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
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.
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
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
5
Q
Used to determine the severity of anemia
A
Hemoglobin (Hgb) levels
6
Q
Anemia Nursing Assessment
-Subjective data
A
- Important health information
- Past health history
- Medications
- Surgery or other treatments
- Dietary history
- Functional health patterns
7
Q
Anemia Nursing Assessment
-Objective data
A
- General
- Integumentary
- Respiratory
- Cardiovascular
- Gastrointestinal
- Neurologic
- Diagnostic findings
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
9
Q
Iron supplements cause stools to darken
A
.
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.
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
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.
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.
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.
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
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
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
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
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 ???
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
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
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
23
Q
Thalassemia Etiology
A
- A group of diseases involving inadequate production of normal hemoglobin
- Therefore decreased erythrocyte production
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
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
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.
27
Q
Thalassemia Clinical Manifestations
Thalassemia major
A
- Life-threatening
- Physical & mental growth often retarded
- Pale & jaundiced
- Splenomegaly, hepatomegaly, & cardiomyopathy
- Symptoms develop in childhood
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
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
