Functions Of Blood

FUNCTIONS OF BLOOD Transport of gases, nutrients, and waste products Transport of processed molecules Transport of regulatory molecules Regulation of pH and osmosis Maintenance of body temperature Protection against foreign substances Clot formation

COMPOSITIONS OF BLOOD

COMPOSITION OF BLOOD PLASMA

91 % water; 7% proteins; 2 % other substances Proteins: Albumins

-58% of the plasma proteins Globulins – 38% of the plasma proteins Fibrinogens – 4% of plasma proteins Ions – Na, Cl, K, hydrogen, hydroxide, bicarbonate ions Nutrients Gases Waste products Regulatory substances

FORMED ELEMENTS

FORMED ELEMENTS Red Blood cell Are disk-shaped and biconcave; no nucleus;

contains hemoglobin Live for about 120 days in males and 110 days for females. Main component is the hemoglobin which is responsible for 98.5% of the oxygen transported in the blood 6.5 – 8.5 µm in diameter Function: transports oxygen and carbon dioxide

White Blood cells Granulocytes 

Neutrophils  Nucleus with 2 to 4 lobes; granules stain light pink or reddish purple .  10 -12 µm in diameter  Function: Phagocytizes microorganisms and other substances

 Eosinophils

Nucleus often bilobed; cytoplasmic granules stain orange-red or bright red  11-14 µm in diameter  Function: Releases chemicals that reduce inflammation and attacks certain worm parasites  Basophils  Nucleus with 2 indistinct lobes; granules stain blue  10-12 µm in diameter  Function: Releases histamine and heparin 

Agranulocytes 



Lymphocytes  Round nucleus; cytoplasm forms a thin ring around the nucleus  6-14 µm in diameter  Function: Produces antibodies and other chemicals for destroying microorganisms; contributes to allergic reactions ; graft rejection, tumor control and regulation of the immune system. Monocytes  Nucleus round, kidney or horseshoe-shaped; contains more cytoplasm  12-20µm in diameter  Function: Phagocytic cell in the blood; becomes the macrophage

Platelets Also called the thrombocytes Cell fragments from the megakaryocytes

surrounded by a plasma membrane and containing granules 2-4 µm in diameter Function: Forms platelet plugs; releases chemicals necessary for blood clotting

PRODUCTION OF FORMED ELEMENTS Hematopoiesis Process of blood cell production Confined mainly to the red bone marrow

after birth All populations of blood cells are derived from a single stem cell and is regulated by specific growth factors

ERYTHROPOIESIS Or Red Blood Cell production Proerythroblasts Give rise to the red blood cell line Red blood cells are the final cells produced

from a series of cell divisions.

The process of cell division requires the B

vitamins folate and B12 for DNA synthesis Iron is required for production of hemoglobin RBC is stimulated by low blood oxygen levels

ERYTHROPOIESIS Erythropoietin Stimulates red bone marrow to produce more

RBC Released from the kidneys secondary to a low blood oxygen levels. Old , abnormal or damaged red blood cells are removed from the blood by macrophages located in the spleen and liver. Iron from the heme is transported in the blood to the red bone marrow and is used to produce new hemoglobin

Hemoglobin Breakdown

ERYTHROPOIESIS Bilirubin A yellow pigment molecule from heme Normally taken up by the liver and

released into the small intestine as part of the bile

PREVENTING BLOOD LOSS Vascular Spasm Is an immediate but temporary

constriction of a blood vessel resulting from contraction of smooth muscle within the wall of the vessel Nervous system reflexes and chemicals (thromboxanes and endothelins) produce vascular spasms.

Platelet plugs Is an accumulation of platelets than can seal up small break in a blood vessel The formation of a platelet plug can be described as a series of steps. Platelets adhesion results in platelets sticking to collagen exposed by blood vessel damage.  Von Willebrand’s factor is a protein produced and secreted by blood vessel endothelial cells and mediates platelet adhesion.  Platelet release reaction – platelet release chemicals (ADP and thromboxanes) which activate other platelets which also release the same chemicals to activate more platelets. 

As platelets become activated they express surface receptors called fibrinogen receptors which can bind to fibrinogen .  Platelet aggregation- fibrinogen forms bridges between the fibrinogen receptors of numerous platelets resulting in the formation of a platelet plug. 

Blood Clotting Also called the coagulation which is a network of threadlike protein fibers called the fibrin. The formation of a blood clot depends on proteins found in the plasma called clotting factors. Most clotting factors are manufactured in the liver , and many require vitamin K for their synthesis.

Control of Clot formation The blood contains anticoagulants Antithrombin and Heparin These inactivate the thrombin. Without the thrombin, fibrinogen is not

converted to fibrin, and no Clot is formed.

Clot Retraction and Fibrinolysis Clot Retraction After a clot is formed , it begins to condense into a more compact structure. Contraction of the extensions of the platelets pulls on the fibrin and responsible for the retraction. Serum 

Is the plasma without the clotting factors that is squeezed out of the clot during clot retraction.

Retraction of the clot pulls the edges of the damaged

blood vessel together.

Fibrinolysis Clots are dissolved by this process

ABO Blood Groups

Diagnostic Tests and Assessments  Red blood cell count  Hemoglobin and hematocrit  Hemoglobin measures the hemoglobin

available in circulation, which is the gas-carrying capacity of an erythrocyte  Hematocrit is the ratio of the RBC volume to the volume of whole blood

Diagnostic Tests and Assessments  RBC indexes  MCV (mean corpuscular volume):

estimates size of the RBC  MCH (mean corpuscular hemoglobin): measures the content of Hgb in RBCs from a single cell  MCHC (mean corpuscular hemoglobin concentration): a more accurate measurements of the Hgb content of RBC as it measures the entire volume of RBCs

Diagnostic Tests and Assessments  Serum ferritin, transferrin, and total iron-

binding capacity (TIBC):  these tests are used to evaluate iron levels  ferritin measures the iron in plasma. Which is

also a direct reflection of total iron stores  transferrin is the major iron-transport protein

Diagnostic Tests and Assessments  White blood cell count  Abnormal elevation of the WBC is

referred to as leukocytosis  Leukopenia is a decrease in the number of white blood cells  Differential count refers to the breakdown of the different types of cells

Diagnostic Tests and Assessments  Coagulation studies  Bleeding time: normal range is 1 to 4

minutes; it is used in evaluation of platelet function; extended bleeding times are seen with thrombocytopenia and aspirin therapy

Diagnostic Tests and Assessments  Prothrombin Time (PT): is the rapidity of

blood clotting; normal range is 11 to 16 seconds; PT evaluates extrinsic coagulation pathway which include factors 1, II, V, VII, X  Partial thromboplastin time (PTT): normal range is 60 to 70 seconds, which evaluates the intrinsic coagulation pathway of fibrin clot formation

Diagnostic Tests and Assessments  Activated partial thromboplastin time (APTT):

normal range is 30 to 45 seconds;  a modified PTT, preferred because it is quicker to perform  used in heparin therapy and in the evaluation of hemophilia  increased in anticoagulation therapy, liver disease, vitamin K deficiency, and disseminated intravascular coagulation (DIC)

Diagnostic Tests and Assessments  Fibrinogen: normal range is 150 to 400

mg/dL; it is a soluble plasma protein that is decreased in DIC and fibrinogen disorders and increased in acute infections, hepatitis, and oral contraceptive use

Diagnostic Tests and Assessments  Fibrin degradation products (FDP): normal

value is <10 ug/mL; FDP is increased in fibrinolysis, thrombolytic therapy, and DIC  Fibrin D-dimer: normal is 0 to 0.5 ug/mL;

D-dimer is the most sensitive indicator to differentiate DIC from primary fibrinolysis; it is elevated in DIC

Diagnostic Tests and Assessments  Bone marrow examination  Specimens obtained during a bone marrow

examination may include those obtained by aspiration or biopsy  Sites for bone marrow aspiration may include: sternum, iliac crest (most common), and tibia; the most common site for bone marrow biopsy is the posterosuperior iliac spine; the sternum also is used  Aspiration is the most common procedure for obtaining a marrow sample

Diagnostic Tests and Assessments  The client is positioned based on the site

selected by the physician;  the skin and periosteum are anesthetized to decrease pain with anesthetic such as procaine; the marrow aspiration needle is then inserted; after the marrow cavity is entered, the marrow stylet is removed from the needle and a sterile syringe is attached;  the syringe plunger is drawn back until marrow appears in the syringe

Diagnostic Tests and Assessments  During the withdrawal of aspirate, the client will

experience sharp pain often described as a burning pain  After the needle is removed, a pressure dressing is applied over the puncture site, where only minimal bleeding should occur; if the patient has thrombocytopenia, pressure is applied for 3 to 5 minutes  The nurse should check on the facility`s procedure manual as to the disposition of specimens

Diagnostic Tests and Assessments  Most clients experience little, if any, pain

or discomfort after the procedure; some persons will complain of tenderness and ache at the aspiration site for a few days

Diagnostic Tests and Assessments The procedure for a bone marrow biopsy is

essentially the same as for aspiration; the biopsy needle most commonly used is a Jamshidi needle; which allows a second needle, called a stylet to be inserted within in the initial biopsy needle and a core of marrow to be collected and withdrawn through the sleeve of the needle; after the procedure, clients are assessed for bleeding from the puncture site

Diagnostic Tests and Assessments  Lymphangiography  Is visualization of the lymph system

radiographically after injection of a dye  It is used primarily in staging of Hodgkin`s and non-Hodgkin`s lymphoma

Diagnostic Tests and Assessments  Lymph node biopsy  Can either be done utilizing a closed

needle biopsy done at the bedside or an open biopsy performed in the operating room  The purpose is to obtain lymph tissue for histologic analysis

Administration of blood and blood products

Administration of blood and blood products  Check the agency`s policy and procedure

pertaining to blood transfusion and transfusion of blood products  Verify the physician`s order for the transfusion noting the blood product ordered, the time specified for transfusion (if any), and any medications to be given before transfusion

Administration of blood and blood products  Check that the client has given consent for

receiving blood transfusion  check that a typing and crossmatch has been performed  Obtain blood from the blood bank when an intravenous access line is available; the IV line should be maintained with normal saline while waiting for the blood or blood product to be delivered to the nursing unit

Administration of blood and blood products Return blood to the blood bank immediately if transfusion is not possible; blood may not be returned to the blood bank after 20 minutes Do not keep blood or blood products in the nursing unit refrigerator; blood is refrigerated under strict and controlled conditions only in the blood bank

Administration of blood and blood products  Validate data on the blood or blood

product with another nurse; the client`s ID bracelet should match the blood bank number on the unit of blood  Validate with another nurse that the client`s name, ID number, blood type, and Rh match the unit of blood to be transfused

Administration of blood and blood products  Note the expiration date indicated on

the blood product  Observe the unit of blood for bubbles or discoloration; return unit of blood to the blood bank if break in the bag is noted or if signs of contamination are evident

Administration of blood and blood products Obtain pre-transfusion vital signs, and the vital signs 15 minutes after the transfusion is initiated and immediately after the completion of the transfusion; A pre-transfusion temperature of 100 degree F or higher should be reported to the physician before initiating the transfusion; any increase in 2 degree F in the client`s temperature may indicate a transfusion reaction and should be reported to the physician

Administration of blood and blood products  Start blood transfusion slowly,

administering 25 to 50 mL during the first 15 minutes; most untoward reactions occur during the first 15 minutes; stay with the client during this period of time

Administration of blood and blood products Do not administer any medications through

the blood transfusion tubing; use tubing specific for the blood product being transfused; a blood filter is used to prevent clots and other particles from entering the venous system Use only agency-approved blood-warming devices; do not warm blood in hot water or microwave ovens

Administration of blood and blood products  Blood products should not be infused

longer than 4 hours; the longer a blood product is in room temperature, the greater the chances of bacterial contamination  Discard tubings and bags used in the transfusion in biohazard receptacle  Follow the agency`s protocol for any suspected transfusion reactions

Protocol for suspected blood transfusion reaction  Check the specific policy and protocol of the agency  If blood transfusion reaction is noted or suspected,

stop the infusion immediately; change IV tubing and keep vein open with normal saline; the IV access might be needed for the administration of emergency drugs  Assess the client for other signs and symptoms of transfusion reaction  Notify the physician and the blood bank

Protocol for suspected blood transfusion reaction  Send the unit of blood and tubing used to

the blood bank; this will help determine the cause of the reaction  Urine and blood samples will be required; follow the agency`s protocol  Administer drugs that are prescribed and continue to monitor the client  Document the reaction and interventions

Iron-deficiency anemia (IDA)

Iron-deficiency anemia (IDA)  Description:  anemia that results when the supply of

iron is inadequate for optimal formation of RBCs related to excessive iron loss caused by bleeding, decreased dietary intake, or malabsorption

Iron-deficiency anemia (IDA)  Etiology and pathophysiology 

Iron deficiency accounts for 60 percent of anemias in clients over age 65; the most common cause of IDA is blood loss from gastrointestinal or genitourinary system

Iron-deficiency anemia (IDA) 



Normal iron excretion is less than 1 mg/day through the urine, sweat, bile, feces, and from desquamated cells of the skin; the average woman loses 0.5 mg of iron daily or 15 mg monthly during menstruation is the most common cause of iron deficiency in women, while gastrointestinal bleeding is the most common cause in men Anemia reduces the oxygen-carrying capacity of the blood, producing tissue hypoxia

Iron-deficiency anemia (IDA)  Iron is stored in the body as ferritin, an

iron-phosphorus-protein complex that contains about 23 percent iron; it is formed in the intestinal mucosa, when ferritin iron joins with the protein apoferritin; ferritin is stored in the tissues; primarily in the reticuloendothelial cells of the liver, spleen, and bone marrow

Iron-deficiency anemia (IDA)  Develops slowly through three phases:

body`s stores of iron used for erythropoiesis are depleted, insufficient iron is transported to the bone marrow and iron deficient erythropoiesis begins, allowing small hemoglobin deficient cells to enter the peripheral circulation in large numbers; iron is needed on the hemoglobin so the oxygen molecule will attach

Iron-deficiency anemia (IDA) 



Adequate iron in the RBC is essential since the oxygen molecule attaches to it An average diet supplies the body with 12 to 15 mg/day of iron, of which only 5 to 10 percent is absorbed

Iron-deficiency anemia (IDA)  Assessment 

Clinical manifestations (usually develop gradually with the client not seeking attention until the hemoglobin drops to 7 to 8 g/dL)  Fatigue  Weakness  Shortness of breath

Iron-deficiency anemia (IDA) 

 

  

Pallor (ear lobes, palms, and conjunctiva) Brittle spoon-like nails Cheilosis (cracks in the corners of the mouth) Smooth, sore tongue Dizziness Pica (craving to eat unusual substances such as clay or starch)

Iron-deficiency anemia (IDA) 

Diagnostic and laboratory tests 

Is considered a microcytic and hypochromic anemia (small RBC diameter<6 with decreased pigmentation) with an increase in the red cell size distribution width (RDW)

Iron-deficiency anemia (IDA) 



Erythrocytes are small (microcytic) and pale (hypochromic); mean corpuscular volume (MCV; measures size) is decreased and mean corpuscular hemoglobin (MCH) or mean corpuscular hemoglobin concentration or MCHC (calculated value of the hemoglobin present in the RBC compared to its size) will be decreased; the MCV, MCH, and MCHC should be analyzed only when the hemoglobin is low Low serum iron level and elevated serum iron-binding capacity or low serum ferritin levels

Iron-deficiency anemia (IDA)  Therapeutic management 

The cause for the anemia is usually explored; stools are examined for occult blood; endoscopic examination and other diagnostic procedures may be performed to rule out possible sources of bleeding, which is a common cause of iron deficiency

Iron-deficiency anemia (IDA)   



Increase intake of iron-rich foods Vitamin supplementation Administration of oral iron preparation in the form of ferrous sulfate Parenteral administration of iron

Iron-deficiency anemia (IDA)  Priority nursing diagnoses:  Activity intolerance  Risk for decreased cardiac output  Risk for injury  Ineffective health maintenance

Iron-deficiency anemia (IDA)  Planning and implementation  Administer oral iron preparation with orange juice or vitamin C to increase absorption; antacids interfere with the absorption of iron  Administer parenteral iron deep intramuscularly via the Z-track method  Identify/implement energy-saving techniques, e.g., shower chair, sitting to perform tasks  Promote quiet environment to facilitate sleep/rest

Iron-deficiency anemia (IDA) 







Monitor for dizziness, suggest position changes be made slowly Provide/recommend assistance with activities/ambulation as needed; allowing patient independence as much as needed Monitor laboratory studies, e.g., Hgb/Hct, RBC count Administer medications, blood or blood products as indicated; monitor closely for transfusion reactions

Iron-deficiency anemia (IDA) 



 

Encourage/assist with good oral hygiene before and after meals, using soft bristled toothbrush for gentle brushing of fragile gums Determine stool color, consistency, frequency, and amount Encourage fluid intake of 2,500 to 3,000 mL /day Discuss use of stool softeners, bulk-forming laxatives, mild stimulants, or enemas if indicated; monitor effectiveness

Iron-deficiency anemia (IDA) 





Oral liquid form of iron can stain the teeth; clients should not use a straw or place spoon at the back of the mouth to take the supplement and rinse mouth thoroughly afterward Caustion client that bowel movement may appear greenish black/tarry Deep IM, Z-track administration of medication; use separate needles for withdrawing and injecting the medication

Iron-deficiency anemia (IDA) 



Caution regarding possible systemic (allergic) reactions to the medications, e.g., (flushing, nausea/vomiting, myalgias) and the importance of reporting symptoms Refer to appropriate community resources when indicated, e.g., social services for food stamps. Meals on wheels

Iron-deficiency anemia (IDA)  Medication therapy 

Usual therapy is oral ferrous sulfate (FeSO4) 300 to 325 mg t.i.d., given 1 hr before meals for 6 months; other oral forms may include ferrous gluconate (Fergon) and ferrous fumarate (Ircon, Femiron)

Iron-deficiency anemia (IDA) 



If the client is unable to tolerate oral therapy, iron dextran (INFeD) may be given by deep IM (Z-track) route or as IV therapy; there is risk of anaphylaxis with parenteral administration; therefore, before a full dose is given a small test dose is administered Transfusion of packed RBCs may be necessary if anemia is severe

Iron-deficiency anemia (IDA)  Client education  Teach clients to maintain good nutrition; the elderly and those with limited economic means may have dietary deficiencies requiring referrals to appropriate agencies (e.g., Means on Wheels)  Teach client to take iron on an empty stomach; absorption of iron is decreased with food; absorption may be enhanced when taken with an acidic beverage (such as one with vitamin C); but avoid grapefruit juice

Iron-deficiency anemia (IDA) 





Inform clients that their stools will appear black with the oral intake of iron Teach the client to report to the healthcare provider persistent GI symptoms secondary to iron intake Clients should be informed that iron preparations cause constipation; the addition of a stool softener may be necessary; other measures such as increasing oral intake of fluids and fiber will prevent constipation

Iron-deficiency anemia (IDA)  Review required diet alterations to meet

specific dietary needs; foods high in iron include organ meats (beef or calf`s liver, chicken liver), other meats, beans (black, pinto, and garbanzo), leafy green vegetables, raisins, and molasses

Megaloblastic anemia  Vitamin B12 deficiency anemia 

Description:  a type of anemia characterized by macrocytic red blood cells

Megaloblastic anemia 

Etiology and pathophysiology 



Enevitably develops after total gastrectomy, with 15 percent of clients developing pernicious anemia after partial gastrectomy or gastrojejunostmy Lack of vitamin B12 alters the structure and disrupts the function of the peripheral nerves, spinal cord, and brain

Megaloblastic anemia 



Lack of vitamin B12 impairs cellular division and maturation especially in rapidly proliferating RBCs Pernicious anemia is the body`s inability to absorb vitamin B12 because of a lack of intrinsic factor, a substance secreted by the parietal cells of the gastric mucosa

Megaloblastic anemia 

Assessment 

Clinical manifestations:  signs and symptoms include pallor or slight jaundice with a complaint of weakness  smooth, sore, beefy red tongue (glossitis), with diarrhea

Megaloblastic anemia paresthesias

(altered sensations such as numbness, or tingling in the extremities), impaired proprioception (difficulty identifying one`s position in space, which may progress to difficulty with balance) clients with this anemia tend to be fair-haired or prematurely gray

Megaloblastic anemia 

Diagnostic and laboratory tests 





Macrocytic (megaloblastic) anemia (RBC diameter>8) Laboratory examination shows an increase in the MCV and MCHC Gastric secretion analysis reveals achlorhydria: the absence of free hydrochloric acid in a pH maintained at 3.5

Megaloblastic anemia  24 hour urine for Schilling test (a

vitaminB12 absorption test that indicates if a client lacks intrinsic factor by measuring the excretion of orally administered radionuclide labeled B12) confirms the diagnosis of pernicious anemia

Megaloblastic anemia 

Therapeutic management 

Review required diet alterations to meet specific dietary needs; if the deficiency is caused by a vegetarian diet, fortified soy milk may be added to the diet, or oral supplements of B12 may be added

Megaloblastic anemia  If the deficiency is caused by gastric

malabsorption such as deficiency of intrinsic factor, lifelong replacement therapy is required; an intramuscular injection of B12 is required and in some situations megadoses or oral vitamins may be given

Megaloblastic anemia  Priority nursing diagnoses:  Risk for injury  Activity intolerance  Altered oral mucous membrane

Megaloblastic anemia  Planning and implementation:  the major nursing consideration in the

care of the client with this type of anemia is client education pertaining to nutrition and medications; the client should be assessed carefully for neurologic deficits and incorporate in the plan of care interventions relating to prevention of injury

Megaloblastic anemia  Medication therapy:  parenteral vitamin B12, 100 to 1,000

micrograms subcutaneously daily for 7 days, then once a week for 1 month, then monthly for the remainder of life is usually prescribed to clients with this type of anemia

Megaloblastic anemia 

Client education 





Inform client that the burning sensation felt after parenteral dose of vitamin B12 is temporary Discuss dietary sources of vitamin B12 like dairy products, animal proteins, and eggs For clients who have pernicious anemia, discuss the regular schedule of parenterally administered vitamin B12 and the importance and necessity for continued treatment

Folic acid deficiency anemia Description: anemia caused by a deficiency of folic

acid resulting in the interruption of DNA synthesis and normal maturation of red blood cells

Folic acid deficiency anemia 

Etiology and pathophysiology 



Causative etiology: poor nutrition, malabsorption syndrome, medications that impede the absorption (oral contraceptives, anticonvulsants, methotrexate [MTX]), alcohol abuse, and anorexia Alcoholics and those receiving total parenteral nutrition are at risk

Folic acid deficiency anemia 





Pregnant women, infants, and teenagers are also at risk for the development of folic acid deficiency Clients on hemodialysis are also at risk for the development of folic acid deficiency Lack of folic acid causes the formation of megaloblastic cells; these cells are fragile

Folic acid deficiency anemia 

Assessment 

Clinical manifestations:  pallor, progressive weakness, fatigue, shortness of breath, cardiac palpitations  GI symptoms are similar to B12 deficiency, but usually more severe (glossitis cheilosis, and diarrhea)  neurological symptoms seen in B12 deficiency are not seen in folic acid deficiency and therefore assist in the differentiation of these two types of anemia

Folic acid deficiency anemia 

Diagnostic and laboratory tests 

 

Macrocytic (megaloblastic) anemia (RBC diameter>8) MCV high with low hemoglobin Low serum folate level

Folic acid deficiency anemia 

Therapeutic management: 



includes dietary counseling and the administration of folic acid

Priority nursing diagnoses:    

Activity intolerance Constipation Diarrhea Risk for infection

Folic acid deficiency anemia 

Planning and implementation 





Identify/implement energy-saving techniques, e.g., shower chair, sitting to perform tasks Monitor for dizziness, suggest position changes be made slowly Provide/recommend assistance with activities/ambulation as needed, allowing client independence as much as needed

Folic acid deficiency anemia 





Monitor laboratory studies, e.g., Hgb/Hct, RBC count Encourage/assist with good oral hygiene before and after meals, using soft bristled toothbrush for gentle brushing of fragile gums Refer to appropriate community resources when indicated, e.g., social services for food stamps, Meals on Wheels, Alcoholics Anonymous

Folic acid deficiency anemia  Medication therapy:  oral folate, 1 to 5 mg/day for 3 to 4

months  folate should be given along with vitamin B12 when both are deficient

Folic acid deficiency anemia 

Client education 

Discuss with client the dietary sources of folic acid such as green leafy vegetables, fish, citrus fruits, yeast, dried beans, grains, nuts, and liver

Folic acid deficiency anemia 



Teach clients who are at risk for the development of folic acid deficiency (alcoholism, clients on hemodialysis and certain drugs) to increase their dietary intake through diet selection and supplementation Discuss with client strategies to decrease pain associated with glossitis such as eating bland and soft foods

Aplastic anemia  Description:  aplastic anemia is a form of anemia

resulting in decreased production of bone marrow elements, namely erythrocytes, leukocytes, and platelets

Aplastic anemia  Etiology and pathophysiology  Affects all age groups and both genders  Two classifications of aplastic anemia include congenital or acquired  Congenital aplastic anemia is caused by a chromosomal alteration  Acquired form of the disease may be caused by radiation, chemical agents and toxins, drugs, viral and bacterial infections, pregnancy, and idiopathic  In about 50 percent of cases is unknown

Aplastic anemia  There is a decrease or cessation of

production of RBCs (anemia), WBCs (leucopenia), and platelets (thrombocytopenia);  the decrease may result from damage to bone marrow stem cells, the bone marrow itself, and the replacement of bone marrow with fat; depending on the causative factor, the condition may be acute to chronic

Aplastic anemia

 Assessment 

Clinical manifestations  Pallor  Fatigue  Palpitations  Exertional dyspnea  Infections of the skin and mucous membranes  Bleeding from gums, nose, vagina, or rectum  Purpura (bruising)  Retinal hemorrhage

Aplastic anemia 

Diagnostic and laboratory tests 

 

Blood counts reveal pancytopenia (decreased RBC, WBC, and platelets) Decreased reticulocyte count Bone marrow examination reveals decrease in activity of the bone marrow or no cell activity

Aplastic anemia  Therapeutic management 

   

Identification of the cause of bone marrow suppression Bone marrow transplantation Immunosuppression Transfusion of leukocyte-poor RBCs Splenectomy

Aplastic anemia  Priority nursing diagnoses:  Risk for infection  Risk for bleeding  Activity intolerance

Aplastic anemia  Planning and implementation  

 

 

Institute reverse isolation Limit visitors and potential sources of infection Monitor for evidence of bleeding Avoid invasive procedures including rectal temperatures Provide frequent rest periods Monitor tolerance to activities

Aplastic anemia  Medication therapy 



Agents that suppress lymphocyte activity such as antilymphocyte globulin (ALG), antithymocyte globulin (ATG), and cyclosporine (Sandimmune) Immunosuppresive agents such as prednisone and cyclophosphamide (Cytoxan)

Aplastic anemia  Client education 



Teach client ways to prevent infection such as avoiding crowds, maintaining good hygiene, handwashing, and elimination of uncooked foods from the diet Discuss ways to prevent hemorrhage such as using a soft toothbrush, avoiding contact sports, and use of an electric razor

Aplastic anemia 





Emphasize the avoidance of drugs that increase bleeding tendency such as aspirin Teach client to balance activity with adequate rest periods to avoid fatigue Teach client about symptoms to report to the healthcare provider including signs of infection, bleeding, and increasing intolerance to activity

Sickle cell disease  Definition: 

a hereditary, chronic form of hemolytic anemia

 Etiology and pathophysiology 

Eight percent of African-americans are heterozygous (carriers) for sickle cell anemia thereby inheriting one affected gene or the sickle cell trait

Sickle cell disease 



One percent of African-Americans are homozygous (identical genes) for the disorder, thereby inheriting a defective gene from both parents or sickle cell anemia and are likely to experience sickle cell crisis Sickle cell trait (heterozygous state) is a generally mild condition that produces few, if any, manifestations

Sickle cell disease 



Sickle cell anemia is caused by an autosomal genetic defect (one gene affected) that results in the synthesis of hemoglobin S Produced by a mutation in the beta chain of the hemoglobin molecule through a substitution of the amino acid valine for glutamine in both beta chains

Sickle cell disease 

During decreased oxygen tension in the plasma, the hemoglobin S causes the RBCs to elongate, become rigid, and assume a crescent, sickled shape causing the cells to clump together, obstruct capillary blood flow causing ischemia and possible tissue infarction

Sickle cell disease Conditions likely to trigger a sickle cell crisis

include: hypoxia, low environmental and/or body temperature, excessive exercise, high altitudes, or inadequate oxygen during anesthesia Other causes of sickle cell crisis include: elevated blood viscosity/decreased plasma volume, infection, dehydration, and/or increased hydrogen ion concentration (acidosis)

Sickle cell disease 



With normal oxygenation, the sickled RBCs resume their normal shape; repeated episodes of sickling and unsickling weaken the cell membrane, causing them to hemolyze and be removed Crisis is extremely painful and can last from 4 to 6 days

Sickle cell disease  Assessment  Clinical manifestations  Pallor  Jaundice  Fatigue  Irritability  Large joints and surrounding tissue may become swollen during crisis  Priapism (abnormal, painful, continuous erection of the penis) may occur if penile veins are obstructed  Pain

Sickle cell disease  Therapeutic management    

Bone marrow transplantation Blood transfusions Management of pain Use of chemotherapy drug hydroxyurea (Droxia) to increase hemoglobin F and decrease sickling

Sickle cell disease  Priority nursing diagnoses:  Pain; Ineffective tissue perfusion  Impaired gas exchange  Risk for infection  Knowledge deficit

Sickle cell disease  Planning and implementation 



Teach clients ways to prevent development of sickle cell crisis Refer to appropriate agency for genetic counseling and family planning

Sickle cell disease Monitor for complications such as vasoocclusive disease (thrombosis), hypoxia, CVA, renal dysfunction, priapism leading to impotence, acute chest syndrome (fever, chest pain, cough, pulmonary infiltrates, and dyspnea), and substance abuse  Management of infection  Administer care with attention to culture; avoid racial bias or cultural insensitivity 

Sickle cell disease  Medication therapy 









Nifedipine (Procardia) may be used for priapism Hydroxyurea (Droxia) to increase hemoglobin F and decrease sickling Narcotic (opioid) analgesics during the acute phase of sickle cell crisis, often at large doses Broad-spectrum antibiotics to manage acute chest syndrome Folic acid supplement

Sickle cell disease  Client education 

Teach client ways to prevent sickle cell crisis; these instructions should include:  Maintain adequate fluid intake; clients with sickle cell disease should maintain an oral intake of at least 4 to 6 quarts/day; avoid conditions that might predispose them to dehydration

Sickle cell disease Avoid high altitudes  Prevent and promptly treat infection  Stress-reduction strategies  Avoid exposure to cold  Avoid overexertion  Discuss the importance of adhering to vaccination schedules for pneumococcal pneumonia, haemophilus influenza type B, and hepatitis B  Importance of regular medical follow-up 

Polycythemia  Description:  an increase in the number of circulating

erythrocytes and the concentration of hemoglobin in the blood; also known as polycythemia vera, PV, or myeloproliferative red cell disorder, polycythemia can be primary or secondary

Polycythemia Etiology and Pathophysiology a. Primary Common in men of European Jewish descent Neoplastic stem cell disorder characterized by increased production of RBCs, granulocytes, and platelets With the over production of erythrocytes, increased blood viscosity results in congestion of blood in tissues, the liver, and spleen Thrombi form, acidosis develops, and tissue infarction occurs as a result of the diminished circulatory flow of blood caused by the increased viscosity

Polycythemia b. Secondary Most

common form of polycythemia vera The disturbance is not in the development of red blood cells but in the abnormal increase of erythropoietin, causing excessive erythropoiesis The increase in red blood cell production caused by increased erythropoietin release is a physiologic response to hypoxia; hypoxia stimulates the release of erythropoietin in the kidney

Polycythemia 



Chronic hypoxic states may be produced by prolonged exposure to high altitudes, pulmonary diseases, hypoventilation, and smoking The results of an increased RBC production include the increased viscosity of blood, which alters circulatory flow

Polycythemia 



Assessment a. Clinical manifestations Plethora: a ruddy (dark, flushed) color of the face, hands, feet, ears, and mucous membranes resulting from the engorgement or distention of blood vessels Symptoms associated with increased blood volume including headaches, vertigo, blurred vision, and tinnitus Distended superficial veins

Polycythemia  







Itching unrelieved by antihistamines Symptoms associated with impaired tissue oxygenation including angina, claudication, or dyspnea Erythromyalgia, or burning sensation of the fingers and toes Splenomegaly in majority of those with primary polycythemia vera Epistaxis, GI bleeding

Polycythemia Diagnostic and laboratory tests Elevated hemoglobin and erythrocyte count Decreased MCHC Increased WBC and basophilia Increased platelets Elevated leukocyte alkaline phosphatase Elevated uric acid Elevated cobalamin levels Increased histamine levels Bone marrow examination shows

hypercellularity

Polycythemia Therapeutic management Management of the underlying condition

(such as COPD) causing the chronic hypoxia Repeated phlebotomy to decrease blood volume; the goal is to keep the hematocrit less than 45 to 48 percent Hydration to decrease blood viscosity

Polycythemia Priority nursing diagnoses: Impaired gas exchange Pain Risk for infection

Polycythemia Planning and implementation Assist in phlebotomy Measures to relieve pruritus including cool and

tepid baths Accurate monitoring of fluid intake and output Nursing measures to prevent thrombotic events including early ambulation, passive leg exercise when on bed rest, avoid crossing legs, and maintaining adequate hydration Administration of medications for the prevention of complications including anticoagulants

Polycythemia Medication therapy Myelosuppressive agents to inhibit bone

marrow activity including hydroxyurea (Hydrea), melphalan (Alkeran), and radioactive phosphorus Allopurinol to manage gout Antiplatelet agents to prevent thrombotic complications

Polycythemia Client education Teach client about the importance of

maintaining good hydration; the client should drink at least 3 liters of fluid per day Teach client about the disease and ways in which it can be controlled, such as smoking cessation Discuss signs and symptoms of complications associated with the disorder including signs of vaso-occlusive states (MI, CVA) and bleeding that require immediate medical attention

Polycythemia  Teach client to prevent bleeding states such

as using a razor, using soft bristled toothbrush, not flossing, and avoiding the use of aspirin and aspirin-containing products  Emphasize the importance of a regular medical check-up  Teach client to avoid products that contain iron  Discuss ways of preventing thrombosis

Thrombocytopenia  Definition:  a decrease in the number of circulating

platelets or a platelet count of less than 100,000 platelets per milliliter of blood resulting in problems of hemostasis

Thrombocytopenia  Etiology and pathophysiology  The decrease in the number of

circulating platelets may be a result of three mechanisms: decreased production, increased destruction, or increased consumption  The cause of decreased production of platelets may be inherited or acquired

Thrombocytopenia  Increased destruction of platelets may be

caused by an immune system defect; the platelets become coated with an antibody; when these antibody coated platelets reach the spleen, they are recognized as foreign and are destroyed  platelets normally have a circulating life of 8 to 10 days but this immune response shortens their life cycle; this condition is referred to as immune thrombocytopenic purpura (ITP);

Thrombocytopenia  The acute form of this disorder is more common in

children whereas the chronic form is more common in women between the ages of 20 to 50  Other causes of increased destruction of platelets include non-immune related factors such as infection or drug-induced effects  A decrease in the number of functional platelets leads to bleeding disorders; cerebral and pulmonary hemorrhage can occur when platelet counts drop below 10,000/mm3

Thrombocytopenia Assessment a. Clinical manifestations Petechiae and purpura most commonly found in the anterior thorax, arms, and neck Epistaxis, gingival bleeding, menorrhagia, hematuria, and gastrointestinal bleeding Signs of internal hemorrhage

Thrombocytopenia Diagnostic and laboratory tests Decreased hemoglobin and hematocrit if

bleeding is present Decreased platelet count Prolonged bleeding time Bone marrow examination to determine the etiology; may reveal decreased platelet activity or increased megakaryocytes

Thrombocytopenia Therapeutic management a. Treatment of the underlying cause or removal of the causative agent b. Use of immunosuppressive and chemotherapeutic agents in case of ITP c. Platelet transfusion if there is active bleeding; little benefit in ITP d. Splenectomy in ITP

Thrombocytopenia  Priority nursing diagnoses:  Risk for injury  Bleeding  Fatigue  Altered oral mucous membrane

Thrombocytopenia  Planning and implementation  Institute bleeding (thrombocytopenic) precautions  Avoid intramuscular or subcutaneous injections  Avoid indwelling catheters  If absolutely necessary use smallestgauge needles for injections or venipunctures; apply pressure on injection sites for 5 minutes or until bleeding stops  Discourage straining at stool, vigorous coughing, and nose blowing

Thrombocytopenia 









Avoid rectal manipulation such as rectal temperatures, suppositories, or enemas Discourage the use of razors; use only electric shavers Use soft-bristled toothbrush or toothettes and avoid flossing Put side rails if necessary and avoid tissue trauma Avoid the use of aspirin and drugs that interfere with blood coagulation

Thrombocytopenia 

  

Monitor for signs of bleeding; test stools for occult blood Monitor CBC and platelet counts Administer platelets as ordered Monitor response to therapy

Thrombocytopenia  Medication therapy 





steroids and immunoglobulins may be used to suppress the immune response in ITP Immunosuppressive agents may be used such as vincristine (Oncovin) and cyclophosphamide (Cytoxan) Platelet growth factor such as oprelvekin (Neumega)

Thrombocytopenia  Client education  Teach the client and family to monitor for signs of bleeding and when to contact the primary care provider  Include instructions on bleeding precautions such as the use of softbristled toothbrush, avoidance of flossing, prevention of tissue trauma and injury including vigorous sexual intercourse, and using an electric razor for shaving

Thrombocytopenia 





Teach client to avoid drugs that contain aspirin and others that interfere with coagulation Discuss medication dosing, schedule, and side effects Teach the importance of regular medical follow-up and platelet monitoring

Hemophilia  Description:  a group of hereditary clotting factor

disorders characterized by prolonged coagulation time that results in prolonged and sometimes excessive bleeding

Hemophilia  Etiology and pathophysiology  Hemophilia A and B are X-linked recessive disorders transmitted by female carriers, displayed almost exclusively in males  Hemophilia A (classic hemophilia) is a deficiency in Factor VIII (an alpha globulin that stabilizes fibrin clots; it is the most common form of hemophilia  Hemophilia B (Christmas disease) is a deficiency in Factor IX; (a vitamin dependent beta globulin essential in stage 1 of the intrinsic coagulation system as an influence on the amount of thromboplastin available)

Hemophilia

Hemophilia 





Despite the difference in factor deficiency, hemophilia A and B are clinically identical In clients with hemophilia A and B, platelet plugs are formed at the site of bleeding, but the clotting factor impairs the coagulation response and the capacity to form a stable clot Von Willebrand`s factor (vWF), which is necessary for factor VIII activity and platelet adhesion; this disorder affects men and women equally

Hemophilia  Assessment  Clinical manifestations  Persistent and prolonged bleeding from small cuts and injuries  Delay of onset of bleeding after an injury  Subcutaneous ecchymosis and subcutaneous hematomas  Gingival bleeding

Hemophilia 

 



Gastrointestinal bleeding, which may be manifested by hematemesis (vomiting blood), occult blood in the stools, gastric pain, or abdominal pain Urinary tract bleeding (hematuria) Pain, paresthesias, or paralysis resulting from nerve compression of the hematomas Hemarthrosis (joint bleeding, swelling and damage)

Hemophilia 

Diagnostic and laboratory tests 

 



Specific factor assays are used to determine the type of hemophilia present APTT is increased in all types of hemophilia Bleeding time is prolonged in von Willebrand`s disease Decreased factor VIII in hemophilia A, vWF in von Willebrand`s disease, and factor IX in hemophilia B

Hemophilia  Therapeutic management 





Treatment is the replacement of the deficient coagulation factor(s) Hemophilia A: cryoprecipitate containing 8 to 100 units of factor VIII per bag at 12-hour intervals until bleeding ceases; freeze-dried concentrate of factor VIII may also be given Hemophilia B: plasma or factor IX concentrate given q 24 hours or until bleeding ceases

Hemophilia 







Von Willebrand`s disease: cryoprecipitate containing 8 to 100 units of factor VIII per bag at 12-hour intervals until bleeding ceases; desmopressin (DDAVP) given intravenously may also be used Supportive treatment for hemarthrosis including arthrocentesis and physiotherapy Control of topical bleeding with hemostatic agents, pressure, and application of ice Management of complications associated with hemorrhage

Hemophilia  Priority nursing diagnoses:  Risk for injury, bleeding  Decreased cardiac output  Deficient fluid volume  Risk for ineffective therapeutic regimen

management

Hemophilia  Planning and implementation 







Teach the client and family about the disease and therapeutic regimen Refer for genetic counseling and family planning Refer to the National Hemophilia Foundation for support and counseling Monitor for signs of complications including hemarthrosis and intracranial bleeding

Hemophilia 





Assist in management of pain associated with hemarthrosis; measures include joint immobilization , and administration of analgesics; aspirin and drugs affecting coagulation are avoided Control bleeding and maintain hemostasis through direct pressure, application of topical hemostatic agents, and application of ice Administer medications as prescribed

Hemophilia  Client education 

Discuss with client and family signs and symptoms requiring immediate medical attention, which includes severe joint pain, trauma or injury, and signs of uncontrolled internal bleeding

Hemophilia Teach the client and family precautions

to prevent bleeding including the use of soft bristled toothbrush, avoid flossing, use of electric razor, avoiding contact sports or activities most likely to cause injury, and avoidance of aspirin and other drugs that interfere with coagulation

Hemophilia 





Teach the client about the importance of wearing a Medic-Alert bracelet indicating the hemophilia Emphasize the need to maintain good dental hygiene to decrease the necessity of invasive dental procedures Emphasize the importance of adhering to scheduled visits and follow-up care with the primary health provider

Disseminated intravascular coagulopathy (or coagulation)

Disseminated intravascular coagulopathy (or coagulation)  Description:  disseminated intravascular coagulopathy or

consumption coagulopathy is a syndrome characterized by abnormal initiation and acceleration of clotting and simultaneous hemorrhage; the paradoxical bleeding that occurs is a result of the consumption of clotting factors and platelets; the syndrome is usually precipitated by an underlying pathologic condition

Disseminated intravascular coagulopathy (or coagulation)  Etiology and pathophysiology 



Mortality rate associated with DIC is as high as 80 percent with the most frequent sequela being hemorrhage The syndrome is precipitated by conditions such as widespread tissue damage, hemolysis, hypotension, hypoxia, and metabolic acidosis

Disseminated intravascular coagulopathy (or coagulation) The

underlying condition causes initiation and widespread formation of clots in the vascular system either through the activation of factor XII, factors II and X, or the release of tissue thromboplastin; substances necessary for clotting are used at a more rapid rate than they can be replaced

Disseminated intravascular coagulopathy (or coagulation) As the clotting continues, the

fibrinolytic pathway is activated to dissolve the clots formed; clotting factors become depleted while fibrinolysis continues; platelets decrease, clotting factors II, V, VIII, and fibrinogen are depleted

Disseminated intravascular coagulopathy (or coagulation) 



Fibrin degradation products (FDP) are released as a result of fibrinolysis; fibrin degradation products (FDP), which are potent anticoagulants used to lyse the clots further, increase the bleeding state With the depletion of clotting factors and the increase in fibrin degradation products, stable blood clots no longer form and hemorrhage occurs

Disseminated intravascular coagulopathy (or coagulation)  Assessment  Clinical manifestations  Diagnostic and laboratory tests  Prothrombin time: prolonged  Partial thromboplastin time: prolonged  Thrombin time: prolonged  Fibrinogen: decreased  Platelets: decreased  Fibrin split (degradation) products: elevated  Factor assays (factor V, VII, VIII, X, XIII): reduced  D-dimers: elevated

Disseminated intravascular coagulopathy (or coagulation)

Disseminated intravascular coagulopathy (or coagulation)

coagulopathy (or coagulation)  Therapeutic management 





The priority of therapeutic management is to initiate treatment of the underlying medical condition that precipitated DIC Supportive treatment for the manifestations of DIC such as the control of bleeding; lifethreatening hemorrhage may be treated by administering specific blood components based on the identified deficiency: platelets for thrombocytopenia; cryoprecipitate to replace fibrinogen, and factors V and VII; and fresh frozen plasma to replace all clotting factors except platelets Use of heparin or antithrombin III (AT-III) to control intravascular clotting

Disseminated intravascular coagulopathy (or coagulation)  Priority nursing diagnoses:  Impaired gas exchange  Ineffective tissue perfusion  Risk for deficient fluid volume  Pain  Decreased cardiac output

Disseminated intravascular coagulopathy (or coagulation)  Planning and implementation 





Assess client carefully for evidence of bleeding and altered tissue oxygenation Institute thrombocytopenic precautions (refer to previous discussion on thrombocytopenia) Monitor intake and output hourly

Disseminated intravascular coagulopathy (or coagulation) 







Administer blood products as indicated by the healthcare provider Monitor for signs of complications such as renal failure, pulmonary embolism, cerebrovascular accident, and acute respiratory distress syndrome Monitor effectiveness of therapy and pharmacologic interventions Provide emotional support to client and family

Disseminated intravascular coagulopathy (or coagulation)  Medication therapy 





Heparin and antithrombin III, although their use is controversial; these drugs are usually indicated to manage thrombosis Epsilon aminocaproic acid (Amicar) to inhibit fibrinolysis Blood products (FFP, platelets, and cryoprecipitate)

Disseminated intravascular coagulopathy (or coagulation)  Client education  Teach the client and family regarding the syndrome and explain treatments and interventions  Teach the client to report symptoms of complications including abdominal pain, headache, visual disturbances, and pain  Discuss with the client and family thrombocytopenic precautions (see client education in the discussion of thrombocytopenia)

Leukemia

Definition: a malignant disorder of the blood-

forming tissues of the bone marrow, spleen, and lymph system characterized by unregulated proliferation of WBCs and their precursors

Leukemia  Etiology and pathophysiology  The type of WBC affected (granulocyte, lymphocyte, monocyte) and the duration of the disease (acute or chronic) is the basis of the classification of the different types of leukemia: if the majority of the leukemia cells are primitive, the leukemia is classified as acute; if the leukemic cells are mostly mature (well-differentiated), the leukemia is classified as chronic

Leukemia 

Acute lymphocytic/lymphoblastic leukemia (ALL) 



Peak incidence at 2 to 4 years of age Immature granulocytes proliferate and accumulate in the marrow

Leukemia 

Chronic lymphocytic leukemia (CLL) 



More common in men and mainly between the ages of 50 and 70 Abnormal and incompetent lymphocytes proliferate and accumulate in the lymph nodes and spreads to other lymphatic tissues and the spleen; most of the circulating cells are mature lymphocytes

Leukemia 

Acute myelogenous/myelocytic leukemia (AML) 



All age groups are affected with a peak incidence at age 60 There is uncontrolled proliferation of myeloblasts, which are the precursors of granulocytes; they accumulate in the bone marrow

Leukemia 

Chronic myelogenous leukemia (CML) 





Uncommon in people under 20 years of age; the incidences rises with age There is uncontrolled proliferation of granulocytes in increased circulating blast (immature) cells; the marrow expands into long bones because of this proliferation and also extends into the liver and spleen In most cases the Philadelphia chromosomes, a characteristic chromosomal abnormality, is present

Leukemia  Abnormal or immature WBCs do not

function properly because of the massive proliferation of these abnormal immature cells; abnormal cells can continue to multiply, infiltrate, and damage the bone marrow, spleen, lymph nodes, liver, kidneys, lungs, gonads, skin, and central nervous system (CNS)

Leukemia  Normal bone marrow becomes diffusely

replaced with abnormal or immature WBCs, interfering with the bone marrow`s ability to produce other types of cells such as erythrocytes and thrombocytes; the bone marrow becomes functionally incompetent with resulting bone marrow suppression

Leukemia  Acute leukemia has a rapid onset,

progresses rapidly, with a short clinical course; left untreated, death will result in days or months; the symptoms of acute leukemia relate to a depressed bone marrow, infiltration of leukemic cells into other organ systems, and hypermetabolism of leukemia cells

Leukemia Chronic leukemia has a more insidious onset

with a more prolonged clinical course; clients with the chronic form of leukemia are usually asymptomatic early in the disease; the life expectancy may be more than 5 years; symptoms of chronic leukemia relate to hypermetabolism of leukemia cells infiltrating other organ system; the cells in this type of leukemia are more mature and function more effectively

Leukemia  Assessment  Clinical manifestations           

Fever Night sweats Bleeding Ecchymoses Lymphadenopathy Weakness Fatigue Pruritic vesicular lesions Anorexia Weight loss Shortness of breath

Leukemia        

Decreased activity tolerance Bone or joint pain Visual disturbances Gingival bleeding Epistaxis Pallor Splenomegaly Hepatomegaly

Leukemia 

Diagnostic and laboratory tests  









Increased WBC (in CLL and CML) A normal, decreased or increased WBC (in ALL and AML) Decreased reaction to skin sensitivity tests (anergy) Bone marrow tests reveal excessive blast cells in AML Philadelphia chromosome found in 90 to 95 percent in clients with CML; BCR/ABL gene is present in virtually all clients with CML Bone marrow biopsy and aspirate is the definitive diagnostic test

Leukemia  Therapeutic management 



Induction of remission with chemotherapy and radiation therapy Bone marrow and stem cell transplantation

 Priority nursing diagnoses: 

Risk for infection: Risk for bleeding; Imbalanced nutrition; less than body requirements; Fatigue, Activity intolerance; Pain; Anticipatory grieving

Leukemia  Planning and implementation 





Review and institute the care of a client receiving chemotherapy Review and implement the nursing care of a client undergoing radiation therapy Assist in bone marrow biopsy; apply pressure on the site for 5 minutes or until bleeding stops; frequently assess the site for signs of bleeding up to 4 hours after the procedure

Leukemia  

 



Institute neutropenic and bleeding precautions Plan activities to prevent fatigue; provide measures for uninterrupted rest and sleep Provide for diversionary activities Maintain good nutrition; enlist the assistance of a dietician in maximizing and meeting the nutritional needs of the client Assist the client in maintaining good personal hygiene; measures to promote oral hygiene should be instituted

Leukemia 







Provide emotional support to the client and family; refer to appropriate agency, organization, or professional for counseling and support Administer drugs that are prescribed and monitor for side effects Monitor laboratory results to evaluate effectiveness of interventions and therapy Prepare the client for bone marrow transplantation if this is included in the treatment plan

Leukemia  Medication therapy:  chemotherapeutic drugs include

alkylating agents (Busulfan [Myleran]), anthracyclines (Doxorubicin [Adriamycin]), antimetabolites (Fludarabine [Fludara]), corticosteroid (Prednisone), plant alkaloids (Vincristine [Oncovin]) and others

Leukemia  Client education  Teach client and family about precautions to prevent bleeding  Teach client and family about neutropenic precautions as previously discussed  Teach client to maintain good oral hygiene including measures to keep the oral cavity moist; these measures can include rinsing mouth with saline, lubricating the lips and oral mucosa with water-soluble lubricants every 2 hours; alcoholbased mouthwash solutions should be avoided; sponge-tipped applicators should be used for oral hygiene if the neutrophil and platelet counts are low

Leukemia 



Teach client measures to prevent perirectal complications; the area should be washed and cleansed thoroughly after each bowel movement Discuss with client and family therapeutic plans and interventions

Malignant lymphomas  Definition:  lymphoma is a group of malignant

neoplasms that affects the lymphatic system resulting in the proliferation of lymphocytes; lymphomas can be classified as Hodgkin`s disease and non-Hodgkin`s lymphoma

Malignant lymphomas  Etiology and pathophysiology 

Hodgkin`s disease  More common in men and has two peaks; 15 to 35 years of age and 55 to 75 years of age; incidence is higher in whites than in African-Americans  The cause of the disease is unknown although several factors have been identified to contribute to the development of the disease; these factors include infection with the Epstein-Barr virus (EBV), familial pattern, and exposure to toxins

Malignant lymphomas 



Hodgkin`s disease is characterized by the presence or Reed-Sternberg cell, a multinucleated and gigantic tumor cell thought to be of lymphoid origin The tumor originates in a lymph node (in majority of cases from the cervical nodes) and infiltrates the spleen, lungs, and liver

Malignant lymphomas 

Non-Hodgkin`s lymphoma  Most common form of lymphoma; affects usually adults from 50 to 70 years old; it is more common in men than women and in whites  There is no known cause but the incidence of non-Hodgkin`s lymphoma is linked to viral infections, immune disorders, genetic abnormalities, exposure to chemicals, and infection with Helicobacter pylori

Malignant lymphomas 



Non-Hodgkin`s lymphoma has a similar pathophysiology to Hodgkin`s disease, although Reed-Sternberg cells are absent and the method of lymph node infiltration is different In majority cases, the disease involves malignant B cells; the lymphoma usually originates outside the lymph nodes; tthe lymphoid tissues involved become infiltrated with malignant cells; the cells that make up the lymphoid tissue become abnormal and crowd out normal cells

Malignant lymphomas  Assessment  Clinical manifestations  Hodgkin`s disease  Usually begins with a firm and painless enlargement of one or more lymph nodes on one side of the neck  Fatigue  Weakness  Anorexia  Dysphagia  Dyspnea  Pruritus

Malignant lymphomas 

    



Development of severe but brief pain at the site of Hodgkin`s after ingestion of alcohol Cough Jaundice Abdominal pain Bone pain B symptoms: fever without chills; night sweats, and unintentional 10 percent weight loss Enlarged lymph nodes, liver, and spleen

Malignant lymphomas 

Non-Hodgkin`s lymphoma     



Painless lymph node enlargement B symptoms (see above) Abdominal pain, nausea, vomiting Hematuria Peripheral neuropathy, cranial nerve palsies, headaches, visual disturbances, changes in mental status, and seizures Shortness of breath, cough, and chest pain

Malignant lymphomas 

Diagnostic and laboratory tests 

Hodgkin`s disease  Normocytic, normochromic anemia  Neutrophilia, monocytophilia, and lymphopenia  Presence of Reed-Sternberg cells in excisional bone biopsy

Malignant lymphomas 





Mediastinal lymphadenopathy revealed by chest x-ray, CT scan, and radioisotope studies Mediastinal mass and pulmonary infiltrates may be seen on chest xray Absent or decreased response to skin sensitivity testing known as anergy

Malignant lymphomas 

Non-Hodgkin`s lymphoma  Lymphocytopenia  X-ray may reveal pulmonary infiltrates  Lymph node biopsy helps to identify the cell type and pattern

Malignant lymphomas  Therapeutic management  Hodgkin`s disease  Lymphangiography is used to evaluate abdominal nodes  Staging laparotomy is performed to obtain specimen of retroperitoneal lymph nodes and to remove the spleen

Malignant lymphomas Staging of the disease to determine the extent of

the disease and appropriate therapy is instituted Stage 1 indicates involvement of a single lymph node region Stage IV (for Hodgkin`s disease only) indicates diffuse or disseminated involvement of extralymphatic organs, with or without lymph node involvement (liver, lung, marrow, skin)

Malignant lymphomas 





Radiation therapy for stages 1A, 1B, 11A, and 11B Combination chemotherapy for stages III, IV, and all B stages Combination radiation and chemotherapy for stages 1A and 1B

Malignant lymphomas 

Non-Hodgkin`s lymphoma 

 





Staging of the disease is undertaken; this is based on data obtained from CT scans and bone marrow biopsies Combination chemotherapy Radiation alone or in combination with chemotherapy for stage 1 and II Biologic therapy with alpha interferon, interleukin-2 and tumor necrosis factor Administration of rituximab (Rituxan), a monoclonal antibody against the CD20 of malignant B lymphocytes, which causes cell lysis and death

Malignant lymphomas  Priority nursing diagnoses:  Risk for infection  Activity intolerance  Ineffective protection  Fatigue  Imbalanced nutrition: less than body

requirements  Disturbed body image  Hopelessness

Malignant lymphomas  Planning and implementation  Institute nursing interventions for clients on chemotherapy or radiation therapy  Assist in balancing activity with periods of rest  Provide and assist in maintaining good nutritional state  Provide measures to diminish the discomfort associated with pruritus  Provide interventions to enable client to deal with body image changes such as alopecia, weight loss, and sterility  Plan interventions for the prevention of infection

Malignant lymphomas  Medication therapy  

Chemotherapeutic agents Biologic therapy agents

Malignant lymphomas  Client education  Discuss with client and family the nature of the disease, the course of therapy, and associated interventions  Teach the client and family about the medications prescribed, precautions, and side effects  Teach the client and family symptoms necessitating immediate medical interventions such as the occurrence of bleeding, infection, or fever