Anemia Flashcards
1
Q
What is Anemia
A
A deficiency in the
Number of erythrocytes (RBCs)
Quantity of hemoglobin
Volume of packed RBCs (hematocrit)
Not a specific disease
Manifestation of a pathologic process
2
Q
Causes of Anemia
A
3
Q
RBC function
A
Transport oxygen (O2) from lungs to systemic tissues Carry carbon dioxide from the tissues to the lungs
4
Q
How is Anemia Classified by
A
laboratory review of
Complete blood count (CBC)
Reticulocyte count
Peripheral blood smear
5
Q
Anemia Clinical Manifestations
Caused by the body’s response to tissue hypoxia
A
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.
6
Q
Anemia Integumentary Manifestations
A
Pallor-Pale
Jaundice
Pruritus
7
Q
Causes of Pallor
A
↓ Hemoglobin
↓ Blood flow to the skin
8
Q
Causes of Jaundice
A
↑ Concentration of serum bilirubin
9
Q
Causes of Pruritus
A
↑ Serum and skin bile salt concentrations
10
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
11
Q
Anemia Nursing Assessment Subjective Data
A
Important health information
Past health history
Medications
Surgery or other treatments
Dietary history
Functional health patterns
12
Q
Anemia Nursing Assessment Objective Data assessment
A
General
Integumentary
Respiratory
Cardiovascular
Gastrointestinal-bleed
Neurologic-AMS
Diagnostic findings
13
Q
Anemia Nursing Diagnoses
A
Fatigue-Not enough oxygen
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
14
Q
Anemia Decreased Erythrocyte Production
A
Erythropoietin (EPO) is a glycoprotein primarily produced in the kidneys (10% in the liver).- Stimulates production of RBC’s in the bonemarrow
15
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.
16
Q
Iron-Deficiency Anemia Etiology
A
Inadequate dietary intake
5% to 10% of ingested iron is absorbed.
Malabsorption
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
Hemodialysis
Pregnancy contributes to this condition.Why?
black stool
17
Q
How much blood does it take to make stool black?
A
50-75 mL blood loss
18
Q
Iron-Deficiency Anemia Clinical Manifestations
A
General manifestations of anemia
Pallor is the most common finding.
Glossitis is the second most common.
Cheilitis
19
Q
What is glossitis
A
Inflammation of the tongue- Low level of iron=low myoglobin. Important for muscle.
20
Q
What is Cheilitis
A
Inflammation of the lips
21
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
22
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
23
Q
How to do replace iron
A
Nutritional therapy
Oral or occasional parenteral iron supplements
Transfusion of packed RBCs-Hg below 7 or symptomatic, sickle cell
Iron rich foods: Leafy/whole greans, apples, lettuce, eggs, also look in book
24
Q
Iron-Deficiency Anemia Drug Therapy Oral Iron
A
Ferrous Sulfate- Give 1 hour before meals because it absorbs better
Inexpensive
Convenient
Factors to consider
Enteric-coated or sustained-release capsules are counterproductive. Not absorbed well. Absorbed best in the jejunum
Daily dose is 150 to 200 mg.
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Oral Iron Factors to be considered
***_Best absorbed as ferrous sulfate in an acidic environment
Liquid iron should be diluted and ingested through a straw. Stains your teeth_***
Side effects
Heartburn, constipation-Need stool softeners or laxatives, diarrhea, ***_black stools-expected side effect_***
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Iron-Deficiency Anemia Drug Therapy Parenteral iron
***_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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Iron-Deficiency Anemia Nursing & Collaborative Management At-risk groups
Premenopausal women
Pregnant women
Persons from low socioeconomic backgrounds
Older adults
Individuals experiencing blood loss
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Iron-Deficiency Anemia Nursing & Collaborative Management Teaching
***_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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What is Thalassemia
A group of diseases involving inadequate production of normal hemoglobin
Therefore decreased erythrocyte production
30
Thalassemia Etiology
Common in ethnic groups near the Mediterranean Sea and in equatorial or near-equatorial regions of Asia, Middle East, and Africa
Problem with globulin protein
Abnormal Hgb synthesis
Hemolysis also occurs.
One thalassemic gene
***_Thalassemia minor-Usually requires no treatment. Body adapts_***
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.
32
Thalassemia Clinical Manifestations Thalassemia major
Life-threatening
Physical & mental growth often retarded
Pale & jaundiced
Splenomegaly, hepatomegaly, & cardiomyopathy
Symptoms develop in childhood.
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
33
Thalassemia Collaborative Care
***_No specific drug or diet is effective in treating thalassemia._***
Thalassemia major
Blood transfusions or exchange transfusions
Spelenectomy
34
Megaloblastic Anemias
Group of disorders
Caused by impaired DNA synthesis
Presence of megaloblasts
Majority result from deficiency in
Cobalamin (vitamin B12)
Folic acid
35
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.
***_GI tract/ulcer can cause issues with IF sercretion_***
36
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
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Cobalamin Deficiency other 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
38
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: With Cobalamin deficency not folic acid deficiency
Weakness, paresthesias of feet & hands, ↓ vibratory and position senses, ataxia, muscle weakness, and impaired thought processes
39
Cobalamin Deficiency Diagnostic Studies
***_Macrocytic RBCs have abnormal shapes and fragile cell membranes._***
Serum cobalamin levels are decreased.
Normal serum folate levels and low cobalamin levels suggest megaloblastic anemia is due to cobalamin deficiency.
Upper GI endoscopy with biopsy of gastric mucosa
40
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._***
41
Folic Acid Deficiency
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._***
42
Folic Acid Deficiency Common Causes
Dietary deficiency
Malabsorption syndromes
Drugs
Increased requirement
Alcohol abuse and anorexia
Loss during hemodialysis
Serum folate level is low.
Serum cobalamin level is normal.
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Serum folate normal levels
3 to 25 mg/mL (7 to 57 mol/L)
44
Folic Acid Deficiency Treatment
***_Treated by replacement therapy
Usual dose is 1 mg per day by mouth._***
Encourage patient to eat foods with large amounts of folic acid.
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Megaloblastic Anemia Nursing & Collaborative Management
***_Early detection and treatment
Ensure safety_***
Focus on compliance with treatment
Regular screening for gastric cancer
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Aplastic Anemia
***_Pancytopenia_***
Hypocellular bone marrow
Ranges from chronic to critical
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What is Pancytopenia
***_Decrease in all blood cell types
Red blood cells (RBCs)
White blood cells (WBCs)
Platelets_***
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Aplastic Anemia Etiology
Low incidence
2 Major Types
Congenital
Chromosomal alterations
***_Acquired-75% are idiopathic_***
Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections
49
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-increased heart rate
***_Neutropenia –Really high risk for infection-Even low grade fever can be serious at risk for septic shock_***
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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)
51
Aplastic Anemia Nursing & Collaborative Management
Identify and remove causative agent (when possible).
Provide supportive care until pancytopenia reverses.
Prevent complications from infection.
Prevent hemorrhage.
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.
52
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.
***_Blood transfusions: Transfusion Rx, Stop infusion, flush the line, need consent for blood transfusion, stay with patient 15 minutes, As a student cannot verify blood-Give to prevent hypovolemic shock_***
53
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
54
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
55
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.
56
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
57
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
58
Chronic Blood Loss
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
59
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.
60
Hemolytic Anemia General manifestations of anemia
***_Fatigue –Teach to rest often to avoid fatigue_***
Specific manifestations including
Jaundice-increased bilirubin
Enlargement of the spleen and liver
Maintenance of renal function is a major focus of treatment. ***_Caused by HG being filtered in kidney and causing blockage acute tubular necrosis_***
61
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
62
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.
***_Give oxygen, hydration, and make sure we are addressing their pain. They may require high doses of pain medication_***
63
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.
Give Immunizations to prevent illness_***
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.-Give hydration and oxygen_***
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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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Clinical Manifestations of Sickle Cell Disease Picture
66
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
Acute chest syndrome
67
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 Looking for Joint deformities or flattening
Magnetic resonance imaging (MRI)- To look for stroke
Doppler studies- To assess for DVT’s
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-Decreases Oxygen
***_Maintain adequate fluid intake
Treat infections promptly- flu vaccine_***
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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- Anticoagulation_***
***_Administration of fluids and electrolytes_***
***_- hypotonic solution 0.45 % NS- To expand volume_***
Transfusion therapy
***_Chelation_*** therapy with repeat exacerbations-Filtering of the blood
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Sickle Cell Disease Nursing & Collaborative Management pain management
Under-treatment is a major problem
Often pain medication tolerant
Require continuous & breakthrough analgesia with morphine & hydromorphone
Multimodal & interdisciplinary approach involving emotional & adjunctive measures
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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.- This is a chemo drug. Only chemo certified person can administer_***
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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What is Polycythemia
Production of increased number of RBCs
Hyperviscosity-Thick
Hypervolemia
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What are the two types of Polycythemia
***_Primary- Polycythemia Vera_***
Secondary polycythemia
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***_What is Primary- Polycythemia Vera_***
***_RBC, WBC, and platelets involved_***
- insidious
- Splenomegaly
- hepatomegaly
- hypercoagulation
- genetic link
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What is Secondary polycythemia
***_Hypoxia driven- Increases RBC production or hypoxia independent- Where there could be a benign or malignant tumor_***
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Polycythemia-clinical manifestations
Headache, vertigo, dizziness, tinnitus, visual disturbances- Secondary to HTN
Paresthesias and erythromelalgia- painful burning and redness of hands and feet
79
Polycythemia complications
Stroke
Embolization
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Polycythemia-Diagnostics
Elevated Hgb, RBC
Low to normal EPO level (secondary has high level)
Elevated WBC
Elevated platelets, cobalamin, uric acid, alkaline phosphate
Bone marrow examination
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Polycythemia-Nursing management
Evaluate fluid intake and output
Assist with phlebotomy
Patient teaching on medications
Assess nutritional status
***_Ambulation to prevent DVT_***
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Polycythemia- interprofessional care
***_Phlebotomy main stay treatment- Remove blood 300-400 ml every other day
Hydration therapy
Avoid iron supplementation_***
Myelosuppressive agents
***_Low dose aspirin-Remember_***
Anagrelide (Agrylin ) orally- inhibit platelet aggregation
Allopurinol-Increased uric acid mimics gout
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