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LEUKEMIA
• Literally means “white blood”
• neoplastic proliferation of one particular cell type

LIQUID TUMORS (granulocytes, monocytes, lymphocytes, or

megakaryocytes)
• defect originates in the hematopoietic stem cell, the
( L E U K E M I A & LY M P H O M A )
myeloid, or the lymphoid stem cell.

B Y : R . A B A D, R N

LEUKEMIA LEUKEMIA
CAUSE: uknown BLEEDING PRECAUTIONS
ETIOLOGY: Potential bleeding* and injury secondary to thrombocytopenia/altered
• Genetic coagulation due to:
• Viral pathogenesis • Malignant invasion in bone marrow
• Radiation exposure from benzene and alkylating • Bone marrow suppression resulting from chemotherapy (particularly
agents [Melphalan (Alkeran)] alkylators, antitumor antibiotics, antimetabolites) and radiation therapy
• Hypersplenism
• Disseminated intravascular coagulation (DIC)
• Altered coagulation

LEUKEMIA
BLEEDING PRECAUTIONS
Assessment:
• Integument: Petechiae (usually located on trunk, thighs), ecchymoses or
hematomas, conjunctival hemorrhages, bleeding gums, bleeding at puncture
sites (venipuncture, lumbar puncture, bone marrow)
• Cardiovascular: Hypotension, tachycardia, complaints of dizziness,
epistaxis
• Pulmonary: Respiratory distress, tachypnea
• Gastrointestinal: Hemoptysis, abdominal distention, rectal bleeding
• Genitourinary: Vaginal or urethral bleeding
• Neurologic: Headache, blurred vision, mental status changes
LEUKEMIA
BLEEDING PRECAUTIONS
LABORATORY TESTS
• Monitor complete blood count (CBC), platelets daily (at least); coagulation
panel.
• Notify physician if platelet count is <10,000/mm3 or if count has changed
significantly from previous count (including coagulation), or whenever
patient becomes symptomatic.
• Ensure patient’s blood was human leukocyte antigen (HLA) typed before
transfusions or chemotherapy begins if admitted for induction therapy (eg,
for acute leukemia).
• Obtain 1-hour posttransfusion platelet count if warranted.
• Test all urine, emesis, stools for occult blood.

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LEUKEMIA
BLEEDING PRECAUTIONS
NURSING INTERVENTION:
Prevent Complications
• Avoid aspirin and aspirin-containing medications or other medications
known to inhibit platelet function, if possible.
• Do not give intramuscular injections.
• Do not insert indwelling catheters.
• Take no rectal temperatures; do not give suppositories, enemas.
• Use stool softeners, oral laxatives to prevent constipation.
• Use smallest possible needles when performing venipuncture.
• Apply pressure to venipuncture sites for 5 min or until bleeding has
stopped.
LEUKEMIA
BLEEDING PRECAUTIONS
NURSING INTERVENTION:
Prevent Complications
• Permit no flossing of teeth and no commercial mouthwashes.
• Use only soft-bristled toothbrush for mouth care.
• Use only toothettes for mouth care if platelet count is<10,000/mm3, or if gums
bleed.
• Lubricate lips with water-soluble lubricant every 2 hr while awake.
• Avoid suctioning if at all possible; if unavoidable, use only gentle suctioning.
• Discourage vigorous coughing or blowing of the nose.
• Use only electric razor for shaving.
• Pad side rails as needed.
• Prevent falls by ambulating with patient as necessary.

LEUKEMIA LEUKEMIA
BLEEDING PRECAUTIONS BLEEDING PRECAUTIONS
NURSING INTERVENTION: NURSING INTERVENTION:
Control Bleeding Evaluation and Expected Patient Outcomes
• Apply direct pressure. • Patient demonstrates an absence of bleeding as evidenced by
• For epistaxis, position patient in high Fowler’s position; apply ice absenceof spontaneous petechiae, ecchymoses, epistaxis, hemoptysis,
pack to back of neck and direct pressure to nose. bleeding gums, conjunctival hemorrhage, vaginal bleeding, hematuria,
guaiac positive stool, blurred vision, orthostatic hypotension, and
• Notify physician for prolonged bleeding (eg, unable to stop prolonged bleeding from puncture sites.
within 10 min).
• Patient demonstrates an absence of bleeding as evidenced by the
• Administer platelets, fresh frozen plasma, packed red blood cells, presence of vital signs within normal limits and intact neurologic
as prescribed. status.

ACUTE LEUKEMIA ACUTE MYELOID LEUKEMIA

• occurs within weeks • results from a defect in the hematopoietic stem cell
• WBC is halted at the blast phase that differentiates into all myeloid cells: monocytes,
• progresses very rapidly granulocytes (neutrophils, basophils, eosinophils),
• death occurs within weeks and months without erythrocytes, and platelets.
aggressive treatment • most common nonlymphocytic leukemia
• undifferentaited form of AML has poorer prognosis
CHRONIC LEUKEMIA and tends to be more resistant to treatment
• can extend for years AGE: All are affected with peak incidence in at age 60
years

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ACUTE MYELOID LEUKEMIA ACUTE MYELOID LEUKEMIA

CLINICAL MANIFESTATIONS: ASSESSMENT AND DIAGNOSTINC FINDINGS:
• Fever • CBC results show a decrease in both erythrocytes and
• Infection platelets.
• total leukocyte count can be low, normal, or high
• weakness • percentage of normal cells is usually vastly decreased
• fatigue • excess immature blast cells
• can be further classified into seven different subgroups, based
• bleeding tendencies on cytogenetics, histology, and morphology (appearance) of
• pain from enlarged liver and spleen the blasts.
• Clinical course and treatment differ substantially with only one
• hyperplasia of the gums subtype: Acute Promyelocytic Leukemia (APL, or AML-M3).
• bone pain from the expansion of bone marrow • DIC in later stages

ACUTE MYELOID LEUKEMIA ACUTE MYELOID LEUKEMIA

MEDICAL MANAGEMENT
COMPLICATIONS
Goal: To achieve complete remission
• Bleeding
common sites of bleeding: Chemotherapy
1. Induction therapy - requires hospitalizationa for several weeks
GI, Pulmonary and intracranial
High doses of :
(infection and fever increases the likelihood of bleeding)
– cytarabine (Cytosar, Ara - C)
– Daunorubicin (DaunoXome)
– Motioxantrone (Novantrone)
– idarubicin (Idamycin)
– etoposide (VP-16, VePesid)
During this time, the patient is typically very ill, with bacterial, fungal, and occasionally viral
infections, bleeding, and severe mucositis, which causes diarrhea and a marked decline in
the ability to maintain adequate nutrition.

ACUTE MYELOID LEUKEMIA ACUTE MYELOID LEUKEMIA

MEDICAL MANAGEMENT MEDICAL MANAGEMENT
3. Consolidation therapy (Post-remission Therapy) 5. Monoclonal Antibody Therapy
Goal: eliminate residual leukemia cells that are clinically detectable –targets all cells that secretes CD33
–cytarabine (Cytosar, Ara-C) Calicheamicin ( a potent antitumor antibiotic)
–induction treatment at lower dosages
Medication:
4. Bone Marrow Transplantation
–when a tissue match is obtained an even more aggressive
gemtuzumab ozogamicin (Mylotarg)
regimen of chemotherapy sometimes in combination with – less toxic than conventional induction therapy
radiation therapy regimens

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ACUTE MYELOID LEUKEMIA ACUTE MYELOID LEUKEMIA

SUPPORTIVE CARE
–Blood trasfusion (RBC, platelets)
–treating infections (bacterial and fungal)
–Administering granulocytic growth factors (filgaastim,
Neupogen, sargramostin (Leukine) can chorten the
duration of neutropenia
–for patients with significant comorbidity such as poor
cardiac, pulmonary and renal or hepatic function
Rx:
Hydroxyurea (Hydrea) is used to to control the increase of
blast cells
PROGNOSIS
–Despite aggressive chemotherapy 70% of patient s
with AML experience a relapse with only 11% survive
10 years or longer
–Bone Marrow Transplantation has shown to cure 25% to
50% of patients who are at high risk of relapse or who
have relapsed
–in patients who are given Hydrea - death follows
within months due to infection and bleeding

ACUTE MYELOID LEUKEMIA CHRONIC MYELOID LEUKEMIA

COMPLICATIONS OF TREATMENT: • arises from a mutation in the myeloid stem cell.
1. Tumor Lysis Syndrome • uncontrolled proliferation of cells, the marrow expands into the
–increase in uric acide and formation of renal stones may • cavities of long bones
progress to acture renal failure
• Extramedullary hematopoiesis in the lliver in spleen resulting in
2. Hyperkalemia and Hypocalcemia
enlargement of these organs
–leads to cardiac dysrhythmias, hypotension, neuromuscular
effects such as muscle cramps weakness, tetany/spasms ETIOLOGY:
Genetic
Patients require high fluid intake, alkylization of urine, prophylaxis Age
with allupurinol ( uncommon to people <20 /o but increases risk with age 40-50 y/o)

CHRONIC MYELOID LEUKEMIA CHRONIC MYELOID LEUKEMIA

STAGES : CLINICAL MANIFESTATIONS:
• usually asymptomatic
1. Chronic • Leukocytosis
• Decreased tissue perfusion which leads to shortness of
2. Transformation breath and confusion
• Enlarged tender spleen
3. Accelerated / Blast Crisis • Enlarged Liver
• Malaise
• Anorexia
• Weight loss

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CHRONIC MYELOID LEUKEMIA CHRONIC MYELOID LEUKEMIA

MEDICAL MANAGEMENT: MEDICAL MANAGEMENT:
1. Tyrosine kinase inhibitor – imanitib mesylate (Gleevac) Less aggressive therapeutic approach
Considerations:
1. hydroxyurea (Hydrea)
• Antacids and grapefruit juice may limit drug absorption, and large
2. Busulfan (Myleran)
doses of acetaminophen can cause atotoxicity
2. interferon-alfa (Roferon-A) and cytosine Extreme Leukocytosis
• expected outcome is correction of the chromosomal • Leukopheresis - patient’s blood is removed and separated, with the
abnormality, administered subQ leukocytes withdrawn, and the remaining blood returned to the
patient)
3. BMT
4. Induction Therapy • anthracycline (daunomycin)

CHRONIC MYELOID LEUKEMIA ACUTE LYMPHOCYTIC LEUKEMIA

COMPLICATIONS OF TREATMENT • uncontrolled proliferation of immature cells
• profound fatigue (lymphoblasts) derived from the lymphoid stem cell
• depression • cell of origin is the precursor to the B lymphocyte in
• anorexia, approximately 75% of ALL cases
• Mucositis • T-lymphocyte ALL occurs in approximately 25% of
• inability to concentrate ALL cases.
• BCR-ABL translocation is found in 20% of ALL blast
cells

ACUTE LYMPHOCYTIC LEUKEMIA ACUTE LYMPHOCYTIC LEUKEMIA

ETIOLOGY: CLINICAL MANIFESTATION:
1. Genetics • Neutropenia
2. Age • Leukopenia / Leukocytosis
• common in young male children peak incidence is at 4 years old • Thrombocytosis
• Anemia
• Increasing age is associated with diminished survival
• Enlarged liver and spleen
• Bone pain
• Headache
• Vommiting

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ACUTE LYMPHOCYTIC LEUKEMIA CHRONIC LYMPHOCYTIC LEUKEMIA

MEDICAL MANAGEMENT: • most common form of leukemia in the United States and
Europe
1. Corticosteriods
2. Vinca Alkaloids
• typically derives from a malignant clone of B lymphocytes
3. Prophylaxis:
• In contrast to the acute forms of leukemia, most of the
leukemia cells in CLL are fully mature and appears to escape
a) Cranial irradiation
apoptosis as a result, there is an excessive accumulation of
b) Intrathecal chemotherapy – methorexate (Folex) cells in the marrow and the circulation
4. BMT
• antigen CD52 is prevalent on the surface of many of these
4. PBSCT leukemic B cells

CHRONIC LYMPHOCYTIC LEUKEMIA CHRONIC LYMPHOCYTIC LEUKEMIA

Early Stage: COMPLICATION:
• elevated lymphocyte count is seen and can exceed 100,000/mm3
• Asymptomatic
• Autoimmune hemolytic anemia
Late Stages
• Idiopathic thrombocytopenic purpura
• Lymphadenopathy
• Hepatomegaly and Splenomegaly
*In the autoimmune process the RES destroys the body’s own
RBCs or platelets

CHRONIC LYMPHOCYTIC LEUKEMIA CHRONIC LYMPHOCYTIC LEUKEMIA

CLINICAL MANIFESTATION: MEDICAL MANAGEMENT
• Lymphocytosis Chemotherapy with:
• RBC is normal in early stages and ddecreases as the it goes to its • corticosteroids
later stages • chlorambucil (Leukeran)
• Lymphadenopathy – severe and sometimes painful • cyclophosphamide (eg, Cytoxan)
• Splenomegaly • vincristine (eg, Oncovin)

• Infections –Bacterial, Viral – Herpes Zoster is widely disseminated
• Anergy – decreased reaction to skin sensitivity tests
• “B symptoms” include: fever, drenching sweating at night, unintentional
weight loss
• doxorubicin (eg, Adriamycin)
• fludarabine (Fludara) – SE: prolonged marrow suppression
Monoclonal Antibody - rituximab (Rituxan)
• alemtuzumab (Campath) targets the CD52 antigen commonly found on CLL cells and that it is
effective in clearing the marrow and circulation of these cells without affecting the stem cells.

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CHRONIC LYMPHOCYTIC LEUKEMIA AGNOGENIC MYELOID METAPLASIA (AMM)

MEDICAL MANAGEMENT • chronic myeloproliferative disorder that arises from
Prophylaxis • neoplastic transformation of an early hematopoietic
Antibacterials stem cell characterized by marrow fibrosis or scarring,
1. trimethoprim
splenomegaly, extramedullary hematopoiesis (typically
2. sulfamethoxazole [Septra]
spleen, liver, or both), leukocytosis and
Immunoglobulin may be given to selected patients
thrombocytosis, and anemia.
• Patients with AMM have increased angiogenesis
* needs to be continued for in the next 2 months post chemo (formation of new blood vessels) within the marrow

AGNOGENIC MYELOID METAPLASIA (AMM) AGNOGENIC MYELOID METAPLASIA (AMM)

ETIOLOGY - unknown MEDICAL MANAGEMENT:
• BT (PRBC)
Age: >60 y/o
• Corticosteroid + Androgen
CLINICAL MANIFESTATIONS: • Iron chelation Therapy
•Pancytopenia • Hydroxourea to control WBC and platelet counts
•Splenomegaly and reduce the size of the spleen
• Splenic irradiation
•Hypermetabolic State • BMT for younger and much healthier individuals

AGNOGENIC MYELOID METAPLASIA (AMM) AGNOGENIC MYELOID METAPLASIA (AMM)

NURSING DIAGNOSIS: NURSING MANAGEMENT:
1. Pain management
1. Altered Body Image
2. Diet should be small and frequent which is is high
2. Fatigue in protien
3. Altered nutrition: Less than body 3. Limit ADLs – energy conservation techniques
requirement 4. Educatiing patient about infection control and
appropriate interventions if infection is present

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LYMPHOMAS HODGKIN’S DISEASE

• neoplasms of cells of lymphoid origin •a relatively rare malignancy that has an
• tumors usually start in lymph nodes but can involve impressive cure rate.
lymphoid tissue in the spleen, the gastrointestinal tract
RF:
(eg, the wall of the stomach), the liver, or the bone
marrow. •Male
• Lymphomas can be broadly classified into two •>50 y/o
categories: Hodgkin’s disease and non-Hodgkin’s ETIOLOGY : Unknown
lymphoma (NHL)

HODGKIN’S DISEASE HODGKIN’S DISEASE

• a relatively rare malignancy that has an impressive cure rate. Reed-Sternberg cell
• unicentric in origin in that it initiates in a single node. • malignant cell of Hodgkin’s disease
RF: • gigantic tumor cell that is morphologically unique and is thought to be
• Male of immature lymphoid origin.
• >50 y/o TWO TYPES HODGKIN’S DISEASE
ETIOLOGY : Unknown 1. Nodular Sclerosis - occur more often in young women, poor
• Viral : EBV fragments are found in 40% to 50% of patients prognosis
• First degree relatives have a higher-than-normal frequency of the 2. Mixed Cellularity - occurs more commonly in men and causes more
disease constitutional symptoms but has a better prognosis

HODGKIN’S DISEASE HODGKIN’S DISEASE

CLINICAL MANIFESTATIONS CLINICAL MANIFESTATIONS
1. Lymphadenopathy 2. Pruritus
• painless enlargement of one or more lymph nodes on one side of the 3. Sever pain after alcohol intake – case: unknown
neck
4. Pain due to nerve compresion by tumor
• Nodes are firm but not hard
• Pulmonary effusion
• Most common sites cervical, supraclavicular, and mediastinal nodes
• Jaundice
• mediastinal mass may be seen on chest x-ray; occasionally, the mass is
large enough to compress the trachea and cause dyspnea • Abdominal pain
• Bone pain
• 5. B Symptoms

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HODGKIN’S DISEASE HODGKIN’S DISEASE

CLINICAL MANIFESTATIONS ASSESSMENT AND DIAGNOSTIC FINDINGS

6. Mild anemia 1. Assessment of the lymphatic chain

2. Assessment of the size of the spleen and liver
7. Impaired cellular immunity as evidenced by absent or
Imaging Studies
decreased reaction to sensitivity skin tests 1. Chest X-ray
2. CT Scan of the chest
3. Bone Scans
Laboratory
• CBC, platelet count, ESR, and liver and renal function studies

HODGKIN’S DISEASE HODGKIN’S DISEASE

ASSESSMENT AND DIAGNOSTIC FINDINGS MEDICAL MANAGEMENT
SURGICAL 1. Early Stage (Stage IA and !!A)
1. Excisional Lymph node biopsy Chemotherpay for 2-4 months followed Radiation therapy
2. Bone Marrow Biopsy
2. Advance Stages (III and IV and all B stages)
3. Staging Laparotomy
ABVD Chemotherapy
4. Lymphangiography
Adriamycin, bleomycin,Vinblastine, dacarbazine

HODGKIN’S DISEASE HODGKIN’S DISEASE

MEDICAL MANAGEMENT LONG TERM COMPLICATIONS OF THERAPY
If patient relapses: • Immune dysfunction
1. BMT • Herpes infections (zoster and varicella)
2. PBSCT • Pneumococcal sepsis
• Acute myeloid leukemia (AML)
• Myelodysplastic syndromes (MDS)
• Non-Hodgkin’s lymphoma
• Solid tumors

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HODGKIN’S DISEASE HODGKIN’S DISEASE

LONG TERM COMPLICATIONS OF THERAPY LONG TERM COMPLICATIONS OF THERAPY
• Thyroid cancer • Avascular necrosis
• Thymic hyperplasia • Growth retardation
• Hypothyroidism • Infertility
• Pericarditis (acute or chronic) • Impotence
• Cardiomyopathy • Dental caries
• Pneumonitis (acute or chronic)

NON-HODGKIN’S LYMPHOMA NON-HODGKIN’S LYMPHOMA

• heterogeneous group of cancers that originate from the
neoplastic growth of lymphoid tissue
• Most NHLs involve malignant B lymphocytes; only 5% involve
T lymphocytes
• true localized disease is uncommon.
• fourth most common type of cancer diagnosed in the United
States and the fifth most common cause of cancer death
• 8th common cause of cancer death in the Phils. as of 2015
Risk increases with age (50-60 years peak incidence)
Cause : Unknown
• increased incidence of NHL in people with immunodeficiencies or
autoimmune disorders, viral infections (including Epstein-Barr virus
and HIV), or exposure to pesticides, solvents, or dyes.

NON-HODGKIN’S LYMPHOMA NON-HODGKIN’S LYMPHOMA

CLINICAL MANIFESTATIONS ASSESSMENT AND DIAGNOSTIC FINDINGS
Early Stage: asymptomatic Histopath (Biopsy)
Advanced Stage: Bone Marrow
Lymphadenopathy Imaging Studies
B Symptoms CSF Studies
Weight loss

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NON-HODGKIN’S LYMPHOMA NON-HODGKIN’S LYMPHOMA

MEDICAL MANAGEMENT NURSING MANAGEMENT
1. Radiation – cranial irradiation 1. Minimize risk of infection
2. Chemotherapy intrathecal 2. Patient edcucation about pre post
chemotherapy
3. Interferon
3. Regular screening for development of second
4. Monoclonal treatment – antibody CD20
malignancies
5. Rituximab
6. BMT and PBSCT – for patients youngar than 60

MULTIPLE MYELOMA MULTIPLE MYELOMA

•malignant disease of the most mature form of B CLINICAL MANIFESTATIONS
lymphocyte, the plasma cell specific • Bone pain that increases in rest and movement – classic symptom

immunoglobulin secreted by the myeloma cells is
detectable in the blood or urine and is referred
to as the monoclonal protein, or M protein
•Plasmacytomas can occur in the sinuses, spinal
cord, and soft tissues. Median survival time is 3
to 5 years
• Osteoporosis -> Fractures -> Spinal cord compression-> PAIN
• Hypercalcemia – plasma cells releases osteoclasts stimulating factor
• Renal failure – destruction of renal tubules by immunoglobulin
molecule
• Anemia – marrow has less spce for RBC production
• Leukopenia – due to plasmacytomas invasion of the bone marrow
• Increased serum viscosisity due to secretion IgA

MULTIPLE MYELOMA MULTIPLE MYELOMA

ASSESSMENT FINDING AND DIAGNOSTICS
• elevated monoclonal protein spike in the serum seen in
serum electrophoresis or UA
• Bence Jone protein – in Urine
• Lytic bone lesions in X-ray
• BIOPSY – Gold Standard
Presence of sheets of plasma cells – hallmark sign
1. Chemotherapy (primary tx)
• dexamethasone (Decadron) combined with melphalan
(Alkeran), cyclophosphamide (Cytoxan), doxorubicin
(Adriamyein), vincristine (Oncouin), and BCNU
(Carmustine).
2. Radiation – useful in strenghtening the bone
3. Monoclonal treatment with Interferon

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MULTIPLE MYELOMA MULTIPLE MYELOMA

4. bisphosphonates, such as pamidronate (Aredia) and NURSING DIAGNOSIS:
zoledronic acid (Zometa) – for bone strenghtening 1. Acute Pain
5. thalidomide (Thalomide) – sedative that has an 2. Activity Intolerance
antimyeloma effect
3. Risk for infection

MULTIPLE MYELOMA
NURSING MANAGEMENT
1. Pain management
2. Health teaching about :
• activity restrictions
• s/s of hypercalcemia
END
• Maintaining mobility
• Hydration
• Infection control

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