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Anemia powerpoints Flashcards

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1
Q

Anemia

  • Not a specific disease
  • Manifestation of a pathologic process
  • Classified by laboratory review of?
A
  • Classified by laboratory review of
  • Complete blood count (CBC)
  • Reticulocyte count
  • Peripheral blood smear
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2
Q

Anemia Clinical Manifestations

A
  • Caused by the body’s response to tissue hypoxia
  • Manifestations vary based on rate of development, severity of anemia, presence of co-existing disease.
  • Hemoglobin (Hgb) levels are used to determine the severity of anemia.
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3
Q

Anemia Integumentary Manifestations

A 
- Pallor
↓ Hemoglobin 
↓ Blood flow to the skin
- Jaundice
↑ Concentration of serum bilirubin
- Pruritus 
↑ Serum and skin bile salt concentrations
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4
Q

Anemia Cardiopulmonary Manifestations

A
  • Result from additional attempts by 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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5
Q

Used to determine the severity of anemia

A

Hemoglobin (Hgb) levels

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6
Q

Anemia Nursing Assessment

-Subjective data

A
  • Important health information
    • Past health history
    • Medications
    • Surgery or other treatments
    • Dietary history
  • Functional health patterns
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7
Q

Anemia Nursing Assessment

-Objective data

A
  • General
    • Integumentary
    • Respiratory
    • Cardiovascular
    • Gastrointestinal
    • Neurologic
    • Diagnostic findings
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8
Q

Anemia Nursing Diagnoses

A
  • Fatigue
  • Imbalanced nutrition: Less than body requirements
  • Ineffective self-health management
    • Assume normal activities of daily living
    • Maintain adequate nutrition
    • Develop no complications related to anemia
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9
Q

Iron supplements cause stools to darken

A

.

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10
Q

Anemia Gerontologic Considerations

A
  • Common in older adults
  • Chronic disease
  • Nutritional deficiencies
  • Signs and symptoms may go unrecognized or may be mistaken for normal aging changes.
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11
Q

Anemia Decreased Erythrocyte Production

A
  • 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
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12
Q

Erythrocyte Production

A
  • Life span of an RBC is 120 days.
  • Three alterations in erythropoiesis may decrease RBC production:
    1) Decreased hemoglobin synthesis
    2) Defective DNA synthesis in RBCs
    3) Diminished availability of erythrocyte precursors.
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13
Q

Iron-Deficiency Anemia

A
  • 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 body’s iron.
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14
Q

Iron-Deficiency Anemia Etiology

A
  • Inadequate dietary intake
  • 5% to 10% of ingested iron is absorbed.
  • Malabsorption
  • Iron absorption occurs in the duodenum.
  • Diseases or surgery that alter, destroy, or remove the absorption surface of this area of the intestine cause anemia.
  • Blood loss
  • 2 mL whole blood contain 1 mg iron.
  • Major cause of iron deficiency in adults
  • Chronic blood loss most commonly through GI and GU systems
  • Hemolysis
  • Pregnancy contributes to this condition.
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15
Q

Iron-Deficiency Anemia Clinical Manifestations

A
  • General manifestations of anemia
  • Pallor is the most common finding.
  • Glossitis is the second most common.
  • Inflammation of the tongue
  • Cheilitis
  • Inflammation of the lips
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16
Q

Iron-Deficiency Anemia Diagnostic Studies

A
  • Laboratory findings
  • Hgb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets
  • Stool guaiac test
  • Endoscopy
  • Colonoscopy
  • Bone marrow biopsy
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17
Q

Iron-Deficiency Anemia Collaborative Care

A
  • Goal is to treat the underlying disease causing reduced intake or absorption of iron.
  • Efforts are aimed at replacing iron.
  • Nutritional therapy
  • Oral or occasional parenteral iron supplements
  • Transfusion of packed RBCs
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18
Q

Iron-Deficiency Anemia Drug Therapy

A
  • Oral iron
    • Inexpensive
    • Convenient
    • Factors to consider
      • Enteric-coated or sustained-release capsules are counterproductive.
      • Daily dose is 150 to 200 mg
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19
Q

Iron-Deficiency Anemia Drug Therapy
Oral iron
Factors to consider

A
  • Best absorbed as ferrous sulfate in an acidic environment
  • Liquid iron should be diluted and ingested through a straw.
  • Side effects
  • Heartburn, constipation, diarrhea

Teaching Opportunity ???

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20
Q

Iron-Deficiency Anemia Drug Therapy

Parenteral iron

A
  • Indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance
  • Can be given IM or IV
  • IM may stain skin
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21
Q

Iron-Deficiency Anemia Nursing & Collaborative Management
-At risk groups

A
  • Premenopausal women
  • Pregnant women
  • Persons from low socioeconomic backgrounds
  • Older adults
  • Individuals experiencing blood loss
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22
Q

Iron-Deficiency Anemia Nursing & Collaborative Management

A
  • Diet teaching
  • Supplemental iron
  • Discuss diagnostic studies.
  • Emphasize compliance.
  • Iron therapy for 2 to 3 months after hemoglobin levels return to normal
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23
Q

Thalassemia Etiology

A
  • A group of diseases involving inadequate production of normal hemoglobin
  • Therefore decreased erythrocyte production
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24
Q

Thalassemia Etiology

A

Common in ethnic groups near the Mediterranean Sea and in equatorial or near-equatorial regions of Asia, Middle East, and Africa

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Thalassemia Etiology
- Problem with globulin protein * Abnormal Hgb synthesis - Hemolysis also occurs. - One thalassemic gene * Thalassemia minor - Two thalassemic genes * Thalassemia major
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Thalassemia Clinical Manifestations | Thalassemia minor
- Asymptomatic frequently - Moderate anemia * Microcytosis * Hypochromia - Body adapts to reduction of Hgb – thus no treatment is indicated.
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Thalassemia Clinical Manifestations | Thalassemia major
- Life-threatening - Physical & mental growth often retarded - Pale & jaundiced - Splenomegaly, hepatomegaly, & cardiomyopathy - Symptoms develop in childhood
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Thalassemia Clinical Manifestations | Thalassemia major
- As the bone marrow responds to the deficit of O2-carrying capacity of the blood, RBC production is stimulated, & marrow becomes packed with immature erythroid precursors that die. - Chronic bone marrow hyperplasia - Hepatitis C
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Thalassemia Collaborative Care
- No specific drug or diet is effective in treating thalassemia. - Thalassemia major * Blood transfusions or exchange transfusions with chelating agents that bind to iron to reduce iron overloading * Splenectomy
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Megaloblastic Anemias
- Group of disorders * Caused by impaired DNA synthesis * Presence of megaloblasts - Majority result from deficiency in * Cobalamin (vitamin B12) * Folic acid
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Megaloblastic Anemia Nursing & Collaborative Management
- Early detection and treatment - Ensure safety - Diminished sensations to heat and pain from neurologic impairment - Focus on compliance with treatment - Regular screening for gastric cancer
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Megaloblastic Anemia Cobalamin Deficiency
- Intrinsic factor (IF) * Protein secreted by the parietal cells of the gastric mucosa - IF is required for cobalamin absorption in the distal ileum. * If IF is not secreted, cobalamin will not be absorbed.
33
Cobalamin Deficiency Etiology
- Most commonly caused by pernicious anemia * Which is caused by an absence of IF * Insidious onset * Begins in middle age or later * Predominant in Scandinavians and African Americans
34
Cobalamin Deficiency Etiology | Can also occur in the following situations:
- GI surgery - Chronic diseases of the GI tract - Chronic alcoholics - Long-term users of H2-histamine receptor blockers and proton pump inhibitors - Strict vegetarians
35
Cobalamin Deficiency Clinical Manifestations
- General manifestations of anemia develop slowly due to tissue hypoxia. - Gastrointestinal manifestations: * Sore tongue, anorexia, nausea, vomiting, & abdominal pain - Neuromuscular manifestations: * Weakness, paresthesias of feet & hands, ↓ vibratory and position senses, ataxia, muscle weakness, and impaired thought processes
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Cobalamin Deficiency Collaborative Care
- Parenteral or intranasal administration of cobalamin is the treatment of choice. - Patients will die in 1-3 years without treatment. - This anemia can be reversed with ongoing treatment but long-standing neuromuscular complications may not be reversible.
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Megaloblastic Anemia Folic Acid Deficiency
- Also a cause of megaloblastic anemia - Folic acid is required for DNA synthesis. * RBC formation and maturation - Clinical manifestations are similar to those of cobalamin deficiency, but absence of neurologic problems differentiates them.
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Folic Acid Deficiency common causes
- Dietary deficiency - Malabsorption syndromes - Drugs - Increased requirement - Alcohol abuse and anorexia - Loss during hemodialysis
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Folic Acid Deficiency
- Serum folate level is low. * Normal is 3 to 25 mg/mL (7 to 57 mol/L). - Serum cobalamin level is normal. - Treated by replacement therapy * Usual dose is 1 mg per day by mouth. - Encourage patient to eat foods with large amounts of folic acid.
40
Anemia of Chronic Disease Anemia of Inflammation | -Caused by
- Chronic inflammation - Autoimmune and infectious disorders - HIV, hepatitis, malaria - Heart failure - Malignant diseases - Bleeding episodes
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Anemia of Chronic Disease Anemia of Inflammation | -Associated with
- Underproduction of RBCs - Mild shortening of RBC survival * Normocytic, normochromic, and hypoproliferative RBCs - Usually a mild anemia but can become severe if the underlying disorder is untreated
42
Anemia of Chronic Disease | Anemia of chronic disease findings
- Anemia of chronic disease findings * ↑ Serum ferritin * ↑ Iron stores * Normal folate and cobalamin levels - Treating underlying cause is best. * Rarely blood transfusions * Conservative use of erythropoietin therapy
43
Aplastic Anemia
- Pancytopenia * Decrease in all blood cell types - Red blood cells (RBCs) - White blood cells (WBCs) - Platelets - Hypocellular bone marrow - Ranges from chronic to critical
44
Aplastic Anemia Etiology
- Low incidence * Affecting 2 of every 1 million persons - 2 Major Types * Congenital: Chromosomal alterations * Acquired: Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections
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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
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Aplastic Anemia Diagnostic Studies
- Diagnosis confirmed by laboratory studies * Low Hgb, WBC, and platelet values * Low reticulocyte count * Prolonged bleeding time * Elevated serum iron and TIBC * Hypocellular bone marrow with increased fat content (yellow marrow)
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Aplastic Anemia Nursing & Collaborative Management
- Identify and remove causative agent (when possible). - Provide supportive care until pancytopenia reverses. - Prevent complications from infection. - Prevent hemorrhage.
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Aplastic Anemia Nursing & Collaborative Management
- Prognosis of severe untreated aplastic anemia is poor. * Median survival is 3 to 6 months. * 20% survive longer than 1 year. - Treatment options * Immune therapies and bone marrow transplantation can be curative.
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Anemia Caused by Blood Loss Acute and Chronic
- Anemia resulting from blood loss may be caused by either acute or chronic problems. - Acute blood loss occurs as a result of sudden hemorrhage. - The sources of chronic blood loss are similar to those of iron-deficiency anemia.
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Acute Blood Loss
- Causes of sudden hemorrhage * Trauma - Complications of surgery - Conditions or diseases that disrupt vascular integrity * Hypovolemic shock * Compensatory increased plasma volume with diminished O2-carrying RBCs
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Acute Blood Loss Clinical Manifestations
- Caused by the body’s attempts to maintain adequate blood volume and meet oxygen requirements - Clinical signs and symptoms are more important than laboratory values. - Pain * Internal hemorrhage: Tissue distention, organ displacement, nerve compression * Retroperitoneal bleeding: Numbness, Pain in the lower extremities - Shock is the major complication.
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Acute Blood Loss Diagnostic Studies
- With sudden blood volume loss, values may seem normal or high for 2 to 3 days. - Once the plasma volume is replaced, low RBC concentrations become evident. - Low RBC, Hgb, and Hct levels show up and reflect actual blood loss.
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Acute Blood Loss Collaborative Care
- Replacing blood volume to prevent shock - Identifying the source of the hemorrhage and stopping blood loss - Correcting RBC loss - Providing supplemental iron
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Acute Blood Loss Nursing & Collaborative Management
- May be impossible to prevent if caused by trauma - Postoperative patients * Monitor blood loss. * Administer blood products for anemia. - No need for long-term treatment
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Chronic Blood Loss - Sources of chronic blood loss: - Management involves:
``` - Sources of chronic blood loss: Bleeding ulcer Hemorrhoids Menstrual and postmenopausal blood loss - Management involves Identifying the source Stopping the bleeding Providing supplemental iron as needed ```
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Hemolytic Anemia
- Destruction or hemolysis of RBCs at a rate that exceeds production - Caused by problems intrinsic or extrinsic to the RBCs * Intrinsic forms are usually hereditary and result from defects in RBCs themselves. * RBCs are normal in acquired forms which are more common; damage is caused by external factors.
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Hemolytic Anemia
- General manifestations of anemia - Specific manifestations including * Jaundice * Enlargement of the spleen and liver - Maintenance of renal function is a major focus of treatment.
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Sickle Cell Disease (SCD) | Group of inherited, autosomal recessive disorders
- Characterized by the presence of an abnormal form of Hgb in the RBC - Genetic disorder usually identified in infancy or early childhood - Incurable and often fatal - Predominant in African Americans
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Sickle Cell Disease Etiology and Pathophysiology
- Abnormal hemoglobin, HgbS, causes the RBC to stiffen and elongate. - Erythrocytes take on a sickle shape in response to ↓ O2 levels. - Substitution of valine for glutamic acid on the β-globin chain of hemoglobin
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Sickle Cell Disease Etiology and Pathophysiology | types of SCD
- Sickle cell anemia * Most severe * Homozygous for hemoglobin S (HgbSS) - Sickle cell thalassemia - Sickle cell HgbC disease - Sickle cell trait (HgbAS)
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Sickle Cell Disease Sickling Episodes
- The major pathophysiologic event of this disease - Triggered by low O2 tension in the blood - Infection is the most common precipitating factor. - Initially, sickling is reversible with re-oxygenation.
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Sickle Cell Disease Sickle Cell Crisis
- Severe, painful, acute exacerbation of sickling causes a vaso-occlusive crisis. - Severe capillary hypoxia eventually leads to tissue necrosis. - Life-threatening shock is a result of severe O2 depletion of the tissues and a reduction of the circulating fluid volume.
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Sickle Cell Disease Clinical Manifestations
- Typical patient is asymptomatic except during sickling episodes. - Symptoms may include * Pain from tissue hypoxia and damage * Pallor of mucous membranes * Jaundice from hemolysis * Prone to gallstones (cholelithiasis)
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Sickle Cell Disease Complications
- Infection is a major cause of morbidity and mortality. - The function of the spleen becomes compromised from sickled RBCs. - Autosplenectomy is a result of scarring. - Pneumococcal pneumonia most common - Severe infections can cause aplastic crisis. - Can lead to shutdown of RBC production
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Sickle Cell Disease Complications | Acute chest syndrome
- Pulmonary complications that include pneumonia, tissue infarction, and fat embolism - Characterized by fever, chest pain, cough, pulmonary infiltrates, and dyspnea - Leads to multiple serious complications
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Sickle Cell Disease Diagnostic Studies
- Peripheral blood smear - Sickling test - Electrophoresis of hemoglobin - Skeletal x-rays - Magnetic resonance imaging (MRI) - Doppler studies - X-rays
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Sickle Cell Disease Nursing & Collaborative Management | - Collaborative care is directed toward
- Alleviating symptoms and complications - Minimizing end-organ damage - Promptly treating serious sequelae - Teach patients to * Avoid high altitudes * Maintain adequate fluid intake * Treat infections promptly
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Sickle Cell Disease Nursing & Collaborative Management | - Hospitalized patients in sickle cell crisis
- O2 for hypoxia and to control sickling - Vigilance for respiratory failure - Rest with DVT prophylaxis - Administration of fluids and electrolytes - Transfusion therapy - Chelation therapy with repeat exacerbations
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Sickle Cell Disease Nursing & Collaborative Management - Under-treatment is a major problem. - Pain management
- Often pain medication tolerant - Require continuous & breakthrough analgesia with morphine & hydromorphone - Multimodal & interdisciplinary approach involving emotional & adjunctive measure
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Sickle Cell Disease Nursing & Collaborative Management
- Treat infections. - Administer folic acid. - Hydrea is the only antisickling agent shown to be clinically beneficial. - Hematopoietic stem cell transplantation (HSCT) is the only available cure.
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Sickle Cell Disease Nursing & Collaborative Management | - Patient and caregiver teaching and support are important.
- How to avoid crises - Importance of prompt medical attention - Pain control - Resources for care and support * Therapy * Counseling & support groups
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