adult nursing - anemia
DESCRIPTION
AnemiaHematologicalTRANSCRIPT
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(Relates to Chapter 31, “Nursing Management: Hematologic Problems,” in the textbook)
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A deficiency in the Number of erythrocytes (red blood cells [RBCs])
Quantity of hemoglobin Volume of packed RBCs (hematocrit)
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Diverse causes such as Blood loss Impaired production of erythrocytes
Increased destruction of erythrocytes
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RBC function Transport oxygen (O2) from lungs to systemic tissues
Carry carbon dioxide from the tissues to the lungs
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Not a specific disease Manifestation of a pathologic
processIdentified and classified by
laboratory diagnosis
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Classified as Morphologic
▪ Cellular characteristics▪ Descriptive, objective laboratory information
Etiologic▪ Underlying cause
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Caused by the body’s response to tissue hypoxia
Hemoglobin (Hb) levels are used to determine the severity of anemia
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Pallor ↓ Hemoglobin ↓ Blood flow to the skin
Jaundice ↑ Concentration of serum bilirubin
Pruritus ↑ Serum and skin bile salt concentrations
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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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Mild = Hb 10 to 14 g/dl May exist without symptoms Possible symptoms
▪ Palpitations, dyspnea, diaphoresisModerate = Hb 6 to 10 g/dl
Increased cardiopulmonary symptoms
Experienced at rest or during activity
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Severe = Hb <6 g/dl Involve multiple body systems
▪ Integument ▪ Eyes▪ Mouth▪ Cardiovascular
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Severe = Hb <6 g/dl Manifestations (cont'd)
▪ Pulmonary ▪ Neurologic ▪ Gastrointestinal (GI)▪ Musculoskeletal
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Subjective Data Important health information
▪ Past health history▪ Medications ▪ Surgery or other treatments
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Subjective Data Functional health patterns
▪ Health perception–health management
▪ Nutritional-metabolic▪ Elimination▪ Activity-exercise▪ Cognitive-perceptual ▪ Sexuality-reproductive
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Objective Data General Integumentary Respiratory Cardiovascular Gastrointestinal Neurologic
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Activity intoleranceImbalanced nutrition: Less
than body requirementsIneffective therapeutic
regimen management Potential complication:
Hypoxemia
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Goals Assume normal activities of daily living
Maintain adequate nutrition Develop no complications related to anemia
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Dietary and lifestyle changesBlood or blood product
transfusionsDrug therapy
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Oxygen therapyPatient teaching
Nutrition intake Compliance with drug therapy
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Common in older adults Chronic disease Nutritional deficiencies
Signs and symptoms may go unrecognized or mistaken for normal aging changes
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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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Life span of an RBC is 120 daysThree alterations in
erythropoiesis that decrease RBC production Decreased hemoglobin synthesis Defective DNA synthesis in RBCs Diminished availability of erythrocyte precursors
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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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Inadequate dietary intake 5% to 10% of ingested iron is absorbed
Malabsorption Blood lossHemolysis
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General manifestations of anemia
Pallor is the most common finding
Glossitis is the second most common Inflammation of the tongue
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Laboratory findings Hb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets
Stool guaiac testEndoscopy Colonoscopy
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Goal is to treat the underlying disease Increased intake of iron Nutritional therapy Oral or occasional parenteral iron supplements
Transfusion of packed RBCs
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Oral iron Inexpensive Convenient Factors to consider
▪ Enteric-coated or sustained-release capsules are counterproductive
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Oral iron Factors to consider (cont’d)
▪ Best absorbed as ferrous sulfate in an acidic environment
▪ Liquid iron should be diluted and ingested through a straw
▪ Side effects▪ Heartburn, constipation, diarrhea
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At-risk groups Premenopausal women Pregnant women Persons from low socioeconomic backgrounds
Older adults Individuals experiencing blood loss
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Diet teachingSupplemental ironDiscuss diagnostic studiesEmphasize compliance Iron therapy for 2 to 3
months after the hemoglobin levels return to normal
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An autosomal recessive genetic disorder of inadequate production of normal hemoglobin Common in ethnic groups near the Mediterranean Sea and equatorial regions of Asia and Africa
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Hemolysis also occursProblem with globulin
protein Abnormal Hb synthesis
One thalassemic gene Thalassemia minor
Two thalassemic genes Thalassemia major
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Thalassemia minor Asymptomatic frequently Moderate anemia
▪ Splenomegaly ▪ Mild jaundice
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Thalassemia major Life-threatening Physical and mental growth often retarded
Pale Symptoms develop in childhood
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Thalassemia major (cont’d) Splenomegaly Hepatomegaly Jaundice Chronic bone marrow hyperplasia ▪ Expansion of bone marrow space
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No specific drug or diet is effective in treating thalassemia
Thalassemia minor Body adapts to decreased Hb
Thalassemia major Blood transfusions with IV deferoxamine
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Group of disorders caused by impaired DNA synthesis
Characterized by the presence of large RBCs (megaloblasts)
Majority result from deficiency in Cobalamin (vitamin B12) Folic acid
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Classification Cobalamin (vitamin B12) deficiency
Folic acid deficiency Drug-induced suppression of DNA synthesis
Inborn errors Erythroleukemia
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Intrinsic factor (IF) Protein secreted by the parietal cells of the gastric mucosa
IF is required for cobalamin absorption in the small intestine
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Causes Pernicious anemia
▪ Insidious onset Nutritional deficiencies Hereditary enzymatic defects
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Absence of IFAcid environment required
for IF secretionGI surgery Long-term users of H2-
histamine receptor blockers
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General symptoms of anemia
Sore tongueAnorexiaNauseaVomitingAbdominal pain
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Neuromuscular manifestations Weakness Paresthesias of the feet and hands
↓ Vibratory and position senses Ataxia Muscle weakness Impaired thought process
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RBCs appear largeAbnormal shapesStructure contributes to
erythrocyte destructionDecreased serum
cobalamin levels
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Normal serum folate levels and decreased cobalamin levels suggest megaloblastic anemia due to cobalamin deficiency
Schilling test
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Parenteral administration of cobalamin
Increase in dietary cobalamin does not correct the anemia Still important to emphasize adequate dietary intake
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Familial disposition Early detection and treatment can lead to reversal of symptoms
Ensure that injuries are not sustained because of the patient’s diminished sensations to heat and pain
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Ensure patient compliance with treatment
Evaluate patient for gastric carcinoma frequently
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Also a cause of megaloblastic anemia
Folic acid is required for DNA synthesis RBC formation and maturation
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Common causes Poor nutrition Malabsorption syndromes Drugs Alcohol abuse and anorexia Lost during hemodialysis
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Clinical manifestations are similar to those of cobalamin deficiency
Insidious onsetAbsence of neurologic problemsTreated by replacement therapyEncourage patient to eat foods
with large amounts of folic acid
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Underproduction of RBCsMild shortening of RBC
survival
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Causes End-stage renal disease
▪ Primary factor: ↓ Erythropoietin Chronic liver disease Chronic inflammation Malignant tumors Chronic endocrine diseases
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Anemia of chronic disease findings ↑ Serum ferritin ↑ Iron stores Normal folate and cobalamin levels
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Treating underlying cause is best
Rarely blood transfusionsErythropoietin therapy
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Pancytopenia Decrease of all blood cell types
▪ RBCs▪ White blood cells (WBCs)▪ Platelets
Hypocellular bone marrow
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Low incidence Affecting 4 of every 1 million persons
Manageable with erythropoietin or blood transfusion
Can be a critical condition Hemorrhage Sepsis
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Types Congenital
▪ Chromosomal alterations Acquired
▪ Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections
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Gradual developmentSymptoms caused by
suppression of any or all bone marrow elements
General manifestations of anemia Fatigue, dyspnea
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Confirmed by laboratory studies
Normocytic, normochromic anemia
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Preventing complications from infection and hemorrhage
Untreated prognosis is poor 75% fatal
Treatment options Bone marrow transplantation Immunosuppressive therapy
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Result of sudden hemorrhage Trauma Complications of surgery Disruption of vascular integrity
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Concerns Hypovolemic shock Reduced plasma volume
▪ Diminished O2 because fewer RBCs available
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Cause Body’s attempt to maintain an adequate blood volume and O2
Pain Internal hemorrhage
▪ Tissue distention, organ displacement, nerve compression
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Pain (cont'd) Retroperitoneal bleeding
▪ Numbness ▪ Pain in the lower extremities
Shock is the major complication
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Laboratory data do not adequately assess RBC problems for 2 to 3 days
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Replacing blood volume to prevent shock
Identifying the source of the hemorrhage
Stopping blood lossCorrecting RBC loss
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May be impossible to prevent if caused by trauma
Postoperative patients Monitor blood loss
No need for long-term treatment
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Reduced iron stores Bleeding ulcer Hemorrhoids Menstrual and postmenopausal blood loss
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Management Identify source Stop bleeding Possible use of supplemental iron
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Destruction or hemolysis of RBCs at a rate that exceeds production
Third major cause of anemia, such as Thalassemia
Intrinsic hemolytic anemia Abnormal hemoglobin Enzyme deficiencies RBC membrane abnormalities
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Extrinsic hemolytic anemia Acquired
Sites of hemolysis Intravascular Extravascular
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Jaundice Destroyed RBCs cause increased bilirubin
Enlarged spleen and liver Hyperactive with macrophage phagocytosis of the defective RBCs
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Accumulation of hemoglobin molecules can obstruct renal tubules Tubular necrosis
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Group of inherited, autosomal recessive disorders
Presence of an abnormal form of hemoglobin in the erythrocyte
Hemoglobin S (HbS), abnormal
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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 disorderIncurable disease, often fatal
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Types of SCD Sickle cell anemia
▪ Most severe▪ Homozygous for hemoglobin S (HbSS)
Sickle cell thalassemia Sickle cell HbC disease Sickle cell trait (HbAS)
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Typical patient is asymptomatic except during sickling episodes
Symptoms can be Pain and swelling Pallor of mucous membranes Fatigue
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Gradual involvement of all body systems
Usually fatal by middle age from renal and pulmonary failure
Prone to infection Pneumonia, most common infection
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Peripheral blood smearSickling testElectrophoresis of
hemoglobinDNA testingSkeletal x-raysMagnetic resonance imaging
(MRI)
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Alleviate symptoms of disease complications
Minimize end-organ damageNo specific treatment for
SCDPatient teaching
Avoid high altitudes, maintain fluid intake, treat infections, control pain
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O2 for hypoxia and to control sickling
Pain managementAcute chest syndrome
Antibiotics O2 therapy Fluid therapy
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Folic acid daily supplementsBlood transfusions in crisis Hydroxyurea: Antisickling
agent Erythropoietin in patients unresponsive to hydroxyurea
Bone marrow transplant Can cure some patients with SCD
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Excessive production of red blood cells
Unknown cause Hemorrhage of distended blood
vesselsReddish face with deep‑red
purplish lips, fatigue, weakness, dizziness, headache, enlarged spleen (splenomegaly), and congested liver
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Treatment: Phlebotomy, antineoplastic agents, and radiation therapy
Increased fluid intake Secondary polycythemia
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Platelet count less than 150,000/mm3
Immune thrombocytopenic purpura
Heparin therapy Safety
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For a patient with a low platelet count, whenever a venipuncture is performed, an injection is administered, or an intravenous catheter or needle is discontinued, pressure over the site must be maintained for 10 minutes to prevent continuous oozing.
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EtiologyPathophysiologySigns and symptomsDiagnosis and treatmentNursing management
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Aspirin must never be taken by a patient with hemophilia as it increases the bleeding problems.
Patients must read labels on every over-the-counter preparation to be certain that it does not contain aspirin or acetylsalicylic acid.