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PLASMA
91 % water; 7% proteins; 2 % other substances
Proteins:
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
Nutrients
Gases
Waste products
Regulatory substances
FORMED ELEMENTS
FORMED ELEMENTS
Red Blood cell
Are disk-shaped and biconcave; no nucleus;
contains hemoglobin
Live for about 120 days in males and 110 days for
females.
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
Granulocytes
Neutrophils
Nucleus with 2 to 4 lobes; granules stain light pink or
reddish purple .
10 -12 µm in diameter
10-12 µm in diameter
nucleus
6-14 µm in diameter
cytoplasm
12-20µm in diameter
macrophage
Platelets
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
PRODUCTION OF FORMED
ELEMENTS
Hematopoiesis
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
ERYTHROPOIESIS
Or Red Blood Cell production
Proerythroblasts
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
ERYTHROPOIESIS
Erythropoietin
Stimulates red bone marrow to produce more
RBC
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
Hemoglobin Breakdown
ERYTHROPOIESIS
Bilirubin
A yellow pigment molecule from heme
Normally taken up by the liver and
released into the small intestine as part
of the bile
PREVENTING BLOOD
LOSS
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
platelets.
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
Fibrinolysis
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.
Serum
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.
Fibrinolysis
Clots are dissolved by this process
ABO Blood Groups
Diagnostic Tests and
Assessments
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
Assessments
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
Assessments
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
Assessments
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
cells
Diagnostic Tests and
Assessments
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
Assessments
Weakness
Shortness of breath
Iron-deficiency anemia (IDA)
Pallor (ear lobes, palms, and
conjunctiva)
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
(RDW)
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
amount
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
afterward
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
wheels
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
Fatigue
Palpitations
Exertional dyspnea
membranes
Bleeding from gums, nose, vagina, or
rectum
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
infection
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
(Sandimmune)
Immunosuppresive agents such as
prednisone and cyclophosphamide
(Cytoxan)
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
diet
Discuss ways to prevent hemorrhage
such as using a soft toothbrush, avoiding
contact sports, and use of an electric
razor
Aplastic anemia
Emphasize the avoidance of drugs that
increase bleeding tendency such as
aspirin
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
anemia
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
chains
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
removed
Crisis is extremely painful and can last
from 4 to 6 days
Sickle cell disease
Assessment
Clinical manifestations
Pallor
Jaundice
Fatigue
Irritability
Stress-reduction strategies
Avoid overexertion
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
Thrombocytopenia
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
Thrombocytopenia
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);
Thrombocytopenia
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
Thrombocytopenia
Assessment
a. Clinical manifestations
Petechiae and purpura most commonly
found in the anterior thorax, arms, and
neck
Epistaxis, gingival bleeding,
menorrhagia, hematuria, and
gastrointestinal bleeding
Signs of internal hemorrhage
Thrombocytopenia
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
megakaryocytes
Thrombocytopenia
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
Thrombocytopenia
Priority nursing diagnoses:
Risk for injury
Bleeding
Fatigue
Altered oral mucous membrane
Thrombocytopenia
Planning and implementation
Institute bleeding (thrombocytopenic)
precautions
Avoid intramuscular or subcutaneous
injections
Avoid indwelling catheters
Fibrinogen: decreased
Platelets: decreased
reduced
D-dimers: elevated
Disseminated intravascular
coagulopathy (or
coagulation)
Disseminated intravascular
coagulopathy (or
coagulation)
coagulopathy (or
coagulation)
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
coagulation)
Priority nursing diagnoses:
Impaired gas exchange
Ineffective tissue perfusion
Risk for deficient fluid volume
Pain
Decreased cardiac output
Disseminated intravascular
coagulopathy (or
coagulation)
Planning and implementation
Assess client carefully for evidence of
bleeding and altered tissue
oxygenation
Institute thrombocytopenic
precautions (refer to previous
discussion on thrombocytopenia)
Monitor intake and output hourly
Disseminated intravascular
coagulopathy (or
coagulation)
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
family
Disseminated intravascular
coagulopathy (or
coagulation)
Medication therapy
Heparin and antithrombin III, although
their use is controversial; these drugs
are usually indicated to manage
thrombosis
Epsilon aminocaproic acid (Amicar) to
inhibit fibrinolysis
Blood products (FFP, platelets, and
cryoprecipitate)
Disseminated intravascular
coagulopathy (or
coagulation)
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
thrombocytopenia)
Leukemia
Definition:
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
Leukemia
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
Leukemia
Acute
lymphocytic/lymphoblastic
leukemia (ALL)
Peak incidence at 2 to 4 years of
age
Immature granulocytes
proliferate and accumulate in
the marrow
Leukemia
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
Leukemia
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
Leukemia
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
present
Leukemia
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)
Leukemia
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
suppression
Leukemia
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
Leukemia
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
effectively
Leukemia
Assessment
Clinical manifestations
Fever
Night sweats
Bleeding
Ecchymoses
Lymphadenopathy
Weakness
Fatigue
Pruritic vesicular lesions
Anorexia
Weight loss
Shortness of breath
Leukemia
Decreased activity tolerance
Bone or joint pain
Visual disturbances
Gingival bleeding
Epistaxis
Pallor
Splenomegaly
Hepatomegaly
Leukemia
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
(anergy)
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
Leukemia
Therapeutic management
Induction of remission with
chemotherapy and radiation therapy
Bone marrow and stem cell
transplantation
Priority nursing diagnoses:
Risk for infection: Risk for bleeding;
Imbalanced nutrition; less than body
requirements; Fatigue, Activity
intolerance; Pain; Anticipatory grieving
Leukemia
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
Leukemia
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
Leukemia
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
Leukemia
Medication therapy:
chemotherapeutic drugs include
alkylating agents (Busulfan [Myleran]),
anthracyclines (Doxorubicin
[Adriamycin]), antimetabolites
(Fludarabine [Fludara]), corticosteroid
(Prednisone), plant alkaloids (Vincristine
[Oncovin]) and others
Leukemia
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
low
Leukemia
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
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
spleen
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
pain
Malignant lymphomas
Diagnostic and laboratory tests
Hodgkin`s disease
Normocytic, normochromic anemia
lymphopenia
Presence of Reed-Sternberg cells in
infiltrates
Lymph node biopsy helps to
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
requirements
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
rest
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
infection
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