Adult Nursing - Anemia

(Relates to Chapter 31, Nursing Management:
Hematologic Problems,
in the textbook)
Copyright 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
A deficiency in the
Number of erythrocytes
(red blood cells [RBCs])

Quantity of hemoglobin
Volume of packed RBCs
(hematocrit)
Diverse causes such as

Blood loss
Impaired production of
erythrocytes
Increased destruction of
erythrocytes
RBC function
Transport oxygen (O2) from
lungs to systemic tissues

Carry carbon dioxide from the
tissues to the lungs
Not a specific disease

Manifestation of a pathologic
process
Identified and classified by
laboratory diagnosis
Classified as
Morphologic
Cellular characteristics
Descriptive, objective laboratory
information
Etiologic
Underlying cause
Caused
by the bodys
response to tissue hypoxia
Hemoglobin
(Hb) levels are

used to determine the
severity of anemia
Pallor
Hemoglobin
Blood flow to the skin
Jaundice
Concentration of serum
bilirubin
Pruritus
Serum and skin bile salt
concentrations
Additional
attempts by the
heart and lungs to provide
adequate O2 to the tissues
Cardiac output maintained
by increasing the heart rate
and stroke volume
Mild = Hb 10 to 14 g/dl
May exist without symptoms
Possible symptoms
Palpitations, dyspnea, diaphoresis
Moderate = Hb 6 to 10 g/dl
Increased cardiopulmonary
symptoms
Experienced at rest or during
activity
Severe = Hb <6 g/dl

Involve multiple body systems
Integument
Eyes
Mouth
Cardiovascular
Severe = Hb <6 g/dl

Manifestations (cont'd)
Pulmonary
Neurologic
Gastrointestinal (GI)
Musculoskeletal
Subjective Data
Important health information
Past health history
Medications
Surgery or other treatments
Subjective Data
Functional health patterns
Health perceptionhealth
management
Nutritional-metabolic
Elimination
Activity-exercise
Cognitive-perceptual
Sexuality-reproductive
Objective Data
General
Integumentary
Respiratory
Cardiovascular
Gastrointestinal
Neurologic
Activity intolerance
Imbalanced nutrition:
Less
than body requirements
Ineffective therapeutic
regimen management
Potential complication:
Hypoxemia
Goals
Assume normal activities of
daily living
Maintain adequate nutrition
Develop no complications
related to anemia
Dietary and lifestyle changes

Blood or blood product
transfusions
Drug therapy
Oxygen therapy
Patient teaching
Nutrition intake
Compliance with drug therapy
Common in older adults

Chronic disease
Nutritional deficiencies
Signs and symptoms may
go
unrecognized or mistaken for
normal aging changes
Erythropoietin
(EPO) is a
glycoprotein primarily
produced in the kidneys
(10% in the liver)
Number of stem cells
committed to RBC production

Shortens the time to mature
RBCs
Life span of an RBC is

Three alterations in
120 days
erythropoiesis that decrease

RBC production
Decreased hemoglobin synthesis

Defective DNA synthesis in RBCs
Diminished availability of
erythrocyte precursors
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
Inadequate dietary intake

5% to 10% of ingested iron is
absorbed
Malabsorption
Blood loss
Hemolysis
General
manifestations of
anemia
Pallor is the most common
finding
Glossitis is the second most
common
Inflammation of the tongue
Laboratory findings
Hb, Hct, MCV, MCH, MCHC,
reticulocytes, serum iron, TIBC,

bilirubin, platelets
Stool guaiac test

Endoscopy
Colonoscopy
Goal
is to treat the
underlying disease
Increased intake of iron
Nutritional therapy
Oral or occasional parenteral
iron supplements
Transfusion of packed RBCs
Oral iron
Inexpensive
Convenient
Factors to consider
Enteric-coated or sustainedrelease capsules are
counterproductive
Oral iron
Factors to consider (contd)
Best absorbed as ferrous sulfate in
an acidic environment
Liquid iron should be diluted and
ingested through a straw
Side effects
Heartburn, constipation, diarrhea
At-risk groups
Premenopausal women
Pregnant women
Persons from low
socioeconomic backgrounds
Older adults
Individuals experiencing blood
loss
Diet teaching
Supplemental iron
Discuss diagnostic studies
Emphasize compliance
Iron therapy for 2 to 3
months after the hemoglobin

levels return to normal
An
autosomal recessive
genetic disorder of
inadequate production of
normal hemoglobin
Common in ethnic groups near
the Mediterranean Sea and

equatorial regions of Asia and
Africa
Hemolysis also occurs

Problem with globulin
protein
Abnormal Hb synthesis
One thalassemic gene

Thalassemia minor
Two thalassemic genes
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
Thalassemia major (contd)

Splenomegaly
Hepatomegaly
Jaundice
Chronic bone marrow
hyperplasia
Expansion of bone marrow space
No
specific drug or diet is

effective in treating
thalassemia
Thalassemia minor
Body adapts to decreased Hb
Thalassemia major
Blood transfusions with IV
deferoxamine
Group
of disorders caused by
impaired DNA synthesis
Characterized by the
presence of large RBCs
(megaloblasts)
Majority result from
deficiency in
Cobalamin (vitamin B12)
Folic acid
Classification
Cobalamin (vitamin B12)
deficiency
Folic acid deficiency
Drug-induced suppression of
DNA synthesis
Inborn errors
Erythroleukemia
Intrinsic factor (IF)

Protein secreted by the parietal
cells of the gastric mucosa

IF
is required for cobalamin

absorption in the small
intestine
Causes
Pernicious anemia
Insidious onset
Nutritional deficiencies
Hereditary enzymatic defects
Absence of IF
Acid environment
required
for IF secretion
GI surgery
Long-term users of H2histamine receptor blockers
General
symptoms of
anemia
Sore tongue
Anorexia
Nausea
Vomiting
Abdominal pain
Neuromuscular manifestations
Weakness
Paresthesias of the feet and
hands
Vibratory and position senses
Ataxia
Muscle weakness
Impaired thought process
RBCs appear large

Abnormal shapes
Structure contributes
to
erythrocyte destruction
Decreased serum
cobalamin levels
Normal
serum folate
levels and decreased
cobalamin levels suggest
megaloblastic anemia due
to cobalamin deficiency
Schilling test
Parenteral
administration
of cobalamin
Increase in dietary
cobalamin does not
correct the anemia
Still important to emphasize
adequate dietary intake
Familial disposition
Early detection and treatment
can lead to reversal of

symptoms
Ensure
that injuries are not

sustained because of the
patients diminished
sensations to heat and pain
Ensure
patient
compliance with
treatment
Evaluate patient for
gastric carcinoma
frequently
Also
a cause of
megaloblastic anemia
Folic acid is required for
DNA synthesis
RBC formation and
maturation
Common causes
Poor nutrition
Malabsorption syndromes
Drugs
Alcohol abuse and anorexia
Lost during hemodialysis
Clinical
manifestations are
similar to those of cobalamin
deficiency
Insidious onset
Absence of neurologic problems
Treated by replacement therapy
Encourage patient to eat foods
with large amounts of folic acid
Underproduction of RBCs
Mild shortening of RBC
survival
Causes
End-stage renal disease
Primary factor: Erythropoietin
Chronic liver disease
Chronic inflammation
Malignant tumors
Chronic endocrine diseases
Anemia
findings
of chronic disease
Serum ferritin
Iron stores
Normal folate and cobalamin
levels
Treating
underlying cause is
best
Rarely blood transfusions
Erythropoietin therapy
Pancytopenia
Decrease of all blood cell types
RBCs
White blood cells (WBCs)
Platelets
Hypocellular bone marrow
Low incidence
Affecting 4 of every 1 million
persons
Manageable
with
erythropoietin or blood
transfusion
Can be a critical condition
Hemorrhage
Sepsis
Types
Congenital
Chromosomal alterations
Acquired
Results from exposure to ionizing
radiation, chemical agents, viral
and bacterial infections
Gradual development
Symptoms caused by
suppression of any or all

bone marrow elements
General manifestations of
anemia
Fatigue, dyspnea
Confirmed
by laboratory
studies
Normocytic, normochromic
anemia
Preventing
complications
from infection and
hemorrhage
Untreated prognosis is poor
75% fatal
Treatment options
Bone marrow transplantation
Immunosuppressive therapy
Result
of sudden
hemorrhage
Trauma
Complications of surgery
Disruption of vascular integrity
Concerns
Hypovolemic shock
Reduced plasma volume
Diminished O2 because fewer RBCs
available
Cause
Bodys attempt to maintain an
adequate blood volume and O2

Pain
Internal hemorrhage
Tissue distention, organ
displacement, nerve compression
Pain (cont'd)
Retroperitoneal bleeding
Numbness
Pain in the lower extremities
Shock is the major
complication
Laboratory
data do not
adequately assess RBC
problems for 2 to 3 days
Replacing
blood volume to
prevent shock
Identifying the source of the
hemorrhage
Stopping blood loss
Correcting RBC loss
May
be impossible to prevent
if caused by trauma
Postoperative patients
Monitor blood loss
No
need for long-term

treatment
Reduced iron stores

Bleeding ulcer
Hemorrhoids
Menstrual and postmenopausal
blood loss
Management
Identify source
Stop bleeding
Possible use of supplemental
iron
Destruction
or hemolysis of
RBCs at a rate that exceeds
production
Third major cause of anemia,
such as Thalassemia
Intrinsic hemolytic anemia
Abnormal hemoglobin
Enzyme deficiencies
RBC membrane abnormalities
Extrinsic hemolytic
Acquired
Sites of hemolysis
Intravascular
Extravascular
anemia
Jaundice
Destroyed RBCs cause
increased bilirubin
Enlarged spleen and liver
Hyperactive with macrophage
phagocytosis of the defective

RBCs
Accumulation
of hemoglobin
molecules can obstruct renal
tubules
Tubular necrosis
Group
of inherited,
autosomal recessive
disorders
Presence of an abnormal
form of hemoglobin in the
erythrocyte
Hemoglobin S (HbS),
abnormal
HbS
causes the RBC to stiffen

and elongate
Sickle shape in response to O 2
levels
Substitution of valine for
glutamic acid on the -globin
chain of hemoglobin
Genetic disorder
Incurable disease,
often fatal
Types of SCD
Sickle cell anemia
Most severe
Homozygous for hemoglobin S
(HbSS)
Sickle cell thalassemia
Sickle cell HbC disease
Sickle cell trait (HbAS)
Typical
patient is
asymptomatic except during
sickling episodes
Symptoms can be
Pain and swelling
Pallor of mucous membranes
Fatigue
Gradual
involvement of all
body systems
Usually fatal by middle age
from renal and pulmonary
failure
Prone to infection
Pneumonia, most common
infection
Peripheral blood smear

Sickling test
Electrophoresis of
hemoglobin
DNA testing
Skeletal x-rays
Magnetic resonance imaging
(MRI)
Alleviate
symptoms of
disease complications
Minimize end-organ damage
No specific treatment for
SCD
Patient teaching
Avoid high altitudes, maintain
fluid intake, treat infections,

control pain
O2
for hypoxia and to control

sickling
Pain management
Acute chest syndrome
Antibiotics
O2 therapy
Fluid therapy
Folic acid daily supplements

Blood transfusions in crisis
Hydroxyurea: Antisickling
agent
Erythropoietin in patients
unresponsive to hydroxyurea
Bone marrow transplant

Can cure some patients with
SCD
Excessive
production of red blood
cells
Unknown cause
Hemorrhage of distended blood
vessels
Reddish face with deepred
purplish lips, fatigue, weakness,
dizziness, headache, enlarged
spleen (splenomegaly), and
congested liver
Treatment:
Phlebotomy, antineoplastic
agents, and radiation therapy

Increased fluid intake
Secondary
polycythemia
Platelet
count less than

150,000/mm3
Immune thrombocytopenic
purpura
Heparin therapy
Safety
For
a patient with a low

platelet count, whenever a
venipuncture is performed, an
injection is administered, or an
intravenous catheter or needle
is discontinued, pressure over
the site must be maintained for
10 minutes to prevent
continuous oozing.
Etiology
Pathophysiology
Signs and symptoms
Diagnosis and treatment
Nursing management
Aspirin
must never be taken by a

patient with hemophilia as it
increases the bleeding problems.
Patients must read labels on
every
over-the-counter preparation to
be certain that it does not
contain aspirin or acetylsalicylic
acid.

Adult Nursing - Anemia

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(Relates to Chapter 31, Nursing Management:

(red blood cells [RBCs])

Diverse causes such as

lungs to systemic tissues

Not a specific disease

(Hb) levels are

Severe = Hb <6 g/dl

Severe = Hb <6 g/dl

Dietary and lifestyle changes

Common in older adults

committed to RBC production

Life span of an RBC is

erythropoiesis that decrease

Decreased hemoglobin synthesis

of the most common

Inadequate dietary intake

reticulocytes, serum iron, TIBC,

Stool guaiac test

months after the hemoglobin

the Mediterranean Sea and

Hemolysis also occurs

One thalassemic gene

Thalassemia major (contd)

specific drug or diet is

Body adapts to decreased Hb

Intrinsic factor (IF)

cells of the gastric mucosa

is required for cobalamin

RBCs appear large

adequate dietary intake

can lead to reversal of

that injuries are not

suppression of any or all

adequate blood volume and O2

need for long-term

Reduced iron stores

phagocytosis of the defective

causes the RBC to stiffen

Sickle shape in response to O 2

Peripheral blood smear

fluid intake, treat infections,

for hypoxia and to control

Folic acid daily supplements

Bone marrow transplant

production of red blood

agents, and radiation therapy

count less than

a patient with a low

must never be taken by a

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