Professional Documents
Culture Documents
ANEMIA
1.) Anemia is reduction in either RBCs, amount of hemoglobin,
or hematocrit (% of packed RBC per deciliter of blood)
Anemia is a symptom of an underlying disease.
Causes and types vary:
1.)dietary problemsdeficiency in components necessary
to make RBCiron, vitamin B12 (cyanocobalamin), folic
acid, or intrinsic factor
2.)genetic disorders
4.)excessive bleeding
5.)Immune reactions
6.)Changes in blood chemistry
7.)Toxins in the blood
**Gastrointestinal bleeding common cause of anemia in
adults**
N323 Module B part I
Hematologic Problems
Anemias
Results in: reduction in oxygen transport due to
decrease in hemoglobin production, a decrease
in erythrocytes, or a combination of these
factors.
Reduced oxygen leads to less energy in all cells,
reduced cell metabolism and reproduction.
Compensation mechanisms include tachycardia
and peripheral vasoconstriction
Hematologic Problems
Anemias
General signs of anemia: fatigue, pallor,
dyspnea, and tachycardia
Severe anemia may lead to angina if
oxygen supply to the heart is insufficient
Chronic severe anemia may cause CHF
Other affects may include hair and skin
changes
Cultural considerations:
N323 Module B part I
Diagnostic Assessment
Tests of cell number and function:
Complete blood count
Reticulocyte count
Hemoglobin electrophoresis
Serum ferritin
transferrin
total iron-binding capacity
LABORATORY PROFILE
Test
Significance of abnormal finding
Red blood cell count
Decreased indicate possible
anemia/hemorrhage
Hemoglobin/Hematocrit
Increased indicate possible chronic
hypoxia, or polycythemia vera
Mean cell hemoglobin (MCV)
Increased levels indicate macrocytic cells,
possible anemia. Decreased levels
indicate microcytic cells,
possible iron deficiency anemia
Reticulocyte count
helpful in determining bone marrow function
(immature RBC) **Increased levels indicate
chronic blood lossdesireable in anemic client
or after hemorrhage.
Hemoglobin electrophoresis
as
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Assessment Hematologic
Demographic data (age,
gender)
Family history and genetic risk
Personal history (use of ASA,
NSAIDS, antibiotic useprolonged can lead to bone
marrow suppression)
Diet history
Socioeconomic status
Current health status
(Gordons Hematologic assessment
activity-exercise pattern, and nutritionmetabolic pattern pg 879)
Skin
Head and neck
Respiratory
Cardiovascular
Renal and urinary
Musculoskeletal
Abdominal
Central nervous
system
Psychosocial
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Anemia
Clinical Manifestations
Severe = Hb <6 g/dl
Mild = Hb 10 to 14 g/dl
Involve multiple body
May exist without symptoms
systems
Moderate = Hb 6 to 10 g/dl
Integument
Increased cardiopulmonary symptoms Eyes
Experienced at rest or during activity
Mouth
Cardiovascular
Pulmonary
Neurologic
Gastrointestinal (GI)
Musculoskeletal
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Iron-Deficiency Anemia
One of the most common chronic
hematologic disorders
Iron is present in all RBCs as heme in
hemoglobin and in a stored form
Heme accounts for two thirds of the
bodys iron
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Management
injection
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Iron-Deficiency Anemia
Drug Therapy
Oral iron
Vitamin C aids in iron absorption
Factors to consider (contd)
Best absorbed as ferrous sulfate in an acidic
environment
Liquid iron should be diluted and ingested
through a straw to prevent staining of teeth
Side effects
Heartburn, constipation, black stools,
diarrhea
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Iron-Deficiency Anemia
Nursing Management
At-risk groups
Premenopausal women
Pregnant women
Persons from low socioeconomic
backgrounds
Older adults
Individuals experiencing blood loss
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Iron-Deficiency Anemia
Nursing Management
Diet teaching
Supplemental iron
Discuss diagnostic studies
Emphasize compliance
Iron therapy for 2 to 3 months after
the hemoglobin levels return to normal
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Vitamin B12
liver, organ meats, nuts
dried beans, green leafy
citrus fruit, brewers
Folic Acid
Liver, organ meats, eggs, cabbage
Brocolli, brussel sprouts
N323 Module B part I
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Megaloblastic Anemias
Group of D/O caused by DNA synthesis and
characterized by large RBCs (abnormal =
hemolysis)
Common: Vitamin B12 Cobalamin deficiency
anemia
Pernicious anemia lack of secretion of intrinsic
factor (needs acidic environment) in GI tract which
is necessary for absorption of Vitamin B12
Folic acid anemia
Other causes: certain drugs
N323 Module B part I
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slight jaundice
Smooth, shiny, beefy tongue
weight loss
paresthesia of hands and feet (numbness and
tingling), difficulty w/gait related lack of B12
needed for normal nerve function (impaired
conduction of nerve impulses=demyelination)
peripheral nerves and eventually spinal cord)
N323 Module B part I
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Thalassemia
Etiology
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Thalassemia
Clinical Manifestations
Thalassemia major
Thalassemia minor
Asymptomatic frequently
Moderate anemia
Splenomegaly
Mild jaundice
Thalassemia major
Life-threatening
Physical and mental
growth often retarded
Pale
Symptoms develop in
childhood
Splenomegaly
Hepatomegaly
Jaundice from
hemolysis
Chronic bone marrow
hyperplasia
Expansion of bone
marrow space
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Thalassemia
Collaborative Care
No specific drug or
diet is effective in
treating thalassemia
Thalassemia minor
Body adapts to
decreased Hb
Thalassemia major
Prevention
Genetic counseling
with families with
known history of
Thalassemia
Prenatal checkup
Blood transfusions
with IV deferoxamine
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Cause
Pain
Internal hemorrhage
Tissue distention, organ displacement, nerve compression
Pain (cont'd)
Retroperitoneal bleeding
Numbness
Pain in the lower extremities
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Bleeding ulcer
Hemorrhoids
Menstrual and postmenopausal blood loss
Management
Identify source
Stop bleeding
Possible use of supplemental iron
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Hemolytic Anemia
Destruction or hemolysis
of RBCs at a rate that
exceeds production
Third major cause of
anemia
Intrinsic hemolytic
anemia
Abnormal hemoglobin
Extrinsic hemolytic
anemia
Acquired (mechanical injury
heart bypass, toxins)
Sites of hemolysis
Intravascular
Extravascular
(sickle cell)
Enzyme deficiencies
RBC membrane
abnormalities
N323 Module B part I
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Hemolytic Anemia
Jaundice
Destroyed RBCs
cause increased
bilirubin
Accumulation of
hemoglobin
molecules can
obstruct renal tubules
Tubular necrosis
Hyperactive with
macrophage
phagocytosis of the
defective RBCs
N323 Module B part I
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b.) Glucose-6Phosphate
Dehydrogenase
Deficiency anemia
c.) Thrombotic
Thrombocytopenia
Purpura (TTP) is a
rare autoimmune
reaction in blood
vessels disorder in
which platelets clump
together abnormally in
the capillaries and few
remain in circulation.
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Clinical Manifestations
Cardiovascular changes
Skin changes
Abdominal changes
Musculoskeletal changes
Central nervous system changes
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Diagnosis
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Interventions
include:
Protection of the
client from infection
in sickle cell crisis
Drug therapy
-pain meds, folic
acid replacement -Hydroxyurea (Droxia)
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Administer blood
transfusion if required
Remove constrictive
clothing
Encourage client to keep
extremities extended to
promote venous return
Check circulation of
extremities
Complementary and
alternative therapies
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2. Immune reactions
vessels)
Antigenantibody
reactions destroy
RBCs
Isoimmune reactions
Antibodies develop
against antigens;
blood transfusions
Autoimmune
reactions
Develop antibodies
against their own
RBCs
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Hemochromatosis
Primary hemochromatosis is an
inherited disorder characterized by
excessive iron accumulation due to
increaxed intestinal iron absorption
causing tissue damage.
Symptoms do not develop until organ
damage, often irreversible, develops.
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Anemia
Nursing Implementation
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Polycythemia
Production and
Polcycythemia
Vera=(PV) is a rare
presence of increased
disease with a
RBCs
sustained increase in
2 types:
blood cells (primarily
Primary polycythemia =
red blood cells)
Polycythemia Vera
produced by the bone
marrow
Secondary Polycythemia =
a.) hypoxia driven = high
With unknown origin,
altitude, cardiopulmonary
chromosomal defect in
disease, defection O2
pluripotent stem cells
transport
b.)Hypoxia independent=
renal cysts or tumors
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Polycythemia Vera
Due to hyperviscous
(thicker than normal
blood) the following may
occur:
Key features:
Clients facial skin and
mucous membranes have
a dark, flushed
(plethoric) appearance
Distention of superficial
veins
Weight loss
Intense itching
Hypertension
Fatigue, enlarged
hemorrhoids
Swollen painful joints
Enlarged firm spleen
Infarctions of the heart
(chest pain, heart
failure), kidneys
Strokes
Bleeding tendency
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Polycythemia Vera
Diagnostic Tests
Blood cell counts and
hematocrit markedly
elevated
Hyperuricemia due to
high cell destruction
Bone marrow
hypercellular
Hgb levels to 18 g/dl
Hct of 55% or >
RBC count of 6 mil/mm3
N323 Module B part I
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Collaborative
management:
Phlebotomy (treatment)
blood drawing
Increase hydration
Anticoagulants are part
of therapy to prevent
clot formation
Chemotherapy to
suppress bone marrow
activity
Radiation therapy
Bone marrow
transplantation
Significant number of
individuals with PV go on
to develop acute
leukemia
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Take anticoagulants as
prescribed
Wear support hose
while awake and up
Elevate feet when you
are seated
Exercise slowly and only
on the advice of your
physician
Stop activity at the
first sign of chest pain
Use electric shaver
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Leukemia
Occurs in all age groups
Accumulation of dysfunctional cells due to loss
of regulation in cell division
Fatal if untreated
Often thought of as a childhood disease
The number of adults affected is 10 times that
of children
No single causative agent
Combination of genetic and environmental
influences
N323 Module B part I
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Leukemia
Acute versus chronic
Cell maturity
Acute: Clonal proliferation of immature hematopoietic cells
higher proportion of very immature, nonfunctional cells in
the bone marrow & circulation
Chronic: has higher proportion of mature, WBC and onset
is more gradual, milder signs and thus better prognosis
Acute
Chronic
Chronic leukemia have better prognosis, more
common older person
Classified by cell type
N323 Module B part I
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Unclassified Leukemias
Subtype cannot be identified
Malignant leukemic cells may have
characteristics of
Lymphoid
Myeloid
Mixed
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Overview: Leukemias
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Clinical Manifestations
Laboratory Assessment
To diagnose and classify
Peripheral blood evaluation
Bone marrow evaluation
Definitive test: examination
of cells obtained from
bone marrow aspiration
and biopsy
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Leukemia
Collaborative Care
Goal is to attain remission Infection protection
Complete, partial, or molecular
remission
Bleeding precautions
Chemotherapeutic treatment
Energy management
Four stages of therapy
Induction
Intensification
Consolidation
Maintenance
Drug therapy
Combination chemotherapy
Mainstay treatment
Three purposes
Drug resistance
Drug toxicity using
multiple drugs
Interrupt cell growth
at multiple points
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CHEMOTHERAPY
4 phases:
1st phase =induction
therapy,
--Patient may
become critically ill
Provide
psychological
support as well
High-dose therapy
May be given after
induction therapy
Same drugs at
higher doses
and/or other drugs
--common S/E=
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3rd phase
therapy=Consolidation
therapy, another course of
chemotherapy single or
repeated for 1-2 years
--intent is to cure
--occurs after remission is
achieved
Eliminate remaining
leukemic cells that
may not be
pathologically evident
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Collaborative treatments
for Leukemia
Drug therapy for infection
may include antibacterial,
antiviral, or antifungal.
Analgesics
Radiation to areas of
lymphocytic infiltrates
Transfusions of whole blood
or blood fractions
Monitor vital signs and assess
for fever. A temperature
elevation of 0.5 degrees F
above baseline is significant
for a client with leukopenia
and indicates an infection
until proven otherwise.
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Conditioning regiment
before transplantation
Purpose Donor stem cells infused
intravenously into the
1.)
blood of the recipient;
2.)
Antirejection
Engraftment
medications for one
successful take of
year and then
transplanted cells in
discontinued.
clients bone marrow.
Common complications:
8-12 days if occurs
WBC, RBC, and platelet
count begin to rise
N323 Module B part I
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uncooked foods
Monitoring of daily laboratory
results
Assessment of vital signs
Skin care, respiratory care
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Malignant Lymphomas
Lymphomas are cancers (malignancies) of one type of
WBC called lymphocytes. Lymphomas are solid
tumors involving lymph nodes in lymphatic system and in
blood-forming organs
The 2 main types of lymphoma are Hodgkin's lymphoma
(HL) and non-Hodgkin's lymphoma (NHL).
Non-Hodgkin's lymphoma is more common than
Hodgkin's lymphoma
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Lymphomas
Lymphatic system- network of lymphatic vessels
are lymph nodes, which house collections of
lymphocytes.
Lymphocytes that become cancerous
(lymphoma cells) may remain confined to a
single lymph node or may spread to the bone
marrow, the spleen, or virtually any other organ
Lymphomas can develop from either B or T
lymphocytes.
T lymphocytes are important in regulating the
immune system and in fighting viral infections.
B lymphocytes produce antibodies.
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Hodgkins Lymphoma
Cancer that starts in a single lymph node or a
single chain of nodes, eventually infiltrates
other organslungs, spleen, liver
Marker: Reed-Sternberg cell
Signs and Symptoms: Large, painless lymph
node usually in the neck, axillary, or inguinal,
fever, malaise, night sweats, weight loss, fever
Other s/s depends on stage of disease
One of the most curable cancers
Disease below diaphragm can spread to liver,
above diaphragm confined to lymph nodes for
a time.
Treatment: external radiation alone or with
combination chemotherapy
N323 Module B part I
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Non-Hodgkins Lymphoma
All lymphoid cancers that do not have the ReedSternberg cell
More than 12 types of non-Hodgkins lymphoma
Burkitts, Large B Cell lymphoma highly aggressive
diseases
Low-grade lymphomas less responsive to treatment;
cures are rare
Treatment: radiation therapy and multi agent
chemotherapy, or single-agent therapy
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Autoimmune
Thrombocytopenic Purpura ITP
Idiopathic thrombocytopenic purpura prior name
Autoimmune
disorder, autoantibodies are
produced
Thrombocytes (plateletes) are recognized as
foreign causing macrophages to destroy them
-- trigger unknown
Bone marrow production of platelet is normal,
platelet destruction is increased, leading to
low number of circulating platelets
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Autoimmune
Thrombocytopenic Purpura
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Autoimmune
Thrombocytopenic Purpura
Interventions (Continued)
include:
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Thrombotic Thrombocytopenic
Purpura (TTP)
Rare disorder; platelets clump abnormally together
in the capillaries, results in bleeding problems
elsewhere, pt. may have hemolytic d/o, neurologic
abnormalities,
Inappropriate clotting when trauma occurs
Cause: Autoimmune reaction in blood vessels
causes clumping, certain drug toxicities
Results in tissue ischemia.
Manifestations: renal failure, MI, stroke
Can be fatal if untreated in 3 months
N323 Module B part I
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Thrombotic Thrombocytopenic
Purpura (TTP)
Collaborative management:
Stop autoimmune process to prevent clotting and
clumping, and decreased platelets circulating (bleeding)
Plasma pheresis, fresh frozen plasma transfusion
Drugs: platelet inhibitors ASA, Prostin, Plicamycin
(antineoplastic, antibiotic)
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Type I
Patients have a transient decrease in platelet
count without any further symptoms.
Type II
Cause: autoimmune /allergic reaction to heparin
After heparin is administered to a patient, an
immune complex can form between heparin and
a specific blood factor (platelet factor 4, or "PF4")
that is released by platelets.
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Diagnosis
--decreased platelet counts
--antibody for HIT
Treatment
--D/C Heparin, use other drugs
--Refludan (lepirudin), argotroban (thrombin
inhibitors)
--Fondaparinux
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A. Causes:
infection, septecemia, viral, fungal,
rickettsial, protozoal infections, obstetrical
complications, neoplastic diseases, burns,
trauma, heatstroke, or any other number of
disorders.
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DIC
Diagnostic Tests
PTT/PT prolonged
Reduced fibrinogen, antithrombin, and
platelets
Elevated fibrin-split products, and elevated
D-dimers (cross linked fibrin fragments)
Decreased levels of factors V, VII, VII, X,
XIII
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Disseminated Intravascular
Coagulation(DIC)
Clinical Findings:
abnormal bleeding anywhere in the body,
cutaneous oozing of serum, cyanotic
extremities, petechia, restlessness, anxiety
Complications: acute tubular necrosis, shock,
multi organ failure
Interventions/Treatment: treatment of
underlying disorder, administration of blood,
fresh frozen plasma, platelet, packed RBCs,
heparin therapy (controversial)
N323 Module B part I
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