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Care of Patients with Leukemia and Lymphoma

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1 Care of Patients with Leukemia and Lymphoma
Hematologic Problems Proliferation or accumulation of malignant cells originating from Bone marrow Lymphatic tissue Leukemia – CA bone marrow Lymphoma – CA lymphoid tissue Care of Patients with Leukemia and Lymphoma

2 Leukemia: 2007-2010 U.S. Demographics 44,000 new cases resulting in
21,700 deaths in 2007 43,050 new cases in 2010 Am. Cancer Society 2007 Leukemia & Lymphoma Society 2011

3 Lymphoma 2007: 2007-2010 Demographics
Hodgkin’s Disease 8,000 new cases, 1,000 deaths ( ;1350) Non-Hodgkin’s Lymphoma 63,000 new cases, 18,000 deaths ( ,000;19,000) 2010: 628,000 people living with disease Black, J., Hawks, J., 2009 Lewis, S., Dirksen, S., Heitkemper, M., et al, 2011

4 Immune Response D I F E R N T Infection Control A O Carry O2 Clotting
Lymphoid Infection Control Review of A/P Stem cells differentiate along pathways into lymphoid (B&T cells), Myeloid (granulocytes), Erythroid (RBC’s & platelets) In leukemias, CONTROL of this process is abnormal or missing  abnormal and UNCONTROLLED PROLIFERATION of leukocytes (BLASTS) that CIRCULATE in the blood and INFILTRATE the blood forming organs (liver, spleen and lymph nodes) and other sites throughout the body … like “TEENS CRASHING A PARTY” Carry O2 Erythroid Clotting Megakaryocytes

5 Leukemia Loss of control of cell division → malignant bone marrow cells accumulate or proliferate, causing disorders affecting the blood and blood-forming tissues Etiology is unknown but risk factors alter DNA, preventing cellular maturity Overexposure to ionizing radiation developing after years of exposure Alkylating agents for other cancers in conjunction with radiation therapy Benzene exposure/other toxic chemicals Genetic/Hereditary Factors Down’s Syndrome Twins and siblings Familial tendency CML (Philadelphia chromosome) Exposure Radiation Chemotherapy/Chemicals Human T-cell leukemia virus type 1 (HTLV-1)

6 Leukemia Further classified by type of leukocyte involved
site of origin lymphocytic – lymphatic system myelogenous – bone marrow

7 Leukemia Four major types acute lymphocytic (ALL)
acute myelogenous (AML) chronic myelogenous (CML) chronic lymphocytic (CLL) Treatment Goal: destroy neo-plastic cells & maintain remission. Medical management varies for the 4 types Nursing Principles for 4 types are same Important to determine Rx and prognosis We will focus on ALL in subsequent slides: AML – develops when stem cells over commit to one type of cell – neutrophils Dx: bone marrow biopsy Favorable factors - < 60 years; Spontaneous; WBC < 10,000 mm3 ; Complete remission w/one cycle of chemo CML – includes Philadelphia chromosome Chronic phase - can go on for years with mild symptoms; blasts < 10% Accelerated phase – 6-12 months with progressive symptoms (night sweats, fevers, unexplained wt. loss) blasts 10-30% Blast phase can lead to death; transforms to very aggressive acute myelogenous leukemia; blasts > 30% (Stem cell transplant) CLL – survival < 19 months (with advanced disease) to >10 years (early stage) Lymphocytosis Lymphadenopathy Hepatosplenomegaly Death usually occurs d/t recurrent bacterial and viral disease; generally not curable – Rx delayed until s/sx as Rx is harsh

8 Leukemia Incidence affects all ages: adults 10X more than children age of peak incidence ALL – between 2-9 years old AML – between years old CML – Philadelphia chromosome CLL - most common in Adults ALL – acute lymphoblastic leukemia AML – acute myelogenous leukemia In acute leukemias, single cell transforms, then leukemic cell proliferates, blocking the differentiation of cells in hematopoietic cell line Two major categories Acute – immature (“blast”) cells Chronic – cells more mature but not functional

9 Leukemia - Pathophysiology
Divide more slowly than normal Take longer to synthesize DNA Blocks differentiation of blood cell precursors Compete with normal cell proliferation Leukemic cells apparently divide more slowly and take longer to synthesize DNA than other blood precursors. Not caused by rapid proliferation but by blocking blood cell precursors  accumulate relentlessly in affected clients and then Compete with normal cell proliferation by crowding out marrow and causing other cell lines to cease  pancytopenia Crowd out marrow and cause normal proliferation of other cell lines to cease, Resulting in pancytopenia

10 Acute Leukemia (review) proliferation of immature cells (blasts)
infiltration of blasts into bone marrow rapid onset (6 months-1 year) requires aggressive intervention Defect in maturation

11 Leukemia - Chronic Differentiated, impaired mature neoplastic granulocytes more gradual onset CML Ages 25-60 Peripheral blood test shows Anemia, elevated PMN’s, Lymph’s WNL, Mono’s WNL/low, and elevated Platelets which drop later 3-4 years, then “blast” crisis resembles AML 90% of cases - Philadelphia chromosome (translocation of long arms of chromosomes 9 & 22) Develops more gradually so rarely seen in people < 20 years old Caused by either Unregulated proliferation of hematopoietic cells Disordered cell death (apoptosis) Blast crisis has 70% mortality rate within 6 months, crisis is refractory to treatment CLL – 15 year survival without treatment

12 CML Blastic Phase Increasing #’s of immature myeloid precursor cells (esp. myeloblasts) proliferate Blast cells comprise >20% of blood, >30% in marrow Increased fibrotic tissue in bone marrow Pancytopenia Refractory to treatment, many patients die within 2 mos. of onset

13 Leukemia – Chronic Cont’ed
CLL (immature B lymphocytes) Age: men > 50 years Infiltration of spleen, liver, lymph nodes & bone marrow Survive 15 years without treatment

14 Acute Lymphocytic Leukemia
Abrupt or gradual manifestations weakness, fatigue, headache fever Bleeding, petichae, bruising Bone tenderness RBC’s, Hb WBC’s Platelets pressure in intermedullary space Anorexia  weight loss,  sensitivity to sweet/sour, muscle wasting, dysphagia CBC – WBC can be either up or down… anywhere from 1000 to > 300K. With abnormal blasts. Decreased Hb & platelets Bone Marrow Aspiration is necessary in order to identify the malignant cell type to prescribe treatment. It will show increased marrow cells and increased blasts. LP not done until after induction to avoid introducing leukemic cells into CNS .

15 Treatment of Acute Leukemia
Initial goal is REMISSION: Restoration of Hematopoiesis complete remission no evidence of disease on physical exam, bone marrow or blood work – bone marrow function restored “blasts” cells < 5% partial remission evidence of disease in bone marrow only relapse usually means a more difficult course of disease process with progressively shorter periods of remission ALL – 70-80% of adults achieve remission with 35-40% surviving 2 years AML – 60-70% adults achieve remission with 25% surviving 5 years Treatment chemotherapy, cranial radiation intrathecal (into spinal canal to allow entry into brain) methotrexate – bypasses blood-brain barrier

16 Treatment of Acute Leukemia Induction therapy
Aggressive chemotherapy treatment aimed at all abnormal cells: reduce ‘Blastic Cells’ to less than 5% of total bone marrow cells & return CBC to normal values for at least 1 month :approximately 70% success (in newly dx’d.) :associated with many complications anemia neutropenia thrombocytopenia Induction Therapy is the initial treatment of an intense course of Chemotherapy with goal of complete remission Why?

17 Treatment of Acute Leukemia Post-Induction Therapy
Intensification Therapy eliminate remaining leukemic cells. high doses of same of 1-2 drugs used in induction therapy; combination therapy: Radiation added if infiltration of CNS, skin, testes, rectum, mediastinal mass Consolidation Therapy: after remission, this phase of treatment to kill any possible remaining leukemic cells Maintenance therapy maintain remission using similar drugs Small doses every 3-4 weeks for 1 – 3 years Used mostly for adults with ALL This also includes Radiation Rx as an adjunct to chemo when leukemic cells infiltrate the CNS Skin Rectum Testes Mediastinal masses

18 Post Therapy Management of Complications
Therapy destroys normal and aberrant cells causing pancytopenia Transfusions of Red Blood Cells (RBC’s) IV Antifungal agent Amphotericin B

19 What CM’s would you anticipate?
Tumor Lysis Syndrome Large number of WBC tumor cells destroyed  release of intracellular contents renal involvement  uric acid crystals metabolic effects  serum uric acid, PO4, K,  serum Ca Potentially fatal complication that occurs with rapid cell death: CM’s: Confusion, weakness, numbness, tingling, muscle cramps, oliguria, Bradycardia, EKG dysrhythmias d/t  K,  Ca Rasburicase (Elitek) an antigout agent – oxidizes uric acid crystals What CM’s would you anticipate?

20 Clinical Manifestations
Confusion Weakness Numbness Tingling Muscle cramps & tetany seizures Bradycardia EKG changes Dysrhthmias Uric acid crystalluria Renal obstruction Acute renal failure (ARF)

21 Prevention & Treatment
Prevention is the best treatment identify high risk patients IV hydration prevention of electrolyte imbalances Allopurinol & Rasburicase to  uric acid formation Hemodialysis: ↓ Creatinine levels Leukapheresis: ↓ WBC count

22 Lymphomas: Hodgkin’s and non-Hodgkin’s
Malignant conditions abnormal lymph cell proliferation unknown etiologies: ? viral, immune-related ? starts at one site; spreads through lymphatic system Lymphatics undergo malignant changes and produce tumors in lymphoid tissue Epstein-Barr Virus is implicated Immune deficiency disease…..3rd World 15 year olds to young adult development and declining in older people Reed-Sternberg Cells: distinctive large/giant cells Bi-modal pattern in economically advantaged countries vs disadvantaged countries overall HD ocurance is lower except higher incidence in <15 y.o.

23 Hodgkin’s and non-Hodgkin’s
How do they differ? Non-Hodgkin’s: spreads by skipping lymph node areas (no Reed-Sternberg cells); Hodgkin’s: spreads in “orderly” fashion, has characteristic Reed-Sternberg (giant) cells, found in 2 age groups (mid-20’s and 50+ years) in “1st World” countries

24 Clinical Manifestations
Painless lymph node enlargement Cervical, submaxillary, posterior auricular, parotid , occipital, mediastinal and axillary

25 Hodgkin’s Disease Can start anywhere-most commonly in upper body: chest, neck, axilla Spreads in orderly fashion Reed-Sternberg (giant) Cells Associated with : Genetic Predisposition, Epstein-Barr Virus, Hx of Mononucleosis, Organ Transplant, Immunodeficiency Disease Copstead & Banasik 2009 Also supraclavicular nodes, mediastinal nodes Reed-Sternberg cells (giant cells with 1-2 large nuclei 3. Exact Cause Unknown– associated with decreased immunity and infection (mononucleosis due to Epstein-Barr virus- 2-3 X more prevelant), genetic component (more common in people with Jewish heiratige, and 1st degree relatives, siblings Overall survival 10 years post diagnosis – 77% with radiation and chemo Specific survival depends upon stage on diagnosis

26 Clinical manifestations
Painless swelling of >1 inch Lasting > 6 weeks Unrelated to infectious process Stage B (Systemic) symptoms Older clients Unexplained weight loss (>10% in last 6 months) Unexplained fever >100 F. Drenching night sweats Stage A symptoms Often asymptomatic

27 Staging- Cotswold Staging Classification for Hodgkin’s Disease
Stage I Confined to one node region or lymphoid structure Stage II 2 or more nodal regions same side of diaphragm Stage III Involved lymphoid regions or structures on both sides of diaphragm Stage IV extranodal sites (present in non-lymphoid tissue such as liver, bone marrow) Staging by symptoms A - asymptomatic B - fever, chills, night sweats, weight loss

28 Stage 1 Single lymph node region or lymphoid structure – spleen, thymus, tonsil

29 Stage 2 2 or more lymph node regions on same side of diaphragm

30 Stage 3 Involvement of lymph regions or structures on both sides of diaphram

31 Stage 4 Extra nodal sites Bone Liver

32 PET Scan Positron Emission Tomography Scan can detect malignant tumor cells in the body. A small amount of radioactive glucose is injected into a vein and then the PET scanner rotates around the body, taking pictures of where glucose is being used in the body. More glucose is metabolized by malignant tumor cells than normal cells, leaving more radioactive material as a residue, so they show up brighter in the picture. Cleveland Clinic 2011

33 Treatment of Hodgkin’s Disease
Stages I & II Chemotherapy w/wo RadiationTherapy 95% - complete remission 90% - 95% 5 Year Survival & 20 Years for 70-80% Stages III & IV Chemotherapy Partial remission Follow up with radiation Rx Up to 90% 5 Year Survival

34 Chemotherapy Systemic Chemotherapy:
Administered Orally, Intravenous or Intramuscular for systemic treatment Regional Chemotherapy: injected into the spinal column, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas Cleveland Clinic 2011

35 Radiation Therapy high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. The way the radiation therapy is given depends on the type, location and stage of the cancer being treated. External radiation therapy: uses a machine outside the body to send radiation toward the cancer. Internal radiation therapy: uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. Cleveland Clinic 2011

36 Prognosis – 5 year survival rates
Stage I - >95% Stage II - >95% Stage III – 85-90% Stage IV – 60-90% Factors   survival B stage symptoms WBC > 15,000 Hb < 10.5 Lymphocyte < 600 Male gender > 45 years  serum albumin B stage symptoms: fever, chills, night sweats, weight loss Overall 10 year survival – 77%

37 Late Effects from Childhood and Adolescent Hodgkin Lymphoma Treatment
Side effects may appear months or years after treatment. Regular follow-up exams are important. Late effects may include problems with the following: Development of sex organs in males. Fertility (ability to have children).

38 Late Effects Thyroid, heart, or lung disease.
An increased risk of developing a second primary cancer. Bone growth and development. The risk of these long-term side effects will be considered when treatment decisions are made. Cleveland Clinic 2011

39 Non-Hodgkin’s Lymphoma
low-grade - indolent intermediate and high-grade – aggressive multiple possible causes include EBV, H pylori, immuno-deficency, autoimmune disorders, infectious physical & chemical agents painless lymph node enlargement lymphadenopathy d/t obstruction Copstead & Banasik 2009 Types Etiology CM’s Incidence has increased by 73% between 1973 & Why?? AIDS – NHL 60 times more common in people with AIDS than the general population. Middle aged white Males greatest prevailance Ages 50-60, caucasian Risk Factors: Immune deficiencies, autoimmune diseases, infections, chemical and agents: EBV, HTLV-1, Herpes virus 8, H. pylori

40 Non-Hodgkin’s Lymphoma
Diagnosis History & Physical (H&P) radiologic studies (including PET Scan) CBC, ESR, chemistry panels lymph node, bone marrow biopsy Indications for biopsy Adenopathy for > 3 weeks, progresses in size or spreads to other areas B symptoms that cannot be explained; fever, night sweats, weight loss Abnormal blood tests suggestive of lymphoma (ESR elevation-nonspecific sign of infection) X-rays to suggest extra-nodal sites Immunodeficiency diseases

41 Non-Hodgkin’s Lymphoma
Treatment instituted after staging cure rates vary with each grade International Index used for predicting survival single or combined treatment depending upon stage of disease Purpose: Eradication of tumor cells Radiation and Chemotherapy Higher growth fraction (measure of the number of cells undergoing mitosis in a tissue—ratio between replication/resting cells) in intermediate and high grade tumors, so greater response to radiation and chemo Combination chemo-shrinkage and remission – numerous protocols Low grade – Stage I-II – radiation alone Intermediate grade – Stage III-IV – aggressive chemo especially under 60 years old High grade – immediate and aggressive treatment (lymphoma doubles in bulk in hours days (BMT and stem cell transplants) Normal Lymphocyte count is 16 to 46 % of all WBC’s (Corbett 2004)

42 Nursing Diagnoses Coping, ineffective (individual or family)
Encourage expression of feelings Relaxation techniques/support group Take prednisone in a.m. to prevent insomnia Infection, risk for r/t bone marrow suppression Prednisone: adverse reactions: insomnia, euphoria, increased appetite, n/v, H/A,

43 Nursing Diagnoses Body Image disturbance Wig/hats prior to first chemo
Skin changes/photosensitive Reproductive issues Sperm banking Contraception Menstrual changes and menopausal symptoms

44 Alternative & Complimentary Therapy
Herbals/Tinctures Supplements Chiropractic/ Massage Spirituality Imagery Nutritional Important for the client to inform health care providers of use of alternative treatments – adjust dose of chemo? drug interactions?

45 Transplantation: Bone Marrow and Stem Cell
Indications: Hematologic disorders rare genetic disorders treatment of patients undergoing high-dose chemotherapy for solid tumors Procedure IV administration of bone marrow that contains cells capable of differentiation into RBC’s, WBC’s and Plts. Approximately 20,000+ transplants/year

46 Transplantation: Bone Marrow and Stem Cell
Types of BMT allogenic - from a donor, often from a sibling autologous - transplanting to “self” after marrow is treated syngeneic - from an identical twin HLA: Human Leukocyte Antigen=system of recognition of host/foreign protein recognition Donor marrow tested for matching HLA National Marrow Donor Program maintains registry and conducts donor drives Only perfect match is between identical twins Bone marrow is aspirated from multiple sites, Treated and stored for future use

47 Transplantation: Bone Marrow and Stem Cell
For allogenic BMT patient is conditioned pre-procedure receives high-dose chemo and/or TBI associated with many side effects protective isolation Treated marrow re-infused intravenously Complications infection interstitial pneumonia graft v. host disease (GVHD) host v. graft TBI=total body irradiation GVHD=donor T-lymphocytes form an immunological reaction against host cells Host v. graft: recipient rejects graft from donor or own graft (skin from thigh to arm after a severe burn as an example)

48 Preventing GVHD Suppression of:
Recipient’s immune system before transplant. Drug Therapy: tacrolimus & cyclosporin prevent cell-mediated attacks upon transplant tissues/organs, no adverse effect upon bone marrow function/inflammatory response. Donor's immune cells in recipient after transplant

49 Investigational and Other Treatments
Molecular genetics gene transfer therapy Alternative or complementary therapies diet supplements macrobiotic diet pharmacological therapies psychological therapies

50 Clinical Trials Planned investigation of a new regime
Therapeutic or preventative 4 phases of studies must be completed for FDA approval Role of the Institutional Review Board Informed consent Polit and Beck 2008 Research—utilize research to create an Evidence Based Practice--an evidence building enterprise—design then implement a study—is the study utilizing ethical methods of data collection. 4 Phases: 1. small scale to develop safety measures, 2. preliminary evidence to establish effectiveness of treatment 3. Randomized Clinical Trials (randon/control groups) and gather evidence as to the effectiveness of new treatment/therapy – better than current methods? 4. study effectiveness in general population.

51 Clinical Trials Role of the nurse in clinical trials
Identifying risk study patients Protecting the integrity of the study Documenting in the medical record Advocating for the patient

52 References Medical-Surgical Nursing, Assessment and Management of Clinical Problems; Lewis, S., Dirksen, S., Heitkemper, M., et al, 8th Ed., 2011, Mosby, Inc. Medical-Surgical Nursing, Clinical Management for Positive Outcomes, Black, J., Hawks, J., 8th Ed., 2009 Saunders Pathophysiology, Copstead, L., Banasik, J., 3rd Ed., 2005 Elsevier Leukemia and Lymphoma Society (lls.org retrieved 11/22/11) Polit, D., Beck, C., 2008, Nursing Research, Generating and Assessing Evidence for Nursing Practice, 8th Ed., Lippincott Williams & Wilkins, Philadelphia


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