Cancer Hodgkins Lymphoma > makes up 12% of all lymphomas > malignant condition characterized by abnormal giant multinucleated

cells called as REED STERNBERG CELLS which are located in the lymph nodes. >Occurs to person from 15-35 years old and above 50 years of age >More prevalent in men than in women >Etiology : no known cause but with interacting factors including infection of Epstein-Barr, genetic predisposition and exposure to occupational toxins >Increased with HIV >Normal structure of the lymph nodes are destroyed from hyperplasia of monocytes and macrophages >Main diagnostic: Lymph node biopsy with presence of Reed Sternberg Cells >Clinical Manifestations: Initial development: 1. Firm, movable enlargement of cervical, axillary or inguinal lymph nodes 2. Painless lymphadenopathy unless exert pressure on adjacent nerves. 3. An initial finding associated with night sweats , weight loss fatigue and fever correlates worse prognosis (B symptoms) 4. In advance cases hepatomegaly and spleenomegaly >Diagnostic and staging: excisional lymph node biopsy offers definitive diagnosis >Bone marrow biopsy is performed for staging where REED STERNBERG cells are also found. Lymphoma >Treatment Plan 1. Standard Chemotherapy : ABVD Doxorubicin (Adriamycin), bleomycin, vinblastine and dacarbazine. For patients with favorable early detection will receive 2-4 cycles of chemotherapy With early detection but with symptom B. or intermediate stage (4-6 cycles) Hodgkins Lymphoma >Maybe alternated with MOPP Mechlorethemine, vincristine (Oncovin), procarbazine and prednisone >Intensive chemotherapy with autologous and allogenic HSCT and hematopoeitc growth factors is the treatment for advance hodgkins lymphoma >Nursing Care is usually based on managing problems related to the disease eg: Pain due to tumor, pancytopenia, and other side effects of therapy

Early stage of hodgkins lymphoma has 10 year survival rate with near 90% and advance stage has 10 year survival rate with 50% recovery Psychosocial considerations is focused on nursing care Evaluation of patients for long term effects of therapy is important bec. Delayed consequence of treatment may not be apparent for many years.

Non Hodgkins Lymphoma >Heterogenous group of malignant neoplasms of B or T cells origin affecting all ages. >B cell lymphomas constitutes 90% of NHL >Cause: unkonwn but more predominant with HIV cases, history of prolong immunosuppressive medications EBV and with burkitts lymphoma. >May originate outside the lymph nodes >No hallmark feature of NHL but involves lymphocytes in various stage of development: ex lymphoblastic lymphoma and lymphobalstic leukemia >Has 3 classificationa 1. Low grade indolent lymphomas 2. Intermediate grade (aggressive ) lymphoma 3. High Grade (very aggressive ) lymphoma >Dx and staging . More on extranodal sites thus more diagnostic work up such as MRI, barium enema or GI involvement >Lymph node biopsy establish cell type and pattern >Classified as morphologic, genetic, immunoophenotypic and clinical feature. >Management: involves chemotherapy and radiation therapy. Aggressive lymphomas are more responsive to treatment Patients with low grade (indolent ) lymphomas have a median ovrall survival of 9 years. However if relapse occur several times cure is unlikely >Therapy is indicated with local symptoms from progressive, bulky or painful disease or a compromise organ function st >DOC: Rituximab (MA) every week for the 1 month then every 2 months as maintenance >Chemo DOC: CHOP R- 14 (R q 14 wd G-CSF) Cyclophosphomide, doxorubicin hydrochloride, oncovin and prednisone >Nsg, management: same with HL yet NHL can be more extensive and involves specific organs (CNS, Spleen GI, and bone marrow) Leukemia >A group of malignant disorders affecting the blood and blood forming tissues of he bone marrow, lymph system and spleen. >May occur in all age group

>Results in accumulation of dysfunction cells bec of a loss of regulation and cell division >No single known cause but multifactorial : chromosoamal changes benzene exposure chemotehrapeutic agents (alkykating agents) oncogenic viruses and bacteria constant exposure to radiation. >Classification: Onset and maturity: 1. acute 2. chronic Origin: 1. myelogenous (from granulocytic leukocyte) 2. lymphocytic (lymphocytes or monocytes) 4 types: 1. ALL 2. CLL 3. AML 4. CML Acute Lymphocytic Leukemia Most common in children 5 year event free survival rate is 80% for children and 40% of adults Proliferates in bone marrow of B cell origin CM: fever, with bleeding maybe progressive weakness, fatigue bone and or joint pain and bleeding tendencies. Acute Myelogenous Leukemia Represent sonly of the leukemia but makes 85% of acute leukemias in adults Abrupt and dramatic onset Serious infection and abnormal bleeding from the onset of disease Uncontolled proliferationof myeloblast, hyperplasia of bone marrow CM: related to replacment of normal hematopoeitc cells in the marrow by leukemic myeloblast and to a lesser extent to infiltration of other organs and tissue Chronic Myelogenous Leukemia Excessive development of mature neoplastic granulocytes in the bone marrow Neoplastic granulocytes move into peripheral bloos in massive number and infiltrate the liver and spleen Contains philadelphia chromosomes a disease marker and results from translocation of genetic material Chronic stable phase followed by more acute aggressive phase (blastic phase) Hairy Cell Leukemia 2% of adult leukemia more predominant in males at 40 yrs and above. Cells have hairy appearance

Leukemia >Clinical Manifestations are varied but relates to problems caused by bone marrow failure and formation of leukemic infiltrates 1. results from overcrowding by abnormal cells 2. inadequate production of normal marrow elements >As leukemia progresses, fewer blood cells are produced. The abn WBCs cont to accumulate bec they do not go through normal cell life cycle >Leukemic cells infiltrate to other organs leading to spleenomegaly hepatomegaly lymphadenopathy, bone pain, menigeal irriatation >Diagnostic 1. Peripheral blood evaluation and bone marrow examination are the primary diagnosing and classifying subtypes of leukemia. 2. CT scan and lumbar puncture detect presence of leukemia cells outside blood and bone marrow >Collaborative Care: 1. Age and chromosome analysis often help form the basis of important treatment decision >Phases Chemotherapy in Acute Leukemia 1. Induction therapy 2. Intensification 3. Consolidaton therapy 4. Maintenance therapy 1. Induction Therapy aggressive treatment Attempt to bring out remission. destroy leukemic cell in the tissues, peripheral blood an bone marrow patient is critically ill, bone marrow is severely depressed with chemotherapeutic agents. Common agents: cytarabine, antitummor antibiotics (doxorubicin), daunorubicin, Promyelocytic leukemia tretinoin is used along with chemotherapy. 2. Intensification > high dose therapy maybe given immeditely after inductions (use same drugs but a higher dose). 3. Consolidation therapy >Started after remission is achieved >Purpose is to eliminate leukemic cells that may not be clinically pathologically evident 4. Maintenance >Drug of Choice Combination therapy is the mainstay Purposes 1. Decrease drug resistance 2. Minimize drug toxicity 3. Interrupt cell growth.

Treatment of ALL (COAP) >Cyclophophomide, oncovin, arabinoside and prednisone >Imatinib (target therapy) (targets Philadelphia chromosome) Monoclonal antibodies >CLL Rituximab binds to the B cell antigen Alemtuzumab panlymphocyte antigen on both B and T cells >Myelogenous leukemia Gemtuzumab , ozogomacin, calicheamicin - anti CD3 monoclonal antibodies binds with myeloid tissue ,lkij 5. Hematopoetic Stem Cell therapy >Nursing Care 1. cope effectively with diagnosis, prognosis and treatment regimen 2. attain and maintain adequate nutrition 3. experience less or no complications 4. feel comfortable and supported all over treatment. Multiple Myeloma Aka plasma cell myeloma A condition in which plasma cells infiltrate in the bone marrow and destroy the bone Incidence is 4 per 100,000 and twice as common men than in women, develops after 40 years with an average of 65 yrs Etiology is unknown Involves excessive production of plasma cells . Plasma cells produces immunoglobulins (antibodies) Malignant plasma cells infiltrate the bone marrow and produces abn amounts of Ig (myeloma protein or M protein) Increases abnormal amounts of leukotrienes, cytokines Bence jones proteins from myeloma cells can be detected by the urine Proliferation of malignant plasma protein and overproduction of Igs and proteins result in end organ effects to the bone marrow, bone, kidneys may include spleen, lymph, lymph nodes liver and heart muscles CM: dev slowly insidiously, does not manifest symptom until advance case. Skeletal pain is the major manifestation pain in pelvis, spine and ribs are common and triggered with movement CM: diffuse osteoporosis develop in multiple myeloma, loss of bone integrity, bone degenration and hypercalcemia that might cause renal, GI, neurologic manifestations such as polyuria anorexia, confusionseizure, coma and cardiac problems

>Dx and staging 1. Presence of monoclonal antibody protein cqn be found in urine and blood 2. Distinct lytic bone erosions are seen in Xrays 3. Blood level of B2 microglobulin and albumin measures the prognosis >Collaborative Care It is seldom cured but treatment of symptoms produces remission and prolonged life 1. Corticosteroids, chemotherapy, biologic therapy and hematopoeitic stem cell transplant 2. Ambulation and adequate hydration 3. Control of pain and prevention of pathologic fractures (analgesics, orthopedic support and localized radiation helps reduce pain) 4. Give biphosphates (primadonate, zoledronic and etidronate) to inhibit bone breakdown, skeltal pain and hypercalcemia MOA: inhibits bone resorption w/o inhibitibg bone formation Given in monthly IV infusion Nusring responsibility: patient should be well hydrated 5. vertebroplasty to support degenrtive vertebrae 6. Chemotherapy is alkylating agents w/ VAD (vincristine,doxorubucin (adriamycin), Dexamehtasone ) given once a month for several months before autologous HSCT 7. may be given with Bertezomib (proteasome inhibitor ) for pts with relapse after two prior treatments and resistance to their last treatment 8. Thalidomide (antiangiogenic drug) slow growth of plasma cells and reduce their numbers 9. Allopurinol, furosemide and calcitonin > Nsg. Management 1. Maintaining adequate (UO= 1.5-2L / day) may require intake of 3-4 L per day 2. Be careful when moving or ambulating the patient 3. Pain Management suh as (NSAIDS, acetaminophen and opoid combination) 4. Assesment and prompt treatment for infection Lung Cancer leading cause of cancer related death Risk factor: cigarette smoking (tobacco contains 60 carcinogen in addition to carbon monoxide and nicotine) Changes in bronchial epithelium but usually returns to normal with discontinuation Arises from bronchial epithelial cells and grows slowly it takes 8-10 yrs for tumor to reach 1 cm >Primary lung cancers are often categorizied into two 1, Non small cell lung cancer (NSCLC) 80% 2. Small cell lung cancer (SCLC)20%

Metastasize by direct extension and via blood circulation to bones, brain, liver lymph nodes and adrenals SCLC- causes paraneoplastic syndrome

>CM: asymptomatic usually found in routine xrays, Manifestation depends on the location of Ca and metastatic spread but majority reported with persistent pneumonitis, cough (productive or not) >Late manifestation: Non speciic systemic complication, fatigue, weight loss, anorexia, nausea and vomiting, hoarseness of voice palpable lymph nodes unilateral paralysis of the diaphragm *insert table* >Diagnostic Studies Xrays, CT scan, sputum cytology, bronchoscopy, MRI, Pet Scan, spirometry, lung scan, fine needle aspiration >Staging NSCLC >Used with TNM Staging, >Stage I, II, IIIA are operable >Stage IIIB or IV inoperable with poor prognosis SCLC >Limited (2 yrs) and extensive (7-10 mos) Simplified Staging of Lung Cancer *insert table* >Screening for Lung cancer On going screening for low risk asynmptomatic individual Single view xray and CT scan >Collaborative Care 1. Surgical Therapy 2. Radiation Therapy 3. Chemotherapy 4. Biologic and Target Therapy 5. Other therapies Prophylactic cranial radiation Bronchoscopic laser therapy Photodynamic therapy Airway stenting cryotherapy >Surgical Therapy Surgical resection for NSCLC Stage 1 and II 5 yr survival for stage I with combination of chemotherapy and radiation therapy Surgical surgery may include pneumonectomy, lobectomy, or lung conserving resection or segmental When tumor is considered operable CP status must be evaluated, ABG status and other test

>Radiation therapy Maybe used when intent is cure but pt. is unable to tolerate surgery Can be treated for locally advance, unresectable NSLC Maybe adjuvant for resection of tumor Improved survival rate when given in combination Hyperfractionated, given twice daily and improved survival rate of SCLC Comp: esophagitis, skin irritation, radiation pneumonitis, Can be used to relive symptoms of dyspnea and hemoptysis, and to treat superior ven cava syndrome, treat pain of bone lesion and cerebral metastasis >Chemotherapy Non resectable tumor and for adjuvant therapy Drug combination: Etoposide, carboplatin, cisplatin, pactitaxel, vinorelbine, cyclophosphomide, ifosfamide, docetaxel, gemcitabine, topotecan, and irinotecan improves survival of advanced NSCLC and SCLC >Biologic and target therapy Use to block the growth of molecules invloved in specific aspect of the tumor NSCLC- erlotinib (Tarveca) TI, with epdermal growth receptor Gefitinib >Prophylactic cranial radiation 39% of SCLC metastasize in the cranium >Photodynamic therapy Safe bronchoscopic laser therapy of the lung cancer Profimer (Photofrin) is injected intravenously and selectively concentrates the tumor cells, after 48 hrs the tumor is exposed to light producing toxic amount of oxgen to destroy tumor cells Necrotic tissue then are removed through bronchoscope >Airway Stenting Palliation for dyspnea, cough, or respiratory insufficiency Supports airway wall against collapse and compression and impeded eextension of the tumor to the airway. >Cryotherapy Tse is destroyed through freezing Given through bronchoscopy >Nursing Management: 1. Proper assessment of symptom 2. overall goals for client is to have effective breathing pattern, adequate airway clearancee,

adequate oxygenation of tissues, minimal to no pain, and realistic atittude towards treatment and prognosis 3. Enhance Health Promotion >Five As strategy for patient attempts to smoking ceasation Ask, advise, assess, assist and arrange >Four stages in smoking ceasation 1. pre contemplation (I want) 2. contemplation (I might) 3. preparation (I will) 4. action (I am) Oral Cancer May occur in the lips or any else in the mouth Head and neck squlmous cell carcinoma (HNSCC) is an umbrella trm for cancers in the oral cavity, pharynx and larynx More common after age 40 individuals who smoke are smoke are 7 -10 times most likely to develop oral cancers >Types and Characteris tics Oral Cancer *inset table* >Diagnostic Studies Biopsy with cytologic examination Oral exfoliative cytology Toluidine blue test >Cheemotherep 5 fluoracil, methotrexate, cisplatin, carboplastin, paclitaxel, docetaxel, and bleomycin >Nutritional therapy PeG tube , gastrostomy, parenteral fedings Stomach Cancer (Gastric) Adenocarcinoma of the stomach More prevalent int men with Low socioeconomic status, >Etiology Probably begins with non specific mucusal injury, as a result of aging, autoimmunity, repaeated exposure to irritaants, Associated with diet high in salt smoked foods, pickled vegetables Infection of H pylori causes metabolic changes, then to dysplasia to cancer >Other prdisposing factors such as gastritis, pernicious anemia, adenomatous polyps, smoking and obesity, , have inhereted familial component >Stomach cancer loacated in the cardia or fundus has the lowest prognosis.

>Clinical manifestations, May spread to adjacent organ before any distressing symptoms Anemia. PUD indigestion, , pt appears weak, complains of fatigue, dizzines, SOB, positive occult blood test, dyspepsia, cachectic, , a mass can be detected in the abdominal wall during inspiration, Presence of ascites, poor prognosis >Diagnostics History and physical examination Endoscopy and biopsy Upper GI barium series Exfoliative cytology CBC. Stool exam, liver enzymes, serum amylase and tumor markers (CEA and acarbohydrate antigen CA 19-9) >Collabortive Care 1. correction of nutritional deficiencies 2. PRBC transfusions 3.. surgery 4. adjuvant therapy >Surgery (defkinitive means of cure) 1. Subtotal gastrectomy Billroth I (gastrodoudonostomy) or II (gastojejunostomy) (lesions located in the antrum ) 2. total gastrectomy with esophagojejunostomy >Adjuvant therapy Radiation and chemotherpay Radiation use to relieve tumor mass >Chemotherapy 5 FU cisplastine, leucovorin increases survival after surgery Colorectal cancer >Insidious onset, symptoms may not appear until disease is quite advance, of colractal Ca appeasrs in the rectosigmoid >85% may arise from adenomatous polyps which can be detected nd removed by sigmoidoscopy or colonoscopy >Hereditary nonpolyposis colorectal cancer (HNPCC) Lynch syndrome >Risk factors: low fiber diet, low level of physical activity, fleshy polyps >CM -Ascending colon: cauliflower appearance , with occult blood leads to anemia, referred pain in the epigastric area, weight loss -Distal colon and rectum: ribbon like stool, change in bowel habits, increase sensation of increase bowel habits, fecal smelling breath,

>Surgery: Resection of polyps Hemicolectomy with temporary ileostomy Abdominoperineal resection. Permanent colostomy Total colectomy resection with permanent ileostomy Pre op: high caloric low residue diet for 3-5 days pre op 3-5 days antibiotic of neomycin sulfate >Chemotherapy -Recommended for positive lymph nodes at the time of surgery or has metastatic disease -5 FU with leucovorin, and ironetecan, >Biologic therapy Monoclonal antibodies Cetuximab- target epidermal growth factor Pantimumab- vascular endothelial growth factor Bevacizumab- anti angiogenic agent >Radiation therapy