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Transport of gases, nutrients, and waste products

Transport of processed molecules
Transport of regulatory molecules
Regulation of pH and osmosis
Maintenance of body temperature
Protection against foreign substances
Clot formation

91 % water; 7% proteins; 2 % other substances
Albumins -58% of the plasma proteins
Globulins – 38% of the plasma proteins
Fibrinogens – 4% of plasma proteins
Ions – Na, Cl, K, hydrogen, hydroxide,
bicarbonate ions
Waste products
Regulatory substances
Red Blood cell
Are disk-shaped and biconcave; no nucleus;
contains hemoglobin
Live for about 120 days in males and 110 days for
Main component is the hemoglobin which is
responsible for 98.5% of the oxygen transported in
the blood
6.5 – 8.5 µm in diameter
Function: transports oxygen and carbon dioxide
White Blood cells
 Neutrophils
 Nucleus with 2 to 4 lobes; granules stain light pink or
reddish purple .
 10 -12 µm in diameter

 Function: Phagocytizes microorganisms and other

 Eosinophils
 Nucleus often bilobed; cytoplasmic granules stain
orange-red or bright red
 11-14 µm in diameter

 Function: Releases chemicals that reduce inflammation

and attacks certain worm parasites
 Basophils
 Nucleus with 2 indistinct lobes; granules stain blue

 10-12 µm in diameter

 Function: Releases histamine and heparin

 Lymphocytes
 Round nucleus; cytoplasm forms a thin ring around the

 6-14 µm in diameter

 Function: Produces antibodies and other chemicals for

destroying microorganisms; contributes to allergic reactions

; graft rejection, tumor control and regulation of the
immune system.
 Monocytes
 Nucleus round, kidney or horseshoe-shaped; contains more

 12-20µm in diameter

 Function: Phagocytic cell in the blood; becomes the

Also called the thrombocytes
Cell fragments from the megakaryocytes
surrounded by a plasma membrane and
containing granules
2-4 µm in diameter
Function: Forms platelet plugs; releases
chemicals necessary for blood clotting
Process of blood cell production
Confined mainly to the red bone marrow
after birth
All populations of blood cells are derived
from a single stem cell and is regulated by
specific growth factors
Or Red Blood Cell production
Give rise to the red blood cell line
Red blood cells are the final cells produced
from a series of cell divisions.
The process of cell division requires the B
vitamins folate and B12 for DNA synthesis
Iron is required for production of hemoglobin
RBC is stimulated by low blood oxygen levels
Stimulates red bone marrow to produce more
Released from the kidneys secondary to a low
blood oxygen levels.
Old , abnormal or damaged red blood cells are
removed from the blood by macrophages located
in the spleen and liver.
Iron from the heme is transported in the blood to
the red bone marrow and is used to produce new
Hemoglobin Breakdown
A yellow pigment molecule from heme
Normally taken up by the liver and
released into the small intestine as part
of the bile
Vascular Spasm
Is an immediate but temporary
constriction of a blood vessel resulting
from contraction of smooth muscle
within the wall of the vessel
Nervous system reflexes and chemicals
(thromboxanes and endothelins) produce
vascular spasms.
Platelet plugs
Is an accumulation of platelets than can seal up small
break in a blood vessel
The formation of a platelet plug can be described as a
series of steps.
 Platelets adhesion results in platelets sticking to collagen
exposed by blood vessel damage.
 Von Willebrand’s factor is a protein produced and
secreted by blood vessel endothelial cells and mediates
platelet adhesion.
 Platelet release reaction – platelet release chemicals
(ADP and thromboxanes) which activate other platelets
which also release the same chemicals to activate more
 As platelets become activated they express surface
receptors called fibrinogen receptors which can bind
to fibrinogen .
 Platelet aggregation- fibrinogen forms bridges
between the fibrinogen receptors of numerous
platelets resulting in the formation of a platelet plug.
Blood Clotting
Also called the coagulation which is a network of
threadlike protein fibers called the fibrin.
The formation of a blood clot depends on proteins
found in the plasma called clotting factors.
Most clotting factors are manufactured in the liver
, and many require vitamin K for their synthesis.
Control of Clot formation
The blood contains anticoagulants
Antithrombin and Heparin
These inactivate the thrombin.
Without the thrombin, fibrinogen is not
converted to fibrin, and no Clot is formed.
Clot Retraction and
Clot Retraction
After a clot is formed , it begins to condense into a
more compact structure.
Contraction of the extensions of the platelets pulls on
the fibrin and responsible for the retraction.
 Is the plasma without the clotting factors that is squeezed
out of the clot during clot retraction.
Retraction of the clot pulls the edges of the damaged
blood vessel together.
Clots are dissolved by this process
ABO Blood Groups
Diagnostic Tests and
 Red blood cell count
 Hemoglobin and hematocrit
 Hemoglobin measures the hemoglobin
available in circulation, which is the
gas-carrying capacity of an erythrocyte
 Hematocrit is the ratio of the RBC
volume to the volume of whole blood
Diagnostic Tests and
 RBC indexes
 MCV (mean corpuscular volume):
estimates size of the RBC
 MCH (mean corpuscular hemoglobin):
measures the content of Hgb in RBCs from
a single cell
 MCHC (mean corpuscular hemoglobin
concentration): a more accurate
measurements of the Hgb content of RBC
as it measures the entire volume of RBCs
Diagnostic Tests and
 Serum ferritin, transferrin, and total iron-
binding capacity (TIBC):
 these tests are used to evaluate iron levels
 ferritin measures the iron in plasma. Which is
also a direct reflection of total iron stores
 transferrin is the major iron-transport protein
Diagnostic Tests and
 White blood cell count
 Abnormal elevation of the WBC is
referred to as leukocytosis
 Leukopenia is a decrease in the number
of white blood cells
 Differential count refers to the
breakdown of the different types of
Diagnostic Tests and
 Coagulation studies
 Bleeding time: normal range is 1 to 4
minutes; it is used in evaluation of
platelet function; extended bleeding
times are seen with thrombocytopenia
and aspirin therapy
Diagnostic Tests and

 Prothrombin Time (PT): is the rapidity of

blood clotting; normal range is 11 to 16
seconds; PT evaluates extrinsic
coagulation pathway which include
factors 1, II, V, VII, X
 Partial thromboplastin time (PTT):
normal range is 60 to 70 seconds, which
evaluates the intrinsic coagulation
pathway of fibrin clot formation
Diagnostic Tests and
 Activated partial thromboplastin time (APTT):
normal range is 30 to 45 seconds;
 a modified PTT, preferred because it is quicker to
 used in heparin therapy and in the evaluation of
 increased in anticoagulation therapy, liver
disease, vitamin K deficiency, and disseminated
intravascular coagulation (DIC)
Diagnostic Tests and
 Fibrinogen: normal range is 150 to 400
mg/dL; it is a soluble plasma protein
that is decreased in DIC and fibrinogen
disorders and increased in acute
infections, hepatitis, and oral
contraceptive use
Diagnostic Tests and
 Fibrin degradation products (FDP): normal
value is <10 ug/mL; FDP is increased in
fibrinolysis, thrombolytic therapy, and DIC

 Fibrin D-dimer: normal is 0 to 0.5 ug/mL;

D-dimer is the most sensitive indicator to
differentiate DIC from primary fibrinolysis;
it is elevated in DIC
Diagnostic Tests and
 Bone marrow examination
 Specimens obtained during a bone marrow
examination may include those obtained by
aspiration or biopsy
 Sites for bone marrow aspiration may include:
sternum, iliac crest (most common), and tibia;
the most common site for bone marrow biopsy
is the posterosuperior iliac spine; the sternum
also is used
 Aspiration is the most common procedure for
obtaining a marrow sample
Diagnostic Tests and
 The client is positioned based on the site
selected by the physician;
 the skin and periosteum are anesthetized to
decrease pain with anesthetic such as
procaine; the marrow aspiration needle is
then inserted; after the marrow cavity is
entered, the marrow stylet is removed from
the needle and a sterile syringe is attached;
 the syringe plunger is drawn back until
marrow appears in the syringe
Diagnostic Tests and
 During the withdrawal of aspirate, the client will
experience sharp pain often described as a
burning pain
 After the needle is removed, a pressure dressing
is applied over the puncture site, where only
minimal bleeding should occur; if the patient has
thrombocytopenia, pressure is applied for 3 to 5
 The nurse should check on the facility`s procedure
manual as to the disposition of specimens
Diagnostic Tests and
 Most clients experience little, if any, pain
or discomfort after the procedure; some
persons will complain of tenderness and
ache at the aspiration site for a few days
Diagnostic Tests and
The procedure for a bone marrow biopsy is
essentially the same as for aspiration; the
biopsy needle most commonly used is a
Jamshidi needle; which allows a second
needle, called a stylet to be inserted within
in the initial biopsy needle and a core of
marrow to be collected and withdrawn
through the sleeve of the needle; after the
procedure, clients are assessed for
bleeding from the puncture site
Diagnostic Tests and
 Lymphangiography
 Is visualization of the lymph system
radiographically after injection of a dye
 It is used primarily in staging of
Hodgkin`s and non-Hodgkin`s
Diagnostic Tests and
 Lymph node biopsy
 Can either be done utilizing a closed
needle biopsy done at the bedside or an
open biopsy performed in the operating
 The purpose is to obtain lymph tissue
for histologic analysis
Administration of blood
blood products
Administration of blood and
blood products
 Check the agency`s policy and procedure
pertaining to blood transfusion and
transfusion of blood products
 Verify the physician`s order for the
transfusion noting the blood product ordered,
the time specified for transfusion (if any), and
any medications to be given before
Administration of blood and
blood products
 Check that the client has given consent for
receiving blood transfusion
 check that a typing and crossmatch has
been performed
 Obtain blood from the blood bank when an
intravenous access line is available; the IV
line should be maintained with normal
saline while waiting for the blood or blood
product to be delivered to the nursing unit
Administration of blood and
blood products

Return blood to the blood bank

immediately if transfusion is not
possible; blood may not be returned to
the blood bank after 20 minutes
Do not keep blood or blood products in
the nursing unit refrigerator; blood is
refrigerated under strict and controlled
conditions only in the blood bank
Administration of blood and
blood products
 Validate data on the blood or blood
product with another nurse; the client`s
ID bracelet should match the blood
bank number on the unit of blood
 Validate with another nurse that the
client`s name, ID number, blood type,
and Rh match the unit of blood to be
Administration of blood and
blood products
 Note the expiration date indicated on
the blood product
 Observe the unit of blood for bubbles or
discoloration; return unit of blood to the
blood bank if break in the bag is noted
or if signs of contamination are evident
Administration of blood and
blood products
Obtain pre-transfusion vital signs, and the vital
signs 15 minutes after the transfusion is initiated
and immediately after the completion of the
A pre-transfusion temperature of 100 degree F or
higher should be reported to the physician before
initiating the transfusion; any increase in 2 degree
F in the client`s temperature may indicate a
transfusion reaction and should be reported to the
Administration of blood and
blood products

 Start blood transfusion slowly,

administering 25 to 50 mL during the
first 15 minutes; most untoward
reactions occur during the first 15
minutes; stay with the client during this
period of time
Administration of blood and
blood products
Do not administer any medications through
the blood transfusion tubing; use tubing
specific for the blood product being
transfused; a blood filter is used to prevent
clots and other particles from entering the
venous system
Use only agency-approved blood-warming
devices; do not warm blood in hot water or
microwave ovens
Administration of blood and
blood products
 Blood products should not be infused
longer than 4 hours; the longer a blood
product is in room temperature, the
greater the chances of bacterial
 Discard tubings and bags used in the
transfusion in biohazard receptacle
 Follow the agency`s protocol for any
suspected transfusion reactions
Protocol for suspected blood
transfusion reaction
 Check the specific policy and protocol of the agency
 If blood transfusion reaction is noted or suspected,
stop the infusion immediately; change IV tubing and
keep vein open with normal saline; the IV access
might be needed for the administration of
emergency drugs
 Assess the client for other signs and symptoms of
transfusion reaction
 Notify the physician and the blood bank
Protocol for suspected blood
transfusion reaction
 Send the unit of blood and tubing used to
the blood bank; this will help determine the
cause of the reaction
 Urine and blood samples will be required;
follow the agency`s protocol
 Administer drugs that are prescribed and
continue to monitor the client
 Document the reaction and interventions
Iron-deficiency anemia (IDA)
Iron-deficiency anemia (IDA)
 Description:
 anemia that results when the supply of
iron is inadequate for optimal formation
of RBCs related to excessive iron loss
caused by bleeding, decreased dietary
intake, or malabsorption
Iron-deficiency anemia (IDA)

 Etiology and pathophysiology

 Iron deficiency accounts for 60 percent
of anemias in clients over age 65; the
most common cause of IDA is blood
loss from gastrointestinal or
genitourinary system
Iron-deficiency anemia (IDA)
 Normal iron excretion is less than 1 mg/day through
the urine, sweat, bile, feces, and from desquamated
cells of the skin; the average woman loses 0.5 mg of
iron daily or 15 mg monthly during menstruation is
the most common cause of iron deficiency in women,
while gastrointestinal bleeding is the most common
cause in men
 Anemia reduces the oxygen-carrying capacity of the
blood, producing tissue hypoxia
Iron-deficiency anemia (IDA)
 Iron is stored in the body as ferritin, an
iron-phosphorus-protein complex that
contains about 23 percent iron; it is
formed in the intestinal mucosa, when
ferritin iron joins with the protein
apoferritin; ferritin is stored in the tissues;
primarily in the reticuloendothelial cells of
the liver, spleen, and bone marrow
Iron-deficiency anemia (IDA)
 Develops slowly through three phases:
body`s stores of iron used for
erythropoiesis are depleted, insufficient
iron is transported to the bone marrow
and iron deficient erythropoiesis begins,
allowing small hemoglobin deficient cells
to enter the peripheral circulation in large
numbers; iron is needed on the
hemoglobin so the oxygen molecule will
Iron-deficiency anemia (IDA)
 Adequate iron in the RBC is essential
since the oxygen molecule attaches to
 An average diet supplies the body with
12 to 15 mg/day of iron, of which only
5 to 10 percent is absorbed
Iron-deficiency anemia (IDA)
 Assessment
 Clinical manifestations (usually
develop gradually with the client not
seeking attention until the hemoglobin
drops to 7 to 8 g/dL)
 Fatigue

 Weakness

 Shortness of breath
Iron-deficiency anemia (IDA)
 Pallor (ear lobes, palms, and
 Brittle spoon-like nails
 Cheilosis (cracks in the corners of
the mouth)
 Smooth, sore tongue
 Dizziness
 Pica (craving to eat unusual
substances such as clay or starch)
Iron-deficiency anemia (IDA)
 Diagnostic and laboratory tests
 Is considered a microcytic and
hypochromic anemia (small RBC
diameter<6 with decreased
pigmentation) with an increase in
the red cell size distribution width
Iron-deficiency anemia (IDA)
 Erythrocytes are small (microcytic) and pale (hypochromic);
mean corpuscular volume (MCV; measures size) is decreased
and mean corpuscular hemoglobin (MCH) or mean
corpuscular hemoglobin concentration or MCHC (calculated
value of the hemoglobin present in the RBC compared to its
size) will be decreased; the MCV, MCH, and MCHC should be
analyzed only when the hemoglobin is low
 Low serum iron level and elevated serum iron-binding
capacity or low serum ferritin levels
Iron-deficiency anemia (IDA)
 Therapeutic management
 The cause for the anemia is usually
explored; stools are examined for
occult blood; endoscopic examination
and other diagnostic procedures may
be performed to rule out possible
sources of bleeding, which is a
common cause of iron deficiency
Iron-deficiency anemia (IDA)
 Increase intake of iron-rich foods
 Vitamin supplementation
 Administration of oral iron preparation
in the form of ferrous sulfate
 Parenteral administration of iron
Iron-deficiency anemia (IDA)
 Priority nursing diagnoses:
 Activity intolerance
 Risk for decreased cardiac output
 Risk for injury
 Ineffective health maintenance
Iron-deficiency anemia (IDA)
 Planning and implementation
 Administer oral iron preparation with orange juice
or vitamin C to increase absorption; antacids
interfere with the absorption of iron
 Administer parenteral iron deep intramuscularly
via the Z-track method
 Identify/implement energy-saving techniques, e.g.,
shower chair, sitting to perform tasks
 Promote quiet environment to facilitate sleep/rest
Iron-deficiency anemia (IDA)
 Monitor for dizziness, suggest position
changes be made slowly
 Provide/recommend assistance with
activities/ambulation as needed; allowing
patient independence as much as needed
 Monitor laboratory studies, e.g., Hgb/Hct,
RBC count
 Administer medications, blood or blood
products as indicated; monitor closely for
transfusion reactions
Iron-deficiency anemia (IDA)
 Encourage/assist with good oral hygiene before
and after meals, using soft bristled toothbrush for
gentle brushing of fragile gums
 Determine stool color, consistency, frequency, and
 Encourage fluid intake of 2,500 to 3,000 mL /day
 Discuss use of stool softeners, bulk-forming
laxatives, mild stimulants, or enemas if indicated;
monitor effectiveness
Iron-deficiency anemia (IDA)
 Oral liquid form of iron can stain the teeth;
clients should not use a straw or place spoon
at the back of the mouth to take the
supplement and rinse mouth thoroughly
 Caustion client that bowel movement may
appear greenish black/tarry
 Deep IM, Z-track administration of
medication; use separate needles for
withdrawing and injecting the medication
Iron-deficiency anemia (IDA)
 Caution regarding possible systemic
(allergic) reactions to the medications,
e.g., (flushing, nausea/vomiting,
myalgias) and the importance of
reporting symptoms
 Refer to appropriate community
resources when indicated, e.g., social
services for food stamps. Meals on
Iron-deficiency anemia (IDA)
 Medication therapy
 Usual therapy is oral ferrous sulfate
(FeSO4) 300 to 325 mg t.i.d., given 1
hr before meals for 6 months; other
oral forms may include ferrous
gluconate (Fergon) and ferrous
fumarate (Ircon, Femiron)
Iron-deficiency anemia (IDA)
 If the client is unable to tolerate oral
therapy, iron dextran (INFeD) may be
given by deep IM (Z-track) route or as
IV therapy; there is risk of anaphylaxis
with parenteral administration;
therefore, before a full dose is given a
small test dose is administered
 Transfusion of packed RBCs may be
necessary if anemia is severe
Iron-deficiency anemia (IDA)
 Client education
 Teach clients to maintain good nutrition; the
elderly and those with limited economic means
may have dietary deficiencies requiring referrals
to appropriate agencies (e.g., Means on Wheels)
 Teach client to take iron on an empty stomach;
absorption of iron is decreased with food;
absorption may be enhanced when taken with
an acidic beverage (such as one with vitamin C);
but avoid grapefruit juice
Iron-deficiency anemia (IDA)
 Inform clients that their stools will appear
black with the oral intake of iron
 Teach the client to report to the healthcare
provider persistent GI symptoms secondary
to iron intake
 Clients should be informed that iron
preparations cause constipation; the
addition of a stool softener may be
necessary; other measures such as
increasing oral intake of fluids and fiber will
prevent constipation
Iron-deficiency anemia (IDA)
 Review required diet alterations to meet
specific dietary needs; foods high in iron
include organ meats (beef or calf`s liver,
chicken liver), other meats, beans (black,
pinto, and garbanzo), leafy green
vegetables, raisins, and molasses
Megaloblastic anemia
 Vitamin B12 deficiency anemia
 Description:
 a type of anemia characterized by

macrocytic red blood cells

Megaloblastic anemia
 Etiology and pathophysiology
 Enevitably develops after total
gastrectomy, with 15 percent of clients
developing pernicious anemia after
partial gastrectomy or
 Lack of vitamin B12 alters the structure
and disrupts the function of the
peripheral nerves, spinal cord, and
Megaloblastic anemia
 Lack of vitamin B12 impairs cellular
division and maturation especially in
rapidly proliferating RBCs
 Pernicious anemia is the body`s
inability to absorb vitamin B12
because of a lack of intrinsic factor, a
substance secreted by the parietal
cells of the gastric mucosa
Megaloblastic anemia
 Assessment
 Clinical manifestations:
 signs and symptoms include pallor

or slight jaundice with a complaint

of weakness
 smooth, sore, beefy red tongue

(glossitis), with diarrhea

Megaloblastic anemia
paresthesias (altered sensations
such as numbness, or tingling in the
extremities), impaired
proprioception (difficulty identifying
one`s position in space, which may
progress to difficulty with balance)
clients with this anemia tend to be

fair-haired or prematurely gray

Megaloblastic anemia
 Diagnostic and laboratory tests
 Macrocytic (megaloblastic) anemia
(RBC diameter>8)
 Laboratory examination shows an
increase in the MCV and MCHC
 Gastric secretion analysis reveals
achlorhydria: the absence of free
hydrochloric acid in a pH
maintained at 3.5
Megaloblastic anemia

 24 hour urine for Schilling test (a

vitaminB12 absorption test that indicates
if a client lacks intrinsic factor by
measuring the excretion of orally
administered radionuclide labeled B12)
confirms the diagnosis of pernicious
Megaloblastic anemia
 Therapeutic management
 Review required diet alterations to
meet specific dietary needs; if the
deficiency is caused by a vegetarian
diet, fortified soy milk may be added
to the diet, or oral supplements of
B12 may be added
Megaloblastic anemia
 If the deficiency is caused by gastric
malabsorption such as deficiency of
intrinsic factor, lifelong replacement
therapy is required; an intramuscular
injection of B12 is required and in some
situations megadoses or oral vitamins
may be given
Megaloblastic anemia
 Priority nursing diagnoses:
 Risk for injury
 Activity intolerance
 Altered oral mucous membrane
Megaloblastic anemia
 Planning and implementation:
 the major nursing consideration in the
care of the client with this type of
anemia is client education pertaining to
nutrition and medications; the client
should be assessed carefully for
neurologic deficits and incorporate in
the plan of care interventions relating
to prevention of injury
Megaloblastic anemia
 Medication therapy:
 parenteral vitamin B12, 100 to 1,000
micrograms subcutaneously daily for 7
days, then once a week for 1 month,
then monthly for the remainder of life is
usually prescribed to clients with this
type of anemia
Megaloblastic anemia
 Client education
 Inform client that the burning sensation felt
after parenteral dose of vitamin B12 is
 Discuss dietary sources of vitamin B12 like
dairy products, animal proteins, and eggs
 For clients who have pernicious anemia,
discuss the regular schedule of parenterally
administered vitamin B12 and the
importance and necessity for continued
Folic acid deficiency anemia
anemia caused by a deficiency of folic
acid resulting in the interruption of DNA
synthesis and normal maturation of red
blood cells
Folic acid deficiency anemia
 Etiology and pathophysiology
 Causative etiology: poor nutrition,
malabsorption syndrome,
medications that impede the
absorption (oral contraceptives,
anticonvulsants, methotrexate
[MTX]), alcohol abuse, and anorexia
 Alcoholics and those receiving total
parenteral nutrition are at risk
Folic acid deficiency anemia
 Pregnant women, infants, and
teenagers are also at risk for the
development of folic acid deficiency
 Clients on hemodialysis are also at
risk for the development of folic acid
 Lack of folic acid causes the
formation of megaloblastic cells;
these cells are fragile
Folic acid deficiency anemia
 Assessment
 Clinical manifestations:
 pallor, progressive weakness, fatigue,
shortness of breath, cardiac palpitations
 GI symptoms are similar to B12
deficiency, but usually more severe
(glossitis cheilosis, and diarrhea)
 neurological symptoms seen in B12
deficiency are not seen in folic acid
deficiency and therefore assist in the
differentiation of these two types of
Folic acid deficiency anemia
 Diagnostic and laboratory tests
 Macrocytic (megaloblastic) anemia
(RBC diameter>8)
 MCV high with low hemoglobin
 Low serum folate level
Folic acid deficiency anemia
 Therapeutic management:
 includes dietary counseling and the
administration of folic acid
 Priority nursing diagnoses:
 Activity intolerance
 Constipation
 Diarrhea
 Risk for infection
Folic acid deficiency anemia
 Planning and implementation
 Identify/implement energy-saving
techniques, e.g., shower chair, sitting to
perform tasks
 Monitor for dizziness, suggest position
changes be made slowly
 Provide/recommend assistance with
activities/ambulation as needed,
allowing client independence as much
as needed
Folic acid deficiency anemia
 Monitor laboratory studies, e.g.,
Hgb/Hct, RBC count
 Encourage/assist with good oral
hygiene before and after meals, using
soft bristled toothbrush for gentle
brushing of fragile gums
 Refer to appropriate community
resources when indicated, e.g., social
services for food stamps, Meals on
Wheels, Alcoholics Anonymous
Folic acid deficiency anemia
 Medication therapy:
 oral folate, 1 to 5 mg/day for 3 to 4
 folate should be given along with
vitamin B12 when both are deficient
Folic acid deficiency anemia
 Client education
 Discuss with client the dietary
sources of folic acid such as green
leafy vegetables, fish, citrus fruits,
yeast, dried beans, grains, nuts, and
Folic acid deficiency anemia
 Teach clients who are at risk for the
development of folic acid deficiency
(alcoholism, clients on hemodialysis
and certain drugs) to increase their
dietary intake through diet selection
and supplementation
 Discuss with client strategies to
decrease pain associated with
glossitis such as eating bland and soft
Aplastic anemia
 Description:
 aplastic anemia is a form of anemia
resulting in decreased production of
bone marrow elements, namely
erythrocytes, leukocytes, and platelets
Aplastic anemia
 Etiology and pathophysiology
 Affects all age groups and both genders
 Two classifications of aplastic anemia include
congenital or acquired
 Congenital aplastic anemia is caused by a
chromosomal alteration
 Acquired form of the disease may be caused by
radiation, chemical agents and toxins, drugs, viral
and bacterial infections, pregnancy, and idiopathic
 In about 50 percent of cases is unknown
Aplastic anemia
 There is a decrease or cessation of
production of RBCs (anemia), WBCs
(leucopenia), and platelets
 the decrease may result from damage to
bone marrow stem cells, the bone marrow
itself, and the replacement of bone
marrow with fat; depending on the
causative factor, the condition may be
acute to chronic
 Assessment
Aplastic anemia
 Clinical manifestations
 Pallor

 Fatigue

 Palpitations

 Exertional dyspnea

 Infections of the skin and mucous

 Bleeding from gums, nose, vagina, or

 Purpura (bruising)

 Retinal hemorrhage
Aplastic anemia
 Diagnostic and laboratory tests
 Blood counts reveal pancytopenia
(decreased RBC, WBC, and platelets)
 Decreased reticulocyte count
 Bone marrow examination reveals
decrease in activity of the bone
marrow or no cell activity
Aplastic anemia
 Therapeutic management
 Identification of the cause of bone
marrow suppression
 Bone marrow transplantation
 Immunosuppression
 Transfusion of leukocyte-poor RBCs
 Splenectomy
Aplastic anemia
 Priority nursing diagnoses:
 Risk for infection
 Risk for bleeding
 Activity intolerance
Aplastic anemia
 Planning and implementation
 Institute reverse isolation
 Limit visitors and potential sources of
 Monitor for evidence of bleeding
 Avoid invasive procedures including
rectal temperatures
 Provide frequent rest periods
 Monitor tolerance to activities
Aplastic anemia
 Medication therapy
 Agents that suppress lymphocyte
activity such as antilymphocyte
globulin (ALG), antithymocyte globulin
(ATG), and cyclosporine
 Immunosuppresive agents such as
prednisone and cyclophosphamide
Aplastic anemia
 Client education
 Teach client ways to prevent infection
such as avoiding crowds, maintaining
good hygiene, handwashing, and
elimination of uncooked foods from the
 Discuss ways to prevent hemorrhage
such as using a soft toothbrush, avoiding
contact sports, and use of an electric
Aplastic anemia
 Emphasize the avoidance of drugs that
increase bleeding tendency such as
 Teach client to balance activity with
adequate rest periods to avoid fatigue
 Teach client about symptoms to report
to the healthcare provider including
signs of infection, bleeding, and
increasing intolerance to activity
Sickle cell disease
 Definition:
 a hereditary, chronic form of hemolytic
 Etiology and pathophysiology
 Eight percent of African-americans are
heterozygous (carriers) for sickle cell
anemia thereby inheriting one
affected gene or the sickle cell trait
Sickle cell disease
 One percent of African-Americans are
homozygous (identical genes) for the
disorder, thereby inheriting a defective
gene from both parents or sickle cell
anemia and are likely to experience
sickle cell crisis
 Sickle cell trait (heterozygous state) is
a generally mild condition that
produces few, if any, manifestations
Sickle cell disease
 Sickle cell anemia is caused by an
autosomal genetic defect (one gene
affected) that results in the synthesis
of hemoglobin S
 Produced by a mutation in the beta
chain of the hemoglobin molecule
through a substitution of the amino
acid valine for glutamine in both beta
Sickle cell disease
 During decreased oxygen tension in
the plasma, the hemoglobin S causes
the RBCs to elongate, become rigid,
and assume a crescent, sickled shape
causing the cells to clump together,
obstruct capillary blood flow causing
ischemia and possible tissue infarction
Sickle cell disease
Conditions likely to trigger a sickle cell crisis
include: hypoxia, low environmental and/or body
temperature, excessive exercise, high altitudes,
or inadequate oxygen during anesthesia
Other causes of sickle cell crisis include:
elevated blood viscosity/decreased plasma
volume, infection, dehydration, and/or increased
hydrogen ion concentration (acidosis)
Sickle cell disease
 With normal oxygenation, the sickled
RBCs resume their normal shape;
repeated episodes of sickling and
unsickling weaken the cell membrane,
causing them to hemolyze and be
 Crisis is extremely painful and can last
from 4 to 6 days
Sickle cell disease
 Assessment
 Clinical manifestations
 Pallor

 Jaundice

 Fatigue

 Irritability

 Large joints and surrounding tissue

may become swollen during crisis
 Priapism (abnormal, painful,
continuous erection of the penis) may
occur if penile veins are obstructed
 Pain
Sickle cell disease
 Therapeutic management
 Bone marrow transplantation
 Blood transfusions
 Management of pain
 Use of chemotherapy drug
hydroxyurea (Droxia) to increase
hemoglobin F and decrease sickling
Sickle cell disease
 Priority nursing diagnoses:
 Pain; Ineffective tissue perfusion
 Impaired gas exchange
 Risk for infection
 Knowledge deficit
Sickle cell disease
 Planning and implementation
 Teach clients ways to prevent
development of sickle cell crisis
 Refer to appropriate agency for
genetic counseling and family
Sickle cell disease
 Monitor for complications such as vaso-
occlusive disease (thrombosis), hypoxia,
CVA, renal dysfunction, priapism leading to
impotence, acute chest syndrome (fever,
chest pain, cough, pulmonary infiltrates,
and dyspnea), and substance abuse
 Management of infection

 Administer care with attention to culture;

avoid racial bias or cultural insensitivity
Sickle cell disease
 Medication therapy
 Nifedipine (Procardia) may be used for
 Hydroxyurea (Droxia) to increase
hemoglobin F and decrease sickling
 Narcotic (opioid) analgesics during the
acute phase of sickle cell crisis, often at
large doses
 Broad-spectrum antibiotics to manage
acute chest syndrome
 Folic acid supplement
Sickle cell disease
 Client education
 Teach client ways to prevent sickle cell
crisis; these instructions should include:
 Maintain adequate fluid intake; clients

with sickle cell disease should maintain

an oral intake of at least 4 to 6
quarts/day; avoid conditions that might
predispose them to dehydration
Sickle cell disease
 Avoid high altitudes
 Prevent and promptly treat infection

 Stress-reduction strategies

 Avoid exposure to cold

 Avoid overexertion

 Discuss the importance of adhering to vaccination

schedules for pneumococcal pneumonia,
haemophilus influenza type B, and hepatitis B
 Importance of regular medical follow-up
 Description:
 an increase in the number of circulating
erythrocytes and the concentration of
hemoglobin in the blood; also known as
polycythemia vera, PV, or
myeloproliferative red cell disorder,
polycythemia can be primary or
Etiology and Pathophysiology
a. Primary
Common in men of European Jewish descent

Neoplastic stem cell disorder characterized by

increased production of RBCs, granulocytes,
and platelets
With the over production of erythrocytes,
increased blood viscosity results in congestion of
blood in tissues, the liver, and spleen
Thrombi form, acidosis develops, and tissue
infarction occurs as a result of the diminished
circulatory flow of blood caused by the
increased viscosity
b. Secondary
Most common form of polycythemia vera
The disturbance is not in the development of red blood
cells but in the abnormal increase of erythropoietin,
causing excessive erythropoiesis
The increase in red blood cell production caused by
increased erythropoietin release is a physiologic response
to hypoxia; hypoxia stimulates the release of
erythropoietin in the kidney
 Chronic hypoxic states may be
produced by prolonged exposure to
high altitudes, pulmonary diseases,
hypoventilation, and smoking
 The results of an increased RBC
production include the increased
viscosity of blood, which alters
circulatory flow
 Assessment
 a. Clinical manifestations
Plethora: a ruddy (dark, flushed) color of
the face, hands, feet, ears, and mucous
membranes resulting from the
engorgement or distention of blood vessels
Symptoms associated with increased blood
volume including headaches, vertigo,
blurred vision, and tinnitus
Distended superficial veins
 Itching unrelieved by antihistamines
 Symptoms associated with impaired
tissue oxygenation including angina,
claudication, or dyspnea
 Erythromyalgia, or burning sensation
of the fingers and toes
 Splenomegaly in majority of those with
primary polycythemia vera
 Epistaxis, GI bleeding
Diagnostic and laboratory tests
Elevated hemoglobin and erythrocyte count
Decreased MCHC
Increased WBC and basophilia
Increased platelets
Elevated leukocyte alkaline phosphatase
Elevated uric acid
Elevated cobalamin levels
Increased histamine levels
Bone marrow examination shows
Therapeutic management
Management of the underlying condition
(such as COPD) causing the chronic
Repeated phlebotomy to decrease blood
volume; the goal is to keep the
hematocrit less than 45 to 48 percent
Hydration to decrease blood viscosity
Priority nursing diagnoses:
Impaired gas exchange
Risk for infection
Planning and implementation
Assist in phlebotomy
Measures to relieve pruritus including cool and
tepid baths
Accurate monitoring of fluid intake and output
Nursing measures to prevent thrombotic events
including early ambulation, passive leg exercise
when on bed rest, avoid crossing legs, and
maintaining adequate hydration
Administration of medications for the prevention
of complications including anticoagulants
Medication therapy
Myelosuppressive agents to inhibit bone
marrow activity including hydroxyurea
(Hydrea), melphalan (Alkeran), and
radioactive phosphorus
Allopurinol to manage gout
Antiplatelet agents to prevent
thrombotic complications
Client education
Teach client about the importance of
maintaining good hydration; the client should
drink at least 3 liters of fluid per day
Teach client about the disease and ways in
which it can be controlled, such as smoking
Discuss signs and symptoms of complications
associated with the disorder including signs of
vaso-occlusive states (MI, CVA) and bleeding
that require immediate medical attention
 Teach client to prevent bleeding states such
as using a razor, using soft bristled
toothbrush, not flossing, and avoiding the
use of aspirin and aspirin-containing
 Emphasize the importance of a regular
medical check-up
 Teach client to avoid products that contain
 Discuss ways of preventing thrombosis

 Definition:
 a decrease in the number of circulating
platelets or a platelet count of less than
100,000 platelets per milliliter of blood
resulting in problems of hemostasis
 Etiology and pathophysiology
 The decrease in the number of
circulating platelets may be a result of
three mechanisms: decreased
production, increased destruction, or
increased consumption
 The cause of decreased production of
platelets may be inherited or acquired
 Increased destruction of platelets may be
caused by an immune system defect; the
platelets become coated with an antibody;
when these antibody coated platelets reach
the spleen, they are recognized as foreign
and are destroyed
 platelets normally have a circulating life of
8 to 10 days but this immune response
shortens their life cycle; this condition is
referred to as immune thrombocytopenic
purpura (ITP);
 The acute form of this disorder is more common in
children whereas the chronic form is more common in
women between the ages of 20 to 50
 Other causes of increased destruction of platelets
include non-immune related factors such as infection
or drug-induced effects
 A decrease in the number of functional platelets leads
to bleeding disorders; cerebral and pulmonary
hemorrhage can occur when platelet counts drop
below 10,000/mm3
a. Clinical manifestations
Petechiae and purpura most commonly
found in the anterior thorax, arms, and
Epistaxis, gingival bleeding,
menorrhagia, hematuria, and
gastrointestinal bleeding
Signs of internal hemorrhage
Diagnostic and laboratory tests
Decreased hemoglobin and hematocrit if
bleeding is present
Decreased platelet count
Prolonged bleeding time
Bone marrow examination to determine
the etiology; may reveal decreased
platelet activity or increased
Therapeutic management
a. Treatment of the underlying cause or
removal of the causative agent
b. Use of immunosuppressive and
chemotherapeutic agents in
case of ITP
c. Platelet transfusion if there is active
bleeding; little benefit in ITP
d. Splenectomy in ITP
 Priority nursing diagnoses:
 Risk for injury
 Bleeding
 Fatigue
 Altered oral mucous membrane
 Planning and implementation
 Institute bleeding (thrombocytopenic)
 Avoid intramuscular or subcutaneous
 Avoid indwelling catheters

 If absolutely necessary use smallest-

gauge needles for injections or
venipunctures; apply pressure on
injection sites for 5 minutes or until
bleeding stops
 Discourage straining at stool, vigorous
coughing, and nose blowing
 Avoid rectal manipulation such as rectal
temperatures, suppositories, or enemas
 Discourage the use of razors; use only
electric shavers
 Use soft-bristled toothbrush or
toothettes and avoid flossing
 Put side rails if necessary and avoid
tissue trauma
 Avoid the use of aspirin and drugs that
interfere with blood coagulation
 Monitor for signs of bleeding; test
stools for occult blood
 Monitor CBC and platelet counts
 Administer platelets as ordered
 Monitor response to therapy
 Medication therapy
 steroids and immunoglobulins may be
used to suppress the immune
response in ITP
 Immunosuppressive agents may be
used such as vincristine (Oncovin) and
cyclophosphamide (Cytoxan)
 Platelet growth factor such as
oprelvekin (Neumega)
 Client education
 Teach the client and family to monitor
for signs of bleeding and when to
contact the primary care provider
 Include instructions on bleeding
precautions such as the use of soft-
bristled toothbrush, avoidance of
flossing, prevention of tissue trauma
and injury including vigorous sexual
intercourse, and using an electric razor
for shaving
 Teach client to avoid drugs that
contain aspirin and others that
interfere with coagulation
 Discuss medication dosing, schedule,
and side effects
 Teach the importance of regular
medical follow-up and platelet
 Description:
 a group of hereditary clotting factor
disorders characterized by prolonged
coagulation time that results in
prolonged and sometimes excessive
 Etiology and pathophysiology
 Hemophilia A and B are X-linked recessive
disorders transmitted by female carriers,
displayed almost exclusively in males
 Hemophilia A (classic hemophilia) is a
deficiency in Factor VIII (an alpha globulin
that stabilizes fibrin clots; it is the most
common form of hemophilia
 Hemophilia B (Christmas disease) is a
deficiency in Factor IX; (a vitamin dependent
beta globulin essential in stage 1 of the
intrinsic coagulation system as an influence
on the amount of thromboplastin available)
 Despite the difference in factor deficiency,
hemophilia A and B are clinically identical
 In clients with hemophilia A and B, platelet plugs
are formed at the site of bleeding, but the
clotting factor impairs the coagulation response
and the capacity to form a stable clot
 Von Willebrand`s factor (vWF), which is
necessary for factor VIII activity and platelet
adhesion; this disorder affects men and women
 Assessment
 Clinical manifestations
 Persistent and prolonged
bleeding from small cuts and
 Delay of onset of bleeding after
an injury
 Subcutaneous ecchymosis and
subcutaneous hematomas
 Gingival bleeding

 Gastrointestinal bleeding, which may be

manifested by hematemesis (vomiting
blood), occult blood in the stools, gastric
pain, or abdominal pain
 Urinary tract bleeding (hematuria)
 Pain, paresthesias, or paralysis resulting
from nerve compression of the hematomas
 Hemarthrosis (joint bleeding, swelling and
 Diagnostic and laboratory tests
 Specific factor assays are used to determine
the type of hemophilia present
 APTT is increased in all types of hemophilia
 Bleeding time is prolonged in von
Willebrand`s disease
 Decreased factor VIII in hemophilia A, vWF in
von Willebrand`s disease, and factor IX in
hemophilia B
 Therapeutic management
 Treatment is the replacement of the deficient
coagulation factor(s)
 Hemophilia A: cryoprecipitate containing 8 to 100
units of factor VIII per bag at 12-hour intervals until
bleeding ceases; freeze-dried concentrate of factor
VIII may also be given
 Hemophilia B: plasma or factor IX concentrate
given q 24 hours or until bleeding ceases
 Von Willebrand`s disease: cryoprecipitate containing 8 to
100 units of factor VIII per bag at 12-hour intervals until
bleeding ceases; desmopressin (DDAVP) given
intravenously may also be used
 Supportive treatment for hemarthrosis including
arthrocentesis and physiotherapy
 Control of topical bleeding with hemostatic agents,
pressure, and application of ice
 Management of complications associated with hemorrhage
 Priority nursing diagnoses:
 Risk for injury, bleeding
 Decreased cardiac output
 Deficient fluid volume
 Risk for ineffective therapeutic regimen
 Planning and implementation
 Teach the client and family about the
disease and therapeutic regimen
 Refer for genetic counseling and family
 Refer to the National Hemophilia
Foundation for support and counseling
 Monitor for signs of complications including
hemarthrosis and intracranial bleeding
 Assist in management of pain
associated with hemarthrosis; measures
include joint immobilization , and
administration of analgesics; aspirin and
drugs affecting coagulation are avoided
 Control bleeding and maintain
hemostasis through direct pressure,
application of topical hemostatic agents,
and application of ice
 Administer medications as prescribed
 Client education
 Discuss with client and family signs and
symptoms requiring immediate medical
attention, which includes severe joint
pain, trauma or injury, and signs of
uncontrolled internal bleeding

Teach the client and family precautions

to prevent bleeding including the use of
soft bristled toothbrush, avoid flossing,
use of electric razor, avoiding contact
sports or activities most likely to cause
injury, and avoidance of aspirin and
other drugs that interfere with
 Teach the client about the importance of
wearing a Medic-Alert bracelet
indicating the hemophilia
 Emphasize the need to maintain good
dental hygiene to decrease the
necessity of invasive dental procedures
 Emphasize the importance of adhering
to scheduled visits and follow-up care
with the primary health provider
Disseminated intravascular
coagulopathy (or
Disseminated intravascular
coagulopathy (or
 Description:
 disseminated intravascular coagulopathy or
consumption coagulopathy is a syndrome
characterized by abnormal initiation and
acceleration of clotting and simultaneous
hemorrhage; the paradoxical bleeding that occurs
is a result of the consumption of clotting factors
and platelets; the syndrome is usually precipitated
by an underlying pathologic condition
Disseminated intravascular
coagulopathy (or
 Etiology and pathophysiology
 Mortality rate associated with DIC is as
high as 80 percent with the most
frequent sequela being hemorrhage
 The syndrome is precipitated by
conditions such as widespread tissue
damage, hemolysis, hypotension,
hypoxia, and metabolic acidosis
Disseminated intravascular
coagulopathy (or
The underlying condition causes
initiation and widespread formation of
clots in the vascular system either
through the activation of factor XII,
factors II and X, or the release of tissue
thromboplastin; substances necessary
for clotting are used at a more rapid
rate than they can be replaced
Disseminated intravascular
coagulopathy (or
As the clotting continues, the
fibrinolytic pathway is activated to
dissolve the clots formed; clotting
factors become depleted while
fibrinolysis continues; platelets
decrease, clotting factors II, V, VIII, and
fibrinogen are depleted
Disseminated intravascular
coagulopathy (or
 Fibrin degradation products (FDP) are
released as a result of fibrinolysis;
fibrin degradation products (FDP),
which are potent anticoagulants used
to lyse the clots further, increase the
bleeding state
 With the depletion of clotting factors
and the increase in fibrin degradation
products, stable blood clots no longer
form and hemorrhage occurs
Disseminated intravascular
coagulopathy (or
 Assessment
 Clinical manifestations

 Diagnostic and laboratory tests

 Prothrombin time: prolonged

 Partial thromboplastin time: prolonged

 Thrombin time: prolonged

 Fibrinogen: decreased

 Platelets: decreased

 Fibrin split (degradation) products: elevated

 Factor assays (factor V, VII, VIII, X, XIII):

 D-dimers: elevated
Disseminated intravascular
coagulopathy (or
Disseminated intravascular
coagulopathy (or
coagulopathy (or
 Therapeutic management
 The priority of therapeutic management is to
initiate treatment of the underlying medical
condition that precipitated DIC
 Supportive treatment for the manifestations of
DIC such as the control of bleeding; life-
threatening hemorrhage may be treated by
administering specific blood components based
on the identified deficiency: platelets for
thrombocytopenia; cryoprecipitate to replace
fibrinogen, and factors V and VII; and fresh
frozen plasma to replace all clotting factors
except platelets
 Use of heparin or antithrombin III (AT-III) to
control intravascular clotting
Disseminated intravascular
coagulopathy (or
 Priority nursing diagnoses:
 Impaired gas exchange
 Ineffective tissue perfusion
 Risk for deficient fluid volume
 Pain
 Decreased cardiac output
Disseminated intravascular
coagulopathy (or
 Planning and implementation
 Assess client carefully for evidence of
bleeding and altered tissue
 Institute thrombocytopenic
precautions (refer to previous
discussion on thrombocytopenia)
 Monitor intake and output hourly
Disseminated intravascular
coagulopathy (or
 Administer blood products as indicated
by the healthcare provider
 Monitor for signs of complications such as
renal failure, pulmonary embolism,
cerebrovascular accident, and acute
respiratory distress syndrome
 Monitor effectiveness of therapy and
pharmacologic interventions
 Provide emotional support to client and
Disseminated intravascular
coagulopathy (or
 Medication therapy
 Heparin and antithrombin III, although
their use is controversial; these drugs
are usually indicated to manage
 Epsilon aminocaproic acid (Amicar) to
inhibit fibrinolysis
 Blood products (FFP, platelets, and
Disseminated intravascular
coagulopathy (or
 Client education
 Teach the client and family regarding
the syndrome and explain treatments
and interventions
 Teach the client to report symptoms of
complications including abdominal pain,
headache, visual disturbances, and pain
 Discuss with the client and family
thrombocytopenic precautions (see
client education in the discussion of

a malignant disorder of the blood-
forming tissues of the bone marrow,
spleen, and lymph system characterized
by unregulated proliferation of WBCs and
their precursors
 Etiology and pathophysiology
 The type of WBC affected (granulocyte,
lymphocyte, monocyte) and the duration of
the disease (acute or chronic) is the basis
of the classification of the different types of
leukemia: if the majority of the leukemia
cells are primitive, the leukemia is
classified as acute; if the leukemic cells are
mostly mature (well-differentiated), the
leukemia is classified as chronic
 Acute
leukemia (ALL)
 Peak incidence at 2 to 4 years of
 Immature granulocytes
proliferate and accumulate in
the marrow
 Chronic lymphocytic leukemia (CLL)
 More common in men and mainly between
the ages of 50 and 70
 Abnormal and incompetent lymphocytes
proliferate and accumulate in the lymph
nodes and spreads to other lymphatic
tissues and the spleen; most of the
circulating cells are mature lymphocytes
 Acute myelogenous/myelocytic
leukemia (AML)
 All age groups are affected with a
peak incidence at age 60
 There is uncontrolled proliferation
of myeloblasts, which are the
precursors of granulocytes; they
accumulate in the bone marrow
 Chronic myelogenous leukemia (CML)
 Uncommon in people under 20 years of age;
the incidences rises with age
 There is uncontrolled proliferation of
granulocytes in increased circulating blast
(immature) cells; the marrow expands into long
bones because of this proliferation and also
extends into the liver and spleen
 In most cases the Philadelphia chromosomes, a
characteristic chromosomal abnormality, is
 Abnormal or immature WBCs do not
function properly because of the massive
proliferation of these abnormal immature
cells; abnormal cells can continue to
multiply, infiltrate, and damage the bone
marrow, spleen, lymph nodes, liver,
kidneys, lungs, gonads, skin, and central
nervous system (CNS)
 Normal bone marrow becomes diffusely
replaced with abnormal or immature
WBCs, interfering with the bone marrow`s
ability to produce other types of cells
such as erythrocytes and thrombocytes;
the bone marrow becomes functionally
incompetent with resulting bone marrow
 Acute leukemia has a rapid onset,
progresses rapidly, with a short clinical
course; left untreated, death will result in
days or months; the symptoms of acute
leukemia relate to a depressed bone
marrow, infiltration of leukemic cells into
other organ systems, and
hypermetabolism of leukemia cells
Chronic leukemia has a more insidious onset
with a more prolonged clinical course; clients
with the chronic form of leukemia are usually
asymptomatic early in the disease; the life
expectancy may be more than 5 years;
symptoms of chronic leukemia relate to
hypermetabolism of leukemia cells infiltrating
other organ system; the cells in this type of
leukemia are more mature and function more
 Assessment
 Clinical manifestations
 Fever
 Night sweats
 Bleeding
 Ecchymoses
 Lymphadenopathy
 Weakness
 Fatigue
 Pruritic vesicular lesions
 Anorexia
 Weight loss
 Shortness of breath
 Decreased activity tolerance
 Bone or joint pain
 Visual disturbances
 Gingival bleeding
 Epistaxis
 Pallor
 Splenomegaly
 Hepatomegaly
 Diagnostic and laboratory tests
 Increased WBC (in CLL and CML)
 A normal, decreased or increased WBC (in
ALL and AML)
 Decreased reaction to skin sensitivity tests
 Bone marrow tests reveal excessive blast
cells in AML
 Philadelphia chromosome found in 90 to 95
percent in clients with CML; BCR/ABL gene is
present in virtually all clients with CML
 Bone marrow biopsy and aspirate is the
definitive diagnostic test
 Therapeutic management
 Induction of remission with
chemotherapy and radiation therapy
 Bone marrow and stem cell
 Priority nursing diagnoses:
 Risk for infection: Risk for bleeding;
Imbalanced nutrition; less than body
requirements; Fatigue, Activity
intolerance; Pain; Anticipatory grieving
 Planning and implementation
 Review and institute the care of a client
receiving chemotherapy
 Review and implement the nursing care of a
client undergoing radiation therapy
 Assist in bone marrow biopsy; apply pressure
on the site for 5 minutes or until bleeding
stops; frequently assess the site for signs of
bleeding up to 4 hours after the procedure
 Institute neutropenic and bleeding precautions
 Plan activities to prevent fatigue; provide
measures for uninterrupted rest and sleep
 Provide for diversionary activities
 Maintain good nutrition; enlist the assistance of a
dietician in maximizing and meeting the
nutritional needs of the client
 Assist the client in maintaining good personal
hygiene; measures to promote oral hygiene
should be instituted
 Provide emotional support to the client and family;
refer to appropriate agency, organization, or
professional for counseling and support
 Administer drugs that are prescribed and monitor
for side effects
 Monitor laboratory results to evaluate
effectiveness of interventions and therapy
 Prepare the client for bone marrow transplantation
if this is included in the treatment plan
 Medication therapy:
 chemotherapeutic drugs include
alkylating agents (Busulfan [Myleran]),
anthracyclines (Doxorubicin
[Adriamycin]), antimetabolites
(Fludarabine [Fludara]), corticosteroid
(Prednisone), plant alkaloids (Vincristine
[Oncovin]) and others
 Client education
 Teach client and family about precautions to
prevent bleeding
 Teach client and family about neutropenic
precautions as previously discussed
 Teach client to maintain good oral hygiene
including measures to keep the oral cavity moist;
these measures can include rinsing mouth with
saline, lubricating the lips and oral mucosa with
water-soluble lubricants every 2 hours; alcohol-
based mouthwash solutions should be avoided;
sponge-tipped applicators should be used for oral
hygiene if the neutrophil and platelet counts are
 Teach client measures to prevent peri-
rectal complications; the area should
be washed and cleansed thoroughly
after each bowel movement
 Discuss with client and family
therapeutic plans and interventions
Malignant lymphomas
 Definition:
 lymphoma is a group of malignant
neoplasms that affects the lymphatic
system resulting in the proliferation of
lymphocytes; lymphomas can be
classified as Hodgkin`s disease and
non-Hodgkin`s lymphoma
Malignant lymphomas
 Etiology and pathophysiology
 Hodgkin`s disease
 More common in men and has two

peaks; 15 to 35 years of age and 55 to

75 years of age; incidence is higher in
whites than in African-Americans
 The cause of the disease is unknown

although several factors have been

identified to contribute to the
development of the disease; these
factors include infection with the
Epstein-Barr virus (EBV), familial
pattern, and exposure to toxins
Malignant lymphomas
 Hodgkin`s disease is
characterized by the presence
or Reed-Sternberg cell, a
multinucleated and gigantic
tumor cell thought to be of
lymphoid origin
 The tumor originates in a lymph
node (in majority of cases from
the cervical nodes) and
infiltrates the spleen, lungs, and
Malignant lymphomas
 Non-Hodgkin`s lymphoma
 Most common form of lymphoma; affects
usually adults from 50 to 70 years old; it is
more common in men than women and in
 There is no known cause but the incidence
of non-Hodgkin`s lymphoma is linked to
viral infections, immune disorders, genetic
abnormalities, exposure to chemicals, and
infection with Helicobacter pylori
Malignant lymphomas
 Non-Hodgkin`s lymphoma has a similar pathophysiology
to Hodgkin`s disease, although Reed-Sternberg cells are
absent and the method of lymph node infiltration is
 In majority cases, the disease involves malignant B
cells; the lymphoma usually originates outside the
lymph nodes; tthe lymphoid tissues involved become
infiltrated with malignant cells; the cells that make up
the lymphoid tissue become abnormal and crowd out
normal cells
Malignant lymphomas
 Assessment
 Clinical manifestations
 Hodgkin`s disease

 Usually begins with a firm and painless

enlargement of one or more lymph
nodes on one side of the neck
 Fatigue

 Weakness

 Anorexia

 Dysphagia

 Dyspnea

 Pruritus
Malignant lymphomas
 Development of severe but brief pain
at the site of Hodgkin`s after ingestion
of alcohol
 Cough
 Jaundice
 Abdominal pain
 Bone pain
 B symptoms: fever without chills; night
sweats, and unintentional 10 percent
weight loss
 Enlarged lymph nodes, liver, and
Malignant lymphomas
 Non-Hodgkin`s lymphoma
 Painless lymph node enlargement
 B symptoms (see above)
 Abdominal pain, nausea, vomiting
 Hematuria
 Peripheral neuropathy, cranial nerve
palsies, headaches, visual
disturbances, changes in mental
status, and seizures
 Shortness of breath, cough, and chest
Malignant lymphomas
 Diagnostic and laboratory tests
 Hodgkin`s disease
 Normocytic, normochromic anemia

 Neutrophilia, monocytophilia, and

 Presence of Reed-Sternberg cells in

excisional bone biopsy

Malignant lymphomas
 Mediastinal lymphadenopathy
revealed by chest x-ray, CT scan,
and radioisotope studies
 Mediastinal mass and pulmonary
infiltrates may be seen on chest x-
 Absent or decreased response to
skin sensitivity testing known as
Malignant lymphomas
 Non-Hodgkin`s lymphoma
 Lymphocytopenia

 X-ray may reveal pulmonary

 Lymph node biopsy helps to

identify the cell type and pattern

Malignant lymphomas

 Therapeutic management
 Hodgkin`s disease
 Lymphangiography is used to evaluate
abdominal nodes
 Staging laparotomy is performed to obtain
specimen of retroperitoneal lymph nodes
and to remove the spleen
Malignant lymphomas
Staging of the disease to determine the extent of
the disease and appropriate therapy is instituted
Stage 1 indicates involvement of a single lymph
node region
Stage IV (for Hodgkin`s disease only) indicates
diffuse or disseminated involvement of
extralymphatic organs, with or without lymph
node involvement (liver, lung, marrow, skin)
Malignant lymphomas
 Radiation therapy for stages 1A, 1B,
11A, and 11B
 Combination chemotherapy for
stages III, IV, and all B stages
 Combination radiation and
chemotherapy for stages 1A and 1B
Malignant lymphomas
 Non-Hodgkin`s lymphoma
 Staging of the disease is undertaken;
this is based on data obtained from CT
scans and bone marrow biopsies
 Combination chemotherapy
 Radiation alone or in combination with
chemotherapy for stage 1 and II
 Biologic therapy with alpha interferon,
interleukin-2 and tumor necrosis factor
 Administration of rituximab (Rituxan), a
monoclonal antibody against the CD20
of malignant B lymphocytes, which
causes cell lysis and death
Malignant lymphomas
 Priority nursing diagnoses:
 Risk for infection
 Activity intolerance
 Ineffective protection
 Fatigue
 Imbalanced nutrition: less than body
 Disturbed body image
 Hopelessness
Malignant lymphomas
 Planning and implementation
 Institute nursing interventions for clients on
chemotherapy or radiation therapy
 Assist in balancing activity with periods of
 Provide and assist in maintaining good
nutritional state
 Provide measures to diminish the discomfort
associated with pruritus
 Provide interventions to enable client to deal
with body image changes such as alopecia,
weight loss, and sterility
 Plan interventions for the prevention of
Malignant lymphomas
 Medication therapy
 Chemotherapeutic agents
 Biologic therapy agents
Malignant lymphomas
 Client education
 Discuss with client and family the
nature of the disease, the course of
therapy, and associated interventions
 Teach the client and family about the
medications prescribed, precautions,
and side effects
 Teach the client and family symptoms
necessitating immediate medical
interventions such as the occurrence
of bleeding, infection, or fever