Presentation on leukaemia
- 2. INTRODUCTION
- 3. INTRODUCTION • Cancer of.hematopoetic system are disorder that results form proliferation of maliganant cells . • Malignant cells are originated in the bone marrow thymus and lymphatic tissues • Blood cells that originate in lymph are called lymphoid cells • Leukemia (cancer of bone marrow cells) • Lymphoma(cancer of lymphoid tissues) • The cause of leukemia is not unknown but there is some evidence that genetic influences and viral pathogenesis may be evolved .
- 5. DEFINITION • Leukemia is a malignant disease of the blood forming organs • Leukemia is a malignant progressive disease in which the bone marrow of other forming organs produces increased number of immature abnormal leukocytes these supress the production of normal blood cells leading to anemia and other symptoms. • It is the neoplastic proliferation of one particular cell type (granulocytes;monocytes ;lymphocytes or infrequently erythrocytes and megakaryotes)
- 6. ETIOLOGY AND RISK FACTORS • The exact cause is unknown:- • Several factors are associated with leukemia include:- • Genetic factor:-A high incidence of acute leukemia and chronic lymphocytic leukemia is reported in certain families 1. Heriditary abnormalities aassociated with an increased incidence of leukemia are “Down syndrome “,fancouils aplastic anemia ,trisomy -13etc
- 7. • Over exposure to ionsing radiation and chemicals .It can be a major risk factor for development of leukemia with disease developing years after initial exposure. • Alkylating agent used to treat other cancer specially in combination with radiation therapy increases persons risk of leukemia • Workers exposed to chemical agents such as benzene (an aromatic hydrocarbon)are at much higher risk
- 8. COGENTIAL ABNORMALITIES • Down syndorme • The presence of • Primary immunodeficiency • Infection with human T-cell leukemia virus
- 9. SYMPTOMS
- 10. PATHOPHYSIOLOGY 1. There are four major types on the basis of acute versus chronic the term acute and chronic refers to cell maturity and nature of disease onset 2. Acute lymphocytic leukemia 3. Acute myeloid leukemia 4. Chronic lymphocytic leukemia 5. Chronic myeloid leukemia
- 12. ACUTE LYMPHOCYTIC LEUKEMIA • Most common type of leukemia in children accounts for 15%in adults • In this type immature lymphocytes proliferation in bone marrow most are of bone marrow origin. • It results form an uncontrolled proliferation of immature cells(lymphoblast ) Derive form the lymphoid stem cells. • Age of onset • Before 14years of age • Peak incidence in between 2-9 • In older adults (65-90)
- 13. CLINICAL MANIFESTATION • Fever,pale skin,bleeding anorexia ,fatique and weakness • Bone ,joints ,and abdominal pain • Generalized lymph-adenopathy infection,weight loss • Hepatomegaly,spleenomagely,headache,mouthsores • Increased ICP(nausea,vomitting,lethargy,cranial nerve dysfunction)
- 14. DIAGNOSTIC EVALUATION • Low RBC count,Hb,HCT,low.platelet count • Low or.high WBC count • Transverse lines of rarefraction at the end of metaphysis of long bones on X-rays • Hyper cellular bone.marrow with lymphoblast • Lymphoblast also.possible in CSF • Presence of Philadelphia chrosome (20-25%cases)
- 15. ACUTE MYELOID LEUKEMIA • This type represent only one fourth of all leukemia in which 85%of this type in adults • It is characterized by uncontrolled proliferation of myeloblasts precursor of granulocytes • There is hyper plasia of bone marrow • It results from a defect in the hematopoietic stem cells that differentiates into cell myeloid cells monocytes ,granulocytes,erythrocytes and platelets. • Age of onset • It onset is often adrupt and chromatic patient may have sevior infection and abnormal bleeding from onset of disease • Increase in incidence with advancing agr,peak incidence between 60-70years of age
- 16. CLINICAL MANIFESTATION • Fatique,weakness,headache ,mouth sores,anemia,bleeding,fever ,infection,sternal tenderness,gingival hyperplasma minimal • Hepatospienomegaly and lymphadenopathy • Pain from enlarged liver or spleen ,hyperplasma of gums,the bone pain form exapansion of marrow
- 17. DIAGNOSTIC EVALUATION • Low RBC count,hemoglobin,HCT.low platelet count,low to.high WBC with myelioblast • High LDH Greatly hypercellular bone marrow with myeloblasts
- 18. CHRONIC LYMPHOCYTIC LEUKEMIA • It is common in adults • It is characterized by production of accumulation of functionally inactive but long lived small mature appearing lymphocytes • The type of lymphocytes involved is usually B-cells • The lymphocytes in filterate the organ • In contrast to the acute form of leukemia most of the leukemia cell in chronic lymphocytic leukemia are fully matured • Lymphadenopathy is present throughout the body and there is an increased incidence of infection because t-cell deficiencies or hypo-gamma globulin • Pressure on nerve from enlarged lymph nodes causes pain and even paralysis • Age of onset • 50-70years of age,rare below 30 years of age
- 19. CLINICAL MANIFESTATION • Many patients are asymptomatic and are diagnosed incidentally during routine physical examination or during treatment of other disease • An increased lymphocyte count is also present • Spleenomagely and lymphadenopathy • Hepatomegaly may progress to fever ,night sweats ,weight loss • Patient with CLL have defects in their humoral and cell mediated immune system therfore infection are common • Viral infection such as herpes,roster can become widely disseminated
- 20. DIAGNOSTIC EVALUATION • Mild anemia and thrombocytopenia with disease progression total WBC less than 100000/microliter • Hemolytic anemia (4-11%) • Thrombocytopenia purpura(2-4%) • Hypo gamma globulinemia
- 21. CHRONIC MYELOID LEUKEMIA • It is caused by excessive development of mature neoplastic granulocytes in the bone marrow .The excess neoplastic granulocytes moves into peripheral blood in massive number and ultimately infilterate the liver and spleen • These cells contain a distinctive cytogenetic abnormalities the Philadelphia chromosome which serves as a disease makers and results from translocation of genetic material b/w chromosome 9 and 12 • Age of onset • 25-60 years of age ,peak incidence about 45 years of age
- 22. CLINICAL MANIFESTATION • Clinical feature of luekemia relate to problem caused by bone marrow failure and formation of leukemia infilterate • As leukemia progress • A fewer normal blood cells are produced • Abnormal WBC’s continue to accumulate (don’t through apoptosis ) • The luekemia cells infilterate the patients organ leading to problem such as.speenomegaly ,hepatomegaly ,Lymphadenopathy,bone pain,meingeal and oral lesions • Solid masses resulting form collection of leukemia cells called chloranea can also occur
- 23. DIAGNOSTIC EVALUATION • A history collection • Physical examination • Pheripheral blood evaluation (WBC and platelet count) • Bone marrow examination (sampling form hipbone) • Lumber puncture and ct scan are done to determine the luekemia cells outside of blood and bone marrow
- 26. THE TNM STAGING SYSTEM • The tnm system is most widely used cancer staging system.Most hospitals and medical cancers use the TNM system as their main method of cancer reporting • Example of cancer with different staging systems include brain and spinal cord and blood cancers • In the TNM systems • The T refers to the size and extent of the main tumor • The main tumor is usually called the primary tumor • The N refers to the number of nearby lymph nodes that have cancer • The M refers to whether the cancer has matastasized this means that cancer as spread from the primary tumor to the other parts of the body • When your cancer is described by the TNM system there will be numbers after each letter that give more details about the cancer .for example –TINOMX OR T3NIMO
- 27. • The following explains what the letter and number means :- • Primary tumor(T) • TX;-main tumor cannot found • TO;-main tumor cannot found • T1,T2.T3,T4:-Refers to size and or extent of the main tumor .the higher the number after T ,the larger the tumor Or more It has grown into nearby tissues .T’s may be further divided to provide more detail such as T3a and T3b
- 28. REGIONAL LYMPH NODES (N) • NX:-cancer nearby lymph nodes cannot be measured • NO:-There is no cancer in nearby lymph nodes • N1,N2,N3:-Refers to the number and location of lymph nodes that contain cancer.The higher the number after the N.the note lymph nodes that contain cancer
- 29. DISTANCE METASTASIS • MX:-Metastasis cannot be measured • MO:-Cancer has no spread to other parts of the body • MI:-Cancer has spread to other parts of the body • FOR ACUTE MYELOID LEUKEMIA. • Autologous or allogereic hematopoietic stem transplantation • FOR ACUTE LYMPHOCYTÍC LEUKEMIA • Allogeneic hematopoietic stem cell transplantation • FOR CHRONIC MYELOID LEUKEMIA • Hematopoietic cell transplantation alpha interferon Leukapheresis • FOR CHRONIC LYMPHOCYTIC LEUKEMIA • Spleenoctomy allogereic hematopoietic stem cell transplant
- 30. MEDICAL MANAGEMENT • FOR ACUTE MYELOID LEUKEMIA • THE overall objective of treatment is to achieve complete remission in which there is no evidence of residual leukemia in the bone marrow .Attempts are made by the aggressive administration of chemotherapy called induction therapy • Induction therapy typically involves high doses of cytrabine (cytosar-Ara- L)sometimes etoposide (VP-16Vepeniside )Is added to the regimen • The aim of induction therapy is to eradicate the leukemia cell,but this often accompained by eradication of normal types of myeloid cells :-when the pateint recover from the induction therapy (ie neutrophill and platelet count return to normal )then the patient will receive consolidation therapy.(protremimission theapyy to eliminate any residual leukemia cells that are not clinically detecable and to reduce the chances of recurrence .
- 31. • Another aggressive treatment option is BMT or PBSCT.when a suitable tissue match can be obtained the patient embarks on an even more aggressive regimen of chemothearpy (something in combination with radiation therapy )with the treatement goal of destroying the hematopoietic function of patients bona marrow • Another important option for the patient to consider is supportive care alone .Supportive care may be the only otpion if the pateint hve significant comordidity such as extremely poor cardiac pulmonary renal or hepatic function
- 32. FOR ACUTE LYMPHOCYTIC LEUKEMIA • The Expected outcome of treatment is complete remission .lymphoid blast cell are typically very sensitive to coricocosterloid and to vinca alkaloids therefore these medication are ana integral part of the induction therapy because all frequently invades the central nervous system proplylaxis with cranial irradication or intrathecal chemotherapy • Infection specially viral infection are common the use of corticosteroid to treat all increases the pateints suspectibility to infection • Patient with all tend to have a better response to treatment tne do patients with AML • BMT and PBSCT offers a chance for prolonged reemission or even care,if the illness recurs after the therapy .
- 33. FOR CHRONIC MYELOID LEUKEMIA • CML is a disease that can potentially be cured with BMT and PBSCT • Other therapy depend on the stage of disease • In the chronic phase the expected outcome is correction of the chromosomal abnormalities (ie conversion of malignant stem cell population back to normal )agents that have been used successfully for this purpose and interferon alpha(Roferon-A)and cytosin often in combination theseagents are administered daily as subcutaneous injections • In case of an extreme leukocytes (eg leukocyte count greater than 3000000/mm3 )a more emergent treatment may be required in this instance leukaphieresis in which the patients blood is removed and separated with the leukocytes withdrawn and the remaining blood return to the patient can temporarily reduce the no of leukocytes
- 34. • The transformation phase can be insidious and rapid it marks the process of evolution (or transformation)to the acute form of leukemia (blast crisis ) in the transformation phase the patient may complain of biine pain nd may report fever and weight loss the patient may become more anemic and thrombocytopenic an increased basophill level is detected by the CBC • In the acute CML treatmnet may resemble Induction therapy for aute leukemia patient whose disease evolve into “lymphoid “ blast crisis are more likely to reciter into the chronic phase after the induction therapy for those whose disease evolve in AML therapy is largely ineffective in acheiveing a second chronic phase life threatening infections and bleeding occur frequently in this phase
- 35. FOR CHRONIC LYMPHOCYTIC LEUKEMIA • In early stages the CLL may not require any treatment when symptoms are severe (dreching hight sweats ,painfull,lymphadenopathy )or when the disease progress to layer stages (with resultant anemia and thrombocytopenia)chemotherapy with fludarabjne (fludara)or corticosterioids and chlorambucil (leukeran)is often used .The major side effect of fludarabine is prolonged bone marrow supression manifested by prolonged period of neutropenia lymphopenia and thrombocytopenia.
- 36. NURSING MANAGEMENT • Intervention • Assessing client • Gand washing techniques • Client evaluation • Maintain Oral hygiene • Perineal cleaning for every bowel movement
- 37. DECREASED CARDIAC OUTPUT TO THROMBOCYTOPENIA SECONDARY TO EITHER LEUKEMIA TO TREATEMENT • Institute bleeding precaution • Provide a soft toithbrush for Oral hygiene • Avoid commercial mouth wash containing alcohol • Avoid blowing or picking Jose,straining at bowel movement douching is using tempon using razors • Don’t administer IM S C injections • Don’t insert rectal suppository • Avoid aspirin contaiing • Avoid urinary catheterization I’d needed then only lesser sized
- 38. • Avoid mucosal trauma during suctioning • Remove all.the sharp objects around client • Use pressure reducing mattress proper change the position • Use only paper tape aovoid strong adhesive
- 39. RESEARCH IMATINIB THERAPY IN CHRONIC MYELOID LEUKEMIA • By:-Namrata bhutani (senior resident department of biochemistry VMMC AND safdurjang hospital,new delhi)issue date 1january 2020 • The current aim for CML disease management in the TKI era is to provide age and sex matched normal life duration to CML patient .Despite excellent outcome ,many patient fail to treatment with many of them requiring a third or even further lines of therapy when selecting for such previous TKIS to date more than 40.mutation have been indentified and their early detection is important for clinical treatment with the treatment of the new tyosine kinase inhibitors associated with these mutation the resistance problem seems to diminish as some of the new drug are less prone to resistance the introduction of imantinib opend up of different treatment prespective in CML
- 40. • For thE patient resistant or intolerant to imantib second and third generation TKIS are successfully used in distinct CML disease states .TKI related adverse event could impact the clinical course especially in long term drig administration .The current article reviews the difrenent aspects of imantib therapy in CML pateints
- 41. SUMMARY • Today we discussed About “Leukemia and it’s nursing management “ • Here we studied about defintion of leukemia it’s etiology and risk factors pathophysiology it’s type clinical manifestationits diagnosis surgical management medical management it’s nusing management and a research on CML
- 42. CONCLUSION • Classification os based on the type of cell form which the leukemia development and it’s degree of maturity • This is done by examing the appearance of the malignant cell with light microscopy and by using cytogenetic to characterize any underlyning chromosomal abnormailities • All pateint suffers from any type of cancers should have an extra attention • The nurse should be knowledgeable about different type of treatment so he can provide optimal care
- 43. REFERENCE • Joyce M block,jane hokamson A textbook of medical surgical nursing clinical management page no 2115-2124 • Chintamani Lewis helt Kemper divksen O Berien A textbook of medical surgical nursing page no 722-728 • Medical surgical nursing 12th edition Brunner and Sidharth page no 933_939 • http:/www.nursing.orib.com/pathophysiology of leukemia