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74 Cards in this Set

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decreased WBC count
decreased granulocyte count.
decreased neutrophil count.
is determined clinically by the absolute neutrophil count (ANC).
ANC is calculated from the WBC and Diff
ANC = WBC x (% segs + % bands)
Diagnosis – WBC count
Neutrophil count < 1000 – 1500/ųl
White blood cells
lymphocytes 20-25% and monocytes 3-8%
basophils- .5-1%
neutrophils 60-70%
eosinophils 2-4%
inflammatory response not so responsive!

Watch for c/o
Sore throat
Nonproductive cough
Perirectal discomfort
neutropenia s/s
Why & What
Antibiotic therapy
Growth factor improvement
G-CSF (Neupogen, Neulasta)
GM-CSF (Leukine, Prokine)
Infection control
Monitor for s/s infection
Avoid invasive procedures
Consider thrombocytopenia
neutropenia nursing mgmt
monitor visits and handwashing!!
from themselves
From everything else
Strict hand washing
Private rooms
The gifts that keep on giving
neutropenia care plan
A group of malignant disorders affecting the blood and blood-forming tissues of
Bone marrow
Lymph system
Occurs in all age groups.
Accumulation of dysfunctional cells due to loss of regulation in cell division.
Fatal if untreated
No single causative agent

Associated factors include
Chemical agents
Chemotherapeutic agents
Immunologic deficiencies
leukemia pathophys.
Most common type of leukemia in children.
15% of acute leukemia in adults.
Immature lymphocytes proliferate in the bone marrow (most are B-cell)
Signs and symptoms may appear abruptly
CNS manifestations are common.
Acute Lymphocytic Leukemia (ALL
Excessive mature neoplastic granulocytes in bone marrow
Move into peripheral blood in massive numbers
Ultimately infiltrate liver and spleen
Philadelphia chromosome
Disease specific marker
Chronic, stable phase
Followed by acute, aggressive (blastic) phase
Chronic Myelogenous Leukemia (CML)
Production and accumulation of functionally inactive but long-lived, mature-appearing B-lymphocytes .
Lymph node enlargement is present throughout body
Increased incidence of infection
Complications from early-stage CLL are rare
May develop as the disease advances
Pain, paralysis from pressure caused by enlarged lymph nodes
Chronic Lymphocytic Leukemia (CLL)
25% of all leukemias
85% of the acute leukemias in adults
Abrupt, dramatic onset
Serious infections or abnormal bleeding
Uncontrolled proliferation of myeloblasts
Acute Myelogenous Leukemia (AML)
Varied but usually relate to
Bone marrow failure
Overcrowding by abnormal cells
Inadequate production of normal marrow elements
Inadequate marrow elements cause
↓ Number and function of WBCs
leukemia clinical manifestations
Bone pain
Meningeal irritation
Oral lesions
Solid masses (chloromas)
leukemia cells cause
To diagnose and classify
Peripheral blood evaluation
Bone marrow evaluation
To identify cell subtype and stage
Morphologic, histochemical, immunologic, and cytogenic methods
leukemia diagnostic studies
Chemo is mainstay of treatment
Monoclonal antibodies
Uses genetic technology to target and kill cancer cells.
Antibody binds to a known antigen on the surface of the lymphocyte.
Antibody-antigen complex is destroyed by the immune system.
Stem cell transplantation. Must eradicate pt’s own stem cells first, then replace with HLA matched stem cells.
leukemia treatment
cancer originates in lymphocytes
Lymphoma hogdkins
EBV, genetics, exposure to toxins
↑ in HIV
lymphoma hogdkins etiology
Enlarged lymph nodes
Weight loss
Night sweats
Pruritis – no lesions
Alcohol – causes pain
Cough, dyspnea, stridor
Liver & spleen enlargement
lymphoma hogdkins c.m.
Blood analysis
Bone marrow exams
Radiologic exam
For staging
lymphoma hogdkins diagnostic studies
Leukopenia & thrombocytopenia
noted labs for hodgkins lymphoma
Indolent vs. rapidly developing
Unknown cause
More common in immunosupressed
No hallmark cell
lymphoma non-hodgkins
Painless lymph node enlargement
s/s relative to location
lymphoma non-hodgkins cm's
similar to Hodgkin’s
More diagnostics
lymphoma non-hodgkins diagnostics
Chemotherapy care
Radiation therapy care
Pain control
Aware of type/involvement – specifically for NHL
Psychosocial & spiritual support
lymphoma care
Cancerous plasma cells invade bone marrow and destroy bone.
Cancer cells produce abnormal and excessive amounts of antibodies and cytokines.
Insufficient normal plasma cells reduces immune function.
Skeletal pain is most common presenting symptom.
multiple myeloma
Bone pain, exacerbated by movement.
Pathologic bone fractures.
Myeloma protein can cause renal failure.
Anemia, thrombocytopenia, neutropenia.
multiple lyeloma clinical manifestations
Proteins secreted from malignant plasma cells can be detected in urine.
M antibody protein
Bence-Jones protein
Radiologic studies reveal lytic bone lesions.
Bone marrow analysis reveals large numbers of plasma cells.
mult. myeloma diagnostic studies
Rarely cured, goal is remission and relief of symptoms.
Biological therapy
Hematological Stem Cell Transplant
Management of hypercalcemia and prevention of pathologic bone fractures are important components of therapy.
mult. myeloma treatment
Thrombocytopenia has many causes: immune and nonimmune

Immune thrombocytopenic purpura (ITP)
Platelets become coated with antibodies
Macrophages in spleen destroy platelets
Mucosal (epistaxis, gingival bleeding)
Cutaneous (ecchymoses, petechiae, purpura)
Ecchymoses: “black and blue” bruising.
Petechiae are caused by RBCs leaking out of capillaries into the skin. Look like small, flat red dots on skin.
Purpura are consolidated petechiae.
Prolonged bleeding time
Risk is high for catastrophic hemorrhage (into the brain, retina, joints).
thrombocytopenia c.m.'s
Platelet count < 150,000 per microliter (μl)
< 50,000/μl prolongs bleeding time
< 20,000/μl at risk for spontaneous hemorrhage
Coagulation studies may indicate which part of coagulation cascade (if any) is involved.
Example: PT, aPTT
Bone marrow studies
thrombocytopenia diagnostic studies
To restore intravascular volume
To restore the oxygen carrying capacity of blood
To replace clotting factors and/or platelets
To replace WBC’s
blood therapy
Replaces RBC’s while preventing febrile, non-hemolytic transfusion reaction
Replaces RBC’s while preventing graft vs. host disease
Used in immunocompromised clients
Irradiated RBC’s
Replaces plasma without RBC’s or platelets. Contains most coagulation factors. Used in the control of bleeding
Fresh Frozen Plasma
Stop the transfusion
Maintain IV with NS
Notify physician and blood bank
Obtain blood & urine samples (if ordered)
Monitor VS and urine output
Administer medications as indicated
Return blood bag and tubing to blood bank
In some reactions, the transfusion may be restarted after medication administration
Document transfusion reaction
interventions for blood reactio
Tachypnea, Dyspnea
Heat/pain along vein
Hives, Rash, erythema
N/V/D, abdominal cramping
Chest/back pain
Myalgia with fever
Loss of consciousness
Cardiac arrest
transfusion reactions
Deficiency in RBCs, Hgb, Hct
s/s relative to hypoxia
See table 31-3 pg 686
Primary or secondary problem
Normal RBC lifespan is 120 days.

Erythropoietin (EPO) is a glycoprotein primarily produced in the kidneys (10% in the liver) that regulates RBC production and maturation.
↑ Number of stem cells committed to RBC production.
Shortens the time to mature RBC’s
erythrocyte production
Three alterations in erythropoiesis that decrease RBC production:
Decreased hemoglobin production.

Defective DNA synthesis.

Decreased number of erythrocyte precursors.
erythrocyte production
Dietary intake
Blood loss or hemolysis
Most susceptible
Very young
Poor diets
Women in reproductive years
Iron-deficiency anemia etiology
Early – symptom free
Glossitis-infl. On tongue
Cheilitis-infla. lips
c/o headache, paresthesia-itching
Burning sensation (tongue)
iron def. anemia cm's
Tachycardia, palpitations
Severity based on Hb level.
Hb 10-14 g/dl is mild
Hb 6-10 g/dl is moderate
Hb < 6 g/dl is severe
Guiac test
Collaborative care
Treat the underlying cause
iron def. anemia diagnostics and care
1) Enteric coated or sustained release should not be used
150-200 mg (daily dose) of elemental iron QID or TID
1 hour before meals (give with OJ if possible)
Liquid iron (watch the teeth!) dilute & straw
GI side effects
Heartburn, constipation, diarrhea
iron administration
Can be given parenterally (IM or IV)
Stain skin – change out prep and admin needles
0.5 ml air bubble after solution for IM
IM – deep muscle – Z track method
Do not massage injection site
IV – do not mix with other meds and no faster than 1 ml/min
nursing considerations for iron administration
Ascorbic acid
Other oral iron salts
Ferrous gluconate and ferrous fumarate
iron salts drug interatcions
Person may be heterozygous for defective gene or homozygous.
Heterozygous: one copy of defective gene. Has thalassemia trait or thalassemia minor. May be asymptomatic or have mild disease.
Homozygous: two copies of defective gene. Will have thalassemia major:
An autosomal recessive genetic disorder of inadequate production of normal hemoglobin
Problem is a genetic defect in the globin chain
Alpha chain defective in α-thalassemia
Beta chain defective in β-thalassemia (AKA Cooley’s anemia)
Most often occurs in persons of Mediterranean descent. Middle Eastern, African, and Asian also.
Leads to increased destruction of RBC’s (hemolytic anemia).
Hb Production Disorder: Thalassemia
Microcytic (small), hypochromic(pale) anemia with decreased RBC indices.
Pallor (r/t severe anemia; Hb < 6g/dl)
FTT (inadequate weight gain)
Facial deformities & skeletal abnormalities from hyperplasia of bone marrow.
Darkening of skin
Clinical Signs of Thalassemia
No specific drug or diet is effective in treating thalassemia
Thalassemia minor
Body adapts to decreased Hb
Thalassemia major
Blood transfusions to keep Hb around 10 g/dl.
Chelating agents (Desferal) may be needed to reduce iron overloading.
No Vit C or Iron Supplementation!
Thalassemia Treatment
Decreased intrinsic factor (IF) is usually the cause of Vit B12 deficiency.
IF is secreted by the parietal cells of the stomach. Is necessary for B12 absorption.
May be autoimmune, or caused by anything that decreases acid production in the stomach.
Most common cause: Pernicious anemia.
Cobalamin (Vit B12) Deficiency
due to ineffective hematopoiesis
& autohemolysis of megaloblasts.
WBC and platelet production also affected (pancytopenia).
Neurologic symptoms
Vit B12 deficiency causes demyelination of CNS neurons.
Paresthesias, decreased DTR’s, ataxia, irritability, & memory impairment result .
Pernicious Anemia
Increase in dietary cobalamin by itself does not correct the anemia.
Still important to emphasize adequate dietary intake.
Drug of choice: Cyancobalamin (Lehne, p. 630-631).
Can be given PO if pt can absorb some B12.
IM or SC injection
Nasal Spray
Regular evaluation for gastric carcinoma.
Pernicious Anemia Treatment
Also a cause of megaloblastic anemia
Folic acid is required for DNA synthesis
RBC formation and maturation affected.
Common causes
Poor nutrition
Malabsorption syndromes
Alcohol abuse and anorexia
Lost during hemodialysis
Folic Acid Deficiency
Chromosomal alteration inherited from parents.
Majority are idiopathic.
Result from exposure to ionizing radiation, chemical agents, viral and bacterial infections .
Relatively rare (4 cases per million)
May be chronic (managed with transfusions, EPO) or acute (risk of hemorrhage & sepsis).
Aplastic Anemia Etiology
Destruction or hemolysis of RBCs at a rate that exceeds production.
Third major cause of anemia.
Hemolytic Anemias
RBC defective.
Abnormal hemoglobin (sickle cell disease)
Enzyme deficiencies (G6PD)
RBC membrane abnormalities
Intrinsic hemolytic anemia –
caused by factor other than the erythrocytes.
Extrinsic hemolytic anemia –
Group of inherited, autosomal recessive disorders.
Presence of an abnormal form of hemoglobin in the erythrocyte.
Hemoglobin S (HbS)
Substitution of valine for glutamic acid on the β-globin chain of hemoglobin
HbS causes the RBC to stiffen and elongate.
Assumes sickle shape in response to ↓ O2 levels
Incurable disease, often fatal .
Sickle Cell Disease (SCD)
Typical patient is asymptomatic except during sickling episodes.
Sickle cell crisis is a vasoocclusive crisis. See Lewis, p. 696
Symptoms can be
Pain and swelling of joints.
Pallor of mucous membranes
Sickle Cell Disease (SCD) c.m.s
Supportive care!
Pain management
O2 for hypoxia and to control sickling
IV hydration
Hydroxyurea to prevent sickling (off label use).
Prevention of crisis.
Transfusion if necessary.
Stem cell transplantation.
treatment of sickle cell anemia
Vera: neoplastic transformation of hematopoietic stem cells.
Secondary: chronic hypoxemia.
Results in increased blood viscosity and risk of thrombi.
Treatment is removal of cause, phlebotomy, bone marrow suppressants.
Hypervolemia and hyperviscosity cause symptoms.
HTN: Headache, vertigo, dizziness, tinnitus, visual disturbances.
Blood vessel distention, impaired blood flow, thrombosis and tissue hypoxia cause paresthesias and cardiovascular symptoms.
Generalized pruritus, exacerbated by heat.
Pt. at risk for stroke & hemorrhage.
Polycythemia clinical presentations
Goal is to reduce blood volume and viscosity.
Phlebotomy to reduce HCT to < 48%
IV hydration
Polycythemia Treatment
Polycythemia Treatment suppress bone marrow
Polycythemia Treatment
(lowers blood counts)
Polycythemia Treatment
decreases platelets
vit b-12 defficiency, pernicious anemia, part of the schiling test. Necessary coenzyme needed for metabolic processes including fat and carbohydrate metabolism and protein synthesis, required for RBC formation. Monitor for hypokalemia, monitor for signs of b-12 def. pallor, neuropathy, red tongue, psychosis.
antianemics, iron. SE: seizures, hypotension, nausea, constipation, dark stools, diarrhea, epigastric pain, skin staining, anaphylaxis. ASSESS for anaphylaxis
Ferrous sulfate