MedSurg - Finals PDF

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Summary

This document is a lecture on care of clients with acute and chronic problems, specifically focusing on cancer. The document defines and differentiates between benign and malignant cancers, discusses the causes and mechanisms, and highlights warning signs.

Full Transcript

BSNG 3102 - 1st Semester Lecture BSN 3D - Semis Care of Clients with Acute and A.Y. 2024-2025 Chronic Problems Transcribed by: Kent Adrian J. Gabayran...

BSNG 3102 - 1st Semester Lecture BSN 3D - Semis Care of Clients with Acute and A.Y. 2024-2025 Chronic Problems Transcribed by: Kent Adrian J. Gabayran BENIGN CANCER REMEMBER CONTENT 1:  harmless, does not spread/invade, does not occupy CANCER space, encapsulated  But if located within a vital tube or organ, it can be fatal  Latin word for "crab"  Cell Characteristics: well-differentiated cells that  collective term describing a large of diseases resemble normal cells characterized by uncontrolled growth and spread of abnormal cells  Mode of Growth: grows by expansion and does not infiltrate  serves no useful purpose and may harm the host organism  Rate of Growth: slow  Synonym: Tumor - any swelling  Metastasis: does not spread by metastasis  Appearance: larger, bigger nucleus  General Effects: localized unless interferes with vital function  Pattern of growth: uncontrolled  Tissue Destruction: no tissue damage unless its  Function: serves no purpose location interferes with flow Cancer remains a national health priority in the country  Ability to cause death: does not usually cause death with significant implications for individuals, families, unless its location interferes with vital function communities, and the health system. MALIGNANT CANCER  Third leading cause of morbidity and mortality (Philippine Health Statistics, 2009)  harmful, metastasizes, non-encapsulated  The 6 most common sites of cancer diagnosed in men  But if located within a vital tube or organ, it can be fatal were lung, liver, colon/rectum, prostate, stomach, and  Cell Characteristics: undifferentiated and bear little leukemia. resemblance  The 6 most common sites of cancer diagnosed in  Mode of Growth: grows at the periphery and sends out women were breast, cervix, lung, colon/rectum, ovary processes that infiltrate and destroy surrounding tissue and liver.  Rate of Growth: variable and depends on the level of  189 of every 100,000 Filipinos are afflicted with cancer differentiation, the more anaplastic, the faster its  4 Filipinos die of cancer every hour or 96 cancer growth patients every day  Metastasis: gain access to the blood and lymphatic Neoplasm - an abnormal tissue that grows by cellular channels and metastasizes to the other areas of the proliferation more rapidly than normal and continues to body grow after the stimuli that initiates the new growth ceases.  General Effects: generalized anemia, weakness weight Neo - new, recent loss Plasm - thing formed  Tissue Destruction: extensive tissue damage - produce substances that cause cell damage Cellular Aberration (CA) - departure from what is normal  Ability to cause death: eventually causes death unless Carcinoma - neoplasm derived from epithelial tisues growth can be controlled -oma - denoting a tumor or neoplasm Hyperplasia - an increase in the number of cells Hypertrpophy - increase in size Remission - temporary recovery Relapse - recurrence of symptoms after a period of improvement Exacerbation - increase in severity WARNING SIGNS OF CA  Change in bladder or bowel habits  A lesion or sore that does not heal  Unusual bleeding or discharges  Thickening or lump in the breast  Indigestion or difficulty swallowing  Obvious changes in wart or mole  Nagging cough or persistent hoarseness  Unexplained weight loss  Pernicious anemia 1 REMEMBER CONTENT 2:  Human T-cell lymphotropic virus may cause some lymphocytic leukemias and lymphomas.  Human immunodeficiency virus (HIV) is associated 3 STEP CELLULAR PROCESS with Kaposi’s sarcoma. During initiation, carcinogens (substances that can  Helicobacter pylori is linked to an increased incidence cause cancer), such as chemicals, physical factors, or biologic of gastric malignancy, possibly due to inflammation and agents, cause mutations in the cellular DNA. Normally, these injury of gastric cells. alterations are reversed by DNA repair mechanisms or the CHEMICAL AGENTS changes initiate programmed cellular death (apoptosis)  Tobacco smoke, considered the single most lethal 1001 or cell senescence. Cells can escape these protective chemical carcinogen, causes at least 30% of cancer mechanisms with permanent cellular mutations occurring, deaths. but these mutations usually are not significant to cells until the second step of carcinogenesis  Smoking is strongly linked to cancers of the lung, head and neck, esophagus, pancreas, cervix, and bladder. During promotion, repeated exposure to promoting agents (cocarcinogens) causes proliferation and expansion  Chewing tobacco is associated with oral cavity cancers of initiated cells with increased expression or manifestations and mainly affects men under 40. of abnormal genetic information, even after long latency  The list of suspected carcinogens continues to grow and periods. Promoting agents are not mutagenic and do not includes aromatic amines, aniline dyes, pesticides, need to interact with the DNA. The promotion phase formaldehydes, arsenic, soot, tars, asbestos, benzene, generally leads to the formation of a preneoplastic or benign betel nut, lime, cadmium, chromium compounds, nickel, (noncancerous) lesion. zinc ores, wood dust, beryllium compounds, and During progression, the altered cells exhibit polyvinyl chloride. increasingly malignant behavior. These cells acquire the  The liver, lungs, and kidneys are the most affected ability to stimulate angiogenesis (growth of new blood organs, likely due to their role in detoxifying chemicals. vessels that allow cancer cells to grow), to invade adjacent PHYSICAL AGENTS tissues, and to metastasize.  Physical factors linked to carcinogenesis include CELLULAR TRANSFORMATION AND DERANGEMENT exposure to sunlight or radiation, chronic irritation or THEORY inflammation, and tobacco use. Conceptualizes that normal cell may be transformed into  Excessive ultraviolet (UV) exposure from the sun, cancer cells due to exposure to some etiologic agents especially in fair-skinned, blue- or green-eyed  the exact mechanism by which these agents transform individuals, increases the risk of skin cancers. healthy cells info neoplastic cells remain obscure when  Factors like clothing styles, sunscreen use, occupation, defective cell divides recreational habits, and environmental variables  contain the defective genetic code within the DNA. (humidity, altitude, latitude) influence UV exposure. overtime, defective cells divide and multiply and the  Ionizing radiation exposure can occur through repeated malignancy grows x-ray procedures or radiation therapy. IMMUNE RESPONSE FAILURE THEORY  Improved x-ray equipment reduces the risk of Advocates that all individuals possess cancer cells. However, excessive radiation exposure. the cancer cells are recognized by the immune response  Radiation therapy or exposure to radioactive materials system. So, the cancer cells undergo destruction. Failure of at nuclear sites increases the risk of leukemia, multiple the immune system leads to inability to destroy the cancer myeloma, and cancers of the lung, bone, breast, thyroid, cells. and other tissues.  CA cells continually form within the body  Background radiation, such as radon decay, is  The immune system perceives these CA cells as foreign associated with lung cancer; homes with high radon and destroys them levels should be ventilated to disperse the gas.  However certain conditions either cause a breakdown or overwhelm the immune system  Thus the malignant cells reproduce more rapidly than the immune system can destroy them ETIOLOGY OF CANCER Certain categories of agents or factors implicated in carcinogenesis include viruses and bacteria, physical agents, chemical agents, genetic or familial factors, dietary factors, and hormonal agents. VIRUS AND BACTERIA  Epstein-Barr virus is suspected as a cause of Burkitt’s lymphoma, nasopharyngeal cancers, and some types of non-Hodgkin’s lymphoma and Hodgkin’s disease.  Herpes simplex virus type II, cytomegalovirus, and human papillomavirus types 16, 18, 31, and 33 are linked to dysplasia and cervical cancer.  Hepatitis B virus is implicated in liver cancer. 2 REMEMBER CONTENT 3:  M refers to the extent of metastasis. M0 - no evidence of distant metastasis PRIMARY PREVENTION Mx - distant metastasis cannot be evaluated M1- ascending degrees of metastatic involvement Primary - reducing the risk in a healthy individual including lymph nodes Assisting patients to avoid known carcinogens is one way to A variety of other staging systems are used to describe the reduce the risk for cancer. Another way involves adopting extent of cancers, such as central nervous system cancers, dietary and various lifestyle changes that epidemiologic and hematologic cancers, and malignant melanoma, that the laboratory studies show influence the risk for cancer. TNM system does not describe appropriately. TAKING STEPS TO MINIMIZE CA GRADING refers to the classification of the tumor cells. Increase: Grading systems seek to define the type of tissue from which  fresh vegetables (especially those in the cabbage the tumor originated and the degree to which the tumor family)- roughage and vitamin-rich foods help prevent cells retain the functional and histologic characteristics of CA the tissue of origin. Samples of cells to be used to establish  fiber- reduce the risk of breast, prostate, and colon CA the grade of a tumor may be obtained through cytology (examination of cells from tissue scrapings, body fluids,  Vit A- reduces the risk of esophageal, laryngeal, and secretions, or washings), biopsy, or surgical excision. lung CA. Decrease CLASSIFICATION - based on origin  Practice weight control- obesity is linked to CA of the uterus, gallbladder, breast and colon  carcinoma - originates in epithelial tissues  Decrease fat  adenocarcinoma - glandular tissue (breast, prostate)  Moderate consumption of salt-cured, smoked, and  sarcoma - connective and supporting tissue (bones, nitrate-cured foods- esophageal and gastric CA nerves)  Stop smoking-cigars and cigarettes are carcinogenic  embryonal - embryonic tissue  Reduce alcohol intake - liver CA  lymphomas - lymphatic system  Avoid overexposure to the sun, wear protective  leukemias - blood forming organs clothing and use sunscreen to prevent damage from UV rays-skin CA Metastasis a. Vascular System- cancer cells penetrate blood vessels SECONDARY PREVENTION and circulate until trapped. Cancer cells may penetrate Secondary - early detection and screening the vessel wall and invade adjacent organs and tissues The evolving understanding of the role of genetics in cancer b. Lymphatic System- cancer cells penetrate the lymphatic cell development has contributed to prevention and system and distributed along the lymphatic channels screening efforts. Individuals who have inherited specific c. Implantation- cancer cells implant into a body organ; genetic mutations have an increased susceptibility to cancer. certain cells have an affinity for particular organs and  Needle Biopsy - tumor cells are withdrawn from the body areas tumor by a needle and syringe. Pathologist will examine d. Seeding- a primary tumor sloughs off tumor cells into a the cell body cavity  Incisional Biopsy - small sample TUMOR SPECIFIC ANTIGEN (TUMOR MARKERS)  Excisional Biopsy - removes all the tumor- entire  proteins contained in cell membrane of malignant cells sample  distinguish malignant from benign cell of same type of  Endoscopic Biopsy - direct biopsy through an tissue endoscopy of the area  chemicals in the blood that are produced by certain cancers TUMOR STAGING AND GRADING  Carcinoembryonic antigen (CEA) - colon, rectal, breast, STAGING determines the size of the tumor and the lung existence of metastasis. Several systems exist for classifying  Alpha-fetoprotein (AFP) - testicular, liver, lung, the anatomic extent of disease. pancreas  The TNM system is frequently used.  Prostatic Acid Phosphatase (PAP) - metastatic prostate  T refers to the extent of the primary tumor  Prostate specific antigen (PSA) - primary and T0 - no evidence of tumor metastatic prostate Tis - cancer cells are only growing in the layer of  Cancer Antigen (CA 125) Ovarian - pancreatic cells where they started T1-4 - ascending degrees of increase in tumor size and involvement  N refers to lymph node involvement N0 - no clinical evidence of regional lymph node involvement Nx - regional lymph nodes cannot be evaluated N1-3 - ascending degrees of nodal involvement 3 REMEMBER CONTENT 4:  Interstitial Therapy - utilizes solid radioactive materials seed implants; temporary or permanent: sodium phosphate, iodine 13, 137 cesium, 226 radium, iridium TERTIARY PREVENTION 192, iodine 125, cesium 137, gold 198, radon 222 Tertiary - efforts focus on monitoring for and preventing RADIATION SAFETY recurrence of the primary cancer as well as screening for the 1. Distance - the greater the distance maintained from the development of second malignancies in cancer survivors. radiation source, the less the exposure to ionizing rays Survivors are assessed for the development of second  6 ft distance from the source malignancies such as lymphoma and leukemia, which have 2. Time - the less the time that is spent close to the been associated with certain chemotherapy agents and the radiation source, the less the amount of radiation use of radiation therapy exposure GOALS OF THERAPY  nurses- 30 minutes per 8 hr shift  do not linger  Cure - complete eradication of CA cells 3. Shielding - lead shields lead gloves and aprons  Control - prolonged survival and containment of CA cell  Sealed - can’t contaminate body fluids growth  Unsealed - excreted in body fluids, flush the toilet  Palliation - relief of symptoms several times  Prophylaxis- provide treatment when no tumor is TO PREVENT DISPLACEMENT detectable but client is known to be at risk  bedrest and logrolled MEDICAL MANAGEMENT OF  indwelling catheter - ensure bladder empties CANCERS  low residuediet and antidiarrheals (such as diphenoxylate (Lomotil)) - prevent bowel movement Major objective: during therapy  treat the client effectively with the appropriate therapy ACUTE ADVERSE EFFECTS OF RADIATION THERAPY for a sufficient duration so as cure result with minimal functional and structural impairment  Fatigue and malaise If cure is not possible, alternate goals are:  2 weeks - skin erythema - folds because of warmth and moist GI effects 1. Prevent further metastases  Oral effects: xerostomia 2. Relieve symptoms  Pulmonary: dyspnea, productive cough, 3. Maintain a high quality of life as long as possible  radiation pneumonitis: 1-3 months after SURGERY  Renal/bladder-cystitis, urethritis NURSING RESPONSIBILITY IN RADIATION THERAPY  Surgical removal of the entire CA remains the ideal and most frequently used treatment method  private room  Plays a role in the diagnosis, staging and treatment of  post "Radiation Precaution" sign CA  staff-dosimeter badges equipped  no pregnant women or children allowed in the room RADIATION THERAPY  interrupt cell growth  use of high-energy ionizing rays to treat a variety of CA  ionizing radiation destroys the cell's ability to reproduce by damaging the cell's DNA  Primary - local cure of CA  Adjuvant - before and after the surgery to aid in the destruction of CA cells  Palliative - to relieve pain due to obstructions, pathologic fractures, spinal cord" compression and metastasis. External Radiation (teletherapy) - usually administered by high energy machines or machines containing a radioisotope. Internal Radiation (brachytherapy) - involves the placement of specially prepared radioisotopes directly into or near the tumor itself or into the systemic circulation. Also includes systemic therapy (systemic IV) Sealed Source - delivers a high dose of radiation to a localized area Unsealed Source  Intracavity Therapy - radioisotope is placed on an applicator; inserted into cavity; eg. vagina, cervix 4 REMEMBER CONTENT 5:  fine motor activities zipping pants, tying shoes, buttoning shirt. CHEMOTHERAPHY  paresthesia-tingling, numbness Objective:  reflexes  Systemic intervention and is appropriate when  weakness, ataxia and gait disease is widespread or when the risk of  activities of daily living undetectable disease is high  urinary retention/constipation  Use of medication through oral or intravenous route  tinnitus, decreased hearing acuity to destroy all malignant tumor cells without Genitourinary excessive destruction of normal cells  urine output  Promote control by controlling tumor growth when a cure is not possible.  urinary frequency, urgency, hesitancy Alkylators: busulfan, carmustin, carboplatin, cisplatin  changes in color, odor, clarity Antimetabolites - cytarabine, 5-fluorouracil, methotrexate  hematuria, oliguria, anuria Plant Alkaloids - vincristine  blood urea nitrogen test , creatinine test Taxanes - taxol  antineoplastic agents and their metabolites are found in the excreta and body fluids of client's undergoing NURSING ASESSEMENT IN CHEMOTHERAPY therapy. Integumentary system  gowns and gloves when handling body fluids who  pain, swelling, necrosis, inflammation have received chemotherapy within 48 hours.  skin rash, pruritis NURSING PRECAUTIONS IN CHEMOTHERAPY  assess changes pigmentation 1. Obtain all allergy history from the client  photosensitivity and tearing 2. Obtain baseline vital signs  condition: gums, teeth, buccal mucosa, tongue 3. Administer a test dose when ordered by physician (test  stomatitis, ulceration, bursning, and dysphagia dose) Gastrointestinal System 4. Stay with the client the entire time the drug is being  nausea and vomiting - onset, duration and severity administered  hydration status and electrolyte balance 5. Have emergency equipment and drugs readily available  diarrhea/constipation 6. Establish a free-flowing IV line for the administration of fluids and emergency drugs should the need to arise  anorexia - taste changes and food preferences SIGNS AND SYMPTOMS OF HYPERSENSITIVITY  daily food intake and eating patterns REACTION  jaundice, right upper quadrant pain, liver function, total bilirubin Dyspnea Agitation Hematopoetic System Chest tightness Inability to speak  myelosuppresion Pain Cyanosis  fever greater than 38.3℃ Pruritis Abdominal pain  assign for signs of infection  auscultate lungs for breath sounds Uticaria Nausea  productive cough and shortness of breath Tachycardia Hypotension  asses for thrombocytopenia: 50,000 mm3 - mild risk Dizinness Decreases sensorium for bleeding; 20,000 mm3 - high risk for bleeding Anxiety Flushed appearance  assess for bleeding  assess petechiae, bruising NURSING ACTION DURING HYPERSENSITIVITY REACTION  blood in stool, urine, or emesis a. Immediately stop administration  intracranial bleeding - level of consciousness, responsiveness, vital signs, pupillary reaction b. Maintain IV access with 0.9 NaCl Anemia c. Notify physician  assess skin color turgor and capillary refill d. Maintain airway  dyspnea on exertion, fatigue, weakness, palpitations e. Supine with feet elevated and vertigo f. Vital signs every 2 hrs until stable  advise rest periods g. Administer emergency drug Respiratory and Cardiovascular  lung sounds  dyspnea, shortness of breath  apical pulse, radial pulse  baseline cardiac studies - electrocardiography (ECG), echocardiogram (2d Echo) Neuromuscular 5 REMEMBER CONTENT 6: - Tarry stols, blood in urine - Hemoptysis ADVERSE EFFECTS OF CHEMOTHERAPY AND NURSING - epistaxis INTERVENTION GI EFFECTS Alopecia N&V - antiemetic 6-12 hrs before  Begins 2 weeks after Anorexia  Regrowth about 3-5 months Taste alteration  Use of scalp hypothermia and tourniquet Weight loss Anorexia Oral mucosistis  Chemo changes the reproduction of taste buds Oral hygiene  Absent or altered taste - decrease food intake Low residue diet Fatigue Increase fluid and bulk  Unknown cause - may be related to anemia, weight loss, altered sleep pattern and coping ALOPECIA Nausea and Vomiting Obtain wig  Caused by the stimulation of the vagus nerve by the Ice packs to scalp serotonin released by cells in the upper GIT Scalp tourniquett  Depends on the chemo drug Avoid sunlight to exposed scalp  Patterns: Anticipatory - conditioned response; Acute - Wear hat or scarf 0-24 hours after chemo; Delayed - 1-4 days after Mild shampoo and conditioner Mucositis (-) excessive combing  Destruction of the oral mucosa, causing an Use wide toothed comb inflammation response TOXIC EFFECTS OF CHEMOTHERAPY  Start in burning ssensation Myelosuppresion - Most common and most lethal  Consistent oral hygiene to prevent infection  Wbc before administration of anti neoplastic agents Anemia Nadir - time after chemo administration when platelet and  Suppresion of the stem cell WBC count is at lowest point  Require RBC transfusion or injection of erythropoetin  7-14 days after administration Neutropenia  No active immunization should be given  Neutrophil count is 1500 cells/mm3 or less  Risk for infection if below 500 cells/mm3  Caused by suppression of stem cell  Occurs after 7-14 days from start of chemo Thrombocytopenia  Caused by suppresion of megakaryocytes  Risk for bleeding - 5000mm3  Critical if below 20000  Teach to avoid injury PROTECT AGAINST INFECTION  Maintain adequate nutrition and fluid intake  Avoid crowds, people with infection and clients who have been recently vaccinated with live or attenuated vaccines  Avoid contact with animal excrements such as bird dog feces  Immediately report fever, sore throat, cough, chills, sweating, painful urination  Maintain personal hygiene especially handwashing  Adequate rest and exercise  Avoid indiscriminate use of antipyretics because they can mask fever BLEEDING AND HEMORRHAGE Platelet count us below 20000/mm3 CNS/GI bleeding - below 10000/mm3 Report - bleeding gums - Bruising, petechiae, purpura - Hypermenorrhea 6 REMEMBER CONTENT 7:  High fat diet  Advancing age BONE MARROW  Mother or sister with breast cancer TRANSPLANTATION  Previous breast CA - Remission – do not have signs and symptoms but there is a relapse (cancer is back) Allows the client to receive lethal and potentially more effective doses of chemotherapy and ration therapy without  Being 30 y.o. at the time of full term pregnancy regard to hematopoietic toxicity  High socioeconomic status The damaged bone marrow is replaced by healthy donor  Early menarche and late menopause marrow  Nulliparity IMMUNOTHERAPHY (BIOLOGIC Clinical Manifestations upper outer quadrant THERAPY) - where most breast tissue is located Produces antitumor effects particularly through the action of - lesion- non-tender natural host defense mechanism - Fixed, hard with irregular borders Underlying principle - primarily function of the immune Note: If there is a mass, palpable, and it is not tender and system is to detect and eliminate substances that are painful a breast cancer is suspected. non tender, dixed, hard recognized as “non-self” Lymph nodes on the other hands are palpable and tender BIOLOGIC RESPONSE MODIFIERS (BRM) and moves Agents that are capable of modifying the relationship MASTECTOMY between the tumor and the host by strengthening the host’s immune function  with or without reconstruction and breast conserving surgery combined with radiation therapy 1. restore, augment or modulate the host's normal immune function.  Surgical removal of the breast 2. have direct antitumor effects. MODIFIED RADICAL MASTECTOMY 3. demonstrate other biologic effects.  removal of the entire breast tissue along with axillary lymph nodes Example:  pectoralis major, minor remain intact maintain and a. BCG restore normal function to the hand, arm and shoulder b. monoclonal antibodies - destroy CA cells directly girdle on the affected side c. Cytokines - subtances produced by cells of immune BREAST CONSERVING SURGERY system to enhance the production and function of  Lumpectomy component of the immune system  Partial or Segmental Mastectomy d. Interferons - antiviral and antitumor properties  Wide Excision e. Interleukins - lymphokines, monokines  Quadrantectomy- resection of the involved breast f. Hematopoietic growth factor. quadrant followed by radiation therapy to treat g. Tumor necrosis factor killing activity. residual, microscopic disease h. Retinoids boosts immune function. COMPLICATIONS OF BREAST SURGERY TARGETED THERAPY  Accumulation of blood (hematoma) Such as oral tyrosine kinase inhibitors for lung cancer and  Infection hormone therapy for breast cancer blocks specific genes and  Late accumulation of serosanguieous fluid after drain proteins to disrupt the cancer cells’ ability to grow and removal spread  Nerve trauma with resultant phantom breast sensation- CONTENT 8: numbness, tingling or burning sensations may also occur and may persist for a period of month or possibly BREAST CANCER years after surgery LYMPHEDEMA  90% Female - 10% Male  Disruption of lymphatic and venous drainage chronic  October - Breast Cancer Awareness month - Symbolized swelling of the extremity at any point after Surgery with pink ribbon  To manage: put an arm sling to maintain the position of  3 out of 100 Filipinos develop breast cancer before the the arm , it should be above the level of the heart age of 75 years old  Highest mortality rate among 15 Asian countries (58.6%, 5 year survival rate) Etiology 1. Estradiol and Progesterone - 2 key ovarian hormones which plays an important role in breast cancer 2. Estrogen - tumors grow faster when exposed to estrogen and is associated with the development of Breast CA Risk Factor 7 REMEMBER CONTENT 9:  Predisposing factors: low residue, high fat diet, highly refined foods, familial tendency, pencil like stool, PROSTATE CANCER tenesmus  metabolic and bacterial end products are carcinogenic  most common CA among men and that constipation allows a longer contact with  Represented by light blue ribbon bowel walls thus increasing the probability of CA  Awareness month: September RISK FACTORS ETIOLOGY:  Familial Hx of colon CA  Genetic Tendency  Generic predisposition or inherited syndromes  Hormonal Factors - late puberty; who have a high  Previous colon CA frequency of sexual experience with a history of  Obesity multiple sexual partners; with higher fertility  Cigarette smoking and alcohol  lower amounts of androsterone and higher serum levels of estrogen and estradiol  Being older than 50 years of age  DIET-high fat consumption can alter cholesterol and  Diabetes mellitus associated with insulin resistance steroid metabolism which may increase the risk of CA  Consumption of fresh red meat and processed meat CHEMICAL CARCINOGENS OF PROSTATE CANCER  Over age 40 Viruses - gonorrhea is also associated with an increase  Familial polyps incidence of prostatic CA  Living in highly industrialized societies CLINICAL MANIFESTATIONS  Ulcerative colitis  No symptoms presenting findings and most often those  High fat, low residue diet that is high in refined food of prostatitis  Adematous polyps  Rectal pressure or obstruction from local tumor growth  Inflammatory bowel disease may produce stool changes and painful defecation  Long-term immunosuppression  Painful ejaculations  Sedentary lifestyle PREVENTION PRESENTING SYMPTOMS:  Annual digital rectal exam  change in bowel habits  Transrectal UTZ  Rectal bleeding  Acid phosphatase - 1,000x more  Changes in bowel habits PHARMACOLOGIC INTERVENTION  Intestinal obstructiovis Endocrine Therapy - used based on an observation that prostate epithelial cells atrophy if they are deprived of  Nausea and Vomiting androgens  Abdominal pain  androgens is produced in the testicles and the adrenal  Weight loss glands  Anorexia  Used to remove the source of androgens, suppress  Palpable mass pituitary gonadotropins, interfere with androgen EARLY SIGNS OF COLON CANCER synthesis, and interfere with action of androgen on the  "Pencil" stools tissue  Pain with defecation Androgen Blockers - blocks the action and secretion of androgens which stimulates tumor growth  Rectal bleeding  flutamide  Abdominal pain  gonadotropin releasing hormone  Fatigue  analog leuprolide  Tenesmus - feeling that the bowel is not empty after  goserelin acetate  defecation  finasteride (proscar) DIAGNOSIS Estrogen - Diethylstilbestrol - suppresses the release of  Digital Rectal Exam pituitary gonadotropins and reduces serum testosterone  Stool guaiac test levels  Carcinoembryonic Antigen SURGICAL MANAGEMENT:  X ray, UTZ,CT scan  Transurectal Resection of the Prostate (TURP)  Radical prostatectomy CONTENT 12: COLORECTAL CANCER  Represented by dark blue ribbon  Awareness month: March  CAUSE: unknown 8 REMEMBER CONTENT 13:  Start in lymph nodes but can involve lymphoid tissue in the spleen, GIT, liver or bone marrow LUNG CANCER  2 categories - according to the degree of cell differentiation and the origin of the predominant  Leading cancer killer among men and women in USA malignant cell  About 1 out of 4 cancer deaths from lung CA HODGKIN LYMPHOMA CAUSE:  Rare malignancy, high cure rate  Inhaled carcinogen-cigarette smoke  Initiates in a single node---spreads by contiguous  Other carcinogens- radon gas, occupational and extension along the lymphatic system - malignant cell- environmental agents called Reed-Sternberg cell a gigantic tumor cell that is  arise from a single transformed epithelial cell in the morphologically unique and thought to be of immature tracheobronchial airways, in which the carcinogen lymphoid origin-pathologic hallmark and essential binds to and damage the cell's DNA diagnostic criterion  Cell damage results in cellular changes, abnormal cell  Cause- unknown growth, and eventually a malignant cell  Viral etiology is suspected: Eipstein bar, HIV, Herpes  tends to arise at the sites of previous scarring (TB, virus fibrosis) in the lungs  Seen in patient receiving immunotherapy (renal RISK FACTORS: transplant)  Environmental factors CLINICAL MANIFESTATION OF LYMPHOMA  Genetic predisposition  Usually begins as an enlargement of one or more lymph  Dietary deficits nodes on one side of the neck- painless and firm and  Underlying respiratory diseases - TB, COPD hard CLINICAL MANIFESTATIONS:  Cervical, supraclavicular, mediastinal nodes  Insidiously and is symptomatic until late in the course DIAGNOSTIC TESTS FOR LYMPHOMA s/s depends on the location and size of the tumor,  X-ray degree of obstruction and the existence of metastases  Tracheal compression- dyspnea  COUGH-most common  Pruritus- unknown cause  Change in chronic cough  ESR-increase- means increase disease activity  Dyspnea ASSESSMENT AND DIAGNOSTIC FINDING:  Hemoptysis  Biopsy of the lymph nodes- Reed Sternberg cell  Chest or shoulder pain- chest wall and pleural  Staging involvement  PA- palpate lymph nodes  Pain- metastases to bone  Liver and spleen 10 SYMPTOMS OF LUNG CANCER MEDICAL MANAGEMENT:  Hacking cough  Goal-cure  Shortness of breath  Chemotherapy followed by radiation  Bleeding NON-HODGKIN LYMPHOMAS  Loss of appetite  Originates from the neoplastic growth of lymphoid  Lump in the neck tissue  Chest pain  Vary morphologically  Right side abdominal pain  Clinical Manifestation:  Blood clots all over the body  Lymphadenopathy  Generalized weakness  Not diagnosed until in later stages  Weight loss  Lymphomatous masses can compromise organ function DIAGNOSIS OF LUNG CANCER  Mass in mediastinum - respiratory distress  Chest xray  Abdominal masses - can compromise the ureter-renal  CT Scan dysfunction  Fiberoptic bronchoscopy  Splenomegaly - abdominal discomfort, nausea, early  Fine needle aspiration satiety, anorexia, weight loss MEDICAL MANAGEMENT FOR LUNG CANCER DIAGNOSIS:  Surgery  Hispathology, immunophenotyping, cytogenic analyses of the malignant cells  Radiation  Staging - not an accurate predictor of prognosis  Chemotherapy MANAGEMENT: CONTENT 14:  Radiation and Chemotherapy LYMPHOMA  Neoplasm of cells of lymphoid origin 9 REMEMBER CONTENT 15:  lymphadenopathy  splenomegaly LEUKEMIA  fever- are not always due to infection  prolonged or progressively increasing elevation in ASSESSMENT AND DIAGNOSIS OF ACUTE MYELOID leukocytes unregulated proliferation of leukocytes in LEUKEMIA the bone marrow a. CBC- decrease erythrocytes, platelets  leaves little room for normal cell production b. leukocytes- low, normal, high - vastly decreased  there can be proliferation of cells in the liver, spleen, c. bone marrow analysis- excess more than 20% meninges, lymph nodes, gums and skin immature leukocytes called blast cells - hallmark  increased leukocytes diagnosis  Cause: unknown MEDICAL MANAGEMENT OF ACUTE MYELOID LEUKEMIA RISK FACTORS: Objective:  exposure to radiation or chemicals  achieve remission- no evidence of residual leukemia in  genetic disorders the bone marrow  viral infections  chemotherapy  Radiation/Chemotherapy- cause acute leukemia cell  hematopoietic stem cell transplantation  complication during radiation since bone marrow is  radiation therapy destroyed  supportive care CLASSIFICATIONS OF LEUKEMIA - according to stem cell  hydroxyurea/azacytidine - control the increase of blast involved cells a. Lymphoid - referring to stem cells that produce  antimicrobial therapy lymphocytes  transfusions b. Myeloid - referring to stem cells that produce MAJOR CAUSE OF OF ACUTE MYELOID LEUKEMIA nonlymphoid blood cells  bleeding CLASSIFICATIONS OF LEUKEMIA - according to  Infection symptoms a. Acute - the onset of symptoms is abrupt occurring within a few weeks. Can progress rapidly, with death occurring within weeks to months without aggressive treatment b. Chronic - symptoms evolve over a period of months to years, and the majority of leukocytes produced are mature. Progresses more slowly, the disease trajectory can extend for years CONTENT 16: ACUTE MYELOID LEUKEMIA  results from a defect in the hematopoietic stem cells that differentiate into all myeloid cells: monocytes, granulocytes (neutrophils, basophils, eosinophils) erythrocytes and platelets  develops without warning  symptoms/signs results from the insufficient production of normal blood cells Neutropenia -  fever and infection  weakness and fatigue  dyspnea on exertion  pallor from anemia  petechiae, ecchymosis and bleeding tendencies from thrombocytopenia leukemic cells proliferate within organs leading to:  pain from enlarged liver  hyperplasia of the gums  bone pain from expansion of the marrow  petechiae  Ecchymosis - bruising  gingiva or synovial spaces of joints 10 REMEMBER CONTENT 17:  bone pain  breasts CHRONIC MYELOID LEUKEMIA  CNS-frequent site - cranial nerve palsies  arises from mutation in the myeloid stem cell MEDICAL MANAGEMENT:  normal myeloid cells continue to be produced but there  Obtain remission without excess toxicity and with a is a pathologic increase in the production of forms of rapid hematologic recovery so that additional therapy blast cells wide spectrum of cell types exists within the can be given if needed blood- blast forms to mature neutrophils TREATMENT:  because there is an uncontrolled proliferation of cells, the marrow expands into the cavities of long bones-  radiation femur and cells are also formed in the liver, and spleen  Chemotherapy (extramedullary hematopoiesis)  enlargement- painful CONTENT 19:  results from chromosomal translocation CHRONIC LYMPHOCYTIC LEUKEMIA  section of DNA is shifted from chromosome 22 to  Common malignancy of older adults chromosome  Strong familial predisposition  Location - B-cell receptor (BCR) gene or chromosome  No definitive link to pesticides or chemical exposure 22; Abelson murine leukemia (ABL) gene on  Aggressive in nature - others will have a very short life chromosome 9  Derived from a malignant clone of B lymphocytes  when fused - they produce abnormal CHON that causes  escapes apoptosis (programmed cell death)- resulting leukocytes to divide rapidly in excessive accumulation of the cells in the marrow  BCR-ABL gene - present in all patients and circulation CLINICAL MANIFESTATIONS:  accumulate in the lymph nodes and spleen  vary CLINICAL MANIFESTATIONS:  asymptomatic  Many asymptomatic  leukocytosis- is detected when CBC was performed for  Diagnosed incidentally during a routine PE or during a other reason treatment for another disease  100,000/mm3 WBC -SOB, slightly confused- due to  Increase lymphocyte count (lymphocytosis) decrease perfusion to lungs and brain  RBC and platelets - normal  leukostasis- excessive volume of leukocytes inhibits  Later in the disease- decrease RBC and platelets blood flow through the capillaries  Lymphadenopathy- painful  enlarged, tender spleen  Splenomegaly  occasionally- liver enlarged/tender.  Fever  malaise  Drenching sweats especially at nights  anorexia  Unintentional weight loss  weight loss  T cell function is impaired - causes tumor progression MEDICAL MANAGEMENT: and increase in susceptibility to second malignancy and  Tyrosine kinase inhibitors - blocks signals within the infection- life-threatening infection leukemia cells that express the BCR-ABL protein thus  Defects in complement system increase of infection preventing the series of chemical reaction's that cause  Skin CA the cells to grow and divide  Breast, colorectal, lung and prostate CA CONTENT 18: MANAGEMENT: ACUTE LYMPHOCYTIC LEUKEMIA  Chemotherapy  results from an uncontrolled proliferation of immature  IVIG - to fight infection cells (lymphoblasts) derived from the lymphoid stem NURSING PROCESS cell  Health history  very responsive to treatment  PA  complete remission on response rates are  Lab exam approximately 85% for adults CLINICAL MANIFESTATION  immature lymphocytes proliferate in the marrow - impede in the development of normal myeloid cells---  inhibits normal hematopoiesis - results to decrease granulocytes erythrocytes and platelets  Leukocytes - either increase or decrease immature cells  liver pain  involves meninges - headache/vomiting  Spleen  Testes 11

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