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 .
4.
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
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
11.
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
24.
25.
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