Transcript Focus on Anemia

Zoya Minasyan, RN-MSNEdu
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A deficiency in the
Number of erythrocytes
(red blood cells [RBCs])
 Quantity of hemoglobin
 Volume of packed RBCs (hematocrit)
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Diverse causes such as
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Blood loss
Impaired production of erythrocytes
Increased destruction of erythrocytes
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RBC function
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Transport oxygen (O2) from lungs to systemic tissues
Carry carbon dioxide from the tissues to the lungs
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Classified as
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Morphologic
 Cellular characteristics (erythrocyte size and color )
 Descriptive, objective laboratory information
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Etiologic
 Underlying cause (clinical conditions)
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Caused by the body’s response to tissue hypoxia
Hemoglobin (Hb) levels are used to determine
the severity of anemia.
•Mild states of anemia (Hb 10 to 14 g/dL) may exist
without causing symptoms. Symptoms include
palpitations, dyspnea, and mild fatigue.
•In cases of moderate anemia (Hb 6 to 10 g/dL),
cardiopulmonary symptoms are increased and the
patient may experience them while resting, as well as
with activity.
•The patient with severe anemia (Hb less than 6 g/dL)
has many clinical manifestations involving multiple
body systems.
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Pallor
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↓ Hemoglobin
↓ Blood flow to the skin
Jaundice
↑ Concentration of serum bilirubin
 Pruritus (Itching)
 ↑ Serum and skin bile salt concentrations
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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
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Group of disorders caused by impaired DNA
synthesis
Characterized by the presence of large RBCs
(megaloblasts)
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Easily destroyed because of fragile cell membrane
Majority result from deficiency in
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Cobalamin (vitamin B12)
Folic acid
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Classification
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Cobalamin (vitamin B12) deficiency
Folic acid deficiency
Drug-induced suppression of DNA synthesis
Inborn errors
Erythroleukemia
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Intrinsic factor (IF)
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Protein secreted by the parietal cells of the gastric
mucosa
IF is required for cobalamin absorption in the
small intestine.
Causes
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Pernicious anemia
Gastrectomy
Nutritional deficiencies
Chronic alcoholism
Hereditary enzymatic defects
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GI surgery
Chronic diseases of the GI tract
Long-term users of H2-histamine receptor
blockers
Absence of IF
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 (lack of muscle coordination)
 Muscle weakness
 Impaired thought processes
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Parenteral or intra-nasal administration of cobalamin
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Important to emphasize adequate dietary intake
•
The dosage and frequency of cobalamin administration
may vary. A typical treatment schedule consists of 1000
mg of cobalamin IM daily for 2 weeks and then weekly
until the hematocrit is normal, then monthly for life.
•
High-dose oral cobalamin and sublingual cobalamin are
also available for those in whom GI absorption is intact.
•
As long as supplemental cobalamin is used, the anemia
can be reversed. However, if the person has had longstanding neuromuscular complications, they may not be
reversible.
Early detection and treatment.
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Ensure that injuries are not sustained
because of the patient’s diminished
sensation to heat and pain.
Compliance with treatment.
Evaluate patient for gastric carcinoma.
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Also a cause of megaloblastic anemia
Folic acid is required for DNA synthesis.
RBC formation and maturation
Common causes
Dietary deficiency
 Malabsorption syndromes
 Drugs
 Increased requirement
 Alcohol abuse and anorexia
 Loss during hemodialysis
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Clinical manifestations are similar to those of
cobalamine deficiency.
Absence of neurologic problems
Treated by replacement therapy
Encourage patient to eat foods with large
amounts of folic acid.
•GI disturbances include dyspepsia (upset stomach or
indigestion) and a smooth, beefy red tongue.
•During
diagnostic studies, the serum folate level is
low (normal is 3 to 25 mg/mL)
•Replacement therapy: The usual dose is 1 mg per
day by mouth. In malabsorption states, up to 5 mg
per day may be required.
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Underproduction of RBCs
Mild shortening of RBC survival
Causes
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End-stage renal disease
 Primary factor: ↓ Erythropoietin
Chronic liver disease
 Chronic inflammation
 Malignant tumors
 Chronic endocrine diseases
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Treating underlying cause.
Rarely blood transfusions.
Erythropoietin therapy
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Erythropoietin therapy (Epogen, Darbepoetin) is
used for anemia related to renal disease and may be
used for anemia related to cancer and its therapies.
However, it is used conservatively because the risk
of thromboembolism and mortality is increased in
some patients.
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Pancytopenia
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Decrease in all blood cell types
 RBCs
 White blood cells (WBCs)
 Platelets
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Hypocellular bone marrow
Types
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Congenital
 Chromosomal alterations
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Acquired
 Results from exposure to ionizing radiation, chemical agents,
viral and bacterial infections
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Abrupt or gradual development
Symptoms caused by suppression of any or all
bone marrow elements
General manifestations of anemia
Fatigue, dyspnea
 Cardiovascular and cerebral responses
 Neutropenia-low neutrophil count (WBC, fighting
disease)
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 The patient with neutropenia is susceptible to infection and
is at risk for septic shock and death. Even a low-grade
temperature (>100.4o F) should be considered a medical
emergency.
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Treatment options
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Hematopoietic stem cell transplantation
Immunosuppressive therapy
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Result of sudden hemorrhage
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Trauma
Complications of surgery
Disrupted vascular integrity
Concerns
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Hypovolemic shock
Reduced plasma volume
 Diminished O2 because fewer RBCs are available
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Cause
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Body’s attempt to maintain adequate blood volume
and O2
Pain
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Internal hemorrhage
Tissue distention, organ displacement, nerve
compression
Retroperitoneal bleeding
 Numbness
 Pain in the lower extremities
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Shock is the major complication
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Replacing blood volume to prevent shock
Identifying the source of the hemorrhage
Stopping blood loss
Correcting RBC loss
Providing supplemental iron
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May be impossible to prevent if caused by
trauma
Postoperative patients
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Monitor blood loss.
No need for long-term treatment
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Reduced iron stores
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Bleeding ulcer
Hemorrhoids
Menstrual and postmenopausal blood loss
Management
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Identify source.
Stop bleeding.
Use supplemental iron if needed.
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Destruction or hemolysis of RBCs at a rate that
exceeds production
Intrinsic hemolytic anemia
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Abnormal hemoglobin
Enzyme deficiencies
RBC membrane abnormalities
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Extrinsic hemolytic anemia
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More common than intrinsic
Acquired
Sites of hemolysis
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Intravascular
Extravascular
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Jaundice
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Enlarged spleen and liver
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Destroyed RBCs cause increased bilirubin.
Hyperactive with macrophage phagocytosis of
defective RBCs
Accumulation of hemoglobin molecules can
obstruct renal tubules.
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Tubular necrosis
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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.
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Sickle shape in response to ↓ O2 levels
Substitution of valine for glutamic acid on the βglobin chain of hemoglobin
Genetic disorder
Incurable disease, often fatal
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Typical patient is asymptomatic, except during
sickling episodes.
Symptoms may include
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Pain and swelling
Pallor of mucous membranes
Jaundice
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Gradual involvement of all body systems
Usually fatal by middle age from renal and
pulmonary failure
Prone to infection
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Pneumonia, most common infection
Acute chest syndrome
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Peripheral blood smear
Sickling test
Electrophoresis of hemoglobin(the movement
of charged particles when an electric field is
applied to them)
Skeletal x-rays
Magnetic resonance imaging (MRI)
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Alleviate symptoms of disease complications.
Minimize end target-organ damage.
Avoid high altitudes, maintain fluid intake,
treat infections, help with pain control.
O2 for hypoxia and to control sickling
Pain management
Acute chest syndrome
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Antibiotics
O2 therapy
Fluid therapy
Transfusions, if needed
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Blood transfusions in crisis
Hydroxyurea: Antisickling agent
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Erythropoietin in patients unresponsive to
hydroxyurea
Hematopoietic stem cell transplant
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Can cure some patients with SCD
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Three extrinsic categories
Physical factors
1.
Physical destruction of RBCs results from extreme force
on the cells.
Hemodialysis, prosthetic heart valves
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Immune reactions
2.
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Antigen-antibody reactions destroy RBCs.
Isoimmune reactions
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Autoimmune reactions
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Antibodies develop against antigens; blood
transfusions
Develop antibodies against their own RBCs
Infectious agents and toxins
3.
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Foster hemolysis in four ways
Invading RBCs and destroying contents
Releasing hemolysis substances
Generating an antigen-antibody reaction
Contributing to splenomegaly
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Iron overload disorder
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Increased intestinal iron absorption and increased tissue
iron deposition
Autosomal recessive, C282Y and H63D
Early symptoms-fatigue, abdominal pain, weight
loss.
Later symptoms-liver enlargement, cirrhosis, skin
pigment change (bronzing), cardio-myopathy,
arthritis, testicular atrophy.
Treatment- to remove excess iron from the
body(remove 500ml blood each week for 2-3 years
until iron stores are normal in body)
Avoid vitamin C and iron supplements, uncooked
seafood.
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Involves the vascular endothelium, platelets,
and coagulation factors, which helps to stop
hemorrhage and repair vascular injury.
Three major disorders
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Thrombocytopenia (low platelet count)
Hemophilia (disorder of clotting factors)
Disseminated intravascular coagulation (DIC)
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Reduction of platelets
Prolonged bleeding from minor trauma
Nursing
Monitor for s/s of bleeding
 Monitor for PT, PTT, fibrinogen, platelets count
 Avoid injections (IV, IM, SubQ) to prevent bleeding
 Protect from trauma,
 Administer blood products
 Stop anticoagulants
 Avoid high impact activity (aerobics, contact sports)
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X-linked recessive genetic disorder
Deficient coagulation factor
Hemophilia A caused by Factor VIII deficiency
Hemophilia B factor IX deficiency
Complications related to prolonged bleeding,
uncontrolled hemorrhage after dental
extractions, GI bleeding from gastritis or ulcers,
ecchymosis or hematomas; pain, paralysis from
compression of nerves
Replacement of clotting factors
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Decrease in clotting factor and platelets, which
may lead to hemorrhage.
Is always caused by and underlining disease or
condition. The underlining cause must be
treated for the DIC to resolve.
Assess for petechiae, oozing at IV site, internal
bleeding, heart rate, increasing in abd girth,
change in mental status, pain, decrease in urine
output.
Administer blood product.