Leukemia - unregulated proliferation of leukocytes in the bone marrow

 Leukemias are cancers of white blood cells or of cells that develop into white blood cells. In leukemia,
the white blood cells are not functional. They invade and destroy bone marrow, and they can metastasize
to the liver, spleen, lymph nodes, testes, and brain.
 Blood cells & Bone Marrow
 Overproduction of WBCs
 Ends up with Low RBCs, Low Platelets
o Low H&H, High WBC  Anemia
o Frequent infection
o Unsteady gait, Fatigue
o Bruising, petechiae, easy bleeding
o Weight loss, anorexia
o Bone pain
 Prevent infection!
 Biopsy  posterior iliac crest

o Prolonged bleeding from obvious injury
o Unexplained blood loss
o Feels fatigued and faint with normal activities
o Easily chilled; frequent infections

DIAGNOSTICS
 Blood sample: complete blood count, hemoglobin, prothrombin time, fibrogen levels
 Bone marrow aspiration
 Schilling test: diagnose pernicious anemia, macrocytic anemia, malabsorption syndromes
o Measures vitamin B12 absorption with and without intrinsic factor. It is used to differentiate
between malabsorption and pernicious anemia.
 Lymph node biopsy, ultrasound spleen, lymphangiography
 Radiography, CT, bone scan, MRI

AML – Acute Myeloid Leukemia - Most common leukemia among adults; prognosis is poor.
 Immature Non-functional WBCs
 Acute = Abrupt; AML develops without warning AML Acute Myeloid Leukemia
 Mostly myeloblasts present in bone marrow. Age of onset Onset 15-39 years
usually between 15-39 years Immature Non-functional WBCs
 The complete blood count (CBC) shows a ↓↓↓ erythrocytes Bleeding, fever, infection, weakness,
and ↓↓↓platelets. fatigue, Anemia, pallor
 immature leukocytes, = blast cells Petechiae, echymosis
 Attempts are made to achieve remission of AML by the No contact sports
aggressive administration of chemotherapy, called induction
therapy, which usually requires hospitalization for several weeks. Avoid Contact sports…
 Fever and infection; weakness and fatigue, dyspnea on exertion, and pallor from anemia; and petechiae,
ecchymosis, and bleeding tendencies from thrombocytopenia.
AML-(teen to mid-adult) Teaching-> no contact sports

CML – Chronic Myeloid Leukemia Most prevalent after age 50 years. Prognosis is less than 2 years of
survival from the time of diagnosis. Three phases: chronic (slow growing with mild manifestations);
accelerated (more rapid growing with severe manifestations and
failure to respond to therapy); and blast (very aggressive with
metastasis to organs).
 Mature cells with reduced function
 Slow (insidious) onset
 Mostly granulocytes present in bone marrow; Age of onset
usually in fourth decade

ALL – Acute Lymphocytic Leukemia – B & T lymphocytes

 Immature Non-functional WBCs ALL – Acute Lymphocytic Leukemia
 Acute = Abrupt Common in children ↓15
 Common in children Immature WBCs, reduced function
 Mostly lymphoblasts present in bone marrow. Age of onset LymphBLASTS in Bone Marrow
is usually younger than 15 years

CLL – Chronic Lymphocytic Leukemia older than 50 years of age, strong genetic link. B & T lymphocytes
 Mature cells with reduced function
 Slow (insidious) onset CLL – Chronic Lymphocytic Leukemia
 Plan rest and activities older than 50 years
 Mostly lymphocytes present in bone marrow; Age of Mature WBCs, reduced function
onset is usually older than 50 years Plan rest
LymphoCYTES in Bone Marrow
C’s are ↑50 Mature need rest and are slow
ALL my children are immature
AMidLifeBleed

Assessments
 Anorexia, fatigue, weight loss, dyspnea on exertion, weight loss
 Bleeding , nose, gums rectal, hematuria, increased menstrual flow
 Lymphadenopathy and splenomegaly
 Normal, elevated, or reduced WBCs; decreased ↓↓↓platelets150-450
 Positive Bone Marrow Biopsy: Leukemic Blast -Phase cells; pre-op consents, from iliac crest, painful,
(signs of shock echomosis,
 Severe anemia, infections, fatigue, easy bruising, fever, enlarged spleen and lymph nodes, internal or
external bleeding
 s/s infection ↑BP, febrile
o Risks: infection, hemorrhage, activity intolerance, disturbed body image, anxiety and fear
o Prolonged bleeding -↑5min, go to hospital

Interventions
 Monitor platelet counts.
 Assess for signs of bruising and petechiae; report hematuria or epistaxis.
 Acknowledge client’s anxieties and fears.

What is it, how is it diagnosed?

What labs would be monitored and why?
What precautions are needed
  Remember therapeutic communication!!!!
 Diagnostics
 Bone Marrow Biopsy
◦ A bone marrow analysis shows an excess (more than 20%) of immature leukocytes, called blast
cells; this is the hallmark of the diagnosis.
 Procedures
 Bone Marrow Transplant
 What is it? What risks to donor/recipient?
◦ Autologous bone marrow transplant. The donor is the patient himself or herself.
◦ Allogeneic bone marrow transplant. The donor shares the same genetic type as the patient. ~
higher risk if GVHD~ know S&S of this
Clinical manifestations of acute GVHD include
 diffuse rash progressing to blistering and desquamation similar to second-degree burns;
 mucosal inflammation of the eyes and the entire gastrointestinal tract with subsequent diarrhea that
may exceed 2 L per day;
 biliary stasis with abdominal pain,
 hepatomegaly, and elevated liver enzymes progressing to obstructive jaundice.
 nausea, vomiting, and mucositis
 encephalopathy, hemolytic uremia syndrome, hemolytic anemia, and thrombotic thrombocytopenia
purpura

◦ Umbilical cord blood transplant.

 Immunocompromised
◦ Need to be cautious. Protective Isolation (what does this mean)
 Signs and Symptoms of rejection
◦ Graft-versus-host disease (GVHD) is a potentially life-threatening complication of
allogeneic hematopoietic stem cell transplant (allo-HSCT) driven by alloreactive donor T
cells.2. S&S
◦ GVHD remains a major cause of morbidity and nonrelapse mortality for allo-HSCT
recipients.3,4
◦ There is distinct pathophysiology and presentation of acute GVHD and chronic GVHD.
Acute GVHD can occur at any time, but often occurs in the first few months after
transplant.5
Phases of chemotherapy to treat leukemia
Induction therapy: Intensive combination therapy
 Induce remission: absence of all findings of leukemia, including less than 5% blasts in bone marrow.
Aggressive treatment (possible continuous infusion); IV infusion; CNS and CSF infusion prophylaxis (ALL)
4 to 6 weeks (hospitalization required due to increased risk for infection and hemorrhage)
Consolidation or intensification therapy
Cure by eradicating any residual leukemic cells.
Same medications as induction phase at lower dosage or different combination of medications
About 6 months

Maintenance therapy
Prevent relapse. Lower doses of oral or IV chemotherapy Months to years

Reinduction therapy: for a client who relapses

Place the client back in remission.
Combinations of chemotherapy used to achieve remission
Probability of relapse occurring decreases over time

Complications
 Tumor lysis syndrome refers to the constellation of metabolic disturbances that occurs when large
numbers of neoplastic cells are killed rapidly, leading to the release of intracellular ions and metabolic
byproducts into the systemic circulation
o Make sure to encourage patient to increase fluids 3000-5000 ml per day
o Review lab findings
 The superior vena cava is a major vein in your upper body. It carries blood from your head, neck, upper
chest, and arms to the heart. Superior vena cava syndrome (SVCS) happens when the superior vena
cava is partially blocked or compressed. Cancer is usually the main cause of SVCS. 
o Assessment is key. What S&S would show improvement (think cardiovascular)
 Thrombocytopenia~ is a condition that occurs when the platelet count in your blood is too low.
Platelets are tiny blood cells that are made in the bone marrow from larger cells.

Mnemonic for chemotherapy side effects: BARFS: B for bone marrow depression; A for
alopecia; R for retching (nausea/vomiting); F for fear and anxiety; and S for stomatitis.