Adult Nursing - Anemia

(Relates to Chapter 31, “Nursing Management: Hematologic Problems,” in the textbook)

A deficiency in the Number of erythrocytes (red blood cells [RBCs])

Quantity of hemoglobin Volume of packed RBCs (hematocrit)

Diverse causes such as Blood loss Impaired production of erythrocytes

Increased destruction of erythrocytes

RBC function Transport oxygen (O2) from lungs to systemic tissues

Carry carbon dioxide from the tissues to the lungs

Not a specific disease Manifestation of a pathologic

processIdentified and classified by

laboratory diagnosis

Classified as Morphologic

▪ Cellular characteristics▪ Descriptive, objective laboratory information

Etiologic▪ Underlying cause

Caused by the body’s response to tissue hypoxia

Hemoglobin (Hb) levels are used to determine the severity of anemia

Pallor ↓ Hemoglobin ↓ Blood flow to the skin

Jaundice ↑ Concentration of serum bilirubin

Pruritus ↑ Serum and skin bile salt concentrations

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

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

Severe = Hb <6 g/dl Involve multiple body systems

▪ Integument ▪ Eyes▪ Mouth▪ Cardiovascular

Severe = Hb <6 g/dl Manifestations (cont'd)

▪ Pulmonary ▪ Neurologic ▪ Gastrointestinal (GI)▪ Musculoskeletal

Subjective Data Important health information

▪ Past health history▪ Medications ▪ Surgery or other treatments

Subjective Data Functional health patterns

▪ Health perception–health management

▪ Nutritional-metabolic▪ Elimination▪ Activity-exercise▪ Cognitive-perceptual ▪ Sexuality-reproductive

Objective Data General Integumentary Respiratory Cardiovascular Gastrointestinal Neurologic

Activity intoleranceImbalanced nutrition: Less

than body requirementsIneffective therapeutic

regimen management Potential complication:

Hypoxemia

Goals Assume normal activities of daily living

Maintain adequate nutrition Develop no complications related to anemia

Dietary and lifestyle changesBlood or blood product

transfusionsDrug therapy

Oxygen therapyPatient teaching

Nutrition intake Compliance with drug therapy

Common in older adults Chronic disease Nutritional deficiencies

Signs and symptoms may go unrecognized or mistaken for normal aging changes

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

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

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

Inadequate dietary intake 5% to 10% of ingested iron is absorbed

Malabsorption Blood lossHemolysis

General manifestations of anemia

Pallor is the most common finding

Glossitis is the second most common Inflammation of the tongue

Laboratory findings Hb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets

Stool guaiac testEndoscopy Colonoscopy

Goal is to treat the underlying disease Increased intake of iron Nutritional therapy Oral or occasional parenteral iron supplements

Transfusion of packed RBCs

Oral iron Inexpensive Convenient Factors to consider

▪ Enteric-coated or sustained-release capsules are counterproductive

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

At-risk groups Premenopausal women Pregnant women Persons from low socioeconomic backgrounds

Older adults Individuals experiencing blood loss

Diet teachingSupplemental ironDiscuss diagnostic studiesEmphasize compliance Iron therapy for 2 to 3

months after the hemoglobin levels return to normal

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

Hemolysis also occursProblem with globulin

protein Abnormal Hb synthesis

One thalassemic gene Thalassemia minor

Two thalassemic genes Thalassemia major

Thalassemia minor Asymptomatic frequently Moderate anemia

▪ Splenomegaly ▪ Mild jaundice

Thalassemia major Life-threatening Physical and mental growth often retarded

Pale Symptoms develop in childhood

Thalassemia major (cont’d) Splenomegaly Hepatomegaly Jaundice Chronic bone marrow hyperplasia ▪ Expansion of bone marrow space

No specific drug or diet is effective in treating thalassemia

Thalassemia minor Body adapts to decreased Hb

Thalassemia major Blood transfusions with IV deferoxamine

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

Classification Cobalamin (vitamin B12) deficiency

Folic acid deficiency Drug-induced suppression of DNA synthesis

Inborn errors Erythroleukemia

Intrinsic factor (IF) Protein secreted by the parietal cells of the gastric mucosa

IF is required for cobalamin absorption in the small intestine

Causes Pernicious anemia

▪ Insidious onset Nutritional deficiencies Hereditary enzymatic defects

Absence of IFAcid environment required

for IF secretionGI surgery Long-term users of H2-

histamine receptor blockers

General symptoms of anemia

Sore tongueAnorexiaNauseaVomitingAbdominal pain

Neuromuscular manifestations Weakness Paresthesias of the feet and hands

↓ Vibratory and position senses Ataxia Muscle weakness Impaired thought process

RBCs appear largeAbnormal shapesStructure contributes to

erythrocyte destructionDecreased serum

cobalamin levels

Normal serum folate levels and decreased cobalamin levels suggest megaloblastic anemia due to cobalamin deficiency

Schilling test

Parenteral administration of cobalamin

Increase in dietary cobalamin does not correct the anemia Still important to emphasize adequate dietary intake

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

Ensure patient compliance with treatment

Evaluate patient for gastric carcinoma frequently

Also a cause of megaloblastic anemia

Folic acid is required for DNA synthesis RBC formation and maturation

Common causes Poor nutrition Malabsorption syndromes Drugs Alcohol abuse and anorexia Lost during hemodialysis

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

Underproduction of RBCsMild shortening of RBC

survival

Causes End-stage renal disease

▪ Primary factor: ↓ Erythropoietin Chronic liver disease Chronic inflammation Malignant tumors Chronic endocrine diseases

Anemia of chronic disease findings ↑ Serum ferritin ↑ Iron stores Normal folate and cobalamin levels

Treating underlying cause is best

Rarely blood transfusionsErythropoietin therapy

Pancytopenia Decrease of all blood cell types

▪ RBCs▪ White blood cells (WBCs)▪ Platelets

Hypocellular bone marrow

Low incidence Affecting 4 of every 1 million persons

Manageable with erythropoietin or blood transfusion

Can be a critical condition Hemorrhage Sepsis

Types Congenital

▪ Chromosomal alterations Acquired

▪ Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections

Gradual developmentSymptoms caused by

suppression of any or all bone marrow elements

General manifestations of anemia Fatigue, dyspnea

Confirmed by laboratory studies

Normocytic, normochromic anemia

Preventing complications from infection and hemorrhage

Untreated prognosis is poor 75% fatal

Treatment options Bone marrow transplantation Immunosuppressive therapy

Result of sudden hemorrhage Trauma Complications of surgery Disruption of vascular integrity

Concerns Hypovolemic shock Reduced plasma volume

▪ Diminished O2 because fewer RBCs available

Cause Body’s attempt to maintain an adequate blood volume and O2

Pain Internal hemorrhage

▪ Tissue distention, organ displacement, nerve compression

Pain (cont'd) Retroperitoneal bleeding

▪ Numbness ▪ Pain in the lower extremities

Shock is the major complication

Laboratory data do not adequately assess RBC problems for 2 to 3 days

Replacing blood volume to prevent shock

Identifying the source of the hemorrhage

Stopping blood lossCorrecting RBC loss

May be impossible to prevent if caused by trauma

Postoperative patients Monitor blood loss

No need for long-term treatment

Reduced iron stores Bleeding ulcer Hemorrhoids Menstrual and postmenopausal blood loss

Management Identify source Stop bleeding Possible use of supplemental iron

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

Extrinsic hemolytic anemia Acquired

Sites of hemolysis Intravascular Extravascular

Jaundice Destroyed RBCs cause increased bilirubin

Enlarged spleen and liver Hyperactive with macrophage phagocytosis of the defective RBCs

Accumulation of hemoglobin molecules can obstruct renal tubules Tubular necrosis

Group of inherited, autosomal recessive disorders

Presence of an abnormal form of hemoglobin in the erythrocyte

Hemoglobin S (HbS), abnormal

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

Types of SCD Sickle cell anemia

▪ Most severe▪ Homozygous for hemoglobin S (HbSS)

Sickle cell thalassemia Sickle cell HbC disease Sickle cell trait (HbAS)

Typical patient is asymptomatic except during sickling episodes

Symptoms can be Pain and swelling Pallor of mucous membranes Fatigue

Gradual involvement of all body systems

Usually fatal by middle age from renal and pulmonary failure

Prone to infection Pneumonia, most common infection

Peripheral blood smearSickling testElectrophoresis of

hemoglobinDNA testingSkeletal x-raysMagnetic resonance imaging

Alleviate symptoms of disease complications

Minimize end-organ damageNo specific treatment for

SCDPatient teaching

Avoid high altitudes, maintain fluid intake, treat infections, control pain

O2 for hypoxia and to control sickling

Pain managementAcute chest syndrome

Antibiotics O2 therapy Fluid therapy

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

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

Treatment: Phlebotomy, antineoplastic agents, and radiation therapy

Increased fluid intake Secondary polycythemia

Platelet count less than 150,000/mm3

Immune thrombocytopenic purpura

Heparin therapy Safety

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.

EtiologyPathophysiologySigns and symptomsDiagnosis and treatmentNursing management

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.

Adult Nursing - Anemia

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