Medical-Surgical Nursing Module 9: Oncology Nursing PDF

MEDICAL-SURGICAL NURSING MODULE 9: ONCOLOGY NURSING NCM112 LECTURE 1ST SEMESTER MIDTERMS TRANSES BY: ALLIE ILIGAN INTRODUCTION  Hypertrophy - the enlargement of an...

MEDICAL-SURGICAL NURSING MODULE 9: ONCOLOGY NURSING NCM112 LECTURE 1ST SEMESTER MIDTERMS TRANSES BY: ALLIE ILIGAN INTRODUCTION  Hypertrophy - the enlargement of an organ or tissue from the increase in size Aberration is a deviation from normal. And this is of the cells what is happening to the cells of a person who is afflicted with cancer, a disease characterized  Metaplasia – conversion of one type of as uncontrolled division of abnormal cells which may mature cell into another type of cell (e.g. occur in any part of the body. mucus secreting ciliated pseudostratified Cancer is the second leading cause of death globally columnar epithelial cells of the lungs are and is responsible for an estimated 9.6 million deaths turned into stratified squamous epithelium in 2018. Globally, about 1 in 6 deaths is due to when exposed to cigarette smoke) cancer (WHO, 2018).  Neoplasia – formation of a new, LESSON 1: INTRODUCTION TO ONCOLOGY abnormal growth of tissue; otherwise known as neoplasm; also, tumor  Cancer – an umbrella term for a group of diseases in which certain cells grow and  Malignant tumor – a tumour that multiply uncontrollably eventually forming invades and destroys the tissue in which tissue masses called tumors it originates and has the potential to spread to other sites in the body - a disease process whereby cells proliferate abnormally ignoring  Benign tumor– a tumour that does not growth regulating signals in the invade and destroy the tissue in which it environment surrounding the cells originates or spread to distant sites in the body  Oncology - field or study of cancer  Myelosuppression – a reduction in  Anaplasia – a loss of normal cell blood-cell production by the bone marrow; characteristics or differentiation; different may result in anemia, infection and in shape and organization with respect to abnormal bleeding their cells of origin; usually malignant (The more anaplastic the cell is, the more  Carcinogenesis – process of it is malignant) transforming normal cells into malignant cells  Dysplasia – abnormal and potentially reversible process where there is  Carcinogen -is any substance or agent disordered growth (bizarre cell that promotes cancer. It may be growth) and maturation of cells and the genotoxic. It has the ability to damage the tissues and organs which they make up; genome or disrupt cellular metabolic premalignant processes.  Hyperplasia – the enlargement of an  Mutation – change in the genetic material organ or tissue caused by an increase in of a cell which is not caused by normal the reproduction rate of its cells (not genetic process cancer but may become cancer)  Apoptosis – programmed cell death  Alopecia – hair loss 1  Neutropenia – an abnormal decrease in  Radiation therapy – use of ionizing the number of neutrophils in peripheral radiation to interrupt the growth of blood malignant cells  Leukopenia – a decrease in the  Adjuvant Therapy – treatment given to circulating WBCs patient after the primary treatment, which is usually surgical removal of the tumor  Thrombocytopenia – decrease in the number of circulating platelets  Neoadjuvant Therapy – treatment given before the surgical treatment of the tumor  Pancytopenia - a simultaneous decrease with the aim of improving the results of in the red cells, white cells and platelets in surgery and preventing the development the blood of metastasis  ANC = (Total WBC count x {%  Proto-oncogenes - are normal genes segmented neutrophils + % bands} that help cells grow. / 100  Oncogene - is any gene that causes  Nadir – lowest ANC after cancer. myelosuppression  Angiogenesis - is the creation or - severe risk of infection, ANC of development of new blood vessels less than 1,000 cells/mm3  Vascular endothelial growth factor  Undifferentiated Cell – a primordial cell (VEGF) - is a signal protein produced by that has not assumed the morphologic cells that stimulates the formation of and functional characteristics it will later blood vessels. It is part of the system that acquire restores the oxygen supply to tissues  Remission – absence of signs of cancer when blood circulation is inadequate such as in hypoxic conditions.  Blood Dyscrasias – pathologic condition or disorder in which the constituents of  Epidermal growth factor (EGF) - is a the blood are abnormal or are present in protein that stimulates cell growth and abnormal quantity differentiation by binding to its receptor, EGFR  Chemotherapy – use of medications to kill tumour cells by interfering with cellular  Tumor suppressor genes - are normal functions and reproduction genes that slow down cell division, repair DNA mistakes, or tell cells when to die.  Vesicant – substance that can cause tissue necrosis and damage particularly when extravasated  Extravasation – leakage of medication from the veins into the subcutaneous tissue. 2  THE CELL CYCLE  Cytokinesis – cell’s cytoplasm divides in half forming distinct cells A series of events that take place in a cell  After each cell division, each of the leading to its division and duplication or daughter cells begin the interphase of a replication. new cycle  A vital process by which a single celled  Activation of each phase is dependent on fertilized egg develops into a mature the proper progression and completion of organism as well as the process by which the previous one hair, blood cells and internal organs are renewed TYPES OF CELLS: 2 PERIODS OF CELL CYCLE: 1. Stable cells  Interphase – cell grows accumulating  Cells that multiply only when needed nutrients needed for mitosis and duplicating its DNA  They spend most of the time in the Go  Mitosis – cell splits into 2 distinct cells, phase of the cell cycle often called daughter cells  Can be stimulated to enter the cell cycle when needed PHASES OF CELL CYCLE:  e.g. Liver cells, proximal tubules of the 1. Gap 0/G0 - resting phase where the cell kidneys, endocrine glands has left the cycle and has stopped 2. Labile cells dividing  Multiply constantly throughout life 2. Interphase  e.g. GI lining, bone marrow, hair  Gap 1/G1 – cells increase in size; 3. Permanent cells the G1 checkpoint control  Incapable of reproduction or multiplication mechanism ensures that  e.g. brain cells, heart cells, skeletal everything is ready for DNA muscle cells synthesis Discontinuous Replication - Cells in these  Synthesis/S – DNA replication organs divide at a low wear and tear occurs replacement rate. (ex: liver and kidney)  Gap 2/G2 – during the gap between DNA synthesis and  Renewal rate must compensate the mitosis, the cell will continue to destruction rate grow; the G2 checkpoint control NORMAL CELLS VS. MALIGNANT CELLS mechanism ensures that everything is ready to enter the M NORMAL CELLS MALIGNANT CELLS phase  Sources are  Sources are stem 3. Cell Division/Mitosis/M - cell growth specialized cells cells stops, and cellular energy is focused on  Cells are well  Anaplastic; poor differentiated differentiation the orderly division into 2 daughter cells;  Destruction  More produced than a checkpoint in the middle of mitosis balanced by destroyed (metaphase) ensures that the cell is ready replacement  Less dormant time to complete cell division  Spend time dormant  Move through cell  More resting time in cycle rapidly; mitosis 2 Processes: Go phase of cell occur more  Mitosis – cell chromosomes are cycle frequently  Less rapid cell  More than 2 cells; divided into 2 division abnormal 3   2 cells, normal chromosomes are  Papillomas – from epithelial tissue; chromosomes commonly found cauliflower like projections that erupt  Contained  Invasion and from skin or mucous membrane  Contact inhibition is Metastasis  Contact inhibition is  Warts – hard papillomas (verruca present  Forms intracellular absent vulgaris) junction  Does not form  Adenomas – glandular tumors intracellular junction o prostate, breast  Rampant growth  Cystadenoma – if tumor become cystic  altered cell o breast, ovary membrane  cell membrane contains tumor specific antigen  contains less fibronectin, a cellular cement  nuclei of cancer cells are large and irregularly  Fibromas – composed of fibrous shaped connective tissue  nucleoli structures within the nucleus o affect the skin and mucous that have the membrane RNA is larger and more numerous  less dependent on the availability of a constant oxygen supply Not all tumors are malignant. Some are benign.  Myomas – muscle tumors Certain characteristics differentiate them from o frequently affect smooth muscles one another. But, whenever we talk about such as the uterus (leiomyomas) CANCER, we are referring to MALIGNANT tumors. BENIGN TUMOR VS. MALIGNANT TUMOR Characteristics of Benign Neoplasm:  Well-differentiated  Slow growth  Encapsulated  Non-invasive  Pigmented Nevi (moles) - small, dark  Does NOT metastasize spots occur on the face and neck; maybe  Usually localized covered with coarse hair.  Does not usually cause tissue damage  Nevi – usually present at birth, grow nor death somewhat then become stationary or regress Some types of Benign Neoplasm: 4   Malignant Lymphomas - made up of lymphoid cells; occur in the spleen bowel and lymph nodes  Squamous Cell Carcinoma - typically an aggressive lesion creating ulcerations in  Lipomas local areas and destroying underlying o large but not serious tumor masses tissue; frequently occurs in the lungs, o common sites: buttocks, shoulders, mouth, cervix, lips. neck  Basal Cell Carcinoma - special type of o round and encapsulated squamous cell carcinoma that is slower o easily removed growing and does not create metastasis; appears on facial regions bordered by the ears, upper lip and hairline Characteristics of Malignant Neoplasm:  Undifferentiated  Adenocarcinoma - glandular or glandlike  Erratic and Uncontrolled Growth/Rapid structure cancer; cells have cytoplasm capable of secretory functions; common  Expansive and Invasive in the GIT, female breast, uterus, lungs  Secretes abnormal proteins  Transitional Cell Carcinoma - peculiar  METASTASIZES to cells lining the passages of the urinary  Causes generalized effects tract  Causes tissue damage and death  Sarcomas - from connective tissue Classification of Malignant Neoplasms o highly invasive, metastasize According to Site of Origin: rapidly to distant sites early in their course  Gliomas – from the supporting tissue of o common in youth the CNS (Brain) o may occur in any part of the body  Neuroblastomas - composed of o soft and bulky, has abundant undeveloped nerve cells, common only in blood supply children  Malignant Melanomas- pigmented nevi ----------------------------------------------------------------- of the skin How does cancer develop? Here is where carcinogenesis or the malignant transformation of cells comes in. There are several theories on cancer formation. First is the Genetic Code Theory which states that all individuals have cancer cells known as oncogene. And when this oncogene is exposed 5 to carcinogens, hidden code may be unmasked,  Multiple growth factors such as EGF cell structure changes, and becomes malignant. (epidermal Growth Factor) influence cellular growth and proliferation Another theory is the Immune System Failure  Tumor suppressor gene becomes which says that good immune system prevents mutated and is turned “off” allowing cancer, otherwise malignancy develops. malignant cells to reproduce. When Geneticist, Dr. Isaac Berenblum also gave his suppressor genes become mutated, theory known as Initiation and Promotion they lose their regulatory capabilities. which states that both the carcinogens and Apoptosis will not happen. promoters are needed for cancer to develop,  VEGF (Vascular Endothelial Growth thus it becomes a process that evolves over Factor) promotes tumor angiogenesis time. which nourishes the tumor cells Present day oncology recognizes the three main  P53 (TP53) – frequently mutated phases, otherwise known as the three step tumor suppressor gene cellular process of carcinogenesis:  guardian of genome – responsible in conserving cellular stability by INITIATION, PROMOTION and preventing genome mutation PROGRESSION.  determines whether the damaged cell CARCINOGENESIS: Malignant will live or die Transformation-3 Step Cellular Process  alteration may decrease apoptotic signals, decreasing mutant cell death 1. INITIATION  Mutant TP53 is associated with poor  Initiators (carcinogens) such as prognosis chemicals, physical factors, and 3. PROGRESSION biologic agents alter the genetic  Cellular changes formed during structure of the cellular DNA initiation and promotion exhibit  Normally, cells will either repair or die. increased malignant behavior But occasionally, cells escape these  Invades adjacent tissues and protective mechanisms and metastasizes permanent cellular mutation occurs  These mutations usually are not INVASION significant to cells until the second  Growth of primary tumor to step of carcinogenesis surrounding host tissue 2. PROMOTION  How: mechanical pressure – finger  Repeated exposure to promoting like projections – surrounding tissues agents causes the expression and interstitial spaces of abnormal or mutant genetics  Destructive enzymes- destroy information even after long surrounding tissues, structural tissues latency periods of the vascular membrane  Proto-oncogene, responsible for cellular growth is mutated and METASTASIS – spread of cancer cells transformed to oncogene (gene that  Lymphatic Spread - most common causes cancer) which is switched “on”; mechanism of metastasis thus, cellular growth and proliferation  Hematogenous Spread are stimulated.  Angiogenesis  Direct Extension 6   Seeding or Diffusion  e.g. pleural effusion and ascites 5. Ulceration  Ulceration and necrosis result as the tumor erodes blood vessels and pressure on tissue causes ischemia; infection may soon follow 6. Vascular Thrombosis, Embolus, Thrombophlebitis  tumors tend to produce abnormal coagulation factors that cause increased clotting  individuals with cancer occasionally have thrombophlebitis  pulmonary emboli that result from thrombus formation can SYSTEMIC EFFECTS OF MALIGNANCY be a life threatening or fatal 1. Pressure outcome  as parenchymal tissue is replaced 7. Anemia by neoplastic growth, pressure is  cancer cells produce chemicals exerted on tissues and organs in that interfere with the the area production of red blood cells  obstruction, pain, ischemia and  iron uptake is greater in the necrosis soon follow tumor than that deposited in the 2. Obstruction liver  as tumor continues to grow, hollow  blood loss may result from organs and vessels become bleeding compressed and obstructed 8. Hypercalcemia  esophagus, bronchi, uterus, bowel,  tumors of the bone, multiple blood vessels and lymphatic myeloma, squamous lung system are the common sites cancer and cancer of the breast produce a parathyroid-like 3. Pain hormone that increases or  can be caused by pressure on accelerates bone breakdown nerve endings, distention of organs and release of calcium or vessels, or lack of oxygen to  results from metastasis to the tissues and organs bone  tumor itself may release pain  enhanced by immobilization mediators and dehydration  usually a late sign of cancer 9. Edema 4. Effusion  caused by obstructed blood  when lymphatic flow is obstructed, and lymphatic flow there may be effusion in serous  a result of decreased serum cavities protein from anorexia 7  10. Disseminated intravascular ETIOLOGY OF CANCER: coagulation (DIC) 1. Physical agents  can occur with all tumors but is  Exposure to Radiation more likely with cancer of the  Exposure to sunlight lung, pancreas, stomach and 2. Chemical agents prostate  Smoking  precipitated by the release of  Dietary ingredients tissue thromboplastin or  Drugs endothelial injury 3. Genetics and Family History 11. Anorexia-Cachexia Syndrome  Hallmark of Families with a Hereditary  malignant neoplasms deprive Cancer Syndrome normal cells of nutrition a) Cancer in 2 or more relatives  tumor itself produces alteration b) Cancer in family member in enzyme systems necessary younger than 50 years of age for normal metabolism c) The same type of cancer in  stored fat is lost, and tissues several family members lose nitrogen d) Family members with more  tumor reverts to anaerobic than one type of cancer metabolism, consuming e) Rare cancer in one or more glucose, depleting glycogen family members stores in the liver and 4. Dietary habits converting glucose to lactate  Low-Fiber  there is protein depletion, and  High fat the serum albumin levels  Processed foods decrease  Alcohol  cancer cells may also produce 5. Viruses and Bacteria an anorexigenic substance that  Hepa B, Herpes, Papilloma Virus acts in the satiety center of the  HIV hypothalamus causing anorexia  H. pylori  taste sensations diminish (hypogeusesthia) or become altered (dysgeusia), and the 6. Hormonal agents individual may have an  DES aversion to eating particularly  OCP especially estrogen meat 7. Immunologic Defects 8. Physical Irritation ----------------------------------------------------------------- 9. Precancerous Lesions LESSON 2: DETECTION AND SCREENING 10. Emotions Up to this very moment, one specific, direct  Carcinogens - agents known to cause cause of cancer has not been confirmed cancer or at least are strongly linked to yet. But instead, what is being pointed out as certain kinds of cancer. the cause of cancer is the interplay of different o Known carcinogens include agents and factors viruses, drugs, hormones, chemicals, physical agents ETIOLOGY OF CANCER o Can be genotoxic or promoter substances RISK FACTORS ASSOCIATED WITH CANCER 8   Genotoxic – directly alters DNA and prevention is better than cure and early cause mutation detection leads to early intervention.  Promoter Substances – cause other  Primary Prevention – risk reduction adverse biologic effects such as  Secondary Prevention – early diagnosis, cytotoxicity, hormonal imbalance, altered prompt intervention immunity or chronic tissue damage; do  Tertiary Prevention – care and rehabilitation not cause cancer in the absence of after diagnosis and treatment previous damage cell and require high level and long-term contact. PRIMARY PREVENTION  Avoid known carcinogens  Dietary and lifestyle changes RISK FACTORS ASSOCIATED WITH  Certain medications (tamoxifen)-can CANCER: reduce the incidence of breast cancer by 1. Family History - with inherited cancers 49% in postmenopausal women identified 2. Age – over 55 as being high risk for breast cancer 3. Health Habits (Fisher, 1998)  Smoking – smokers  Increase consumption of fresh vegies  Diet - those eating high  Increase fiber intake cholesterol, low fiber diet  Increase intake of Vit. A and C rich foods 4. Occupational exposure – farmers,  Weight control miners,  Reduce intake of dietary fat sailors, furniture workers, beauticians,  Moderate consumption of preserved zinc mixers, asbestos workers, health foods workers  Stop smoking 5. Residence – urban dwellers  Reduce alcohol intake 6. Precancerous lesions – individuals with  Avoid overexposure to the sun moles, burn scars, polyps, fibrocystic disease of the breast 7. Other Cancer – individuals with history of cancer SECONDARY PREVENTION (Detection and DETECTION AND PREVENTION OF CANCER Screening) During the old times, the focus of cancer care is  Breast on tertiary prevention which is synonymous with o Female 20-39 y/o care and rehabilitation of patients after cancer  Clinical Breast Exam every diagnosis and treatment. In recent practices, the 3 years American Cancer Society, the National Cancer  Self-Breast Exam every Institute, clinicians and researchers are giving month more attention on the primary and secondary o Female equal or greater than 40 prevention of cancer. Primary prevention is y/o focused on risk reduction of cancer among  Clinical Breast Exam, healthy individuals. Secondary prevention deals mammogram every year on detection and screening for early diagnosis  Self-Breast Exam every and prompt intervention with the aim of halting month the cancer process. True to the sayings, 9  o Menopausal female introduced the 7 Warning Signs of Cancer. To  Self-Breast Exam same this date, this is now extended to 9, and now date every month called "CAUTION US".  Colon/Rectum C - Change in bowel/bladder habits o F/M equal or greater than 50 y/o fecal occult blood test every year A - A sore that does not heal and flexible sigmoidoscopy every 5 U - Unusual bleeding/discharge years or colonoscopy every 10 years or double contrast barium T - Thickening or lump in the breast or enema every 5 years elsewhere  Prostate I - Indigestion or difficulty in swallowing o Male: = or > 50 y/o or 40-45 if at risk O - Obvious change in warts or mole PSA and DRE every year N - Nagging or persistent cough or hoarseness  Cervix o F: = or > 21 y/o or within 3 years U - unexplained anemia after starting to have intercourse Pap Test every year if regular pap; S - sudden unexplained weight loss every 2 years if liquid pap test Pelvic examination every year o At age 30, after 3 or more DIAGNOSTIC AIDS AND GRADING & consecutive normal examination, STAGING the PAP test may be performed Diagnostic Aids to Detect Cancer and its every 2-3 years at the discretion of Extent: the physician; human papilloma virus (HPV) test should be included  Tumor marker identification/test at that time  MRI (Magnetic Resonance Imaging)  Cancer Related Check ups  CT (Computerized Tomography) Scan o M/F: = or > 20-39 y/o  Fluoroscopy  examination for cancers of  Ultrasonography the thyroid,  Endoscopy testicles, ovaries, lymph  Nuclear Medicine Imaging (e.g. TBBS Or nodes, oral cavity, skin; Total Body Bone Scan) counselling about health  PET (Positron Emission practices and risk factors Tomography)/PET fusion (PET Scanner every 3 years and CT Scanner in one machine) 40+ y/o – same – every year  Radioimmunoconjugates  Tumor Markers - sometimes called cancer markers in the blood, urine or body The impact of cancer is so devastating to any tissues. These are substances made by individual who will be afflicted by it. The effects cancer cells or by normal cells in are not only limited to physical but also to the response to cancer in the body. Some emotional and the financial aspect of the tumor markers are specific to one type of individual and the family. When diagnosed early, cancer (e.g. PSA- prostate specific such impact may be lessened. And in order to antigen). Others can be found in several do that, the American Cancer Society (ACS) 10  types of cancer (e.g. CEA-Carcino stage I and/or may have spread to nearby Embryonic Antigen). lymph nodes.  Radioimmunoconjugates – Monoclonal  Stage III – Cancer is in the organ where it antibodies are labelled with a radioisotope first started. It may be larger than stage II and injected intravenously into the and may have spread to nearby lymph patient. The antibodies that aggregate at nodes and/or other nearby tissues, the tumor site are visualized with organs or structures. scanners  Stage IV – Cancer has spread to organs  Nuclear Medicine Imaging – Uses in other parts of the body (metastasized). intravenous injection or ingestion of There may be cancer in different organs radioisotope substances followed by but still the same type of cancer as where imaging of tissues that have concentrated it stated. the radioisotopes  Recurrent – cancer has come back (recurred) after it has been treated. It may STAGING AND GRADING come back in the same area or in a Grading different part of the body.  Histologic grade is used to describe what TNM STAGING the cancer looks like using a microscope;  T - stands for the relative tumor size, how much cancer cells look like normal depth of invasion and surface spread; cell extent of the primary tumor  evaluates amount of cell differentiation;  N - presence and extent of lymph node estimates rate of growth based on the involvement mitotic rate; degree of aggressiveness;  M - denotes the presence or absence of classification of the tumor cells distant metastases Staging  used to classify solid tumors and refers to the relative size of the tumor and extent of the disease; spread of the disease STAGES OF CANCER (Note: This list is general; each tumor type has its own and often TNM CLASSIFICATION SYSTEM complex staging system)  PRIMARY TUMOR (T)  Stage 0 or carcinoma in situ – pre- o Tx Primary tumor cannot be malignant or pre-cancer. Abnormal cells assessed are found only in the first layer of cells in o T0 No evidence of primary tumor the place where the changes first started. o Tis Carcinoma in situ (cancer in No invasion yet. place)  Stage I – Cancer is only in the cells o T1, T2, T3, T4 increasing size where it first started, and the area is and/or local extent of the small. Considered early stage and most primary tumor curable.  REGIONAL LYMPH NODES (N)  Stage II – Cancer is in the organ where it o Nx Regional lymph nodes cannot first started. It may be a bit larger than be assessed 11  o N0 No regional lymph node  biopsy – tissue from actual tumor metastasis and/or lymph node near the suspicious o N1, N2, N3 Increasing involvement tumor of regional lymph nodes BIOPSY TYPES:  DISTANT METASTASIS (M) o Mx Distant metastasis cannot be 1. Excisional assessed  for easily accessible tumors o M0 No distant metastasis  entire tumor and surrounding o M1 Dstant metastasis marginal tissues removed CANCER GRADING  decrease chance of seeding the tumor  Grade I – cancer cells resemble normal 2. Incisional cells and aren’t growing rapidly  for too large tumor mass  Grade II – cancer cells don’t look like  wedge of tissue removed for normal cells and are growing faster than analysis normal cells  negative results do not guarantee  Grade III – cancer cells look abnormal absence of cancer and may grow or spread more aggressively Needle (another example)  for suspicious masses that are easily Grade X – grade isn’t known accessible Grade 1 – Well differentiated, low grade  fast, relatively inexpensive, easy to Grade 2 – Moderately differentiated, perform, requires local anesthesia intermediate grade  minimal disruption of surrounding tissues; Grade 3 – Poorly differentiated, high grade decrease seeding chance Grade 4 – Undifferentiated, high grade SURGERY AS A PRIMARY TREATMENT:  results in disfigurement and altered functioning  considered if the tumor can be removed ----------------------------------------------------------------- completely and the chances of cure or LESSON 3: TREATMENT MODALITIES control are good SURGERY Goal:  Surgical removal of the entire cancer –  Remove the entire tumor or as much as is ideal and most frequently used method feasible (Debulking) and any involved  May be the primary method of treatment, surrounding tissue including regional lymph may be prophylactic, palliative or node reconstructive 2 COMMON TYPES: Diagnostic Surgery 1. Local Excision  Definitive method of identifying o mass is small cellular characteristics o includes removal of the mass and a  influence all treatment decisions small margin of normal tissue that is easily accessible 2. Wide or Radical Excision 12  o en bloc dissection SPECIAL TECHNIQUES FOR PREPARING o removal of the primary tumor, LN, CLIENT FOR SURGERY adjacent structures, surrounding Cancer cells can be disseminated by tissues that may be at high risk from manipulation or accidental implantation. tumor spread 1. Before surgery, the area of tumor OTHER TYPES: involvement should not be vigorously  Video Assisted Endoscopic Surgery manipulated or scrubbed.  Salvage Surgery 2. Ulcerated lesions should be covered with  Electrosurgery antiseptic sponges during surgery  Cryosurgery preparation and then covered with a dry  Chemosurgery dressing until excised.  Laser Surgery 3. During surgery any instruments that are in  Stereotactic Radiosurgery contact with tumor cells should be washed and resterilized before reuse for PROPHYLACTIC SURGERY that surgery or other surgeries.  Removing non-vital tissues or organ that 4. Some surgeons may irrigate wounds with arelikely to develop cancer tumoricidal agents before closure  e.g. mastectomy, oophorectomy 5. Arteries and veins supplying the tumor and surrounding tissue should be ligated Factors to be considered: before manipulation and removal  Family history and genetic predisposition  Presence or absence of symptoms  Potential risks and benefits  Ability to detect cancer at an early age  Patient’s acceptance of post-op outcome PALLIATIVE SURGERY  When cure is not possible  Make patient as comfortable as possible  Major goal: high quality of life  e.g. pleural tube placement, abdominal shunt RADIATION THERAPY RECONSTRUCTIVE SURGERY  Uses ionizing radiation to interrupt cell growth  May follow curative or radical surgery  Ionizing radiation breaks the strands of  To improve function the DNA helix leading to cell death  aesthetic  Controls malignant disease when a tumor NURSING MANAGEMENT cannot be removed surgically or when local nodal metastasis is present  Patient must be prepared for surgery  Cells most vulnerable during DNA  Information on what to expect before, synthesis and mitosis (early S, G2 M). during and after surgery must be given o Body tissues undergoing frequent  After surgery, assess patient’s response, cell division are most sensitive monitor for possible complications 13  o Slower growing tissues and tissues  may be increased if concomitant chemo at rest are relatively resistant treatment is administered  Acute local reactions happen when Radiation Dosage normal cells in the treatment area are  dependent on the sensitivity of the target destroyed tissues and on the tumor size  when cell death is greater than cell regeneration Lethal Tumor Dose  will eradicate 95% of the tumor yet preserve normal tissue COMMON TOXICITIES  Radiation Therapy is administered in  Altered skin integrity: alopecia, erythema, small doses (fractionation) over a period desquamation of time to increase likelihood of finding  Alteration in oral mucosa: stomatitis, cells in a mitosis and to allow non- xerostomia, change and loss of taste, malignant cells to repair decreased salivation  Typical treatment protocol: 5 days a week  Esophageal irritation with chest pain and for 4-6 weeks dysphagia if the entire GI mucosa is Palliative Radiation - used to relieve symptoms involved of metastatic disease or to treat oncologic  Anorexia, nausea, vomiting, diarrhea if emergencies like SVC (Superior Vena Cava) with stomach or colon involvement syndrome and SCC (Spinal Cord Compression)  Anemia, thrombocytopenia, leukopenia if sites contain bone marrow 2 TYPES OF RADIATION THERAPY CHRONIC EFFECTS: 1. External Beam Radiation Therapy (EBRT or Teletherapy) - directs high  fibrotic changes which may involve vital energy x-ray beams at a tumor from organs like lungs, heart, CNS, bladder outside the body  usually due to decreased blood supply 2. Internal Radiation Therapy  Irreversible (Brachytherapy) - places radioactive SYSTEMIC EFFECTS material directly inside or next to the tumor. It uses a higher total dose of  fatigue, malaise, anorexia radiation to treat a smaller area in NURSING RESPONSIBILITIES less time than EBRT  Monitor for adverse effects: skin changes TYPES OF INTERNAL RADIATION THERAPY such as blanching, erythema, a) Mechanically Positioned Radiation desquamation, sloughing or hemorrhage, (MPR) – use of seeds, wires, needles, ulceration of mucous membranes, nausea etc. implanted in the body and vomiting, diarrhea or GI bleeding b) Metabolized or Adsorbed Radiation  Assess lungs for rales which may indicate (MAR) - e.g. radioactive iodine ingestion interstitial exudate. Observe for any dyspnea or changes in respiratory pattern  Identify and record any medications that Toxicity the client will be taking during the radiation treatment  localized to the region being irradiated 14  Monitor white blood cell counts, and INTERNAL RADIATION NURSING platelet counts for significant decreases RESPONSIBILITIES CLIENT AND FAMILY TEACHING  Place the client in a private room (EBRT/Telepathy)  Limit visits to 10 to 30 minutes, and have visitors sit at least 6 feet from the client  Wash the skin that is marked as the  Monitor for side effects such as burning radiation site only with plain water; no sensations, excessive perspiration, chills soap; do not apply deodorant, lotions, and fever, nausea and vomiting, or medications, perfume or talcum powder to diarrhea the site during treatment period. Take  Assess for fistulas or necrosis in adjacent care not to wash off treatment marks. tissues.  Do not rub, scratch or scrub treated skin areas. If necessary, use only an electric INTERNAL RADIATION CLIENT AND FAMILY razor to shave the treated area. TEACHING  Apply neither heat nor cold (e.g. heating  While a temporary implant is in place, pad or ice pack) to the treatment site stay in bed and rest quietly to avoid  Inspect the skin for damage or serious dislodging the implant changes, and report these to the  For outpatient treatments, avoid close radiologist or physician. contact with others until treatment has  Wear loose, soft clothing over the treated been discontinued area  If the radiologist indicates the need for  Protect the skin from sun exposure during such measures, dispose of excretory the treatment and for at least 1 year after materials in special containers or in a radiation therapy is discontinued. toilet not used by others  Cover skin with protective clothing during  Carry out daily activities as able; get extra treatment rest if feeling fatigued  Once radiation is discontinued, use sun  Eat a well-balanced diet; frequent, small blocking agents with SPF of at least 15 meals often are better tolerated  External radiation poses no risk to other  Contact the nurse or physician for any people for radiation exposure even with concerns or questions after discharge. intimate physical contact.  Be sure to get plenty of rest and eat a balanced diet. INTERNAL RADIATION  An implant is placed into the affected SAFETY PRINCIPLES FOR INTERNAL tissue or body cavity and is sealed in RADIATION tubes, containers, wires, seeds, capsules or needles.  These recommendations apply to  May be temporary or permanent. caregivers working with clients receiving  May be ingested or injected or be internal radiation (brachytherapy) introduced into the tumor through a  Maintain the greatest possible DISTANCE catheter. from the source of radiation  Spend the minimum amount of TIME close to the radiation source 15   SHIELD yourself from the radiation with remaining tumor cells can be destroyed by the lead gloves and aprons when possible body's immune system.  If pregnant, avoid contact with radiation Chemotherapy - the use of cytotoxic agents in sources treating cancer  If you work routinely near radiation, wear a monitoring device to measure whole- Goals of chemotherapy: body exposure  Cure  Avoid direct exposure with radioisotope  Control containers; for example, do not touch the  Palliation container  Prolong life  Keep clients with implanted radioisotopes  Control symptoms (pain, obstruction) in a private room with private bath and as  Improve quality of life far away from other hospitalized persons as possible Chemotherapy disrupts cell cycle in various  Dispose of body fluids of clients with phases by interrupting cell metabolism and unsealed implanted radioisotopes with replication. It also works by interfering with the special care and in specially marked ability of the malignant cells to synthesize vital containers enzymes and chemicals  Handle bed linen and clothing with care  Phase-specific drugs work during only and according to agency protocol some phases of the cell cycle  Use long handled forceps to place any  Non-phase-specific drugs work through dislodged implants into a lead container the entire  Consult with the radiation therapy cycle department for any questions or problems in caring for clients with radioactive CLASSIFICATION: implants 1. Alkylating Agents - non-phase specific, Three general Guidelines for Controlling basically act on preformed nucleic acids Exposure to Ionizing Radiation: by creating defects in tumor DNA. Toxicity 1. Minimizing exposure TIME results to bone marrow failure, infertility, 2. Maximizing DISTANCE from the radiation nephrotoxicity and hemorrhagic source cystitis(e.g. cisplatin) 3. SHIELDING yourself from the radiation 2. Antimetabolites - phase specific working source best in the S phase and having little effect on Go. Toxic effects do not usually occur until very high level of drugs are CHEMOTHERAPY administered. Most toxic effects relate to rapidly proliferating cells such as cells in Antineoplastic agents or cytotoxic (toxic to the the GIT, hair, skin and WBC’s. S/Sx cells) agents or chemotherapy drugs or anti- include N&V, stomatitis, diarrhea, cancer drugs are used in an attempt to eradicate alopecia, leukopenia (e.g. cancer cells by interfering with cellular functions. methotrexate,5FU) Repeated doses of chemotherapy are 3. Antitumor Antibiotics - non-phase administered over a prolonged period of time to specific. They disrupt DNA replication and achieve regression of tumor. Treatment aims to RNA transcription, create free radicals eradicate enough of the tumor cells so that the which breaks in DNA and other forms of damage. Bind to cells and kill them 16  probably by damaging the cell membrane. o ELF (Leucovorin/ etosoposide/ Main toxic effect is damage to the cardiac fluorouracil) muscle..e.g. doxorubicin. o PE (Paclitaxel/estramustine) 4. Mitotic Inhibitors - prevent cell division  Adenocarcinoma (unknown primary) during the M phase. The toxicity is o Carbo-Tax (carboplatin and characterized by depression of deep paclitaxel) tendon reflex, paresthesia, motor  Breast Cancer weakness, cranial nerve disruption and o AC (doxorubicin & paralytic ileus. e.g.vincristine, etoposide cyclophosphamide) paclitaxel, docetaxel  AT (doxorubicin & paclitaxel) 5. Nitrosureas – cell cycle non-specific; o X+T (capecitabine & docetaxel) alters DNA structure by misreading DNA o TAC (doxorubicin/ code, initiating breaks in the DNA cyclosphosphamide /docetaxel) molecule, cross-linking DNA strands; cross the blood-brain barrier. Toxicities FACTORS AFFECTING TUMOR RESPONSE include delayed and cumulative  Tumor Burden – size of the tumor and myelosuppresion, especially extent of the cancer thrombocytopenia, nausea, vomiting e.g.  Tumor heterogeneity – presence of carmustine, lomustine different tumor cells with distinct profile 6. Topoisomerase I Inhibitors – cell-cycle  Drug resistance specific (S phase); induce breaks in the  Dosing and timing of therapy DNA strand by binding to enzyme o Dosage - based on BSA, previous topoisomerase I, preventing cells from response to chemotherapy dividing. Toxicities include bone marrow or radiation therapy and function of suppression, diarrhea, nausea, vomiting, major organ systems hepatotoxicity e.g. irinotecan, topotecan 7. Hormonal Agents COMMON SIDE EFFECTS OF 8. Miscellaneous Agents - act at different CHEMOTHERAPY phases in the cell cycle. e.g. L-  Gastrointestinal asparaginase, hydroxyurea  Nausea  Vomiting  Diarrhea  Constipation  Stomatitis  Mucositis SAMPLE CHEMOTHERAPY REGIMENS (SITE SPECIFIC)  Colon Cancer  Skin o 5-FU/LV/CPY11  Alopecia (irinotecan/leucovorin/fluorouracil)  Color changes [Saltz Regimen]  Moisture  Gynecologic malignancies  Integrity o Carbo-Tax (paclitaxel/carboplatin)  Nail bed changes  GU malignancies  Rash  Sensitivity to sun light 17  Reproductive and proton pump inhibitor are the  early menopause, common medications being given  temporary or permanent azoospermia ROUTES OF CHEMOTHERAPY  Teratogenic effects  Mutagenic effects  Oral  Central Nervous System  Intravenous  Cognitive function disturbance  Intrathecal  Chemo-brain syndrome  Intracavitary  Vision problem Vesicant Administration (can result to in tissue  Peripheral Nervous System necrosis or formation of blisters) - AVOID  Neuropathy (hands and feet) EXTRAVASATION  Bone marrow  Anemia  Use of Central line is preferable o Fatigue  Patent venous access o Shortness of breath  New peripheral IV  Management: Packed RBC  Verify needle placement in ports transfusion among others  Check for blood return  Thrombocytopenia  Avoid elbows, wrists, lower extremity IV o Bleeding site  Management: Platelet Extravasation Management – DO NOT transfusion among others REMOVE THE LINE!  Neutropenia o Immunocompromised  Stop medication administration  Management: GCSF immediately (Granulokine Colony  Ice application (except vinca alkaloid) Stimulating Factor)  Aspiration of infiltrated medication (by the administration among others physician)  Cardiac  Injection of neutralizing solution (e.g.  Heart muscle damage sodium thiosulfate, sodium bicarbonate)  Respiratory  plastic surgery consult  Pulmonary fibrosis  Genitourinary  Hemorrhagic cystitis  Loss of libido  Kidney  Renal failure PRIOR TO CHEMOTHERAPY HORMONE THERAPY  Check for medical clearance (basis would Hormone therapy is used to treat cancers that be lab results such as CBC and other use hormones to grow, such as prostate and blood chemistries depending on the breast cancers. It is a cancer treatment that drug’s toxicity; ECG and Chest X-ray may slows or stops the growth of cancer that uses also be needed especially before the hormones to grow. initial treatment) Hormones  Pre-meds are given prior to chemotherapy: antiemetic, corticosteroid 18   chemicals produced by glands, such as  treating the glands that produce hormones to the ovaries and testicles keep them from making hormones  help some types of cancer cells to grow,  surgery to remove glands that produce the such as breast cancer and prostate hormones, such as the ovaries that produce cancer estrogen, or the testicles that produce testosterone  HORMONE THERAPY can kill cancer cells, make cancer cells grow more What medications are used for hormone slowly, or stop them from growing therapy?  Hormone therapy as a cancer treatment  Hormone therapy may be used to prevent the may involve taking medications that growth, spread, and recurrence of breast interfere with the activity of the hormone cancer. or stop the production of the hormones  Hormone therapy may involve surgically  The female hormone estrogen can increase removing a gland that is producing the the growth of breast cancer cells in some hormones e.g. orchiectomy, women. oophorectomy  Tamoxifen (Nolvadex) is a medication used in hormone therapy to treat breast cancer by How does Hormone Therapy Work? blocking the effects of estrogen on the growth of malignant cells in breast tissue. However,  Hormone Receptor Test - helps determine tamoxifen does not stop the production of treatment options and helps learn more estrogen. about the tumor.  Drugs approved by the US Food and Drug  This test can help to predict whether the Administration (FDA), called aromatase cancer cells are sensitive to hormones. inhibitors, are used to prevent the  The hormone receptor test measures the recurrence of breast cancer in amount of certain proteins (called hormone postmenopausal women. receptors) in cancer tissue. Hormones (such  Anastrozole (Arimidex) and letrozole as estrogen and progesterone that naturally (Femara), prevent estrogen production. occur in the body) can attach to these o Anastrozole is effective only in proteins. women who have not had previous  If the test is positive, it indicates that the hormonal treatment for breast cancer. hormone is probably helping the cancer cells o Letrozole is effective in women who to grow. In this case, hormone therapy may have previously been treated with be given to block the way the hormone works tamoxifen. and help keep away from cancer cells  Possible side effects of these  If the test is negative, the hormone does not drugs include osteoporosis or affect the growth of the cancer cells, and bone fractures. other effective cancer treatments may be  Fulvestrant (Faslodex) eliminates estrogen given. receptor rather than blocking it used following  If the test indicates that the hormones are previous antiestrogen therapy. affecting the cancer, it may be treated in one o Side effects hot flashes, mild nausea, of following ways: and fatigue.  treating cancer cells to keep them from receiving the hormones they need to grow Prostate Cancer 19   Male hormones, such as testosterone, o vaginal spotting (a blood-stained stimulate prostate cancer to grow. discharge from the vagina that is  Hormone therapy is given to help stop not part of the period) hormone production and to block the o irregular menstrual periods activity of the male hormones. o fatigue  Hormone therapy can cause a tumor to o skin rash shrink and the prostate-specific antigen o loss of appetite or weight gain (PSA) levels to decrease o headaches o vaginal dryness or itching and/or Example of Hormone Therapy for Prostate irritation of the skin around the Cancer: vagina  Bicalutamide (Casodex) –  Taking tamoxifen also increases the risk antiandrogen of endometrial cancer (involves the lining  Estrogen therapy (DES) - removes of the uterus) and uterine sarcoma androgenic hormone that promotes (involves the muscular wall of the uterus) growth of malignancy; relieves  There is also a very small risk of blood symptoms of advanced prostate clots and stroke, eye problems such as cancer, reduces tumor size and pain cataracts, and liver toxicities.  Leuprolide (Lupron) and Goserelin  Tamoxifen should be avoided during (Zoladex) - Luteinizing Hormone Releasing pregnancy. Hormone (LHRH) agonists  LHRH suppresses testicular androgen  Flutamide (Eulexin) – antiandrogen; causes Tamoxifen - used to treat men with breast adrenal androgen suppression cancer What are the side effects of Hormone Men may experience the following side effects: Therapy?  Headaches  For prostate cancer, either the surgical  nausea and/or vomiting removal of the testes or hormone drug  skin rash therapy can improve the cancer. Both  impotence surgery and drugs may cause the  decrease in sexual interest following side effects: o hot flashes o impotence o a loss of desire for sexual relations o male breast enlargement  For breast cancer, some women may TARGETED THERAPY experience side effects from tamoxifen The aim to protect the normal cells from being that are similar to the symptoms some destroyed which both chemotherapy and women experience in menopause. radiation therapy are not able to do gave birth to Side effects of tamoxifen targeted therapy particularly the MONOCLONAL ANTIBODIES or the MoAbs. o hot flashes o nausea and/or vomiting TARGETED THERAPY 20   Aims to minimize the negative effects on therapies interfere with these proteins, healthy tissues by disrupting specific preventing them from telling the cells to cancer cell functions divide. This process helps slow cancer’s  A type of cancer treatment that targets uncontrolled growth. proteins that control how cancer cells  Stop signals that help form blood grow, divide, and spread vessels. Tumors need to form new blood  Advantage compared to using radiation vessels to grow beyond a certain size. In therapy or chemotherapy – only the a process called angiogenesis, these new cancer cells are targeted, leaving the blood vessels form in response to signals healthy cells unaffected; reduced side from the tumor. Some targeted therapies effects called angiogenesis inhibitors are designed to interfere with these signals to Monoclonal antibodies (MoAbs), also known prevent a blood supply from forming. as therapeutic antibodies, are proteins produced Without a blood supply, tumors stay small. in the lab. These proteins are designed to attach Or, if a tumor already has a blood supply, to specific targets found on cancer cells. these treatments can cause blood vessels  Some monoclonal antibodies mark cancer to die, which causes the tumor to shrink. cells so that they will be better seen and  Deliver cell-killing substances to destroyed by the immune system. cancer cells. Some monoclonal  Other monoclonal antibodies directly stop antibodies are combined with toxins, cancer cells from growing or cause them chemotherapy drugs, and radiation. Once to self-destruct. these monoclonal antibodies attach to  Others carry toxins to cancer cells. targets on the surface of cancer cells, the cells take up the cell-killing substances, MONOCLONAL ANTIBODIES causing them to die. Cells that don’t have the target will not be harmed.  Help the immune system destroy cancer cells. One reason that cancer  Cause cancer cell death. Healthy cells cells thrive is because they can hide from die in an orderly manner when they your immune system. Certain targeted become damaged or are no longer therapies can mark cancer cells so it is needed. But cancer cells have ways of easier for the immune system to find and avoiding this dying process. Some destroy them. Other targeted therapies targeted therapies can cause cancer cells help boost your immune system to work to go through this process of cell death. better against cancer. DISADVANTAGES:  Stop cancer cells from growing. Healthy cells in your body usually  Cancer cells can become resistant to divide to make new cells only when they targeted therapy. For this reason, they receive strong signals to do so. These may work best when used with other signals bind to proteins on the cell types of targeted therapy or with other surface, telling the cells to divide. This cancer treatments, such as chemotherapy process helps new cells form only as your and radiation. body needs them. But some cancer cells  Drugs for some targets are hard to have changes in the proteins on their develop. Reasons include the target’s surface that tell them to divide whether or structure, the target’s function in the cell, not signals are present. Some targeted or both. 21  Example of FDA- TARGET Approved MoAbs Marker on cell TYPES OF IMMUNOTHERAPY Alemtuzumab membrane of  Immune checkpoint inhibitors are (Campath) lymphocytes, drugs that block immune checkpoints. monocytes, and These checkpoints are a normal part of macrophages the immune system and keep immune Bevacizumab VEGF (Vascular responses from being too strong. By (Avastin) Endothelial Growth Factor) blocking them, these drugs allow immune Cetuximab (Erbitux) EGF (Epidermal cells to respond more strongly to cancer. Growth Factor)  T-cell transfer therapy, which is a Marker on cell treatment that boosts the natural ability of Rituximab (Rituxan) membrane of the T cells to fight cancer. In this lymphocytes treatment, immune cells are taken from Trastuzumab Growth factor protein the tumor. Those that are most active (Herceptin) on cell membrane against the cancer are selected or Marker on cell changed in the lab to better attack the Ibritumomab-tiuxetan membrane of cancer cells, grown in large batches, and (Zevalin) lymphocytes put back into the body through a needle in a vein. o T-cell transfer therapy may also be IMMUNOTHERAPY called adoptive cell therapy, adoptive immunotherapy, or Although the immune system can prevent or immune cell therapy slow cancer growth, cancer cells have ways to  Treatment vaccines, which work against avoid destruction. Cancer cells may have cancer by boosting the immune system’s genetic changes that make them less visible to response to cancer cells. Treatment the immune system; proteins on their surface vaccines are different from the ones that that turn off immune cells and can change the help prevent disease normal cells around the tumor so they interfere  Immune system modulators, which with how the immune system responds to the enhance the body’s immune response cancer cells. against cancer. Some of these agents Immunotherapy helps the immune system to affect specific parts of the immune better act against cancer. It is good to note that system, whereas others affect the continuous study is still being done regarding immune system in a more general way. this along with other cancer treatment.  Immunotherapy is a type of cancer treatment  Immunotherapy drugs have been that helps the immune system fight cancer. approved to treat many types of cancer. The immune system helps the body fight However, immunotherapy is not yet as infections and other diseases. It is made up widely used as surgery, chemotherapy, or of white blood cells and organs and tissues radiation therapy. of the lymph system.  Immunotherapy can cause side effects,  Immunotherapy is a type of biological many of which happen when the immune therapy. Biological therapy is a type of system that has been revved-up to act treatment that uses substances made from living organisms to treat cancer. 22  against the cancer also acts against  Compression of the spinal cord and its healthy cells and tissues in your body. parts caused by tumors and metastasis ----------------------------------------------------------------- COMMON CAUSES: LESSON 4: ONCOLOGIC EMERGENCIES  Spinal Cord tumors ONCOLOGIC EMERGENCIES are clinical  Bone Metastasis conditions resulting from a structural (anatomic),  Myelomas hematologic or metabolic change caused by  Lymphomas cancer or its treatment that requires immediate SIGNS/SYMPTOMS medical intervention to prevent loss of life or quality of life. It can happen BEFORE or  Back Pain WITHIN the diagnosis.  Motor and Sensory dysfunction  Bladder and Bowel Disturbances SUPERIOR VENA CAVA COMPRESSION SYNDROME (SVC SYNDROME) DIAGNOSTICS  Obstruction of the blood flow return to the  Xray right side of the heart  MRI COMMON CAUSES:  CT scan MANAGEMENT  Tumor Extension  Lymphomas  Multidisciplinary approach  Metastasis  Timely assessment  VAD thrombosis  STAT STEROIDS (SUSPECTED and CONFIRMED) SIGNS/SYMPTOMS  Radiation  Cough, dyspnea, edema, headache, light  Chemotherapy headedness, neck vein distention,  Surgery shortness of breath, spider web veins on face and chest (hallmark sign of SVC) DIAGNOSTICS TUMOR LYSIS SYNDROME  Chest Xray, CT scan  Group of metabolic complications caused by cancer treatment MANAGEMENT  Release of intracellular contents by dying  Radiation tumor cells into the blood  Chemotherapy  It is caused by massive rate of tumor cell destruction from Chemotherapy  Oxygenation  Positioning SIGNS/SYMPTOMS  Diuretics  Hyperkalemia  Accurate Intake and Output  Hyperphosphatemia  Thrombolytic therapy (for VAD  Hyperuricemia thrombosis)  Hypocalcemia SPINAL CORD COMPRESSION (SCC)  Muscle Cramps 23  Joint Pains  Electrolytes Monitoring  Twitching  Kidney Function Monitoring  and their accompanying signs and MANAGEMENT symptoms  Accurate Intake and Output MANAGEMENT  Fluid Restriction  Electrolytes Monitoring  Timely assessment of level of  Hydration consciousness/ muscle weakness/  Diuretic Rescue cramps  Accurate Intake and Output  Sodium Correction  Kayexalate (Sodium Polystrene Sulfonate) - binds K  Sodium Bicarbonate (NaHCO3)- INCREASED INTRACRANIAL PRESSURE alkalinizes urine making it more soluble;  Increase in the pressure within the cranial prevents crystallization vault  Dialysis (severe electrolyte imbalance)  Rasburicase (recombinant urate oxidase) DIAGNOSTICS PREVENTION:  CT SCAN  MRI  Hydrea  PET SCAN  Leukopheresis  Lumbar Puncture  Allopurinol SIGNS AND SYMPTOMS  Altered level of consciousness SYNDROME OF INAPPROPRIATE ANTI  Headache DIURETIC HORMONE (SIADH)  Behavioral Changes  Excess secretion of the antidiuretic  Personality Changes hormone/vasopressin  Vomiting COMMON CAUSES:  Pupil Changes  Motor Changes  Associated with small cell lung cancer MANAGEMENT  Chemotherapy (vincristine/vinblastine)  Morphine use  Surgery  Brain Tumors  Radiation SIGNS AND SYMPTOMS  Steroids  Mannitol  Decreased Urine Output  Vital Signs  Nausea  Neurologic Vital Signs monitoring  Hyponatremia  Positioning  Seizure/Coma  Decreased Plasma Osmolality  Decreased BUN and creatinine HYPERCALCEMIA IN MALIGNANCY  Weight Gain without edema COMMON CAUSES: DIAGNOSTICS 24  Breast abdominal distention, and guaiac-positive  Lung stools  Squamous Cell Head and Neck  dyspnea, hemoptysis, and tachypnea as  Multiple Myeloma a result of acute or slow bleeding into the  Bone Metastasis lungs.  Disruption of the normal bone remodeling  Restlessness, confusion, lethargy, and process altered mental status can be signs of intracranial bleeding SIGNS/SYMPTOMS