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NUR2790 (Exam #1) > Anemia powerpoints > Flashcards

Anemia powerpoints Flashcards

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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25
Q

Thalassemia Etiology

A
  • Problem with globulin protein
  • Abnormal Hgb synthesis
  • Hemolysis also occurs.
  • One thalassemic gene
  • Thalassemia minor
  • Two thalassemic genes
  • Thalassemia major
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26
Q

Thalassemia Clinical Manifestations

Thalassemia minor

A
  • Asymptomatic frequently
  • Moderate anemia
  • Microcytosis
  • Hypochromia
  • Body adapts to reduction of Hgb – thus no treatment is indicated.
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27
Q

Thalassemia Clinical Manifestations

Thalassemia major

A
  • Life-threatening
  • Physical & mental growth often retarded
  • Pale & jaundiced
  • Splenomegaly, hepatomegaly, & cardiomyopathy
  • Symptoms develop in childhood
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28
Q

Thalassemia Clinical Manifestations

Thalassemia major

A
  • 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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29
Q

Thalassemia Collaborative Care

A
  • 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
30
Q

Megaloblastic Anemias

A
  • Group of disorders
  • Caused by impaired DNA synthesis
  • Presence of megaloblasts
  • Majority result from deficiency in
  • Cobalamin (vitamin B12)
  • Folic acid
31
Q

Megaloblastic Anemia Nursing & Collaborative Management

A
  • 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
32
Q

Megaloblastic Anemia Cobalamin Deficiency

A
  • 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
Q

Cobalamin Deficiency Etiology

A
  • 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
Q

Cobalamin Deficiency Etiology

Can also occur in the following situations:

A
  • 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
Q

Cobalamin Deficiency Clinical Manifestations

A
  • 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
36
Q

Cobalamin Deficiency Collaborative Care

A
  • 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.
37
Q

Megaloblastic Anemia Folic Acid Deficiency

A
  • 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.
38
Q

Folic Acid Deficiency common causes

A
  • Dietary deficiency
  • Malabsorption syndromes
  • Drugs
  • Increased requirement
  • Alcohol abuse and anorexia
  • Loss during hemodialysis
39
Q

Folic Acid Deficiency

A
  • 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
Q

Anemia of Chronic Disease Anemia of Inflammation

-Caused by

A
  • Chronic inflammation
  • Autoimmune and infectious disorders
  • HIV, hepatitis, malaria
  • Heart failure
  • Malignant diseases
  • Bleeding episodes
41
Q

Anemia of Chronic Disease Anemia of Inflammation

-Associated with

A
  • 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
Q

Anemia of Chronic Disease

Anemia of chronic disease findings

A
  • 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
Q

Aplastic Anemia

A
  • 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
Q

Aplastic Anemia Etiology

A
  • 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
45
Q

Aplastic Anemia Clinical Manifestations

A
  • 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
46
Q

Aplastic Anemia Diagnostic Studies

A
  • 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)
47
Q

Aplastic Anemia Nursing & Collaborative Management

A
  • Identify and remove causative agent (when possible).
  • Provide supportive care until pancytopenia reverses.
  • Prevent complications from infection.
  • Prevent hemorrhage.
48
Q

Aplastic Anemia Nursing & Collaborative Management

A
  • 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.
49
Q

Anemia Caused by Blood Loss Acute and Chronic

A
  • 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.
50
Q

Acute Blood Loss

A
  • 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
51
Q

Acute Blood Loss Clinical Manifestations

A
  • 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.
52
Q

Acute Blood Loss Diagnostic Studies

A
  • 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.
53
Q

Acute Blood Loss Collaborative Care

A
  • Replacing blood volume to prevent shock
  • Identifying the source of the hemorrhage and stopping blood loss
  • Correcting RBC loss
  • Providing supplemental iron
54
Q

Acute Blood Loss Nursing & Collaborative Management

A
  • 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
55
Q

Chronic Blood Loss

  • Sources of chronic blood loss:
  • Management involves:
A 
- 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
56
Q

Hemolytic Anemia

A
  • 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.
57
Q

Hemolytic Anemia

A
  • General manifestations of anemia
  • Specific manifestations including
  • Jaundice
  • Enlargement of the spleen and liver
  • Maintenance of renal function is a major focus of treatment.
58
Q

Sickle Cell Disease (SCD)

Group of inherited, autosomal recessive disorders

A
  • 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
59
Q

Sickle Cell Disease Etiology and Pathophysiology

A
  • 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
60
Q

Sickle Cell Disease Etiology and Pathophysiology

types of SCD

A
  • Sickle cell anemia
  • Most severe
  • Homozygous for hemoglobin S (HgbSS)
  • Sickle cell thalassemia
  • Sickle cell HgbC disease
  • Sickle cell trait (HgbAS)
61
Q

Sickle Cell Disease Sickling Episodes

A
  • 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.
62
Q

Sickle Cell Disease Sickle Cell Crisis

A
  • 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.
63
Q

Sickle Cell Disease Clinical Manifestations

A
  • 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)
64
Q

Sickle Cell Disease Complications

A
  • 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
65
Q

Sickle Cell Disease Complications

Acute chest syndrome

A
  • 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
66
Q

Sickle Cell Disease Diagnostic Studies

A
  • Peripheral blood smear
  • Sickling test
  • Electrophoresis of hemoglobin
  • Skeletal x-rays
  • Magnetic resonance imaging (MRI)
  • Doppler studies
  • X-rays
67
Q

Sickle Cell Disease Nursing & Collaborative Management

- Collaborative care is directed toward

A
  • 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
68
Q

Sickle Cell Disease Nursing & Collaborative Management

- Hospitalized patients in sickle cell crisis

A
  • 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
69
Q

Sickle Cell Disease Nursing & Collaborative Management

  • Under-treatment is a major problem.
  • Pain management
A
  • Often pain medication tolerant
  • Require continuous & breakthrough analgesia with morphine & hydromorphone
  • Multimodal & interdisciplinary approach involving emotional & adjunctive measure
70
Q

Sickle Cell Disease Nursing & Collaborative Management

A
  • 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.
71
Q

Sickle Cell Disease Nursing & Collaborative Management

- Patient and caregiver teaching and support are important.

A
  • How to avoid crises
  • Importance of prompt medical attention
  • Pain control
  • Resources for care and support
  • Therapy
  • Counseling & support groups

NUR2790 (Exam #1) (17 decks)

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