDO DERM Epitheliu m Gland Melanocy tes Germ cells Connecti ve tissue: Adipose Fibrous Bone Cartilage Muscle: Smooth Striated Nerve cells Endotheli al: Blood vessel Hemat ologic tissue s

BENIGN Papiloma Adenoma Melanoma Testroma

MALIGNAN T Sarcoma Adenocarci noma Malignant melanoma Serninoma

7.

pain: major concern Types of cancer pain: - Acute - Chronic Causes of pain: - direct tumor involvement including metastatic pain - nerve compression - involvement of visceral organs

MESO DERM

Lipoma Fibroma Osteoma Chondrom a Leiomyom a Rhabdo Ganglione uroma Hemangio ma

Liposarcom a Fibrosarco ma Osteosarco ma Chondroms arcoma Leiomyosar coma Rhabdomy osarcom Neuroblast oma (GIT) Kaposis sarcoma, Angiosarco ma Leukemia

8. physical stress: body tries to respond & destroy neoplasm a. fatigue b. weight loss c. anemia d. dehydration e. electrolyte imbalance 9.psychological stress a. cancers equals death sentence b. guilt feelings c. fear d. stigmatized TUMOR CLASSIFICATIONS According tissue/ cell of origin: Most common benign neoplasm Fibrosarcoma may grow anywhere but frequently grow in the uterus Lipomas in adipose tissue, poorly encapsulated and may expand to cause pressure to some tissues as they expand Leiomyomas of smooth muscle Malignant neoplasms Carcinoma arises from epithelial tissues Sarcoma from mesenchymal origins (blood vessels, lymphatic, nerve tissues) Malignant neoplasms Carcinoma in situ confined to the site of origin but can become invasive, eroding surrounding tissues Fibrosarcomas may originate as benign Bronchogenic carcinomas accounts for 90% of all lung cancers, usually at lower trachea and lower bronchi

Granuloc Granulocy ytes tosis Plasma Multiple cells myeloma lymphoc lymphomas ytes insulin (hypoglycemia) not under the homeostasis of the body Somatostin by Delta cells ADH adrenal cortex ACTH, cortisol

Pituitary release ACTH to cortex for it to release cortisol If with lung cancer, release of cortisol causing Cushings syndrome

10

Diagnosis of Cancer History Blood relatives Work history Environmental exposure Previous knowledge and perceptions about cancer Assess clinical manifestations Pressure on surrounding organs or nerves Distortion of surrounding tissue Obstruction of lumen of blood vessels, intestines, ureters etc. Interference with organ function Disturbance of body metabolism Assess Parasitic use of bodys nutritional needs Mobilization of the bodys defensive response Diagnostic evaluation Blood tests Grading Staging Hematologic Hemoglobin - anemia Hematocrit - anemia Leukocytes increased in lymphomas decreased in leukemia Platelets increased in CML, hodgskins decreased in ALL,AML, bone marrow suppression Blood or serum Acid phosphatase N- 0.11-0.6 mU/ml increased in metastatic prostate cancer Alkaline phosphatase N 20-90 mU/ml inc in bone metastasis, liver ca, lymphoma Calcitonin increased in medullary thyroid cancer Calcium N 9-11 mg/dl inc in bone ca LDH N 100-190 mU/ml inc in liver ca, lymphoma, acute leukemia SGPT (AST) N 5-35 mU/ml inc in liver ca SGOT (ALT) N 7-40mU/ml

Uric acid N 1.5-8 mg/dl inc in leukemia, multiple myeloma dec in hodgskins ds, lung ca Tumor markers Alpha fetoprotein N <10 ng/ml inc in lung, pancreatic, colon, gastric, choriocarcinoma Ca 125 N <35 units inc in ovarian and pancreatic ca Carcinoembryonic antigen N 02.5ng/ml for non smokers; <3 ng/ml for smokers inc in colorectal, breast, lung, stomach ca Prostate specific antigen N 0-4 ng/ml inc in prostate ca CA 19-9 inc in pancreatic, colon, gastric ca CA 15-3 inc in breast ca Estrogen receptors inc in breast ca Human chorionic gonadotropin N 0-5 IU/L inc in choriocarcinoma HISTOLOGIC ANALYSIS CLASSIFICATION: GRADING & STAGING GRADING - elevates the amount of differentiation - estimates the growth based on the mitotic rate - grade 1 (least aggressive) to grade 4 (most) Grade 1 cells differ slightly normal & are well differentiated ex. mild dysplasia Grade 2 more abnormal & moderate differentiation ex. moderate dysplasia Grade 3 very abnormal & poorly differentiation ex. severe dysplasia Grade 4 cells are immature & primitive & undifferentiated; origin is difficult to determine ex. anaplasia

STAGING - refers to the size of tumor & extent of the disease, rather than cell appearance Stage 1 cancer in Situ> all characteristic of cancer except invasion Stage 2 tumor is limited to the tissue of origin; localized tumor growth

11

Stage 3 extension local & regional spread Stage 4 metastasis TNM CLASSIFICATION TUMOR T0 no evidence of primary tumor T IS tumor in situ T1-T4 ascending degrees of tumor size & involvement

NODES Nx regional nodes cant be assessed clinically b. Antimetabolites (CCS) N0 no abnormal regional node work best in S phase N1aN2a regional nodes no metastasis displace metabolites or substitute N1b-N3b increasing regional lymph node metabolites onto DNA or RNA molecules involvement methotrexate 5 flouracil METASTASIS 6-mercaptopurine Mo no evidence of distant metastasis M1-M3 ascending degrees of metastatic c. Cytotoxic Antibiotic (CCNS) involvement including distant metastasis disrupt DNA/RNA replication >>TREATMENT MODALITIES Surgery Chemotherapy Radiotherapy Biotherapy Bone Marrow Transplantation --Combined modality or multimodal treatment CHEMOTHERAPY Action: interferes with the ability of the malignant cells to produce needed enzymes & chemicals Affect rapidly dividing cells Combination therapy less side effects destroys more malignant cells create free radicals Doxorubicin Bleomycin Actinomycin d. Plant Alkaloids Vince Alkaloids (CCS) - act on M phase - binds with specific proteins that promotes chromosomes migration Vincristine Vinblastin Etoposide(VP16) - acts on all phases causing metaphase arrest

Classes of Chemotherapeutic Drugs: a. Alkylating agents (CCNS) create defects in the tumor DNA Nitrogen mustard (Mechlorethamine) Nitrosureas (Carmustine) Alkyl Sulfunates (Busulfan) Triazines (Daarbazine) Ethylenimines (Thlopeta)

e.
-

Cell Kill Hypothesis with each cell cycle a percentage of cancerous cells are killed but some remains; repeating chemo kills more cells until those left can be handled by bodys immune system. 2 General classifications: a. Cell cycle non-specific (CCNS) - destroy even the resting cells - act anywhere in the cycle b. Cell cycle specific (CCS)

Hormone and Hormone Antagonist (CCS) acts on G1 Cortocosteroids (prednisone) Hormone Antagonists: *Tamoxifen *Diethylstilbetrol *Antiandrogen (Flutamide)

f.

Miscellaneous agents Cisplatin CCS G1 CCNS binds with DNA

12

Nadir a time in chemotherapy when WBC or platelet count is at its lowest; usually occur in 7-14 days after drug administration

ANC - Absolute Neutrophil Count; WBC x granulocyte

TYPES OF RADIATION ADMINISTRATION: I. External Radiation (Teletherapy) - external beam radiation therapy - patient is exposed to radiation - Never radioactive during this treatment II. Internal Radiation (Brachytherapy) - implantation or insertion of radioactive material into the tumor or dose to the tumor

Neutropenia ANC of less than 1000/mm Infection increases as the ANC decreases below 500/mm

Client Teaching during Nadir: 2 types of Internal Radiation therapy: 1. Adequate nutrition & hydration a. Sealed-Source Radiation Therapy 2. Avoid raw & uncooked foods intracavity & interstitial 3. Avoid crowds, people with Cesium137, Radium226, Radon222, infection & children who have been Iodine125 vaccinated with live attenuated vaccines b. Unsealed-Source Radiation 4. Avoid contact with animal Therapy excrement used in systemic therapy 5. Report signs of infection administered into a cavity or orally 6. Good handwashing may be administered IV (ex. 7. Adequate rest & sleep Phosphate/P32) 8. Avoid indiscriminate use of antipyretics Radiation Safety: 9. Thrombocytopenia risk for Distance the greater the distance from bleeding radiation source, the lesser 10. Less than 20,000/mm - risk the exposure for CNS hemorrhage & massive GI Shielding lead shield bleeding Time limited exposure time 11. Assess for changes in the LOC *generally limited to 30 mins per 8 shift RADIOTHERAPY Target of radiation effects id the DNA Radiation Safety Precaution: Energy produced by radiation is enough to t Sealed source Radiation Therapy break the chemicals bond in DNA Radioisotope is enclosed in a non Cancer cells are unable to repair the radioactive material damage caused by radiation The radioisotope cannot circulate Cellular death by radiation: throughout the body Irreversible loss of proliferative Therefore secretions are not capacity radioactive Production of free radicals Avoid touching the container Radiosensitivity the relative Clients with radioactive implants susceptibility of tissue to require a private room & bath because radiation of risk of dislodgement Rapidly dividing Lead container & a pair of long Well vascularized handled forceps are required in the High oxygen content room. *M & S phase target DNA t Unsealed - source Radiation Therapy

13

 Are placed in colloid suspensions & 5. COLONY-STIMULATING FACTORS comes in direct contact to tissues a group of glycoproteins produced by Radioisotopes are found in excreted vrious cells that stimulate production, body fluids. maturation, regulation, & activation of cells of Trash is placed inside the room & not the hematologic system. removed until discharge Clients are scanned before discharge. a) Granulating colony stimulating factor BIOLOGIC RESPONSE MODIFIERS Stimulates production of neutrophils Route: SQ, IV 1.INTERFERONS are cytokins S./E: bone pain Properties: A. Antiviral Antiproliferative inhibit DNA & CNON synthesis in tumor cells, stimulate expressiom of tumor associated antigens C. Immunomodulatory increases cytotoxic ability & killing potential of NK cells B. * Interleukins produced by lymphocytes & macrophages * Interferon produced by fibroblasts & macrophages Route: IM, IV, SQ b) Granulating-macrophage CSF Approved for neutropenia associated with bone marrow transplantation Stimulates the production & treatment of grtanulocytes, monocytes & macrophages It also stimulates these cells to produce cytokines c) d) Macrophages IL-3 (Multi-CSF) Because it stimulates the growth of neutrophils, monocytes, eosinophils, bsohils, & platelets.

2.INTERLEUKINS IL2
-

a cytokine produced by T-lymphocytes TOXIC & SIDE EFFECTS OF BRMS known to stimulte division of T- it is usually induces the endogenous lymphocytes release of other BRMs (headache, fever, they activate NK cells & lymphokine chills, mylagia,atigue) activated killer (LAK) cells - cause capillary leak syndrome stimulates the release of other cytokines (tachycardia & hypotension) (U interfern, TNF, IL-1, & IL6) - ex. pulmonar edema Approved for treatment - GOAL: reduce venous return Route: IV infusion, SQ, & peritoneal infusion Nursing Care: Oncologic treatment I. Neutropenia 3. MoAbs teachings: practice good hygiene produced by B-lymphocytes that bind with tumor cells II. Thrombocytopenia TUMOR NECROSIS FACTOR a cytokine produced by macrophages toxic to tumor cells by exerting necrotizing effect attack tumor cells while preserving normal cells 4.

teachings: avoid injury (use electric razor) use lubricants during sexual intercourse oral hygiene: soft- bristled toothbrush or sponge oral swabs avoid constipation

14

avoid enemas/rectl suppository/ rectal temperature taking report oral bleeding avoid aspirin, NSAID, IM/SQ injection

Increase fluids Stool softeners & laxatives VII. loss Alopecia temporary hair

management: Oprelvekin (neumega) Occur in 2-3 weeks fter 1st treatment a thrombocytopenia growth factor to prevent its severity; given following Hairgrowth begins 4-6 weeks after myelosuppressive chemotherapy chemo; 8-9 weeks after RT

VIII. Skin reaction Hyperpigmentation disappear for how many days Photosensitivity use sun block Nursing Diagnoses: IV. Nausea & Vomiting 1. Anxiety Anticipated N/V 2. Disturbed body image - loss of body parts; appearance Acute post therapy N/V within 24 changes after therapy - altered functioning Delayed N/V persist or developed - cachetic appearance after 24 - fear of rejection, stigma Referral to dietitian INTERVENTION: Parenteral feeding - explain the meaning of loss Medications: Serotonin receptor - allow denial antagonists (5HT3) - matter of- fact approach Ondansetron (Zofran) - alopecia: discuss the timing, use of Granistron (Kytril) ice cap/ tight head band during Dolasetron ( Anzernet) chemotherapy, referral to support group, reassurance V. Stomatitis 3. Anticipatory grieving - use therapeutic communication Ulceration of the oral mucosal lining skills Care: orla hygiene program is started - encourage client to take control before therapy - honestly answer questions about Moisturation if saliva is scanty illness Avoid alcohol & smoking - prognosis, always encourage hope Culture analysis & antimicrobial 4. Risk for infection Eat soft foods 5. Risk for injury Avoid foods that are very hot/cold foods, 6. Impaired tissue integrity spicy, citrus & juices - small ulcers on the tongue edges & mucous membrane VI. Diarrhea & Constipation - herpes simplex lesions Diarrhea due to GI mucosa damage - fungal infections (thrush) due to RT & chemo - XEROSTOMIA dryness of mouth Low residual diet caused by cessation of normal Perinel hygiene salivary secretions - Management: Gatorade, Constipation due to decreased fuild/ sugarless gum, & blistex, fiber, immobility, tumor pressure on the mouthwash my be used bowel, ordueto medications (Vinc alkaloids & (chlorhexidine) narcotics)

Anemias Blood transfusion Administration of erythropoietin anti diuretics

III.

15

- Acyclovir (Antiviral) - Nystatin or Clotrimazole solution (Anti fungal) - Xylocaine for pain during mouth care 7. caregiver role strain 8. ineffective individual coping 9. ineffective denial 10. Fatigue 11. Fluid volume deficit 12. Hopelessness 13. Impaired social interaction 14. powerlessness 15. ineffective family coping: compromised 16. altered nutrition less than body requirement Oncologic emergencies: 1. Hypercalcemia causes: parathormone, bone metastasis S/S: fatigue, anorexia, nausea, polyurea, constipation, arrhythmias, seizures, coma, death INTERVENTION: ECG (signs of Hypercalcemia) IV fluids (NSS) Stop thiazides Avoid vit. A & D Medications: Plicamycin (Mithracin) Glucocorticoids, Calcitonin (Maicalcin) Superior Vena Cava Syndrome compressed by mediastinal tumors or thoracic tumors ex. small cell cancer or squamous cell cancer venous obstruction pleural effusion edema: face , arms, trachea cerebral edema impaired cardiac filling Managnement: respiratory support, corticosteroids, seizure precaution, chemotherapy & radiator

associated with expanding tumors of the breast, lungs, prostate & lymphoma emergency because of potential - early symptoms: back & leg pain, numbness, paresthesias

-Treatment: radiation, surgical decompression neurologic check every shift prepare for MRI Administer corticosteroids

4.

Septic Shock - causes: tumor necrosis, immnosuppresion, bacteria enters the blood - Treatment: fluid (plasma expanders) Hemodynamic monitoring Oxygen C&S Antibiotics Vasopressors Tumor lysis syndrome - from released intracellular content secondary to destruction of tumor cells - release of K+, ph, nucleic acids - high risk for electrolyte imbalance - Acute renal failure can happen - Treatment: Allopurinol Sodium bicarbonate IV Retention enemas (Kayexalate) D5% N IV dialysis Pericardial Effusion & Neoplastic Cardiac Tamponade - S/S: hypotension - Tachycarida/tachypnea - Dyspnea - Cyanosis INTERVENTION: - Oxygen - Vasopressors

5.

2.

6.

3.

Spinal Cord

Compression

16

- Crash cart of bedside - Pericardiocentesis drawing fluid in pericardial space between the serous membranes - Percardiotomy surgical incision in pericardium

7.

o o o o o o o o

SIADH - in small cell cancer; prostate; adrenal cancer - S/S: Hyponatremia lower than normal concentration of Na in the blood Hypervolemia Increase BP Irritability Confusion Natriuresis urination of Na CANCER Group of diseases in which cells multiply without restraint, destroy healthy tissues and endanger life. The process begins when an abnormal cell is transformed by the genetic mutation of the cellular DNA Genetic factors Deranged genes passed through either autosomal recessive or autosomal dominant transmission Recessive when both parents have abnormal genes Dominant when only one parent have abnormal gene Cont. Genetic factors General characterestics of hereditary CA Early age onset Marked incidence of bilateral cancer in paired organs Greater frequency of dev the same cancer Appearance in two or more members in one generation Cont. genetic factors Leukemia with chromosomal alterations Chronic myelogenous leukemia (CML)- asso ciated wthPhiladelphia chromosome 22 translocation Acute myelogenous leukemia(AML) asso with trisomy 21 found in downs syndrome

- ** It is also possible to inherit a condition that increases risk for developing a certain cancer. - Hormonal influence in carcinogenesis - Making target tissues susceptible to carcinogens - Allowing cancer process to progress - Conditioning effect on the tumor - Hormones can restraint or enhance tumor growth - Precancerous lesions - Have tendency toward a malignant change - Polyps of the colon and rectum, pigmented moles, dysplasia of cervical epithelium - Pagets disease of the bone, senile keratoses, leukoplakias of oral mucosa - Chronic irritation - Believed to be causative factors of cancer - Coal tar products known to contain carcinogens - Belts, girdles,brassiers, shirt collars - Rough jagged teeth - Scalding hot or freezing cold liquids - Indiscriminate use of laxatives - Choice of treatment depends on: - Type of tumor - Extent of disease - Clients physical status - Clients wishes - Combined modality therapy is more effective in destroying cancer cells. - Treatment modalities - Surgery - Radiation - Chemotherapy - Immunotherapy - Surgical therapy - Diagnostic o Obtain tissue for microscopic identification of malignant cells o Cytology specimens cells shed from the tumors surface- aspirate, brushings o Needle biopsy o Incisional biopsy o Excisional biopsy small tumors (2-3cm) o Curative surgery in 55 % of the clients - Palliative surgery o Reduce pain o Relieve obstruction

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Prevent hemorrhage Remove infected and ulcerating tumors Drain abscesses Preventive surgery Subtotal colectomies in clients with ulcerative colitis to prevent colon Ca Radiation therapy Primary modality Local cure in early stage of hodgskins ds, skin ca, cervical ca Adjuvant either preoperatively or postoperatively (colorectal, early breast ca) Palliative to relieve pain caused by obstruction, pathologic fx, spinal cord compression and metastasis Radiation therapy uses high energy ionizing radiation Destroy the cells ability to reproduce by damaging its DNA, delaying mitosis to repair DNA or inducing apoptosis Cells are most vulnerable during the Dna synthesis and mitosis Rapidly dividing cells are most sensitive e.g. bone marrow, lymphatic tissue, GIT, hair cells and gonads Chain of reactions occur in the ECF resulting to the formation of free radicals that interact readily with nearby molecules causing cellular damage Well oxygenated tumors show a much greater response to radiation Types of radiation therapy External RT used outside of the body Teletherapy- radiation delivered from a source at some distance from the target site Adm by high energy x-ray machines or machines containing radioisotope (cobalt 60) With skin sparing effect Internal RT radioisotopes directly placed into or near the tumor or into the systemic circulation Brachytherapy Sealed source- enclosed in a sealed container e.g. cessium 137 Intracavity into a body cavity (24-72 hours) e.g. radium 226 Interstitial in needles, beads, seeds, ribbons or catheters implanted into the tumor e.g. gold 198, iodine 125

- Unsealed RT adm IV , into body cavity, or orally - Radiation dose - Dependent on the sensitivity of target tissues - Tumor dose that will eradicate 95% of the tumor yet preserve normal tissues (lethal dose) - Delivered over several weeks o For healthy tissues to repair o When cells are actively dividing o For periphery of tumor to be reoxygenated - Toxicity to radiation therapy - Localized - Increased if with concomitant chemotherapy - When cellular death exceeds cellular regeneration - On rapidly dividing cells - Common alopecia, erythema, desquamation, stomatitis, xerostomia, loss of taste, decreased salivation - Anemia, leukopenia, thrombocytopenia - Nursing management in RT - Explain about procedure- delivery, equipment, duration, positioning, sensations, radiation precautions - Protect skin and oral mucosa o No lotion, ointments or powder on area o Gentle oral hygiene - Key concepts in RT - Different areas of the body are affected differently - Only the area in the treatment field is affected - Radiation dose is prescribed in units called grays (Gy) - Side effects are decreased by divided doses - Combined modality with chemotherapy and radiation has the potential for enhanced tumor destruction as well as enhanced side effects - GIT, skin and bone marrow are at greatest risk of damage - Radiation therapy is aimed at destroying the malignant tumor without harming the surrounding tissues by: o Fractionation dividing the total radiation dose into small, frequent doses.

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 Increases the probability that tumor cells be in a vulnerable phase of the cell cycle. Allows normal cells time to repair themselves - Side effects do not develop until approx 1014 days into treatment and subsides 2 or more weeks after treatment - Complete blood count during radiation therapy - Skin care of treatment field - Keep skin dry - Do not wash the area until instructed. If permitted wash gently with mild soap and thoroughly pat dry - Do not remove marks on skin - Avoid using powder, lotions, alcohol etc. - Cont. skin care - Wear loose fitting clothing to avoid friction - Do not apply tape - Shave with electric razor. No lotion. - Protect skin from direct sunlight, chlorinated pools, temperature extremes - Consult for specific skin reactions - Key principles for radiation safety - The greater the distance from the radiation source, the less the exposure dose of ionizing rays - Time is limited to 30 min of direct care per shift (8 hrs) - Shielding depends on the source of radiation (lead shielding) - Maintaining maximum distance from the radioactive source and limiting duration of exposure, nurses can safely protect themselves with or without shielding - Film badge provides a measure of whole body exposure - Safety standards for sealed source of internal radioactive implants - Patient in a private room and bath - Shields, a lead container and a long handled forceps in the clients room - If source becomes dislodged, inform radiation safety officer STAT - Safety standards for internal unsealed source of radiation - Private room and bath for patient - All body secretions are radioactive all surfaces are covered with protective covering - Food served on disposable plates

- Trash, linens kept inside the room until after discharged - Toilets flushed several times - To wear a new pair of booties each time anyone enters the room - Wear gloves when handling body fluids - Radiation safety officer scans the patient before discharge - Precautions for the room continues even after discharge until radiation safety officer has lifted restrictions - Indications of Chemotherapy - Disease is widespread - Risk of undetectable disease is high - Tumor cannot be resected and is resistant to RT - Objective of chemotherapy - To destroy malignant tumor cells without excessive destruction of normal cells - Actively dividing cells are most sensitive to chemotherapy - Chemotherapy directly or indirectly disrupts reproduction of cells by altering essential biochemical processes - Cell kill hypothesis only a percentage of cancer cells are killed with each course of chemotherapy. - Combined chemotherapy destroy more malignant cells and produce fewer side effects. Each drug strikes the cancer cells at a different point of the cell cycle. - Cell cycle phase specific drugs - Exert effect within a specific cycle - Schedule dependent - Greatest tumor cell kill when given o Frequent divided doses o Continuous infusion with short cycle time - Cell cycle phase specific drugs - Antimetabolites - Vinca alkaloids Epipodophyllotoxins Taxanes Camptothecins miscellaneous - Antimetabolites - Act in S- phase - Interfere with DNA synthesis - Common side effects: o Myelosuppression o GI o cutaneous

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Antimetabolite drugs Cytarabine (cytosar) 5-florouracil (5-FU) 6 mecaptopurine (6-MP) Methotrexate (MTX) Capecitabine (Xeloda) Pentostatin (Nipent) Gemcitabine (Gemzar) Vinca Alkaloids Camptothecins Act in S-phase Cause double strand DNA damage Common side effects: Myelosuppression Alopecia Diarrhea Epipodophyllotoxins (etoposide) Act in pre-mitotic phases (G2 and S) Induce irreversible blockade of cells and interfere with topoisomerase II enzyme reaction Common side effects: Hypersensitivity Myelosuppression GI, hypotension Taxanes (paclitaxel, docetaxel) Act in G2 and M phase Inhibit cell division Common side effects: Hypersensitivity Myelosuppression Cutaneous Neurologic toxicities Vinca alkaloids (vinblastine, vincristine) Act in late G2 and M phase) Block DNA production Prevent cell division Common side effects: Myelosuppression Autonomic and peripheral neurotoxicity Miscellaneous agents L-asparginase, hydroxyurea, pegasparase,procarbazine, imatinib mesylate Act in various phases (primarily S) Inhibit synthesis Common side effects: Myelosuppression, GI, Hepatotoxicity Cell cycle nonspecific drugs Alkylating agents

- Antitumor antibiotics - Hormonal therapy - Alkylating agents: (busulfan, melphalan, carboplatin, cisplatin etc.) - Cell cycle nonspecific - Break DNA helix strand - Common side effects: o Myelosuppression o Hypersensitivity o Renal, GI, cutaneous, 2nd malignancies - Antitumor antibiotics: bleomycin, doxorubicin - Cell cycle nonspecific - Bind with DNA and inhibit synthesis - Common side effects: o Myelosuppression o GI - Cutaneous - Other organ toxicities - Hormonal therapy - Glucorticoids - Estrogens - Aromatase inhibitor - Anti-estrogen - Progestins - Nitrosureas - Hormones - Cell cycle nonspecific - Alter environment and inhibit tumor growth - Common side effects; o GI o Gynecomastia o Fluid/sodium retention o Menstrual irregularity o Libido changes - Administration of chemotherapy - Depends on the type of agent; required dose; type, location, and extent of tumor - Dosage is based on patients total body surface area, previous response to chemotherapy or radiation, function of major systems - Routes of chemotherapy administration - Intravenous o Peripheral access on large veins o Vascular access devices (VADs) o Implanted and external vascular access cath into a major vein of the upper chest

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o Peripherally inserted central catheter (PICC) through the cephalic or basilic vein - Regional chemotherapy - High concentration of drug directed to localized tumors - Topical applied to skin - Intra-arterial- tumor sites receive maximal exposure with limited serum levels of med - Intracavitary - Intraperitoneal- agent direct to tumor site - Intrathecal into the CNS through an implanted reservoir placed in the ventricle (Ommaya reservoir) - Other routes: o Oral o Subcutaneous o intramuscular - Adverse reactions - Hypersensitivity - Extravasation - Hypersensitivity - Can be serious and life threatening - Commonly implicated: o L-ASPARAGINASE o CARBOPLATIN o CISPLATIN o PACLITAXEL o BLEOMYCIN - PRECAUTIONS TO ENSURE SAFETY - ALLERGY HISTORY - TEST DOSE IF ORDERED - STAY WITH PATIENT THE ENTIRE TIME DRUG IS ADMINISTERED - EMERGENCY EQUIPMENT AND DRUGS AVAILABLE - BASELINE VITAL SIGN - ESTABLISH IV LINE - If with anaphylactic reaction - Immediately stop drug - Maintain IV access with 0.9% saline - Maintain airway - Supine with feet elevated, unless contraindicated - Notify physician - Monitor vital signs every 2 min til stable - Adm epinephrine, diphenhydramine, corticosteroids if ordered - Extravasation or infiltration - Note vesicant potential of drug and its antidote

o o o o o o o -

Assess IV before and after administration Commonly used vesicant drugs: Doxorubicin Vincristine Cisplatin paclitaxel Extravasation Pain, erythema, swelling, and lack of blood return Stop drug administration Aspirate residual drug from tubing, needle and site Administer antidote Do not apply direct manual pressure to site Apply warm or cold compress Observe site regularly for pain, swelling, erythema, induration and necrosis Document the appearance of the site before and after chemotherapy Potential risks from exposure to chemotherapy in the workplace Genotoxicity Carcinogenicity Teratogenicity Serious organ damage Routes of exposure Inhalation of aerosols Absorption through skin Ingestion of contaminated materials Guidelines for safety Wear gloves and gowns during preparation and administration of the drug Use of biologic safety cabinet or laminarflow cabinet for preparation Wear disposable gowns and gloves when handling body secretions of patients who have received chemo within the previous 48 hours. Biotherapy Use of agents derived from biologic sources or agents that affect biologic responses Principles of the immune surveillance theory As multiple genetic mutations occur over years, cells may transform from normal to malignant Cancer cells express antigens on the cell surface (tumor-associated antigens) Immune system recognizes the antigens as non-self

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- Immune response can be mounted in defense - Methods of biotherapeutic action - Enhance immune response - Alter bodys responses that allow cancer cells to grow - Increase vulnerability of cancer cells - Preventing metastasis - Alter pathway of transformation of normal to malignant cells - Enhance repair of normal cells - Change behavior of cancer cells - Biotherapy agents - Cytokines class of protein cell regulators produced by the immune system. - Interferons antiviral,antiproliferative - Interleukins stimulate activation of immune cells - Hematopoietic growth factors stimulate the differentiation, proliferation, maturation, and functioning of hematopoietic cells. - Monoclonal antibodies - Highly specific proteins derived from a single clone of antibody-producing cells that recognize and bind to only one tumor associated antigen - Produce apoptosis - Activate host defenses to mediate antitumor activity - Others - Vaccines - Anti-angiogenesis agents - Bone marrow transplantation - As a primary treatment modality in leukemia - To counter toxic effects of chemotherapy - Damaged marrow is replaced by a healthy marrow - Autologous - Allogenic from a matching donor - Nursing Management - Of problems related to treatment - Oncologic emergencies - Myelosupression - Neutropenia o Nadir when WBC and platelet are at its lowest point after chemotherapy (7-14 days). o ANC = WBC x neutrophils(%)

o Neutropenia is an ANC of less than 1000/mm3 o Monitor temperature o Prompt administration of antibiotics o Teach patient of measures to prevent infection - Measures to prevent infection - Good personal hygiene, esp handwashing - Oral hygiene using alcohol free mouthwash - Adequate nutrition and fluid intake - Do not share eating utensils with anyone - Avoid raw or uncooked foods during nadir - Avoid crowds, people with infections, children recently immunized with live, attenuated vaccines - Avoid contact with animal excreta - Avoid having cut flowers in the home - Adequate rest and sleep - Avoid indiscriminate use of antipyretics - Report sigs and symptoms of infection immediately like cough , fever,sore throat, chills, sweating, frequent or painful urination - Thrombocytopenia - Platelet count of less than 20,000/mm3 - Count recovers within 2 to 6 weeks after the recovery of WBC count - Chemotherapy withheld until platelet count rises to 100,000/mm3 - Measures to prevent bleeding - Be cautious with sharp objects - Lotions to prevent dryness and cracking - Use lubrication during sexual intercourse - Soft toothbrush, or oral swabs - Avoid constipation - Avoid enemas or rectal suppositories - Refrain from taking NSAIDs - If with epistaxis, apply pressure 10-15 min - Avoid IM or H injections - Report presence of petechiae, tarry stools, hypermenorrhea, blood in urine/stools, visual changes, change in LOC - Anemia - Can cause fatigue, headache, dizziness, fainting, pallor, dyspnea, palpitations, tachycardia - Transfusions of PRBC - Administration of erythropoietin - Vitamin B12, folic acid, iron - Balance exercise with rest dec fatigue - Gastrointestinal effects

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Nausea and vomiting Anorexia Stomatitis Diarrhea and constipation Weight loss Nausea and vomiting Stimulation of the afferent pathways or arousal of the ctz in the 4th ventricle of the brain Anticipatory nausea and vomiting Acute post therapy within minutes of the first 24 hrs following therapy Delayed 24 hrs after Measures to prevent nausea/vomiting Add serotonin receptor antagonist Adjust fluid intake Relaxation, exercise, hypnosis, biofeedback, guided imagery Avoid offensive odors Feeding 4-6 times/day Anorexia Protein calorie malnutrition leads to weight loss High protein, high calorie diet Enteral or parenteral feedings Stomatitis Can cause pain, decreased nutritional and fluid intake, infections, malabsorption, diarrhea, delay in therapy Gentle cleaning Moisturization Avoid alcohol and smoking Anesthetics or analgesics for pain Dietary modifications Avoid extremely hot or cold foods, spices, citrus fruits and juices Eat soft foods Nutritional supplements Diarrhea RT GI mucosal damage or chemotherapy Low residue or liquid diet Electrolytes and intake-output monitored Perineal hygiene Antidiarrheal agents Constipation RT decrease in fluid fiber intake, decrease mobility, tumor pressure on bowel, hypokalemia or hypercalcemia Vinca alkaloids (vincristine, vinblastin) slow bowel peristalsis Depression

Measures for constipation Increase fluid intake Stool softeners prophylactically increase physical activity Laxatives prn Integumentary effects Alopecia Skin reactions Alopecia Common side effect Begins 2-3 weeks after treatment New growth begins 4-6 wks after completion of chemotherapy and 8-9 wks after RT - Hair color and texture may change Allow to grieve for hair loss Wear wigs or turbans Baseball caps for men Hearing the experience of others Skin reactions Erythema or urticaria at drug injection site Hyperpigmentation in the nail beds an d mouth, gums or teeth, along the veins used for IV within 2-3 wks after adm of chemo. Continues 10-12 wks after end of therapy Photosensitivity Radiation recall- for those who received RT before chemo Redness, shedding, peeling to blisters and oozing Skin darkened permanently Effects on reproductive system Surgery can affect sexual functioning through impairment of vascular supply, removal of organs, reduction of circulating hormones. Antineoplastic agents increases risks of spontaneous abortion and fetal malformations during first trimester of preg nancy Oncologic emergencies Infection Pain Spinal cord compression Hypercalcemia Tumor-lysis syndrome SIADH DIC Superior vena cava syndrome Cardiac tamponade

o o -

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Infection and pain Life threatening in neutropenia 60-90% of patients with cancer have pain Uncontrolled pain enabling client to live fully cannot be met Hypercalcemia Due to bone resorption (demineralization) Serum calcium level >11mg/dl 80% in solid tumors like breast, lung, head, neck, and renal cancers Difficult to distinguish from other cancer of treatment related symptoms Anorexia, nausea, vomiting, thirst, polyuria Adequate hydration Mobility Report signs and symptoms Control growth of tumor Calcitonin and oral glucocorticoids Tumor lysis syndrome Destruction of large, bulky tumors rapidly releases intracellular potassium, phosphorus, and nucleic acid to circulation Electrolyte imbalances and acute renal failure 1-2 days after treatment starts and ends a week following completion of treatment Aggressive IV hydration before start of treatment Allopurinol Sodium bicarbonate with IV hydration to promote fecal excretion of excess phosphate Remove potassium from the ECF Renal dialysis Weigh daily MIO Report weakness, nausea, diarrhea, flaccid paralysis, muscle cramps, twitching, ECG chnges SIADH From abnormal production of ADH 80% in clients with small cell lung carcinoma Medical emergency when patient has hyponatremia (<120mEq/L) Fluid restriction IV infusion of hypertonic saline (3-5%) MIO DIC With extensive abnormal clots throughout small blood vessels

- Exhaustion of clotting factors and platelets - Mortality rate is 70% - Often caused by gram negative infection or sepsis, release of thrombin or thromboplastin from cancer cells, or BT - Asso with leukemia, adenocarcinomas of lungs, pancreas, stomach, prostate - Spinal cord compression - Direct pressure on or compromise of vascular supply to spinal cord - Back pain in 95% of clients (belt-like) - Motor weakness - Decreased sensation - Constipation, urinary hesitation - RT , or laminectomy as alternative - Adm of steroids - Superior vena cava syndrome - Internal or external obstruction of the SVC - Typically secondary to small cell lung ca (65%) or lymphoma (2%) - Dyspnea, facial swelling,jugular vein distention, swelling of arms, chest pain, dysphagia - Treatment with RT or chemotherapy - Cardiac tamponade - Acute compression of the heart r/t pericardial effusion - N i5-50 ml of fluid - 200-1800 ml of fluid before heart decompensates - Pericardiocentesis - Pericardiotomy may be performed - Developing a hopeful attitude and support to patient and family - Be available and continue to be available esp. during difficult times - Caring attitude - Active listening - Relief from distressing symptoms - Essential information about cancer and care - Maintain a relationship based on trust and confidence; open, honest, caring - Use touch to exhibit caring - Assist in setting realistic, reachable short and long term goals - Assist in maintaining usual lifestyle patterns - Maintain hope o symptoms are not serious o Treatment is curative

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Hope For independence For relief of pain For a longer life For peaceful death Leukemia 5th leading cause of cancer deaths in men; 6th in women Common in white males Malignant disorder of the hematopoietic system involving the bone marrow and lymph nodes Uncontrolled proliferation of leukocytes and their precursors Immaturity of the WBCs leads to decreased immunocompetence and inc susceptibility to infections Etiology unknown Persons with chromosomal aberrations such as downs syndrome have inc inci dence of acute leukemia Chronic exposure to chemicals like benzene, and radiation exposure associated with inc incidence Cytotoxic therapy asso in inc incidence Classification of Leukemias Acute leukemias involve immature cells and are categorized according to predominant cell in the bone marrow

o Acute lymphocytic leukemia (ALL) o Acute nonlymphocytic leukemia (ANLL) or Acute myelogenous leukemia (AML) *rapid onset and short course ending in death if untreated - Chronic leukemias o Chronic lymphocytic leukemia (CLL) o Chronic myelogenous leukemia - *more insidious onset - Median survival is 3-4 years in CML; 2-10 years in CLL Acute lymphocytic leukemia Etiology unknown 80% of persons affected are 2-4 years old Malignant disorder arising from a single lymphoid stem cell, with impaired maturation and accummulation of malignant cells in the bone marrow

- Diagnosis by bone marrow biopsy - The greater the number of immature cells, the poorer is the prognosis - Signs and symptoms anemia, bleeding, lymphadenopathy o Blood smear may show immature lymphoblasts o Platelet count and hematocrit are reduced - Management of ALL - Median survival time (MST) of untreated patients 4-6 months; with current therapy close to 5 years - 50% of children with ALL can be cured - Complete remission in more than 90% of those treated with chemotherapy - Chemotherapeutic protocols for ALL - Induction vincristine and prednisone - Consolidation modified course of intensive therapy to eradicate remaining disease - Maintenance a combination of antimetabolites (6-mercaptopurine and methotrexate) o Vincristine and prednisone are adm intermittently during maintenance program - Cont. management of ALL - Diet high in protein, fiber and fluids - Measures to prevent infection - Signs of bleeding and infection to be reported immediately - Measures to decrease nausea - Oral hygiene to prevent stomatitis - Teach about prescribed regimen - Awareness of the support services available - Acute Myelogenous Leukemia - A disease of the pluripotent myeloid stem cell - Immature myeloblasts in the bone marrow - Often at adolescence and after age 55 yrs - Signs and symptoms same as ALL - WBC count maybe low, normal or high - Bone marrow aspiration show increased myeloblasts - Management of AML - MST 2-3 months if not responsive to tx - Chemotherapy cytarabine, 6-thioguanine, doxorubicin - Complete remission in 50-75% of treated patients; MST 2-3 years

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- 20% in complete remission at 5 years and are capable of prolonged disease free periods - Bone marrow transplantation with HLAidentical allogenic marrow or autologous BMT as an option - Same nursing management with ALL - Chronic Lymphocytic Leukemia - Rare under age 35 years - More common in men - Proliferation of small, abnormal, mature B lymphocytes leading to decreased synthesis of immunoglobulins and depressed antibody response - Begins in the lymph nodes then to other lymphatic tissues and spleen - Peripheral blood smear and bone marrow show increased mature lymphocytes - Onset insidious - Weakness, fatigue, lymphadenopathy, pruritic vesicular lesions, anemia, thrombocytopenia, enlarged spleen - WBC is 20,000-100,000 leading to increased blood viscosity, and clotting may be first manifestation of disease - Management of CLL - MST is 4.5-5.5 years - Treated only when symptoms appearanemia, thrombocytopenia, or enlarged lymph nodes and spleen - Chemo with alkylating agents chlorambucil; glucocorticoids - No treatment is curative - Chronic Myelogenous Leukemia - Accounts for 15-20% of all cases of leukemia - Age onset is in the 50 and 60 years - Equally distributed between the sexes - MST is 5-5.5 years - Benzene and radiation exposure is associated with the disease - Philadelphia chromosome identified in 8095% of patients with CML - Abnormal stem cell leading to uncontrolled proliferation of granulocytic cells - Classic symptoms fatigue, weakness, a norexia, weight loss, splenomegaly - WBC 15,000-500,000 - Peripheral smear show granulocytes in varying degrees of maturity

- Granulocytic hyperplasia in the bone marrow - Chronic indolent phase to accelerated to fulminant neoplastic process - Accelerated phase (blastic) increased granulocytes with anemia and thrombocytopenia - 50-60% progress to blastic phase - Chemotherapy similar to AML if in the blastic phase - Survival rate is poor - Management of CML - Hydroxyurea is the drug of choice - In blast phase anthracyclines and cytosine arabinoside with less than 20% remission - Nursing management focused on measures to prevent infection, promote safety from bleeding, oral hygiene, prevent fatigue, promote effective coping. - Hodgskin Disease - Malignant disorder of the lymph nodes - Unknown cause - Maybe with a genetic component - Epstein- Barr virus associated - Peak incidence in the 30th - Males frequently affected - Reed-Sternberg (RS) is the pathological hallmark - Lymphocyte predominant, nodular sclerosis, mixed cellularity, lymphocyte depletion are the histological subtypes - S/S fatigue, weakness, anorexia, unexplained fever, night sweats, generalized pruritus - P.E.- enlargement of lymph nodes, liver and spleen - Lymphadenopathy common in the cervical, axillary and inguinal nodes - Chest xray may show mediastinal mass - May spread to liver, spleen, vertebrae, uterus and bronchi - Lymphangiography for intra-abdominal nodes - CT scan - Ann Arbor clinical staging by laparotomy - Management of Hodgskins ds - Radiation therapy with 90% for stage I and 80% for stage II - Combination chemotherapy for stages III and IV

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- Commonly used is MOPP regimen mechlorethamine (Nitrogen mustard), Oncovin (vincristine), procarbazine, pred nisone - Cont. - ABVD regimen if relapse occurs Adriamycin(doxorubicin), Bleomycin, Vinblastin (Velban), Dacarbazine - Nursing management re: prevention of infection, preventing injury like bleeding - Non-hodgskins Lymphoma - Lymphoid malignant disease - Unknown cause - Viruses implicated - Men commonly affected are persons above 60 years - Nontender peripheral lymph nodes may appear bulky - Liver and spleen moderately enlarged - Unexplained fever, weight loss, night sweats - Management of NHL - Diagnosis by pathological lymph node examination - Radiotherapy as initial treatment when disease is localized - Chemotherapy for nonlocalized lymphomas - MST is 7-10 years - Therapy induced sterility should be discussed in chemotherapy - For men, sterility is commonly permanent - Sperm banking be discussed before radiation or chemotherapy - With periods of remission and recurrence - Risk factors of Breast Cancer - Age and gender - Menstrual and reproductive history - Hormones and oral contraception - Diet and body weight - Benign breast disease - Radiation hazard - Age and gender - Incidence increases with age - Frequently diagnosed after age 50 r/t increased probability of mutagenic changes over a longer life span - Incidence in first degree relatives - History of premenopausal breast cancer or bilateral disease

- Inherited breast cancer develops at an early age - BCRA gene I transmitted through autosomal dominant pattern of inheritance - With BCRA I, the risk of dev cancer is 50% before age 50 and 80% by age 65 - Menstrual and reproductive history - Early menarche (11-12 yrs) and late menopause (age 55) - Nulliparity or had first child after age 30 - The longer the menstrual history the longer the dividing ductal cells are exposed to hormonal stimulation - Hormones and oral contraception - 40% increased risk in older women receiving hormones for many years - Small increased risk if OCs are begun within 5 years of menarche and taken continually for 10 or more years - Diet and body weight - Fat maybe a promoter of cells being transformed from normal to malignant - Obesity can have a stimulating effect since estrogen is stored in adipose tissue - Some breast cancers are estrogen receptor positive - Benign breast disease - Fibrocystic disease is a risk when there is hyperplasia - Radiation hazard - Young women exposed to radiation show an increased incidence than older women exposed to the same degree of radiation - Pathophysiology - Carcinomas tumors that arise in the epithelial cells of ductal or lobular tissue - In situ carcinoma tumor is confined within a duct or a lobule - Infiltrative tumors that have spread directly into surrounding tissue and may have distant metastasis - Most tumors are located in the upper outer quadrant - Pagets disease , an eczema like inflammation of the nipple and areola may progress to an intraductal carcinoma - Malignant tumor is less mobile or fixed - Retraction or dimpling as tumor infiltrates surrounding tissues - Peau d orange lymphatic obstruction from tumor growth

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Diagnostic evaluation BSE Mammography Ultrasound Biopsy Staging of breast cancer using TNM Bone scan Chest xray Management of breast cancer Chemotherapy cyclophosphamide, methotrexate, 5-fluorouracil (CMF) as the standard regimen Anthracyclines, doxorubicin most effective for advanced breast cancer Radiation therapy eradicates tumor cells left behind after surgery Surgery Modified radical mastectomy standard form of mastectomy surgery Involves removal of the whole breast, some fatty tissue, and dissection of the axillary lymph nodes. Pectoral muscles and surrounding nerves are left intact Precautions after mastectomy Affected arm never used for blood pressure, injections, venipunctures No constricting clothing, jewelry on affected arm Not to carry heavy objects in affected arm Wear gloves when washing dishes Avoid needle pricks and cuts Keep skin moist and soft Wear gloves when gardening Avoid sunburn or use sunscreen liberally Use insect repellent when in an area where stinging insects maybe located Tend to cuts and scratches immediately by washing and applying protective covering Pre-operative care Assisting with treatment decision Assisting with the grieving process Promoting patient participation in the treatment plan Post-operative care Managing pain Preventing infection Promoting mobility of the arm and shoulder Patient /family education re: wound care, assessment of lymphedema, strategies to prevent trauma and infection Colorectal cancer

- Etiology o Familial adenomatous polyposis, an autosomal dominant disorder causing early development of multiple polyps in the colon and rectum o Only 5% of adenomas ever become malignant o Genetic mutation is critical to the development of cancer - Etiology - Inherited factors increase ones vulnerability to specific environmental factors - Low fiber, high fat, protein and refined car bohydrates - Cigarette smoking its amount and duration - Long standing ulcerative colitis and granulomas - Onset is 63 67 years - Men are affected more than women - Whites than african americans - Bowel cancer in two or more first degree relatives - Incidence higher in industrialized western world - pathophysiology - Bowel cancers arise from pre existing benign adenomatous colon polyps - Transformation is slow 1 cm polyp takes 7 years to progress to invasive carcinoma - Adenomas typically round and polypoid - Over time lesions penetrate the colon wall and extend into surrounding tissue - Lungs and liver metastasis - Dukes classification of colorectal cancer - Stage A : confined to bowel mucosa - Stage B : invading muscle wall - Stage C : lymph node involvement - Stage D : metastases or locally unresectable tumor o Stage A with 90% 5-year survival rate Stage D with 5% 5-year survival rate - Clinical manifestations - Frequently asymptomatic and diagnosed incidentally - Symptoms of partial bowel obstructionconstipation or diarrhea; pencil or ribbon shaped stool; senstion of incomplete bowel emptying - Gas or bloating - Occult or rectal bleeding

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o o o o o

Weakness, fatigue, malaise and anorexia Weight loss Abdominal pain Management Digital rectal examination Fecal occult blood tests Sigmoidoscopy Barium enema excellent in outlining large polyps Colonoscopy- the gold standard for diagnosis Cont. Chemotherapy palliative in nature 5 FU Levamamisol or leukovorin with 5 FU to stimulate immune system function and minimize damage to healthy cells In combination with radiation Radiation In rectal cancer Postoperatively to reduce recurrence Preoperatively to shrink the tumor External beam radiation or endocavitary irradiation Surgery Definitive treatment for colorectal cancer Removal of the tumor, surrounding colon and lymph nodes Low anterior resection through an abdominal incision used most extensively Temporary colostomy to allow for bowel rest and healing Dietary management No special diet A period of nothing by mouth and limited oral intake Measures for anorexia Problem of low levels of serum albumin Activity Restricted by anemia and fatigue Pain also limits activity Modify and space activities throughout the day To remain as active as possible Pre-operative care Bowel cleansing required Diet modification- low residue to clear liquid Laxatives, enemas to cleanse colon and suppress bacterial growth

o GoLYTELY (sodium sulfate, polyethylene glycol for osmotic cleansing of bowel o Oral neomycin as standard preparation - Pre-operative teaching - Incisions, NGT and wound drainage - Need for ostomy if applicable - Postoperative pain management-PCA - Pulmonary hygiene - Early ambulation to prevent respiratory and circulatory complications - Post-operative care - Maintaining fluid and electrolyte balance o NGT drainage- output, patency o IV fluids o Daily weight o Monitor electrolyte imbalance o Promoting ventilation - Pain can interfere with lung excursion - Assess for signs of atelectasis - Use of incentive spirometry to open alveoli - Deep breathing hourly in early postop phase - Supporting peristalsis - Temporary paralytic ileus is an expected complication - Auscultate abdomen every 4 hours - Early ambulation - Diarrhea initially but self-limiting - Avoid constipation - Laxatives be avoided if possible - Cancer of the Lung - Either metastatic or primary - Metastasis from colon and kidney common - Metastasis maybe discovered before primary lesion be found - History of smoking for 20 years or more - Exposure to arsenic, radon, asbestos particularly to those who smoke - Genetic predisposition - Cause closely related to smoking - Nearly 90% of persons with lung cancer die within 5 years of diagnosis - Cancer death rate for male cigarette smokers is more than double that for nonsmokers - Effects of smoking on lung cancer risk - Smokers are 10 times more likely to develop lung cancer - Risk associated with smoking increases with number of years person smokes

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- Risk decreases steadily when person stops smoking - Nonsmoking wives of smokers have sig higher risk of lung cancer - Pathophysiology - Most new growths arise from the bronchi - S/S of lesion in the bronchus and lung o 10% asymptomatic o Cough o Hemoptysis o SOB and unilateral wheeze common - Peripheral pulmonary lesions signs and symptoms - Pain on inspiration - Friction rub - Pleural effusion - Edema of face and neck when SVC involved - Fatigue - Clubbing of fingers - Types of lung cancer - Small cell lung carcinoma 15-25% of cases - Non-small cell lung cancer o Adenocarcinoma- most common 35-45% o Squamous cell carcinoma 30-40% o Large cell carcinoma 10% - Management - Histological exam by o Sputum examination o Bronchoscopy o Percutaneous transthoracic needle biopsy o Excision of the lesion - Staging techniques - Imaging techniques chest xray; CT scan; MRI; PET - Thoracentesis - Thoracoscopy and mediastinoscopy - Assessment of surgical risk - Morbidity and mortality higher in those 6065 years of age - Pulmonary reserve- ABGs and PFTs as measurements - Cardiovascular disease - Pneumonectomy for patients age 70 and over esp with surgery of R lung ( does 6070% of breathing) with higher risk - Thoracic surgery - Exploratory thoracotomy - Pneumonectomy- removal of a lung - Lobectomy one lobe of the lung removed - Segmental resection one or more segments removed

- Wedge resection- well circumscribed di seased portion removed - Group work - Identify 3 priority nursing diagnoses with at least 3 interventions each in the care of a patient with: G1 Leukemia G2 Lymphoma G3 Breast cancer (Postoperative) G4 Colon cancer G5 Lung cancer

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