1

DISORDER

ANEMIA

IRON DEFICIENCY ANEMIA

THALASSEMA



Amount of RBC (erythrocytes), hgb
concentration, &/or packed RBC hct.

Most common, chronic hematologic
disorder -young, poor, female

Normal to lose 1 mg of Fe/d in
sweat, urine, GI

Need to replace Fe -> hgb
production reduced

Autosomal recessive genetic
production of Hgb.

Due to absent/reduced globulin
protein.
CAUSE Blood loss (GI ulcer, menorrhagia)
RBC production (stomach, kidney, liver)
RBC destruction (hemolysis) sickle
cell, medication, incompatible blood,
trauma,

Inadequate dietary intake
Malabsorption GI surgery.
duodenum

Blood loss
Hemolysis

Hemolysis

CLINICAL
MANIFESTATION
Pallor
Fatigue
Irritability
Numbness & tingling of extremities
Dyspnea
Sensitivity to cold
Pain and HYPOXIA w/sickle-cell crisis
Early - may have no s/ss

Chronic - most common -
Pallor
Glossitis inflammation of the
tongue
Cheilitis inflammation of the lip

Additional s/s s -
Headache
Paresthesias tingling, numbness

Major life-threatening disease
physical & mental retarted.

Jaundice

DIAGNOSTIC TEST CBC
Mean corpuscular volume (MCV)- size
RBC.
Normocytic normal
CBC
Hgb & Serum Fe

Mean corpuscular volume (MCV)-
CBC =>Microcytic/hypochromic

Hgb electrophoresis separates
Hgb from abnormal. Used to
2

Microcytic small
Macrocytic large

Mean corpuscular Hgb (MCH) amt of
Hgb per RBC
Normochromic normal
Hypochromic-

Mean corpuscular Hgb concentration
(MCHC) Hgb amt relative to the size of
the cell.

TIBC total iron-binding capacity.
Measurement of serum transferrin
(protein binds w/iron & transport it for
storage.
serum iron & TIBC (iron deficiency
anemia

Hgb electrophoresis separates Hgb from
abnormal. Used to detect
THALASSEMIA & SICKLE-CELL
DISEASE

Sickle-cell test evaluates sickling of
RBC in the presence of oxygen tension.


DX procedure
Bone marrow examination dx aplastic
anemia (failure of bone marrow to
produce RBC, platelets, & WBC)
size RBC => Microcytic

Mean corpuscular Hgb (MCH)
amt of Hgb per RBC =>
Hypochromic

Bone Marrow - cell smear
GI - colonoscopy/endoscopy =>stool
for guiac

detect THALASSEMIA &
SICKLE-CELL DISEASE

USUAL TX
(MEDICAL/SURGICAL
MEDICATIONS
O2
Blood transfusion
Erythropoietin (EPOGEN/EPOCRIT)
Iron supplement Ferrous sulfate
(FeSO4)
((Iron Dextran) Imferon - use of Z
track method and 0.5 ml of air
Blood transfusion/exchange
transfusion

Zinc & vit c during Iron
3

FeSO4 and Vitamin B12
Fe rich diet

Diet therapy

Blood transfusion
Chelation therapy - urine
excretion of iron. Used for iron
overloading. Iron supplement
should not be given.
NURSING
IMPLICATIONS
Erythropoietin (EPOGEN/EPOCRIT)
-Observe BP, Cardiovascular
-Monitor Hgb & Hct twice/week

Iron supplement Ferrous sulfate
(FeSO4)
-PO w/ VIT C must take 1 hour b4 meal
-Parenteral iron supplement (Iron
Dextran) for severe anemia Z-track
method
-Monitor Hgb 4-6 weeks
S/E: constipation, diarrhea, heartburn
-Undiluted liquid iron may stain teeth.
Use straw.

(Vitamin B12)
-lack of intrinsic factor in the
stomach/malabsorption syndrome =
parenterally/intranasally continues rest of
their life.
-IM/deep subq. Do not mix w/any meds in
the syringe.

(Fe rich diet)
Liver
Eggs
Meats
Dried fruits
Legumes
Dark green leafy veg
Whole-grain
Enriched bread & cereals

4

Potato

(Vit C)
Citrus fruits
Green leafy veg
Strawberries
Cantaloupe

(B12)
Red meat
Liver
Eggs
Enriched grain

(Folic Acid)
Green leafy veg
Liver
Meat
Fish
Legumes
Whole grains















5

DISORDER

MEGALOBLASTIC ANEMIAS COBALAMIN (VIT B12)
DEFICIENCY
FOLIC ACID DEFICIENCY


impaired DNA synthesis. Large RBC.

Failure of absorption of Vitamin
B12

Not enough folic acid for DNA
synthesis -> RBC formation

CAUSE Pernicious anemia most common

Deficiency of intrinsic factor d/t
atrophy of stomach glandular
mucosa

D/T - variety of problems including
-destruction of parietal cells
-heredity
-GI resection -> ulcers

poor nutrition

malabsorption

alcohol abuse

hemodialysis

growth

CLINICAL
MANIFESTATION
GI:
Sore, red, beefy, & shiny tongue
Anorexia
n/v
abd pain

NEURO:
Muscle weakness
Paresthesias feet & hand
Ataxia - loss of full control of bodily
movements
Impaired thought process

Permanent nerve damage

GI:
Dyspepsia
Smooth, beefy red tongue



no neuro s/ss

DIAGNOSTIC TEST Mean corpuscular volume (MCV)-
size
Macrocytic Anemia -> CHF and
Angina

Blood work

Bone Marrow

Serum Folate level - below 4
6

Blood tests - lg, fragile RBCs

GI analysis

Schilling test measures vit B12
absorption & w/o intrinsic factor.
Malabsorption or pernicious anemia.
-Inject Intrinsic factor

Bone Marrow

Unconjugated Bilirubin ->
hemolysis



ng/ml

Serum Cobalamin - normal

HCl in gastric analysis


USUAL TX
(MEDICAL/SURGICAL
MEDICATIONS
Replacement Therapy


NURSING
IMPLICATIONS
Make sure no injuries will sustain d/t
Neurologic impairment diminished
sensations to heat and pain

Protect pt falling, burns, trauma

Monitor skin frequently detect redness
Need for
B12(CYANOCOBALAMIN)
injections rest of life-> fatal in about
2 years if not received
-IM for 2 weeks then weekly Hct
normal then monthly.
-PO GI absorption intact

Need for Fe and Folic Acid PO

Diluted HCl with meals for vitamin
metabolism

Blood transfusions


Nutritional Support ->teaching
1 mg/day PO
5md/day malabsorption

(Folic Acid)
Green leafy veg
Liver
Meat
Fish
Legumes
Whole grains

7

(B12)
Red meat
Liver
Eggs
Enriched grain

(Folic Acid)
Green leafy veg
Liver
Meat
Fish
Legumes
Whole grains

Rehab for neuro disability
permanent




















8


DISORDER

ANEMIA OF CHRONIC DISEASE APLASTIC ANEMIA


Anemia of inflammation, underproduction of RBCs &
mild shortening of RBC survival.

Pt has peripheral PANCYTOPENIA (blood cell types
RBC, WBC, platelets)

Life threatening, stem cell disorders

CAUSE Renal disease
Autoimmune hemolysis
Myelosuppresion
Medication (chemo/radiation)
HIV, hepatitis, malaria, bleeding episodes,
hypopituitary, hypothyroid, adrenal, Addison.
30% congenital

70% acquired -
exposure to ionizing radiation, chemicals, meds

CLINICAL
MANIFESTATION
fatigue, dyspnea, cardiac, cerebral

Neutropenia - increased susceptibility to infection

Thrombocytopenia - increased bruising (petechiae,
ecchymosis, epistaxis)

DIAGNOSTIC TEST serum ferritin
iron
Normal folate &cobalamin
hgb, WBC, platelet
reticulocyte
bleeding time

May serum iron & total iron-binding capacity

MCV Normocytic
MCH normochromic anemia
Bone marrow biopsy
Aspiration
Pathologic exam

USUAL TX Severe blood transfusion Severe blood transfusion
9

(MEDICAL/SURGICAL
MEDICATIONS
Erythropoietin therapy (Epogen) Erythropoietin therapy (Epogen)
NURSING
IMPLICATIONS
Erythropoietin (EPOGEN/EPOCRIT)
-Observe BP, Cardiovascular
-Monitor Hgb & Hct twice/week

Based on causative agent - remove and wait for condition
to resolve

Need to prevent infection, bleeding

Can be treated with BMT




























10

DISORDER

ACUTE BLOOD LOSS CHRONIC BLOOD LOSS


Hemorrhage hypovolemic shock Similar to iron deficiency anemia
CAUSE Trauma
Surgery

Bleeding ulcer
Hemorrhoids
Menstrual
Postmenauposal blood loss
CLINICAL
MANIFESTATION
10% - none

20% - no s/s @ rest, tachycardia w/exercise. Postural
hypotension

30%- normal supine BP & pulse @ rest. Postural
hypotension & tachycardia w/exercise

40% - BP, CVP, CO. cold clammy skin, rapid &
thready pulse

50%- shock & death

Pain & numbness LE

DIAGNOSTIC TEST Sudden blood volume loss - lab may be normal 2-3
days

Actual blood loss - RBC, Hb, Hct.

USUAL TX
(MEDICAL/SURGICAL
MEDICATIONS
-Replace blood loss

-Identify source of hemorrhage & stop blood loss

IV ER dextran, hetastarch, albumin, &/or crystalloid
electrolyte (Ringers Lactate

Blood transfusion packed RBC
-Identify source of hemorrhage & stop blood loss

-Supplemental iron PO / parenteral

11


Supplemental iron PO / parenteral

NURSING
IMPLICATIONS
Post-op pt:
Monitor for blood loss via drainage tubes, dressings

































12

DISORDER

SICKLE CELL ANEMIA ACQUIRED HEMOLYTIC ANEMIA


Inherited

Autosomal recessive disorder

Unstable bonding of Hgb molecule when O2 tension is
low

Hypoxia -> changes in RBC shape -> sickle shaped -
>clogging of vessels -> further ischemia -> infarction
of body systems

Low O2 conditions -> precipitate sickling

Increased blood viscosity -
-dehydration

Sickled cells clump and block BVs -> ischemia ->
necrosis ->cell death

Hemolysis of RBC from extrinsic factor


CAUSE Cell clamping Trauma
Antibody reaction
Infectious agents and toxic
CLINICAL
MANIFESTATION
Dark skin (grayish cast), pallor
Pain abd & long bones, hand, foot, joint, back, chest
Jaundice

Complication:
Infection
Stroke
URI
Leg ulcers


DIAGNOSTIC TEST Peripheral blood smear
13

serum bilirubin

Hg electrophoresis
CXR skeletal deformities
MRI dx stroke d/t blocked cerebral vessel from SCD
Doppler studies dx DVT
USUAL TX
(MEDICAL/SURGICAL
MEDICATIONS
Hydration
O2
Pain relief (Morphine).
Meperidine (Demerol) contraindicated cause toxicity.
s/e: seizure

Antibiotics

Transfusions

Anti-sickling agents - Droxia(hydroxyurea),
chemotherapy drug. Fetal Hgb, erythrocytes volume
& hydration, neutrophils

Bone Marrow transplant - HSCT


NURSING
IMPLICATIONS
Avoid high altitudes,
adequate fluids
Tx infections

Chronic leg ulcers:
Bed rest
Antibiotics
Warm saline soaks, mechanical /enzyme debridement
Grafting

Priapism (abnormal erection)
Pain mgt
Nifedine (Procardia) CCB















14

*O2 hypoxia->respiratory failure common cause
death
*Rest
*Fluid/electrolytes
*Transfusion

Teaching:
Eye exam
Avoid crisis
Avoid high altitudes
Seek med attention counteract URI
Pain contro
need for preventative vaccines - Flu, pneumonia,
HIB(influenza)



































15

DISORDER

HEMOCHROMATOSIS POLYCYTHEMIA


Iron overload disorder RBC

Impaired d/t:
viscosity (hyperviscosity)
volume (hypervolemia)
CAUSE Genetic defect

Secondary to thalassemia & sideroblastic anemia
(heterogeneous disorder where in the bone
marrow cannot produce enough RBC)

Liver disease

Multiple blood transfusions

PRIMARY OR
POLYCYTHEMIA
VERA
SECONDARY POLYCYTHEMIA
EPO/no

Chronic
myeloproliferative
disorder from
chromosomal
mutation

WBC & platelets

viscosity &
volume

Congested organs
(splenomegaly,
hepatomegaly)
clotting


EPO

HYPOXIA -
DRIVEN
HYPOXIA -
INDEPENDENT
High altitude

Cadiopulmonary
Disease

Defective O2
transport



Renal Cysts

Extrarenal tumor


CLINICAL
MANIFESTATION
Early:
Fatigue
Arthralgia
Impotence
Abdominal pain
Weight loss

HTN
Headache, vertigo, tinnitus, angina, CHF
Blood vessel distention
CVA d/t thrombosis
Purititus
16

Later:
iron liver enlargement
Organs affected

Physical Examination:
Enlarged liver & spleen
Pigmentation changes (bronzing)

Hemorrhage
Plethora - ruddy complexion
Hyperuricemia -> gout

DIAGNOSTIC TEST iron serum, TIBC, serum ferritin

Molecular testing confirm dx

Liver biopsy if not definitive
RBCs

WBCs

histamine levels

Bone marrow -> hypercellularity of RBCs, WBC, platelets

USUAL TX
(MEDICAL/SURGICAL
MEDICATIONS


Phlebotomy - hct less than 45%-48%

NURSING
IMPLICATIONS
Iron removal - 500 ml of blood each week for 2
to yrs until iron WNL.

Mgt of organ involvement (DM, HF)

iron consumptions avoid
VIT C
Iron supplements
Uncooked seafood
Iron rich foods

Hydration therapy - blood viscosity

Avoid iron supplements














17


DISORDER

THROMBOCYTOPENIA HEMOPHILIA & VON WILLEBRAND DISEASE



platelet below 150,000 /uL(150 x 10^9/L) Hereditary bleeding disorder
CAUSE Genetic Wiskott-Aldrich syndrome

Acquired ingestion of food, herbs, drugs (aspirin)

Myleosuppressive -chemotherapy

IMMUNE
THROMBO-
CYTOPENIC
PURPURA
THROMBOTC
THROMBO-
CYTOPENIC
PURPURA
HEPARIN-
INDUCED
THROMBO-
CYTOPENIA
aka immune
thrombocytopenic
purpura (ITP)

-autoimmune




Clamping
(agglutination)
platelets

Hemolytic
uremic
syndrome


-autoimmune
-drug toxicity

Med ER -
bleeding &
clotting
60,000/uL

Aka heparin-
induced
thrombocytopenia
& thrombosis
syndrome (HITTS)

Problem:
-Venous & arterial
thrombosis
-DVT & PE

Defective/deficient coagulation factors

A factor VIII B x-mas
disease, factor
IX
VWD factor
VIII & platelet
dysfunction
Female
transmission
carriers
Female
transmission
carriers
Both genes

Congenital
bleeding
disorder
CLINICAL
MANIFES-
TATION
Bleeding :
mucosal epistaxis, gingival

cutaneous petechiae (small, flat, pinpoint, red/reddish-brown
micro hemorrhage),
purpura (reddish skin bruises),
Severe ecchymoses, subcu hematomas

Acute Hemarthrosis - bleeding in joint-> crippling

Slow, persistent, prolonged bleeding from minor
trauma/cuts
18

superficial ecchymoses (larger purplish lesion, flat/raised, pain &
tenderness)

hemorrhage major complication

Delayed bleeding after minor injuries

Uncontrollable hemorrhage after dental extractions/use of
hard tooth brush

Epistaxis

GI bleed from ulcers/gastritis

Hematuria from GU trauma

Splenic rupture from falls or abd trauma

Neuro s/s d/t compartment syndrome

COMPLICATIONS:
S/S seen mainly in childhood
Usually death early d/t complications
Life span up to 68 before AIDS
HIV+ d/t cryoprecipitates/factor concentrates
Increased incidence of Hepatitis B and C

DX TEST Normal : 150-400 x 10^3/uL

Platelet below 150,000 /uL (150 x 10^9/L) prolong bleeding
below 50,000/uL (50 x 10^9/L) trauma/injury
below 20,000/uL (20 x 10^9/L) life-threatening
below 10,000/uL (10 x 10^9/L) platelet transfusion

Peripheral blood smear distinguish ITP & TTP

PT & aPTT may be normal even severe. If => DIC

Bone marrow r/o leukemia, aplastic anemia, other
myeloproliferative disorders

Usually dxd d/t abnormal bleeding note soon after birth

PT & TT no impairment
Platelet count
PTT prolonged intrinsic
Bleeding time

VIII, IX, vWF
19

USUAL TX:
MED/SURG



















IMMUNE
THROMBO-
CYTOPENIC
PURPURA
THROMBOTC
THROMBO-
CYTOPENIC
PURPURA
HEPARIN-
INDUCED
THROMBO-
CYTOPENIA
Therapy below
30,000.

Corticosteriods
(prednisone)
Intracranial bleeding
(high-dose
methylprednisolone)

Splenectomy

IVIG
Anti-Rho (D)

Platelet transfusion
below 10,000
Identify & tx
cause

Plasmapheresis
(plasma
exchange)

High prednisone

Dextran

Chemotherapy
Splenectomy



Identify & tx cause


Corticosteroid

Platelet transfusion


give prophylactically and during acute crisis

cryoprecipitate - factor VIII - Hemophilia - A

factor IX - factor IX concentrate - Hemophilia - B -
Christmas Disease

NURSING
IMPLI-
CATIONS
Discourage OTC aspirin meds

Teach : pt bleeds easily
Notify Dr bleeding occurs black tarry BM, vomit, urine, etc

Avoid subq injection if cant avoided use small gauge needle &
apply direct pressure 5-10 mins

Female menstrual blood count sanitary napkins
prevent and tx bleeding

Need for genetic counseling

Control of acute bleeding incidents
-Stop bleeding, direct pressure/ice, packing gelfoam/fibrin
foam, apply topical hemostatic agents
- administer coagulation factor
- joint bleeding=>pack joint ice, give analgesics
(acetaminophen, codeine). No Aspirin.
-bleeding cease=> encourage mobilization ROM, PT,
-avoid weigh bearing until swelling gone.
- S/E Hyponatremia cause desmopressin
-tx airway

20

May need PT after joint bleed

Ambulatory/Home care - Medic Alert bracelet
most care will be given at home
refer to National Hemophilia Society
need for long term teaching
need for careful oral care
participation in non-contact sports - golf,
swimming







DISORDER

DISSEMINATED INTRAVASCULAR COAGULATION


Serious bleeding disorder resulting from abnormally initiated and accelerated clotting ->
Subsequent in clotting factors/platelets -> uncontrollable hemorrhage.

Not a disease
CAUSE
CLINICAL
MANIFES-
TATION
Bleeding - no h/o bleeding
Petechiae, oozing at IV sites
Weakness, malaise, fever
Hemoptysis
Hypotension
GI bleeds - upper and lower
Mental Status changes
Fibrin in microvasculature - sm clots
Bleeding and thrombotic s/s in DIC -> to many additional s/s

DX TEST clotting times (PT, PTT, aPTT, TT)
platelets and fibrinogen
D-Dimer assay - marker of the degree of fibrinolysis
21

RBC fragmented in smears
Fibrin split products => platelet dysfunction, disruption of coagulation, increased clot destabilization

USUAL TX:
MED/SURG



















correct underlying cause O2, volume replacement

administer blood products carefully below 20,000 or 50,000 platelet
below 100mg fibrinogen level => Cryoprecipitate & fibrinogen
Fresh frozen plasma (FFP) expect platelet.

protect from additional bleeding heparin/low-molecular-weight heparin (LMWH)

NURSING
IMPLI-
CATIONS
Need to dx/tx quickly

Treatment is controversial - Ns needs to know what is the most current tx

Chronic DIC without active bleeding -> no tx needed - tx underlying disease process -> cure - may need long term heparin not
po meds

DIC with bleeding -> support with blood products -> FFP, cryo, platelets - need to stabilize pt to find underlying cause of DIC

Thrombosis present -> treat with heparin - controversial also Amicar/EACA - platelets, cryo, FFP

Various investigational drugs being used
22

DISORDER

NEUTROPENIA MYELODYSPLASTIC SYNDROME


WBC (granulocytes, monocytes, lymphocytes)

NORMAL: 4000 to 11,000/uL
Below 1000 cells/uL (1 x 10 ^9/L)
Below 500 cells/uL severe
Group of related hematologic disorders characterized by a
change in the quantity and quality of bone marrow
elements.

Pre-leukemia
CAUSE Drug- induced

Hematologic disorder:
Aplastic anemia
Leukemia
Myelodysplastic syndrome

Autoimmune disorder:
SLE
RA

Infections:
Viral (HIV, influenza, measles, hepatitis)
Bacterial (TB, typhoid fever)
Parasitic

Miscellaneous :
sepsis,
bone marrow infiltration
cobalamin & folic acid deficiency
transfusion
hemodialysis

Neoplastic transformation of the pluripotent hematopoietic
stem cells w/in the bone marrow.

Inadequate numbers of ineffective functioning circulating
granulocytes/platelets
CLINICAL
MANIFES-
TATION
Redness, heat, swelling classic sign inflammation

Pus skin/pulmonary infiltrates CXR

Low grade fever =>septic shock

Infection

Bleeding

23

Greater 100.4F (38C)

Neutrophil below 500 MED ER
DX TEST H/P E

WBC count below 4,000/uL

Bone marrow aspiration

Peripheral blood smear
Bone marrow biopsy
USUAL TX:
MED/SURG

Identify infection
Antibiotic therapy (even low grade fever)
Hematopoietic growth factors
Serial bone marrow and peripheral blood examinations

Antibiotic therapy

Transfusion w/blood products along w/ iron chelators to
prevent iron overload
NURSING
IMPLI-
CATIONS
Hand washing & patients hygiene

Private room w/ positive pressure/ high-efficiency particulate air
(HEPA)

Community isolation

Wear mask going outside

Avoid uncooked meats, seafoods, eggs, unwashed fruits,
vegetables

Bathe/shower daily

No gardening/ clean up pets.

Notify DR:
100.4 F (38C)
Chills/feel hot
Swelling, redness, discharge, new pain body

24

Urine/BM changes
Cough, sore throat, mouth sore, blisters


































25

DISORDER

LEUKEMIA


Cancer of WBC/ cells develop into WBC

Group of malignant disorders affecting the blood and blood forming tissues of bone marrow, lymph system and spleen.

Accumulation of dysfunctional cells because of a loss of regulation in cell division.

Fatal if untreated.

Acute lymphocytic
leukemia (ALL)
Acute myelogenous
leukemia (AML)
Chronic lymphocytic
leukemia (CLL)
Chronic myelogenous
leukemia (CML)
children but 5 year survival
rate

adults can be cured.
Adults;

prognosis is poor.
older than 60.

not occur in children
disease progresses slowly in
three phases over
time.
Adults.
uncommon in children;
less than two years of
survival from time of
diagnosis.

CAUSE chromosomal changes, chemical agents, chemo agents, viruses, radiation, immunologic deficiencies
S/S CNS s/s common -> serious problems

Bone pain

Joint swelling

Enlarged liver and spleen

Weight loss
Fever

Poor wound healing (infected lesions)

Signs of anemia (fatigue, pallor, tachycardia, dyspnea on exertion)

Signs of bleeding (ecchymoses, hematuria, bleeding gums)

26

Complications:
high uric acid, infections

DX TEST White blood cell (WBC) Count Often elevated (20,000 to 100,000/mm3) with
immature WBCs in leukemia prior to treatment; decreased with treatment

Hemoglobin, hematocrit, and platelets
Bleeding times

Bone marrow aspiration and biopsy

USUAL TX
(MED/SUR)
Chemotherapy
Client Education
Inform S/E
nausea and vomiting persist. Nutritional consult.
use frequent oral hygiene and use a soft toothbrush. Avoid alcohol-based mouthwash.
Report signs and symptoms of infection or illness immediately to provider.
Inform client that hair loss (alopecia) occurs 7 to 10 days after treatment begins. Encourage client to select hairpiece before
treatment starts.

Colony-stimulating medications such as filgrastim (Neupogen)
- Stimulate the production of leukocytes
-Monitor for signs of bone pain. Monitor CBC twice weekly to check leukocyte level. Use cautiously with clients who have bone
marrow cancer.
-Inform nurse if bone discomfort occurs.
PHASE GOAL PROCEDURE TIME
Induction therapy
Places client at high
risk for infection and
hemorrhage following
this phase
To induce remission
defined as absence of
all signs of leukemia
including less than 5%
blasts in bone marrow
CNS prophylaxis
administered as
chemotherapy to the
CSF (intrathecal) or as
radiation to the brain
and spinal cord
Lasts 4 to 6 weeks
Consolidation or
intensification therapy
To eradicate any
residual leukemic cells
High doses of
chemotherapy
Lasts about 6 months
27

frequently
administered
Maintenance therapy Prevention of relapse Use of oral
chemotherapy
Lasts 2 to 3 years
Reinduction therapy
for the client who
relapses
Primary purpose is to
place the client back in
remission
Combinations of
chemotherapy used to
achieve remission
Probability of relapse
occurring decreases
over time
RN/I Monitor for any signs of infection or bleeding and report immediately.

Prevent infection.
Frequent, thorough hand hygiene is a priority intervention.
Place the client in a private room.Screen visitors carefully.
Encourage good nutrition (low-bacteria diet-Avoid salads, raw fruits, and vegetables) and fluid intake.
Monitor WBC counts.
Encourage good personal hygiene.
Avoid crowds if possible.
These interventions are especially important during chemotherapy induction and for clients who have received a bone marrow
transplant.

Prevent injury.
Monitor platelet counts.
Assess the client frequently for obvious and occult signs of bleeding.
Protect the client from trauma (avoid injections and venipunctures, apply firm pressure, increase vitamin K intake).
Teach the client how to avoid trauma (use electric shaver, soft bristled toothbrush, avoid contact sports).

Conserve the clients energy.
Encourage rest, good nutrition, and fluid intake.
Ensure the client gets adequate sleep.
Assess the clients energy resources/capability.
Plan activities as appropriate.

Interdisciplinary Care
- Oncology services may be consulted for chemotherapy.
- Nutritional services may be contacted for weight loss or gain of client related to medications or diagnosis.
- Rehabilitation team may be consulted if client has prolonged weakness and needs assistance with increasing level of activity.

28

Bone marrow transplantation
Bone marrow is destroyed or ablated using radiation or chemotherapy.
Closely matched donor stem cells are infused to replace destroyed cells.
Autologous cells are the clients own cells that are collected before chemotherapy.
Syngeneic cells are donated from the clients identical twin.
Allogeneic cells are obtained from an HLA-matched donor, such as a relative or from umbilical cord blood.
Following transplantation, the client is at high risk for infection and bleeding until the transfused stem cells begin producing
white blood cells again.


DISORDER

HODGKINS LYMPHOMA NON- HODGKINS LYMPHOMA


Malignant condition proliferation of abnormal giant,
multinucleated cells (REED STERNBERG CELLS)
located Lymph Nodes
Variety of diseases
No hallmark cells
All types have lymphocytes arrested in various stages of
development
5th leading cause of death
Can originate outside of lymph nodes

CAUSE Unknown
Factors:
Infection w/ Epstein-Barr virus (EBV)
Genetic
Toxins
HIV

S/S Disease above diaphragm confined periods of time
Below diaphragm- spreads extralymphoids(liver)
Enlargement of nodes
nontender and moveable
Wt loss, fatigue, fever, night sweats
painless enlarged lymph nodes

29

Pain at disease site with ingestion of alcohol
Progression of disease -> hepatosplenomegally
Anemia
DX TEST Blood analysis -
Lymph node biopsy -
Bone marrow aspiration -
Radiologic Evaluation

Dx and tx similar to Hodgkins

USUAL TX
(MED/SUR)
Treatment d/t stage
Stage I and II -
chemo and radiation
Stage III and IV -
radiation and aggressive chemo
BMT (bone marrow transplant)


RN/I Same as leukemia















30

DISORDER

MULTIPLE MYELOMA SPLEEN DISORDER


Neoplastic plasma cells infiltrate the bone marrow and
destroy bone.

More common in men than women.

Usually develops after age 40.


CAUSE Chronic inflammation, chronic hypersensitivity reactions,
viral influences

production of plasma cells _ activated B cells that
produce immunoglobulins but neoplastic cells invade
bone marrow and produce amts of IgA, IgG, IgD or IgE
-> myeloma protein

Also produce abnormal amts of cytokines -> increased
bone destruction

Plasma cells destroy bone, invade lymph nodes, liver
spleen and kidneys

Splenomegaly (enlarged spleen) => hypersplenism
Peripheral cytopenias (anemia, leukopenia, thrombocytopenia)
Genetics (SCD, thalassemia)
Infection & inflammations
Infiltrative disease leukemia, polycythemia vera,
Congestion cirrhosis, HF, splenic thrombosis



S/S Skeletal pain (pelvic, spine, ribs)

Osteolytic lesion skull, vertebrae, ribs

Bony degeneration cause calcium lost from bones
(hypercalcemia)

Pathological fxs

Hypercalcemia -> GI, renal or neurological changes

Hyperurecemia -> renal failure s/t tubular obst

Painful

31

S/S of anemia, thrombocytopenia, granulocytopenia d/t
bone marrow cell replacement

DX TEST Lab -
-High serum protein levels
-Pancytopenia, hyperuricemia, hypercalcemia, elevated
creatinine
-Bence Jones protein found in urine

Rads -
-est degree of bone involvement

Bone Marrow -
-show increased numbers of plasma cells

Analgesic administration

USUAL TX
(MED/SUR)
Need for increased fluids and ambulation

Control of pain

Chemo used to reduce #s of plasma cells
-alderan, cytoxan, leukeran, steroids

Rads used for palliation of localized lesions

BMT/stem cell transplantation can be curative
-other possible tx under investigation


Splenectomy
RN/I Focus of care - boney involvement and sequelae from
bone breakdown
give pamidronate(Aredia), fluids ( 3-4 L/d)

exercise -> Ca reabsorption

steroids help with Ca excretion

Observe hemorrhage following surgery:
Shock, fever, abdominal distention
IgM
IgG & IgA normal

Postsplenectomy:
Lifelong risk of Infection- pneumococcus
Reduce the risk immunize
32

monitor effects of hyperuricemia - Allopurinol

d/t potential bone fxs -> care when moving

pain management and skin care

psychosocial needs -> chronic illness/losses





































33