Chapter 23: Concepts of Inflammation and the Immune Response Purpose of Immunity to neutralize, eliminate, or destroy organisms that invade

the internal environm ent. without harming the body Self- tolerance Immune system cells distinguish self from non-self proteins and cells, which inc lude infected body cells, cancer cells, and organisms. This ability to recognize self versus non-self is necessary to prevent healthy b ody cells from being destroyed along with invaders and is known as self-toleranc e. Failure to recognize ‘self’ = autoimmune disorder Each person is unique; Antigens are unique for each person (if someone else anti gen gets into your body then antigen antibody reaction takes place ) Antigens ar e protein on the surface of our cells and when stimulated antibodies are made! Question: At what point is our immune Fx the best? A) Infancy B) Teenager; C) 20 to 30 years D) 50 years and older (Nutrition and Age effect immune fx) Answer C; -This is why you don’t see many 30 yr olds in hospital. Infants are not good with immune system b/c they don’t have one yet and an older adult has a lesser due to w orn out system and older age; Chronic diseases and conditions of immune system can wear a system out; Good nut rition is needed for a good immune system; So elders and malnutrition have decreased immune system fx; Important lab values: serum albumin; protein; Prealbumin; ferritin (IRON); Hgb; Clinical observation of good nutrition: BMI; muscle strength; skin color; skin i ntactness; brittle dry nails; thin hair, etc; eyes (dry, sunken) WBC needs protein to develop!! Corticosteroids depress immune system; chemotherapy; Human Leukocyte Antigens Complex (HLA) HLA = A unique universal product code for each person Antigens are a normal part of the person; and act to stimulate an immune respons e when they enter another person’s body These antigens specify the tissue type of a person. If an ‘encountered cell does not match the persons universal product code (HLA’s) th en the immune system activates to neutralize, destroy, or eliminate the foreign invader Self-recognition Human Leukocyte Antigens Complex (HLA) Discovers of these complexes came from the trying to understand organ rejections during transplantation. Immune function effected by nutrition, drugs, disease, age; patients in the extr emes of age have decreased function Organization of the Immune System Not confined to one organ or area of the body Immune system cells come from the bone marrow.

Stem cells – undifferentiated cells (pluripotent) Bone marrow starts with the stem cells; (stem cell can differentiate into any bl ood cell needed for body) Maturational pathway of any stem cell depends on body needs and presence of spec ific-hormones (cytokines, factors) Leukocytes (WBC) – protect body from invasion Provide protection through defense actions Erythrocytes Thrombocytes Three process needed for immunity 1. Inflammation immediate, but short term; non-specific; may be localized or systemic; helps to start the full immune response 2. Anti-body mediated immunity B-lymphocytes ‘Humoral’ immunity 3. Cell-mediated immunity T lymphocytes Inflammation * Provides immediate protection against the effects of tissue injury a nd foreign proteins. * The capability for inflammatory response is critical to health and w ell-being. * Causes visible symptoms and can rid the body of harmful organisms. * Tissue damage may result from excessive inflammatory response. * Does NOT mean that infection is present Inflammatory process is NOT infectious but the infectious process is always infl ammatory; (Tissue injury great example, twisted ankle, heart attack, blisters – in flammatory process with no infection.. no foreign bacteria, etc that caused it) (Infectious is invading) inflammation inhibits arterial blood supply and can cau se tissue damage (localized); Some patients have a systemic inflammatory respons e (injury localized) body responses to the injury, arteries dilate, BP drop, you’l l see shock!!!; UO low, even when a dr does IV antibiotic they don’t get better (i f its just inflammation it wont help) this is all called SIRS (Will put pt in IC U) excessive inflammation; Leukocytes * Normal WBC count ~ 5,000 – 10, 000 * Differential normals (must have ~ 3000 granulocytes to fight infections) * Granulocytes (glandular in their cytoplasm) Infection fighting cells** Segmented Neutrophils (Segs, aka PMNs) ~ 60% w/out these you’d always be sick! BI G GUY!! Phagocytosis takes place by these guys; 1st responder EMS of white cells ; * Bands < 5% (left-shift when ↑ ) Basophils < 1% secrete heparin and antihistamine and others; (heparin that keep s capillary from making clots, temp, so the other cells can get to site of injur y) Histamine to vasodilate (more cells can get there); Allergic response (hypers ensitivity response) and increase with parasitic infestation; Eosinophils < 2% * Lymphocytes ~30% * Monocytes ~ 3 % Long Bones/Hip w/ Bone Marrow Bipsy (Hip bone is more activity); Typically on th

e site cleanse sites, topical pain med; (Bic pen size needle); when needle penet rates down into bone marrow it hurts (esp as aspirating); Lidacain, fetal posit ion (facilitate exposure to get down into muscle to bone) 10-15 min, Risk for Hemorrhage (pressure, place on back, can use ice; visualize and palpate site; * Bone Marrow Biopsy Jamshidi needle for Bone Marrow aspiration and biopsy * Cell Types of Involved in Inflammation Neutrophils Monocyte/ Macrophage (migrate and live in tissues as macrophages) Basophils Eosinophis Infection * Infection is usually accompanied by inflammation; however, inflammat ion can occur without invasion by organisms. * Inflammation does not always mean that an infection is present. Sequence of Inflammatory Responses * SIGNS of Inflammation: warmth, redness, swelling, pain, and decreas ed function; (rush of blood to site, fluid in interstitial space) * Stage I (vascular): change in blood vessels * Phase I: constriction * Phase II: hyperemia and edema * Stage II (cellular exudate): neutrophilia, pus - If there is a infec tion the white cells surround and engulf (clinically indication that that’s happen is pus); if someone is neutropenic there is no destroying; * Stage III (tissue repair and replacement) Question Pt arriving at ER after injured in accident is experiencing swelling an d pain at site. Nurse predicts the pt is experiencing which stage of inflammator y response? III II; Stage I Answer C- Stage I phase II Antibody-Mediated Immunity - B-Lymphocytes Released from BM and mature in lymphoid tissue (spleen, lymph nodes, t onsils) Make specific antibodies against specific organisms or toxins * An antigen enters the body; B cell recognizes antigen as non-self (n ow sensitized) and divides forming a) plasma cells that produce antibodies & b) memory cells; antibodies circulate within blood & body fluids (humoral, b/c the y circulate in body fluids) * Immunoglobulins = gamma globulins: IgG[KE1] , IgA, IgM, IgE, IgD Disease multiple myloma Immune Response: Two categories of Humoral Responses

1. Innate – natural within the person * Can be a barrier to invasion or can be a destroyer * Cannot be developed, or transferred from another, not adaptive * Inflammatory response is innate * No long term memory of the event * Pathogen – PAMP – PRR--- Innate leukocyte --- Phagocytosis * ----Target cell lysis . Adaptive – in response to invasion * Active- body makes the antibodies Natural – without human interference, the body makes the antibody to the antigen a

fter an invasion; longest lasting & most effective (get exposed and healthy B c ells make antibodies – and then if exposed again then they attack and destroy the invading antigen) Artificial – through immunization - invasion by an attenuated antigen; may requir e ‘booster’ to retain protection; dead but enough properties to make antibodies to t hat virus * Passive – antibodies passed from one person to another (breast milk, or i njection with antibodies made by another person/animal) short term Humoral Immunity (B Lymphocyte) help against bacteria, etc. w/ antibody * Acquired as a result of previous exposure * Has the ability not only to distinguish self from nonself, but to re cognize and destroy specific foreign agents based on the distinct antigenic prop erties * Mediated by the B lymphocytes (B cells) * Every effective again extracellular microbes and their toxins * B cells differentiate into antibody-secreting plasma cells Cell-Mediated Immunity: TLymphocyte * Help protect the body by differentiating self from non-self cells; non -self cells most easily recognized by cell-mediated immunity are cancer cells an d those self cells infected by organisms that live within host cells. * Important in preventing the development of cancer and metastasis after exposure to carcinogens. * Have many subsets, each with specific functions * Cancer (bad t lumph) Helper/Inducer T-cells * Most correct name is CD4+ * Helper/inducer T-cells easily recognize self cells versus non-self c ells. * Secrete lymphokines that enhance activity of other WBCs * Help increase immune function * Help maturation of WBCs * Helper/inducer T-cells act as organizers in “calling in arms“ of various squads of WBCs involved in inflammatory, antibody, and cellular defensive actio ns to destroy or neutralize antigens. * 600-1,200 CD4 cells per cubic millimeter of blood * HIV to AIDs means they don’t have sufficient CD4 cells!!!! (T count wa s _____) Suppressor * * * * une system * T-Cells Called theT8 + or the TS cells Help regulate cell-mediated immunity Prevent overreatction to non-self cells/proteins Secrete inhibitory lymphokines to inhibit growth and activity of imm cells If balance of T8 > T4 then person at ↑ risk infection

Cytotoxic T Cells * TC cells - a subset of suppressor cell * Most effective against self cells infected by viruses or protozoa (p arasites) Cytokines *

Hormones produced by WBCs (monokines and lymphokines)

* Once the cytokine binds to a receptor site, the responder cells chan ges its activity * Control inflammatory and immune responses * Examples: interleukins, interferons, colony stimulating factors, an d tumor necrosis factors (chart pg 375) * CMI helps protect body by differentiating self from non-self & rids body of abnormal malignant cells and cells invaded with harmful organisms. Cance r is a failure of the CMI ! Transplant Rejection: Role of NK and cytotoxic T cells to destroy * Hyperacute graft rejection: begins immediately and can’t be stopped (n ot reversible) Occur if not matching up blood properly or if receipent has had m any blood transfusion or freq transplanted organ; * Acute graft rejection; within 1 -3 months; S/S organ dysfunction (sc ar tissue developed so over time not good fx) * Chronic rejection: chronic inflammation with scarring and replacemen t of normal tissue with fibrous tissue * Treatment of transplant rejection: immunosuppressive therapy: Cyclo sporin (Sandimmune®), Imuran®, & steroids (prednisolone); Monoclonal antibodies (nterleukin 2 antagonist) bi nds to the IL-2 receptor sites & inhibits T cell growth * Maintenance: Tacrolimus (Prograf®) Pt receiving therapy w/ cyclosporine after transplant. Nurserec possible outcome of long-term immunosupp. Therapy w/ this drug is? A low cost therapy for suppre ssion of organ rejection; Possible serum sickness and anaphylaxis; risk for inf ection; Increased risk for cancer development. Chapter 27 Altered Cell Growth and Cancer Development Pathophysiology Hypertrophy is cell growth that causes tissue to increase in size by enlarging e ach cell. Hyperplasia is growth that causes tissue to increase in size by increasing the n umber of cells. Neoplasia is any new or continued cell growth not needed for normal development or replacement of dead and damaged tissues. Characteristics: Normal vs Malignant Cells Normal Slow cell division Morphologically like the ‘parent’ Small nucleus Perform specific functions Adhere tightly together Do not move away from site of origin; contact inhibition (touching, growth is inhibited); stick together; O Only divide & replace when needed and stop dividing when cell touches cell Have 23 pairs of chromosomes Malignant Rapid cell division Are anaplastic (poorly differentiated = undifferentiated) Need to look for terms like anaplasia (another name for differentiations) cancer tx depends on how much it looks like parents cells; Large nucleus Have no useful purpose; only thing its good for is replicating (more growth of c

ells) Don’t adhere to one another and will spread via blood, lymphatics, and body tissue s; Have no contact inhibition Expand and invade other tissues # chromosome pairs </ >/ = 23 - The faster the cells divide, the faster the growth of the tumor. As more cells accumulate, the normal tissue b/c disrupted. Cancers spread by invasion and metastasis. Invasion = the direct migr ation and penetration by cancer cells into neighboring tissues. Metastasis= the ability of cancer cells to penetrate into lymphatic and blood vessels, circulat e through the bloodstream, and then invade normal tissues elsewhere in the body. Steps: Cancer cells invade surrounding tissues and blood vessels Cancer cells are transported by the circulatory system to distant sites Cancer cells reinvade and grow at new locations Blood from gut goes to liver and the liver takes out nutrients, and toxins etc. if someone has gut cancer, the spread goes from gut to liver, then thru the hear t to the lungs; Naming – helps to determine site of origin Carcinomas, the most common types of cancer, arise from the cells that cover ext ernal and internal body surfaces. Lung, breast, and colon are the most frequent cancers of this type in the United States. Sarcomas are cancers arising from cells found in the supporting tissues of the b ody such as bone, cartilage, fat, connective tissue, and muscle. Lymphomas are cancers that arise in the lymph nodes and tissues of the body s im mune system. Leukemias are cancers of the immature blood cells that grow in the bone marrow a nd tend to accumulate in large numbers in the bloodstream. Learn these: Adeno = epithelial gland; hepato = liver; lipo= fat; lympho = lymp hoid tissue; osteo = bone; rhabdo = muscle; squamous = skin; (others = chondro = cartilage; erythro = red blood cells; hemangio = blood vessels; melano = pigme nt cell; myelo= bone marrow) If you hear sqaumous or basal skin cancers they are NOT life threatening (don’t sp read to tissues); the American Cancer society does not report these, this kind w ill be melanoma skin cancer!! Cancer Development Carcinogenesis/oncogenesis are names for cancer development Malignant transformation occurs through the following steps: Initiation (damage to DNA from carcinogens); T-lymphocytes is suppose to come in and destroy Promotion (enables CA cell to divide & grow) Progression (continued growth, may change features) Metastasis (spread to new locations via extension, local seeding, blood, lymphat ics) Carcinogenesis: transformation Oncogene activation – cause normal Δ → CA (cancer) Carcinogens: chemical (tobacco, hair dye), physical (radiation from sun, x-ray, chronic irritation), viral, dietary (excesses & deficits) – Excess nitrates and preservatives and “smoked” foods cause GI malignates) Deficits - Low Vit A, low fibers causes slower movement (HIGH FIBER, wheat, barl ey, beans, grains, crucierous veggies - Bro, cali, cabbage, brussel sprouts) oat s, fruit, “raw” fruits, uncooked stuff and the peelings) High Fiber foods: Wheat, barley, beans. Grains crucicerous veggies, oats, fruit , “raw” foods & uncooked stuff Crucicerous – broccoli, coliflower, cabbage, brussel sprouts Personal factors, immune function, age, and genetic risk


Chemicals, radiation, viruses, and heredity all trigger changes; DNA mutation genes can be mutated in several different ways; Oncogenes stimulate dev of cancer by instructing cells to make protein that stim ulate excessive cell growth and division (Normal cells regulate cell growth Tumor Suppresor genes- If tumor suppressor genes absent cancers develop. Indivi dual who inherit and increased risk of dev cancer often are born with defective copy of a tumor suppressor gene. The person then may develop cancer b/c there n o suppression to growth of abnormal cells Immuntherapy tries to stimulate T-suppressor cells Metastasis (blood or lymphatics) Metastasis occurs through a progression of steps: Extension into surrounding tissues Blood vessel penetration Release of tumor cells Invasion ü Local seeding (ovarian cancer) ü Bloodborne metastasis ü Lymphatic spread Breast – bone/lung/brain; lung – bone/brain; GI – liver/lung; prostate – bone If someone has lung cancer an it spreads to the brain it is really lung cancer i n the brain and we must treat it as lung cancer; Question: What is one of the common site of metastasis for breast cancer? A. Brain B. Lymph nodes C. Pancreas D. Pelvic Rationale: Breast cancer commonly metastasizes to bone, lung, liver, and brain. The lymph nodes are common for lung and melanoma. Pancreas is common for lung, prostate to pelvic nodes, and colon cancer to liver. Why cancer is dangerous? Cancer cells can spread to distant parts of the body. For ex melanoma ( a canc er of pigment cells) arising in skin can have cells that enter the bloodstream a nd spread to distant organs like liver or brain. Cancer cell growing in the brai n or liver can disrupt the fx of vital organs an are potentially life threatenin g; Question? Malignant tumor has metastasized from lung to brain? What type of canc er is in brain? Lung cancer in brain; use primary site when naming; Cancer Classification Cancer grading and staging help diagnosis, treatment, & prognosis. Grading on the basis of appearance and activity: compares the CA cell with its n ormal parent tissue. G1 – well differentiated, G4 – poorly differentiated, anaplasti c Staging classifies size of the CA, determines exact location and degree of metas tasis at diagnosis. TNM (T – size of tumor; N – number of involved lymph nodes; M – me tastatsize to another organ system); Stage 1 limited disease, Stage 4 disease has spread; Stage refers to size of tu mor! & extent of how much cancer does the person have Question: Single most important risk factors is: Bring a women Family Hx Cig Smoking Advancing age Rationale: Gender DOES NOT have a factor; AGE, according to the American Cancer Society, advancing age is most important risk factor!! External Factors & Carcinogenesis Chemicals Tobacco ETOH (alcohol can be a contributor) Physical

Chronic irritation Radiation UV (sun, tanning beds) Ionizing (natural elements – radon, uranium, radium) Bacterial H-pylori (upper GI cancer) ulcers & GI malignances Viral Epstein-Barr –Burkitt’s lymphoma Human papillomavirus (HPV) - genital Dietary High intake red meat & fats High intake preservatives, additives including nitrites Low intake of fiber, cruciferous vegetables, Vit A, Vit C (25 fiber/day) Tobacco Use and Cancer: Among factors that cause cancer, tobacco smoking is grea test public hazard. Cig smoke contains more than two dozen different chemicals capable of causing cancer. 1 out of every 3 cancer death relating to cigarette s moking Lag Time – carcinogens initiate genetic alterations & Proliferations. Time is requ ired. There can be a delay of several decades between exposure to a carcinogen a nd the onset of cancer. For ex, exposure to carcinogens from smoking cigarettes generally doesn’t develop into cancer for 20-30 years. ( Someone who was seriousl y sun burned at 5 may not get skin cancer til they are 40) When test is + for CA gene mutation, risk for CA development is HIGH, but test i s NOT diagnostic for cancer!! Consider implications 1st; cancers with genetic im plications: Breast, ovarian, some colon, esophageal/stomach Cancer Risk & Aging: B/c a # of mutations usually must occur for cancer to arise , chances of dev cancer increase as a person gets older b/c more time has been a vailable for mutations to accumulate. Ex 75 old person is 100X more likely to d ev colon cancer than a 25 yr old. B/c person are living longer than they did 50100 year ago they have longer exposure time to factor that may promote gene chan ges linked to cancer. ACUTE LUEKEMIA in a 2 yr old is curable but in an adult is not as promising; But Cancer is more likely to be seen in older adults; Cancer Prevention: Primary Avoidance of Carcinogens Sun, tobacco, asbestos Modification of risk factors Dietary modification, sexual practices Chemoprevention (to disrupt steps in CA development, reverse gen damage, halt pr ogression of transformation) Vit C/E, NSAIDS, Removal of ‘at risk’ tissues (moles, colon polyps, mastectomy) Healthy diet – increase fruit & veggies, and fibers – 5-9 servings of fruits and veg gies daily; Cancer Prevention: Secondary Screenings BSE (monthly) & Mammogram yearly p 40 Pap (yearly) TSE (15 – 35 monthly) PSA & DRE (yearly p 50) Fecal Occult Blood Testing (FOBT) (yearly) & Colonscopy (@ 50 then q 5 -10 year s) Gene therapy – in the future Question: Primary prevention would be Yearly mammography for women older than 40 yr Using skin protection during sun exposure at beach Colonscopy at age 50 Yearly PSA and DRE for men older than 50 Answer is B, prevention!! C A U T I O N

Change in bowel or bladder habits A sore that doesn’t heal Unusual bleeding Thickening or lump Indigestion or difficulty swallowing Obvious change in a wart or mole Nagging cough or hoarseness Cancer may no have any warning: That is why screening for some cancers is import ant. Cancer doubling time (BSE) palpable mass; your fingers cant detect a mass in bre ast til its around size of green pea (b4 big enough to be palpable in a breast i t may have been there for years and divided around 30 some times) Get Mammograpy after period; Cervical PAP – Early detection of cancer of uterine c ervix; Prostate –DRE & PSA or TSE for testicaular cancer; Colon – FOBT & Colonscopysmall amt of stool and test for blood Question : In affluent countries, what percentage of people diagnosed with cance r each year are cured of their disease? 50% (after 10 years without cancer, the y are considered cured, some are after 5) General Disease-Related Consequences of Cancer Complications RT metastasis If untreated, cancer ¡ Impairs immune and hematopoietic function, esp w BM invasion > ↓ WBCs, RBCs, plat elets ¡ Alters gastrointestinal structure and function > obstruction, liver failure, ca chexia (don’t want to eat and lose lots of wt) ¡ Motor and sensory deficits > nerve compression, bone involvement, SC compressio n (Spinal Cord) ¡ Weakness and nerve involvement ¡ Decreases respiratory function, esp. when lungs involved ¡ Increased clotting (when long sitting, riding, job, etc is not present) vComplementary Therapy – enhance affects if pt has positive outlook, mind and body are def connected (psychoneuroimunology); Support pt more likely to do well; in oncology we want to integrate therapeutic approaches; Power of prayer** v Nutritional therapy Well balanced diet Nutritional support Supplements Tube Feedings TPN v Transfusion support RBC FFP Platelets – can donate these (unless you take aspirin b/c it decreases stickin ess) Surgery as Cancer Treatment Oldest form of cancer treatment used for: ¡ Prophylaxis ¡ Diagnosis ** Get tissue to determine if malignant ¡ Cure- if they can get all tissues they can cure it (all visible evidence of dis ease) ¡ Control (cytoreductive = debulking) – remove bulk of disease not likely to cure ( You would do this for comfort measure like if it was blocking fecal matter etc) ¡ Palliation- diminish symptoms; debulking can be palliating too; ¡ Determining efficacy of therapy ¡ Reconstruction Considered as local therapy When it spreads by blood or lymph it may be in new location but amt is so limite d that we don’t catch it (pt undergoes resection of colon, it hasn’t treated the pos sible spread of somewhere else)

Nursing care of surgical client Basic physical care same as for any other surgical client – remember your ABCs Emotional impact of surgery – “what will they find?” “will they get it all?” “how can I liv without my ……..?” Uncertainty Grief – loss of body part, body function, loss if life Radiation Therapy for Cancer Purpose: to destroy cancer cells with minimal exposure of the normal cells to th e damaging actions of radiation Mechanism of action ¡ Cells are damaged by the radiation either outright or become unable to divide R adiation therapy works by damaging cells. Normal cells are able to repair themse lves, whereas cancer cells cannot. Killing effects of radiation Types of Radiation Therapy Teletherapy – external beam therapy (Pt NOT radioactive; must be in same position w/ every tx; usually 5X for 4-6 weeks) Brachytherapy – Short, closeup therapy & Sourse is within client, Continuous (LD) or intermittent (HD) Client is radioactive, durin LD tx until isotope is eliminated – 48hr Unsealed = given IV, PO, instillation; ex I^131 (radioactive iodine) Iodine is t x for thyroids; Sealed – implanted within tumor Some stay in place forever b/c isotope life is so short Preloaded – when placed in OR (placed in prostate) Pregnant ladies cant be in here Afterloaded – special applicators placed, then radioactive implant loaded; excreta are not radioactive; Preg lady can be in here Considered as Local therapy Radiation pysicsis (person who understands when too much radiation is bad for he althy cells) Side Effects of Radiation Therapy Vary according to the site Local skin changes and hair loss that will likely be permanent depending on the total absorbed dose Systemic effects: ¡ Altered taste sensations ¡ Fatigue related to increased energy demands Inflammatory responses in healthy tissue cause tissue fibrosis and scarring Bone marrow, hair and GI are fastest in dividing cells; if getting prostate “radia tion” wont lose hair on but if radiation around lymph nodes they will have bone ma rrow problems (have problems with esophageal and heart) Heart doesn’t respond to r adiation; Lens of eye can tolerate radiation; Nursing Care of Clients Undergoing Radiation Therapy Teach accurate objective facts to help client cope. ¡ Alopecia, Bone Marrow suppression, proctitis, myocardititis, pneumonitis, fatigu e Administer skin care. Do not remove markings. Do not use lotions or ointments. Avoid direct exposure of the skin to the sun. Care for xerostomia (dry mouth). FOR LIFE!!! Good dental hygiene; hard candies, liquids; Destruction of sweat glands Bone exposed to radiation is more vulnerable to fracture. Loose fitting clothing, no exposure to heat or cold, Splash PAT; no LOTION, Per fume, aftershave; no shaving Question: A pt who is receiving radiation therapy for breast cancer would experi ence which side ffect?

Sever fatigue : all pt with radiation can develop fatigue and can be debilitatin g and may last for weeks to months. Mucositis Mouth ulcers Hair Loss Nausea and vomiting Tandum (device that fits in vaginal cannal and opens uterine cervix so when she gets back to room the radiation seeds are placed in oval openings on side) Someone with the implanted things (little smaller than speculum) will have a fol ey and low residue diet (fiber) HOB lower Brachytherapy – protect thyself!! Monitor amt of time you spend with pt, distance b/t you and radiation source and protect with shielding; 30 min for the brady pt (more than 1 pt assigned to this pt) PRIVATE ROOMS!!!!! Skin care (dos and don’ts)

Types of RADIATION THERAPY Teletherapy = external beam therapy ¡ Pt is NOT radioactive ¡ Pt must be in same position every treatment ¡ Usually 5 times a week for 4 – 6 weeks Brachytherapy = short, close-up therapy & source is within the client, continuou s (LD) or intermittent (HD) ¡ Client is ‘radioactive’ during the LD treatment until isotope is eliminated ~ 48 ho urs ¡ Unsealed = given IV, PO, instillation; ex. I131 ¡ Sealed – implanted within the tumor ¢ Some stay in place forever because the isotope life is so short ¢ Preloaded ¢ Afterloaded – special applicators then radioactive implant loaded; excreta are no t radioactive

Protect ‘thyself’ (lead lying canaster and long tongs to pick up seeds) Nursing Care when Clients Undergo Sealed Source Radiation Therapy Private room No children under 16 No staff that is pregnant/ no pregnant visitors Visitors ½ hour a day Stay 6 feet from source Never touch radiation source with bare hands Be careful to NOT dislodge source All body secretions are radioactive – contact radiation safety officer if pt vomit s Floor where client walks, covered with protective covering Foods on disposable plates Flush toilet several times Trash/linens kept in room until client is D/C PPE – gloves & booties Limited contact Chemotherapy Treating cancer with chemical agents Considered as Systemic therapy, providing opportunity to kill metastatic cells Major role in cancer therapy Typically given IV, although some may be given orally; particularly lung cancer that’s very fast growing but it is very very receptive to chemo;

Bone marrow (LETHAL), hair and GI can be hurt most by chemo; Mechanism of Action Chemotherapy – ability of the drugs to damage DNA and interfere with cell division of the cancer cells Tumors most sensitive to drugs are those with rapid growth Will affect healthy cells as well as cancer cells Normal cells affected more are those that have rapid growth such as skin, hair, intestinal tissue, spermatocytes, and blood forming cells Used to cure and increase survival time; prolong good quality of life Some selectivity for killing cancer cells over normal cells Cell cycle specific (means it only works on the cells in that specific cell cycl e) Some cells will be in G0 – variable Quiescence; Prednisone gets them out of G0 – it activates them and gets the off the “fat rockers” wont kill them but puts them in active cycling phase; S Phase specific it will affect cells that are actively making DNA but wont affect the ones in G1 G2, etc; S (DNA synthesis 39%); G2 (Prep for mitosis 19%); M (Mitosis and cell division 2 %); G0 Quiescence (variable); G1 (Synthesis of components req for DNA synthesis 40%) we give combo drugs so we can hit multiple cell specifics Chemotherapy Drugs Antimetabolites --closely resemble normal metabolites and are “counterfeit” metaboli tes that fool cancer cells into using the antimetabolics in cellular reactions w hich impairs cell division. 5-FU (well tol. Drugs, wont lose hair or get sick) Methotrexte (Mtx. SENSITIVITY NEED SUNSCREEN), 6-Mercaptopurine Antitumor antibodies--damage the cells’ DNA and interrupt DNA or ribonucleic acid (RNA synthesis); Not a micro; S phase very phase specific; VERY LIKELY TO CAUSE THE SIDE EFFECTS!! Bleomycin- unusal toxicity to lungs (lil to heart) after a certain dose that’s all they can have for life.. watch COPD patients; Doxirubicin- (Adriamycin/Red devi l) lose hair after 10 days, its cardiac toxic and they can only have a max dose/ life; Mitomycin C- lose of Calcium; Alkylating agents--cross link DNA, making the two DNA strands bind tightly toget her inhibiting cell division Busulfan (Cisplatin) – Easliy tolerated! Nephrotoxic so they need Creatinine (24hr urine) clearance; Chlorambucil, Cytoxan- Hemorrhatic cystisis, CCNU, Alkaran Antimitotic agents--made of plant sources, interfere with the formation of micro tubules, interfering with mitosis during cell division Taxol – comes from tree bark,ethical issues with forest; Vincristine (periwinkle plant), slow peripheral nerve production, neurotoxicity; (sensation, muscle contraction,same issue as DM pt) slow gut; Vinblastine – cause neurotoxicity same as vincristine; Topoisomerase inhibitors--Enzyme need for DNA synthesis and cell division; Allow s DNA to be copied, than it reattaches the DNA together ; Causes DNA breakage an d cell death VP16, VM 26 Miscellaneous chemotherapeutic agents--Inhibition of important enzyme systems; C ompetition for important substances in metabolic pathways Asparaganiase, Hydroxyurea

Combination chemotherapy--Increase effectiveness of several drugs; to produce cu mulative effects; may prescribe one from each and prednisone to get max cell kil l; each cancer ‘Rescue’ agent ¡ Leucorvan Folic acid used w/ Mext. Rescue healthy cells from excessive damage f rom Mext (not a chemo really Folic acid) Timing of this drug is critical… know exa ctly how soon after you admin Mxt when you should get this drug Side Effects: alopecia, N/V, bone marrow suppression Chemotherapy & the Cell Cycle Noupegn- stimulates bone marrow to stimulate white cells Nator max effect on bone marrow (Plasma, Leucocytes and platelets and erythrocyt es in a tube separated) At low point they are at risk for infection; Treatment Issues Nadir- point after administration of drug that person bone marrow is most depres sed; NEEDS CBC prior to next tx cycle We need to know that bone marrow has recovered and the WBC is normal range) Need 3,000 granulocytes (neutrophils) to fight off; Most tx aren’t daily Drug dosage – based on client’s body size (M2) Ht and Wt Ø If they are 1.8M^2 and its 2mg we just multiply; Don’t have to know how to calcul ate M2; Drug schedule – timed to maximize cell kill; what tx plan for the pt Drug administration – ¡ Extravasation of a Vesicants (causes severe tissue damage if infiltrates) (Students don’t admin chemo) ¡ Put in new IV before doing chemo… lots of pt get picc line, central, etc to dimin ish pain of stuck all the time and risk of extravasation is almost none; ¡ Mixing pharmacist and administering RN protect self (absorbed through skin & mucous membranes; therefore wear spec ial PPE) ¡ Special precaution with chemobio wastes kit REMEMBER PROTECT THYSELF w/ chemo drugs Verification of drug, route, dose, and schedule/ Cal check twice. Extensive client education Exposure from Resp inhal Skin absorption Oral ingestion OSHA guidelines PPE (gowns, gloves) during prep and admin Laminar-flow hoods during prep Gowns and gloves handing body secretion of clients within 38 hr after chemothera py Hematopoietic Growth Factors Epoetin (Epogen/Procrit) Filgrastim (Neupogen) WBC stimulator, feel like ya got flu Pegfilgrastim (Neulasta) Oprelvekin (Neumega) – platelet release (At risk for bleeding) Steriods ü Prednisone stimulates bone marrow (activates G0 cells)

Antiemetics Prochlorperazine (Compazine) Act CRAZY (Pyscho) Promethazine (Phenergan) makes you sleepy; burn if rectal; slow if over IV and c an cause psycho stuff; Metoclopramide HCL (Reglan) – increases Gastric emptying, antiemetic properties as well; Ondansetron HCL (Zofran) – least side effects; common IV push THC (meranaol) – generic of marijuana; Routes of Admin (SYSTEMIC therpy) Port-a-cath: occlusive dressing; aseptic tech; IV Oral (not many) Intrathecal – (b/c most meds do not cross Blood-Brain barrier) if pt has brain tumors then it must be directly placed in epidural so it is put in CSF; If frequent use then they use ommaya reservoir (port-a-cath type techniq ue, access by placing needle thru scalp into reservoir and med goes into ventric les Intravessicles (into bladder) Intra hepatic (into kidney) Femoral artery (osteogenic carcoma, save leg) heating/cooling; Inhalation Side effects of chemo- Side Effects of Chemotherapy Alopecia or hair loss – wigs, caps, Mucositis/stomatitis in the entire gastrointestinal tract In mouth or whole GI tract (Candida every shift, ulcers in mouth) Listerine is t oo strong (heavy alcohol), do cheap mouth washes and dilute with water b/c alcoh ol is a drying agent; lemon & glycerin swabs (lemon eats enamel away and glycerin is alcohol); Use sof t bristle toothbrush.. gentle mouthcare; Nystatin (magic mouthwash) will be administered if they have candida (an tifungal); Bendryl, textrcycline, Lidacain (numbs mouth) Stomatitis- not eating, pain, popsicle and ice works great before eating food; r isk for infection and then into blood stream causing fungal septicemia; If mouth looks red the other GI tracts looks same, swallow nystatin and magic mouth wash ; Nausea and vomiting If you know the drugs causes N/V give antiemetic; give another; serve cold food instead of hot; Fluid and electrolyte; nutrition; Skin Changes Anxiety, sleep disturbance Altered bowel elimination Decreased Mobility Bone marrow suppression Leukopenia – granulocyte; neutropenic precautions Wear glown gowns masks, Nec. Private room; No fruit baskets, no flowers, etc. (k itchen orders, no salads, etc. MUST BE COOKED!!) pan cultures (cultures every or ifice, urine, blood, sputum, stool, etc.) Broad spectrum get culture before you admin med, (unless they cant produce sputum) Vitals q4 Thrombocytopenia – Risk for bleeding (lower platelet count higher risk 100,000 & < ALL BIG RISKS) no invasive procedures; maybe platelet transfusion; No hard dry crunchy foods; s oft toothbrush or toothit; neumovax IM don’t do it for bleeding risks; (try to do IM with small 23s, put lots of pressure, use deltoid, maybe use ice bag), check vomit and stool and urine cause they can bleed anywhere b/c they don’t clot; NO AS PIRIN or plyvax (no stickiness) Anemia – Lack of oxygen delivery – confusion, headache, seizure, chest pain, angina,

heart rate increases and irregular; constipation no bowel sounds, bloody diarrh ea, abdominal cramps; fatigue & muscle cramps (claudiation – pain when walking, an gina of legs) May need transfusion, iron, PO iron dark teeth delivery w/ straw, black stool, V it C inhances iron absorption, cast iron skillet b/c iron gets into food; IM iro n (z-track) irritant and stain tissues; IV iron (Venofer) infusion, brown liquid , must be protected from light and can cause anaphylaxis (swelling at IV sight, respiratory stridor, bp drops, start drugs slow to see how pt tolerates it; FOOD S in iron: Meat/fish/poultry, oranges, cantaloupe, strawberries, broc, tomato, p otato, green peppers, grains ; DON’T GIVE spinach, chard, beet greens, rhubarb and sweet potato Question: What is the expected outcome rt hair loss for pt who is undergoing che motherapy? Hair loss may be permanent Hair regrowth usually begin about 1 month after completion of chemotherapy; New hair growth will likely be identical to previous hair growth in color and te xture Hormonal Manipulation Some hormones make hormone-sensitive tumors grow more rapidly. Some tumors actually require specific hormones to divide, therefore decreasing t he amount of these hormones to hormone-sensitive tumors can slow the cancer grow th rate and increase survival time. Side Effects of Hormone Therapy Androgens and antiestrogen receptor drugs cause masculinizing effects in women. For men and women receiving androgens, acne may develop, hypercalcemia is common , and liver dysfunction may occur with prolonged therapy. Feminine manifestations often appear in men who take estrogens, and gynecomastia can occur.

Tamoxifem- antiestrogen (hair growth, menopausal (hot flash, night sweat) Immunotherapy: Biological Response Modifiers Drugs that modify the client’s biologic responses to tumor cells Cytokines: enhance the immune system Interleukins, interferons Side effects: generalized and sometimes severe inflammatory reactions, periphera l neuropathy, skin rashes, increased depression Gene Therapy Experimental as a cancer treatment Renders tumor cells more susceptible to damage or death by other treatments Injection into tumor cells, enabling the immune system to better recognize cance r cells as foreign and kill them Monoclonal antibodies Antisense drugs Oncologic Emergencies 1. Sepsis – Can cause shock 2.Disseminated intravascular coagulation (DIC) – BLEEDING; Collaborative management includes: ¡ Prevention (the best measure) ¡ Intravenous antibiotic therapy (for sepsis) ¡ Anticoagulants, cryoprecipitated clotting factors (for DIC)

3. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) – reabsorb water, excret e less water; H20 is reabsorbed to excess by the kidney and put into system circulation. SIADH is most commonly in CA of the lung Showing hyponatremia (from dilution) showing in neuro; Collaborative management includes: ¡ Fluid restriction ¡ Increased sodium intake ¡ Drug therapy with demeclocycline that works in opposition to antidiuretic hormone 4. Spinal Cord Compression Tumor directly enters the spinal cord or the vertebrae collapse from tumor degra dation of the bone. Tumors in the spine become a problem when they compress the spinal cord or nerve s. This can lead to serious complications such as paralysis and loss of bladder and bowel control. Others can destroy the vertebral bone that supports the spina l cord making it unstable. Incontinence; Cant walk; loss of motor and sensory fx; Collaborative management includes: ¡ Early recognition and treatment ¡ Palliative ¡ High-dose corticosteroids ¡ High-dose radiation ¡ Surgery ¡ External back or neck braces to reduce pressure in the spinal cord If there is a vertebral tumor with spinal cord compression this is a EMERGENCY!! ! IV steroid (decrease inflammation); Mid night, pt suddenly has bowel bladder incontinent (breast and bone metastisis) 2-3 hr to get tumor OUT or undergone tx to try to preserve spinal cord!! 5. Hypercalcemia Occurs most often in clients with bone metastasis (bone is releasing Ca++) From tumors that secrete PTH From Bedrest Generally develops slowly and body adapts but can be life threatening Abnormal cardiac display (QT short) Signs and symptoms of hypercalcemia may include: Nausea / vomiting Fatigue/Lethargy Stomach pain/constipation Anorexia Extreme thirst Dry mouth Moodiness/ Irritability Confusion Frequent urination Extreme muscle weakness Irregular heart beat Coma Paralytic ileus Abnormal behavior Treatment for hypercalcemia FLUIDS Oral glucorticoids, calcitonin, mitramycin C, diuretics Dialysis 6. Superior Vena Cava Syndrome (life threatening) SVC is compressed or obstructed by tumor growth in upper chest (lymph nodes, lun g cancer, etc blocks blood return in SVC into right Atrium). Block blood to ches t and arms and head Condition can lead to a painful, life-threatening emergency. Signs include edema of face, edema of arms and hands, dyspnea, erythema, and epi staxis. JVD, airway #1;

Late-stage signs include hemorrhage, cyanosis, change in mental status, decrease d cardiac output, and hypotension. Collaborative management includes high-dose radiation therapy, but surgery only rarely. 7. Tumor Lysis Syndrome Large numbers of tumor cells are destroyed rapidly; resulting in intracellular contents being released into the bloodstream faster than the body can eliminate them. a.Hyperuricemia (Gout/uric acid kidney stones) When lots of cells die uric acid is released an at risk for gout, stones, etc. give allopurinol Collaborative management includes: ¡ Prevention ¡ Hydration ¡ Drug therapy (for hyperuricemia) Allopurinol (Zyloprim); Probenecid (Benemid); Colchicine; NSAIDs b. Hyperkalemia (Tall Tented T wave) Drug therapy (for hyperkalemia) Kayexylate Loop or thiazide diuretics Regular Insulin (IV) [and D50%] The nurse is assessing for tumor lysis syndrome in a pt who has been receiving c hemo? Hyperkalemia & hyper urcemia