ANEMIA, MEGALOBLASTIC ANEMIA, B12 DEFICIENCY, FOLIC ACID DEFICIENCY, ANEMIA OF CHRONIC DISEASE , APLASTIC ANEMIA, ACUTE /CHRONIC BLOOD LOSS, SICKLE CELL DISEASE Zoya Minasyan, RN- MSN-Edu
Dec 24, 2015
ANEMIA, MEGALOBLASTIC ANEMIA, B12 DEFICIENCY, FOLIC ACID DEFICIENCY,
ANEMIA OF CHRONIC DISEASE , APLASTIC ANEMIA, ACUTE /CHRONIC BLOOD LOSS, SICKLE CELL DISEASE
Zoya Minasyan, RN-MSN-Edu
Anemia
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
Causes of Anemia; GI
Anemia
RBC function Transport oxygen (O2) from lungs to systemic
tissues Carry carbon dioxide from the tissues to the
lungs
Anemia
Classified as Morphologic
Cellular characteristics (erythrocyte size and color )
Descriptive, objective laboratory information Etiologic
Underlying cause (clinical conditions)
Anemia: Clinical Manifestations
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.
Anemia: Manifestations Pallor
↓ Hemoglobin ↓ Blood flow to the skin
Jaundice ↑ Concentration of serum bilirubin Pruritus (Itching) ↑ 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
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Megaloblastic Anemias
Group of disorders caused by impaired DNA synthesis
Characterized by the presence of large RBCs (megaloblasts) Easily destroyed because of fragile cell
membrane Majority result from deficiency in
Cobalamin (vitamin B12) Folic acid
Megaloblastic Anemias
Classification Cobalamin (vitamin B12) deficiency Folic acid deficiency Drug-induced suppression of DNA synthesis Inborn errors Erythroleukemia
Cobalamin Deficiency 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 Gastrectomy Nutritional deficiencies Chronic alcoholism Hereditary enzymatic defects
Cobalamin Deficiency: Etiology
GI surgery Chronic diseases of the GI tract Long-term users of H2-histamine
receptor blockers Absence of IF
Cobalamin Deficiency Clinical Manifestations
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
Cobalamin Deficiency: Collaborative Care
Parenteral or intra-nasal administration of cobalamin
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 long-standing neuromuscular complications, they may not be reversible.
Cobalamin Deficiency: Nursing Management
Early detection and treatment.
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.
Folic Acid Deficiency
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
Folic Acid Deficiency
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.
Anemia of Chronic Disease
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 of Chronic Disease
Treating underlying cause. Rarely blood transfusions. Erythropoietin therapy
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.
Aplastic Anemia
Pancytopenia Decrease in all blood cell types
RBCs White blood cells (WBCs) Platelets
Hypocellular bone marrow Types
Congenital Chromosomal alterations
Acquired Results from exposure to ionizing radiation,
chemical agents, viral and bacterial infections
Aplastic Anemia: Clinical Manifestations
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) 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.
Treatment options Hematopoietic stem cell transplantation Immunosuppressive therapy
Acute Blood Loss
Result of sudden hemorrhage Trauma Complications of surgery Disrupted vascular integrity
Concerns Hypovolemic shock Reduced plasma volume
Diminished O2 because fewer RBCs are available
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Acute Blood LossClinical Manifestations
Cause Body’s attempt to maintain adequate blood
volume and O2
Pain Internal hemorrhage Tissue distention, organ displacement, nerve
compression Retroperitoneal bleeding
Numbness Pain in the lower extremities
Shock is the major complication22
Acute Blood LossCollaborative Care
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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Acute Blood LossNursing Management
May be impossible to prevent if caused by trauma
Postoperative patients Monitor blood loss.
No need for long-term treatment
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Chronic Blood Loss
Reduced iron stores Bleeding ulcer Hemorrhoids Menstrual and postmenopausal blood loss
Management Identify source. Stop bleeding. Use supplemental iron if needed.
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Hemolytic Anemia
Destruction or hemolysis of RBCs at a rate that exceeds production
Intrinsic hemolytic anemia Abnormal hemoglobin Enzyme deficiencies RBC membrane abnormalities
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Hemolytic Anemia
Extrinsic hemolytic anemia More common than intrinsic Acquired
Sites of hemolysis Intravascular Extravascular
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Sequences of Events in Hemolysis
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Hemolytic Anemia
Jaundice Destroyed RBCs cause increased bilirubin.
Enlarged spleen and liver Hyperactive with macrophage phagocytosis of
defective RBCs Accumulation of hemoglobin molecules
can obstruct renal tubules. Tubular necrosis
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Sickle Cell Disease (SCD)
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 ↓ O2 levels Substitution of valine for glutamic acid on the β-
globin chain of hemoglobin Genetic disorder Incurable disease, often fatal
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Sickle Cell Hemoglobin Aggregates and Alters Shape of RBC
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Sickle Cell DiseaseClinical Manifestations
Typical patient is asymptomatic, except during sickling episodes.
Symptoms may include Pain and swelling Pallor of mucous membranes Jaundice
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Clinical Manifestations of Sickle Cell Disease
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Sickle Cell Disease: Complications
Gradual involvement of all body systems Usually fatal by middle age from renal
and pulmonary failure Prone to infection
Pneumonia, most common infection Acute chest syndrome
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Sickle Cell Disease: Diagnostic Studies
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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Sickle Cell Disease: Nursing Management
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
Antibiotics O2 therapy Fluid therapy Transfusions, if needed
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Sickle Cell Disease: Nursing Management
Blood transfusions in crisis Hydroxyurea: Antisickling agent
Erythropoietin in patients unresponsive to hydroxyurea
Hematopoietic stem cell transplant Can cure some patients with SCD
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Acquired Hemolytic Anemia
Three extrinsic categories1. Physical factors
Physical destruction of RBCs results from extreme force on the cells.Hemodialysis, prosthetic heart valves
2. Immune reactions Antigen-antibody reactions destroy RBCs. Isoimmune reactions
Antibodies develop against antigens; blood transfusions
Autoimmune reactionsDevelop antibodies against their own RBCs
3. Infectious agents and toxins Foster hemolysis in four ways
Invading RBCs and destroying contents Releasing hemolysis substances Generating an antigen-antibody reaction Contributing to splenomegaly 38
Blood cell Disorders: Hemochromatosis
Iron overload disorder 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.
Problem with Hemostasis
Involves the vascular endothelium, platelets, and coagulation factors, which helps to stop hemorrhage and repair vascular injury.
Three major disorders Thrombocytopenia (low platelet count) Hemophilia (disorder of clotting factors) Disseminated intravascular coagulation (DIC)
Thrombocytopenia
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)
Hemophilia
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
Disseminated intravascular coagulation (DIC)
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.