Chapter 7 Care of the Patient with a Blood or Lymphatic Disorder

Chapter 7 Care of the Patient with a Blood or Lymphatic Disorder
Mosby items and derived items © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Overview of Anatomy and Physiology
Characteristics of blood Consistency 45% blood cells 55% blood plasma pH 7.35 to 7.45 Volume 10 to 12 pints Blood is the necessary life force in the human body. In ancient times it had a mystical allure. What are the primary functions of blood?

Red blood cells (RBCs) Erythrocytes Transport oxygen and carbon dioxide White blood cells (WBCs) Leukocytes Body defenses: destruction of bacteria and viruses Thrombocytes (platelets) Initiate blood clotting The three primary types of blood cells are the red blood cells, white blood cells, and platelets. Red blood cells give the blood its red coloring. What is the relationship between the red blood cell and hemoglobin? What is the normal red blood cell count in the body? What testing processes measure the key properties of the red blood cells? White blood cells are colorless cells whose main functions involve defense of the body. What are the categories of the white blood cells? What laboratory tests are used to measure the white blood cell levels? The smallest blood cells are the platelets.

Figure 7-1 Human blood cells.
(From Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology. [6th ed.]. St. Louis: Mosby.) Human blood cells.

Hemostasis: A body process that arrests the flow of blood and prevents hemorrhage Injury Hemorrhage Grouping platelets Thromboplastin released Converts prothrombin to thrombin Links with fibrinogen Formation of fibrin Traps RBCs and platelets Forms clot Hemostasis is vital to the maintenance of the blood supply. If altered significantly, death will result. Identify and explain the actions that take place in the process of hemostasis.

Figure 7-2 Blood clotting.
The onset of injury immediately initiates the process of blood clotting. Although the process appears lengthy, it occurs instantly in the healthy individual. What analogies can be used to describe this process? (From Thibodeau, G.A., Patton, K.T. [2007]. The human body in health and disease. [3rd ed.]. St. Louis: Mosby.) Blood clotting.

Blood types (groups) Determined by the presence or absence of specific antigens on the outer surface of the RBC Type A Type B Type AB Universal recipient Type O Universal donor At birth, the blood type is already determined by the type of antigens on the outer portion of the blood cell. A person with type B blood has no anti–B antibodies but instead has B antigens. How many students know their blood types? Draw a diagram to demonstrate the genetic determination of blood types.

Rh factor Rh antibodies may be located on the surface of the RBC Rh positive: Antibodies are present Rh negative: Antibodies are not present The majority of the population is Rh positive. The assessment and monitoring of Rh factor is very important during pregnancy. Discuss the use of RhoGAM.

Lymphatic system Functions Maintenance of fluid balance Production of lymphocytes Absorption and transportation of lipids from the intestine to the bloodstream

Lymphatic system Lymph and lymph vessels Lymph is a specialized fluid formed in the tissue spaces transported by way of the lymphatic vessels and reenters the circulatory system Lymphatic tissue Lymph nodes Act as filters, keeping particulate matter such as bacteria from entering bloodstream The lymphatic system is composed of the lymph, nodes, and tissue. When and how are lymph nodes assessed? Where are they located? What is indicated when they are enlarged?

Lymphatic system (continued) Lymphatic tissue (continued) Tonsils Produce lymphocytes and antibodies: trap bacteria Spleen Reservoir for blood; forms lymphocytes, monocytes, and plasma; destroys worn-out RBCs; removes bacteria by phagocytosis Thymus Immune system before and a few months after birth; atrophies at puberty The tonsils are two small, kidney-shaped organs in the rear of the throat. Their function is to trap bacteria. How does their function correspond with one of the leading causes of illness in children?

Principal organs of the lymphatic system.
Figure 7-4 (From Thibodeau, G.A., Patton, K.T. [2007]. Anatomy and physiology. [6th ed.]. St. Louis: Mosby.) Principal organs of the lymphatic system.

Disorders of the Hematological and Lymphatic Systems
Diagnostic tests Complete blood count (CBC) Red cell indices Peripheral smear Schilling test Megaloblastic anemia profile Lymphangiography Bone marrow aspiration or biopsy Potential alterations in immunity can cause extreme physiological distress. Discuss the listed diagnostic examinations. When are they used?

Anemia Definition Disorder characterized by RBC and hemoglobin and hematocrit levels below normal range Causes delivery of insufficient amounts of oxygen to tissues and cells Etiology/pathophysiology Types of anemia Blood loss Impaired production of RBCs Increased destruction of RBCs Nutritional deficiencies Hemoglobin is the oxygen-carrying component in the blood cells. What are the normal values of the body’s hemoglobin levels? Do the values for men and women differ?

Anemia (continued) Clinical manifestations/assessment Anorexia Dyspepsia Cardiac dilation Disorientation Shortness of breath Dyspnea Fatigue Headache The manifestations associated with anemia can vary between individuals. At what level do signs and symptoms become apparent? Why does the patient experience shortness of breath, fatigue, and headaches?

Anemia (continued) Clinical manifestations/assessment (continued) Insomnia Pallor Palpitation Systolic murmur Tachycardia Vertigo What assessments can be used to identify a patient whose anemia is a long-term condition?

Anemia (continued) Medical management Depends on the cause Correction of the disease process may correct or lessen the anemic condition Treatment is often specific to the particular anemia Can give PO ferrous sulfate Causes constipation and black stool The physiological impact on the patient experiencing anemia can be great. What are nursing interventions that can be instituted to assist the client during this phase? What education should be provided the patient? Some religions do not permit the administration of blood transfusions. What is the role of the nurse when confronted with this dilemma?

Hypovolemic anemia Etiology/pathophysiology Abnormally low circulating blood volume due to blood loss 500-mL loss can be tolerated 1,000-mL loss can cause severe complications Severity and signs and symptoms depend on how rapid the blood is lost Hypovolemic anemia can occur as a result of surgery or trauma. Initially the body does compensate, but as the losses continue, the body’s organs become affected. How much circulating blood does the average adult have? How is the volume of circulating blood related to the body’s hemoglobin level?

Hypovolemic anemia (continued) Clinical manifestations/assessment Weakness Stupor; irritability Pale, cool, moist skin Hypotension Tachycardia (rapid, weak, thready pulse) Hypothermia Hemoglobin less than 10 g/100 mL Hematocrit less than 40% When the body is no longer able to compensate for the loss in blood value, outward signs and symptoms become observable. The nursing assessment can identify the presence of pain. Why might pain occur with hypovolemic anemia?

Hypovolemic anemia (continued) Medical management/nursing interventions Control bleeding Treat shock O2, elevate lower extremities, keep warm Replace fluid Blood transfusion, plasma, dextran, lactated Ringer’s Monitor vital signs Identification of the problem in a timely manner is key to instituting treatment. When are sudden changes in blood volume able to be detected in blood studies? If there is delay, why does this happen?

Pernicious anemia Etiology/pathophysiology Absence of the intrinsic factor from stomach Intrinsic factor is essential for the absorption of vitamin B12 Deficiency of vitamin B12 affects growth and maturity of all body cells Vitamin B12 is also related to nerve myelination May cause progressive demyelination and degeneration of nerves and white matter Pernicious anemia is a serious disease. If not correctly managed, it will result in death. The condition is due to a lack of intrinsic factor. The intrinsic factor is produced by the gastric cells in the body. Who is at risk for the development of this disease? Why is this population at an increased risk?

Pernicious anemia (continued) Clinical manifestations/assessment Extreme weakness Dyspnea Fever Hypoxia Weight loss Jaundice (destruction of RBCs) Pallor GI complaints Excessive weakness is reported overwhelmingly. What is the underlying cause of this fatigue? When collecting data from the patient who has presented with the clinical manifestations associated with pernicious anemia, what questions should be asked?

Pernicious anemia (continued) Clinical manifestations/assessment (continued) Dysphagia Sore, burning tongue Smooth and erythematous Neurological symptoms Tingling of the hands and feet Disorientation Personality changes; behavior problems Partial or total paralysis After completing a systems assessment, laboratory testing will be ordered to support the diagnosis of pernicious anemia. What tests can be anticipated?

Pernicious anemia (continued) Medical management/nursing interventions Vitamin B12 (cyanocobalamin) 1,000 units Daily for 1 week Weekly for 1 month Monthly for life Folic acid supplement Iron replacement RBC transfusion Diet: high in protein, vitamins, and minerals The treatment/management of pernicious anemia involves lifelong medication. What information should the nurse provide to the patient?

Aplastic anemia Etiology/pathophysiology Decrease of bone marrow function Primary Congenital Secondary Viral invasion Medications Chemicals Radiation; chemotherapy There are two classifications of aplastic anemia. In up to 30% of the cases, it is genetic and is present at the time of birth. Many more cases are not tied to any particular cause. Autoimmune involvement is suspected in these diagnoses.

Aplastic anemia (continued) Clinical manifestations/assessment Pancytopenic Repeated infections with high fevers Fatigue, weakness, malaise Dyspnea Palpitations Bleeding tendencies The incidence of aplastic anemia is rare. An estimated 4 in 1 million people are affected. The mortality rate is high. What can the majority of aplastic anemia–related deaths be attributed to?

Aplastic anemia (continued) Medical management/nursing interventions Identify and remove cause Platelet transfusion for severe thrombocytopenia Splenectomy for hypersplenism Steroids and androgens Antithymocyte globulin Bone marrow transplant When a patient presents with the clinical manifestations associated with the development of aplastic anemia, what diagnostic tests will be ordered to confirm the diagnosis? What results will signal a positive finding?

Iron deficiency anemia Etiology/pathophysiology RBCs contain decreased levels of hemoglobin Insufficient intake of iron Excessive iron loss Caused by chronic bleeding—intestinal, uterine, gastric

Iron deficiency anemia (continued) Clinical manifestations/assessment Pallor Fatigue; weakness Shortness of breath Angina; signs and symptoms of heart failure Glossitis; burning tongue Pagophagia Headache Paresthesia The clinical manifestations of iron deficiency anemia are a result of the reduced oxygenation of the body’s red blood cells. When collecting data from the patient, what questions should the nurse include?

Iron deficiency anemia (continued) Medical management/nursing interventions Pharmacological management Ferrous sulfate 900 mg daily Oral or injection (Z-track) Ascorbic acid Diet high in iron What foods are high in iron? A complete blood cell count can be ordered to determine the presence of iron deficiency anemia. Treatment will include both dietary modifications and pharmacological therapies. What information should be provided to the patient about taking iron supplements? What dietary education will be indicated?

Sickle cell anemia Etiology/pathophysiology An abnormal, crescent-shaped RBC Severe, chronic, incurable condition Autosomal recessive Disease Homozygous Trait Heterozygous Sickle cell anemia is the most common genetic order in the United States. Review the genetic transmission of this disorder.

Sickle cell anemia (continued) Clinical manifestations/assessment Precipitating factors Dehydration Change in oxygen tension in the body Loss of appetite Irritability Weakness Abdominal enlargement Joint and back pain Edema of extremities In most cases, the patient who has sickle cell anemia is free of clinical manifestations between birth and the first 10 to 12 weeks. What phenomenon will explain the delay in the onset of symptoms?

Sickle cell anemia (continued) Medical management/nursing interventions No specific treatment—alleviate symptoms Oxygen Rest Fluids Analgesics Bone marrow transplant Most people having sickle cell anemia experience periods of remissions and exacerbations. When the condition “flares up,” treatment is needed. What is the nurse’s role in providing care to the patient with sickle cell anemia? What are primary concerns during a sickle cell crisis?

Polycythemia (erythrocytosis) Polycythemia vera Characterized by hyperplasia of the bone marrow Manifestations Increases in circulating erythrocytes, granulocytes, and platelets Elevated WBC count Diagnostic tests CBC Alkaline phosphatase levels Uric acid levels Histamine levels What populations are most often diagnosed with polycythemia vera? Patients with polycythemia vera are at an increased risk for infarctions to vital organs. What pathology best explains this complication?

Polycythemia (erythrocytosis) Polycythemia vera Medical management/nursing interventions Pharmacological management Myelosuppressive agents Radioactive phosphorus Reduction of blood viscosity Intake and output Assessment of nutritional status Therapeutic ‘donation’ Identify two nursing diagnoses for the patient diagnosed with polycythemia vera.

Agranulocytosis Etiology/pathophysiology Severe reduction in the number of granulocytes WBC less than 200/mm3 Medications Chemotherapy ** Radiation Neoplastic disease Viral and bacterial infections Agranulocytosis is a severe condition that can result in death. How do the identified causes act as a catalyst for the disease?

Agranulocytosis (continued) Clinical manifestations/assessment Symptoms of infection Ulcerations of mucous membranes Bronchial pneumonia Urinary tract infection Medical management/nursing interventions Remove cause of bone marrow depression Prevent or treat infections Meticulous handwashing Strict asepsis When a patient presents with clinical manifestations consistent with agranulocytosis, what diagnostic tests can be anticipated? If the condition is present, what will the test results show? What are two nursing diagnoses applicable to this patient population?

Leukemia Etiology/pathophysiology Malignant disorder of the hematopoietic system Excess leukocytes accumulate in the bone marrow and lymph nodes Cause unknown Classification Acute or chronic Proliferating cells (lymphocytic, monocytic, etc.) The exact cause of leukemia is not known. There are, however, strongly supported theories to explain its cause. What are some of these theories? Identify populations who are at greatest risk for the development of leukemia.

Leukemia (continued) Clinical manifestations/assessment Anemia Thrombocytopenia; leukopenia Enlarged lymph nodes Splenomegaly Medical management/nursing interventions Pharmacological management Leukeran Hydroxyurea Corticosteroids Cytoxan Chemotherapy; radiation Bone marrow transplant Patients diagnosed with leukemia can present a variety of differing signs and symptoms. What questions should be asked by the nurse to facilitate the health intake assessment? What prognosis is associated with leukemia?

Thrombocytopenia Etiology/pathophysiology Condition in which the number of platelets is reduced below 100,000/mm3; may be due to decreased production or decreased survival of the platelets Clinical manifestations/assessment Petechiae Ecchymoses Platelets below 100,000/mm3 Bleeding from mucous membranes Thrombocytopenia occurs when the number of healthy circulating platelets is significantly reduced. What conditions/factors can be attributed to a diagnosis of thrombocytopenia? When collecting data from the patient, what questions will assist in gathering subjective data to aid in the diagnostic process?

Thrombocytopenia (continued) Medical management/nursing interventions Pharmacological management Corticosteroid therapy Gamma globulin Immunosuppressive therapy Splenectomy Platelet transfusions Avoid trauma Diagnostic tests used to confirm the presence of thrombocytopenia include complete blood counts and bone marrow studies. What nursing implications are associated with these tests? When medication therapies are initiated, explain how they will work to manage this disorder.

Hemophilia Etiology/pathophysiology Hereditary coagulation disorder, characterized by a disturbance of clotting factor Hemophilia A; hemophilia B X-linked hereditary trait Clinical manifestations/assessment Internal and external bleeding Hemarthrosis Excessive blood loss from small cuts and dental procedures Hemophilia is an inherited disorder. Explain the genetic transmission of the disorder.

Hemophilia (continued) Medical management/nursing interventions Minimize bleeding—avoid trauma Relieve pain—no aspirin Transfusions Factor VIII or IX concentrate Cryoprecipitate (rich in factor VIII) Manufactured factor VIII or IX Small, seemingly minor injuries can become life-threatening in the hemophiliac. What activities of daily living can become serious for the hemophiliac patient? What are the responsibilities of the nurse in providing care to this patient?

von Willebrand’s disease Etiology/pathophysiology Inherited bleeding disorder characterized by abnormally slow coagulation of blood; mild deficiency of factor VIII Similar to hemophilia; not limited to males Clinical manifestations/assessment Spontaneous episodes of GI bleeding Epistaxis Gingival bleeding von Willebrand’s disease is a disorder of coagulation. How does this disease differ from hemophilia? How are the disorders similar?

von Willebrand’s disease (continued) Medical management/nursing interventions Pharmacological management Desmopressin (DDAVP) Cryoprecipitate Fibrinogen Fresh plasma Minimize bleeding—avoid trauma Relieve pain—no aspirin

Disseminated intravascular coagulation Etiology/pathophysiology Overstimulation of clotting and anticlotting processes in response to disease or injury Clinical manifestations/assessment Bleeding; hemoptysis Dyspnea Diaphoresis Cold, mottled digits Purpura on the chest and abdomen Petechiae What are examples of situations that can lead to the development of DIC? In addition to the outwardly obvious clinical manifestations, what subjective signs might exist in the patient?

Disseminated intravascular coagulation (continued) Medical management/nursing interventions Pharmacological management Heparin—considered somewhat controversial Treat underlying cause Cryoprecipitate Protect from bleeding and trauma Despite the overwhelming blood loss that results with the onset of DIC, treatment involves the administration of heparin and fibrinolytic inhibitors. How will these medications act to correct the disease process?

Multiple myeloma Etiology/pathophysiology Malignant neoplastic immunodeficiency disease of the bone marrow Clinical manifestations/assessment Bone pain; pathological fractures Infection Anemia; bleeding Hypercalcemia Renal failure Neoplastic plasma cells invade the bone marrow of the patient diagnosed with multiple myeloma. The loss of bone tissue causes the onset of bone pain and fractures. What populations are at the highest risk for the development of multiple myeloma?

Multiple myeloma (continued) Medical management/nursing interventions Symptomatic; not curable Pharmacological management Corticosteroids Analgesics Radiation Chemotherapy IV fluids The disorder is managed with symptomatic therapies. In addition to the pharmacologic measures, what nursing interventions should be initiated to provide care to this population? Review the prognosis of the patient with multiple myeloma.

Lymphangitis Etiology/pathophysiology Inflammation of one or more lymphatic vessels Usually occurs from acute streptococcal or staphylococcal infection in an extremity Clinical manifestations/assessment Fine red streaks from the affected area Edema Chills; fever Local pain Headache; myalgia What nursing diagnoses are appropriate for this patient population? Lymphangitis is a disorder that has a good prognosis after treatment.

Lymphangitis (continued) Medical management/nursing interventions Penicillin Moist heat Elevate extremity

Lymphedema Etiology/pathophysiology Primary or secondary disorder Accumulation of lymph in the soft tissue Clinical manifestations/assessment Massive edema and tightness of affected extremity Pain The onset of lymphedema is a painful disorder in which there is an accumulation of lymph in the soft tissue. What causes this buildup of lymph and subsequent edema?

Lymphedema (continued) Medical management/nursing interventions Pharmacological management Diuretics Antibiotics Compression pump Elastic stocking or sleeve Restricted sodium diet Avoid constrictive clothing Meticulous skin care Identify the goals of treatment for the patient diagnosed with lymphedema. Outline important points for patient education relating to the diagnosis of lymphedema.

Hodgkin’s disease Etiology/pathophysiology Inflammatory or infectious process that develops into a neoplasm Affects males twice as frequently as females Reed-Sternberg cells What characteristics do people affected with Hodgkin’s disease share? How do non-Hodgkin’s and Hodgkin’s lymphoma differ?

Hodgkin’s disease (continued) Clinical manifestations/assessment Enlargement of cervical lymph nodes Anorexia Weight loss Pruritus Low-grade fever Night sweats Anemia Leukocytosis

Hodgkin’s disease (continued) Medical management/nursing interventions Stage I or II (localized) Radiation Stage III or IV (generalized) Chemotherapy Combination A staging process is also used in Hodgkin’s disease. Staging is used to determine the needed treatment plan. What are the goals of treatment? What is the prognosis for patients diagnosed with Hodgkin’s disease?

Figure 7-5 (From Belcher, A.E. [1992]. Blood disorders, Mosby’s clinical nursing series. St. Louis: Mosby.) Nodal involvement by stage in Hodgkin’s disease (based on modified Ann Arbor Staging System).

Non-Hodgkin’s lymphoma Etiology and pathology A group of malignant neoplasms Characterized as a neoplasm of the immune system Cause is unknown Tumors usually start in lymph nodes and spread to lymphoid tissue in the spleen, liver, GI tract, and bone marrow NHL is the most common hematological cancer. Its rate of occurrence is increasing. What groups of patients are at a higher risk for the development of non-Hodgkin’s lymphoma? What populations are associated with the development of non-Hodgkin’s lymphoma? What theories are supported concerning the underlying cause for the disease?

Non-Hodgkin’s lymphoma (continued) Clinical manifestations/assessment Painless, enlarged cervical lymph nodes Fever; susceptibility to infection Weight loss; anorexia Anemia Pruritus Fatigue Malaise After a review of the patient’s health history, diagnostic tests will be ordered to confirm a diagnosis. What tests can be anticipated? What results will accompany a positive diagnosis?

Non-Hodgkin’s lymphoma (continued) Diagnostic tests Bone scan CBC ESR Coombs’ test Chest roentgenogram CT scan Gallium scan Biopsies

Non-Hodgkin’s lymphoma (continued) Medical management/nursing interventions Accurate staging of the disease is crucial to determine treatment regimen Radiation Chemotherapy Bone marrow transplant Tumor necrosis factor (TNF) After a diagnosis is confirmed, the disease will be staged. Staging serves to identify the advancement of the disease. Treatment options are based upon the stage of the disease process. Discuss the four stages of the disease.

Nursing Process Nursing diagnoses Infection, risk for
Injury (trauma) risk for (bleeding, falls) Fatigue Knowledge, deficient Pain, acute and chronic Tissue perfusion, ineffective Gas exchange, impaired Activity intolerance Coping, ineffective Skin integrity, impaired Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc. 62

Antineoplastic Medications
Adverse Reactions Dose-dependent GI: nausea, vomiting, diarrhea, and anorexia Bone marrow depression System-specific toxicity Alopecia Drug-specific: consult manufacturer’s guidelines If a patient is experiencing bone marrow depression secondary to chemotherapeutics, what symptoms would be exhibited? What body systems are at high risk for chemotherapy toxicity? If the patient is experiencing peripheral neurotoxicity, what subjective finding is common? Adverse reactions may not occur for several days after treatment. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Antineoplastic Medications
Nursing Implications and Patient Teaching Patient and Family Teaching Chemotherapy/product education Adverse effects When to report symptoms to the health care provider Nutrition Signs of dehydration Hair loss Support groups What education will the LPN/LVN include for home storage of chemotherapy drugs? After surgery for cancer, the patient should be provided education on muscle strengthening and the use of a prosthesis if one has been prescribed. What resources can the nurse suggest for patients who are experiencing hair loss secondary to chemotherapy use? What are signs of dehydration? What symptoms and/or adverse effects will the nurse advise the patient/family to report to the healthcare provider? Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Anticoagulants Two Categories Coumarin and indandione derivatives
Limit the formation of blood coagulation factors II, VII, IX, and X in the liver by interfering with vitamin K Heparin sodium Increases the action of antithrombin III (heparin cofactor) on several other coagulation factors to slow new clot development Heparin and coumarin and indandione derivatives interfere with the blood clotting chain at multiple sites. Neither of these categories of medication dissolves existing clots. Blood clots that are “fixed” in the body are called “thrombi.” Blood clots moving throughout the circulation are called “emboli.” All emboli eventually end up traveling to the lungs, heart, and brain, because that is the normal route of circulation and where major damage can occur. Low-molecular-weight heparin is a special formulation used in special circumstances, such as prevention of deep vein thrombosis after surgery. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Anticoagulants (cont.)
Action and Uses Prevent new thrombus formation Stop existing thrombi from growing in size Prophylactic: postsurgery involving the heart or circulatory system Patients with heart valve disease, some dysrhythmias, and receiving hemodialysis Patients on prolonged bed rest or with a history of thrombus formation There are many indications for anticoagulant therapy. When a clot (thrombus) lodges in the circulatory system, blood flow is diminished or cut off to the area. This results in tissue and organ impairment and/or death. It is beneficial to “thin the blood” in patients with heart valve disease or some dysrhythmias to facilitate circulation in these impaired areas and prevent blood from pooling and clotting. Patients on hemodialysis have an internal access device that is placed in an area that has a high degree of circulation. As this is an invasive technique, and hemodialysis is essential to maintain the patient’s life, anticoagulants are used to keep the device open. Heparin is used for acute therapy because it is given IV or SQ. Heparin is also used if the patient is pregnant. Warfarin (Coumadin) is used for long-term therapy. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Adverse Reactions Warfarin (Coumadin): alopecia, rash, urticaria, cramping, diarrhea, intestinal obstruction, nausea, paralytic ileus, vomiting, excessive uterine bleeding, hemorrhage, leukopenia, fever Heparin sodium: hypertension, headache, hematoma, conjunctivitis, tearing of eyes, rhinitis, hemorrhage, thrombocytopenia, dyspnea, chills, fevers, alopecia, persistent or prolonged erection, hypersensitivity There are many adverse reactions to anticoagulant therapy. Patients requiring these drugs are typically compromised. It is important to closely assess patients for leukopenia and thrombocytopenia, which would put them at additional risk. Early signs of overdosage or internal bleeding include bleeding from gums while brushing teeth, excessive bleeding or oozing from cuts, unexplained bruising or nosebleeds, and unusually heavy or unexpected menses in women. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Drug Interactions Nursing Implications and Patient Teaching Calculation procedure of heparin is critical Monitoring blood values Coumadin = prothrombin time (PT); therapeutic is 1.5 to 2.5 × normal or an INR of 2.0 to 3.0 Heparin = activated partial thromboplastin time (aPPT); therapeutic is 2.5 to 3 × the control value Many drugs alter the effect of anticoagulants. Coumarin and indandione derivatives increase the effect of heparin as do alcohol, aspirin, NSAIDs, and dextran. Antihistamines, digitalis, nicotine, and tetracycline decrease the anticoagulant effect of heparin. ASA, corticotropin, ethacrynic acid, glucocorticoids, and NSAIDs increase the risk of GI bleeding with heparin. Adrenocorticosteroids, antacids, antihistamines, barbiturates, oral contraceptives, estrogens, griseofulvin, haloperidol, meprobamate, primidone, rifampin, thiazide diuretics, and vitamin K decrease the action of Coumadin. Oral hypoglycemics taken with anticoagulants may increase the effect of either the hypoglycemic or anticoagulant. Close monitoring and evaluation by the health care provider are essential when patients are taking these medications. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Protamine Sulfate Action
Strong, alkaline protein that neutralizes effects of heparin Results immediate, last 2 hours or more Uses Treatment of heparin overdose After surgical procedure where heparin was used Adverse Reactions When a patient requires use of the heart-lung machine (extracorporeal circulation), large doses of heparin are used. Protamine sulfate is used to counteract the heparin when the machine is discontinued. Adverse reactions to this medication include bradycardia, dyspnea, lassitude, hypotension, transitory flushing, and feeling of warmth. An overdose of this medication produces anticoagulant effects. Protamine sulfate is only given by a physician, IV, over 1 to 3 minutes. Typical dosage is 50 mg or less over a 10-minute period. What teaching would the LVN/LPN offer the patient and family? Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Thrombolytic Agents Action
Convert plasminogen to the enzyme plasmin, which breaks down fibrin clots, fibrinogen, and other plasma proteins anywhere in the body Uses Acute myocardial infarctions Acute pulmonary emboli Acute ischemic stroke Acute arterial occlusion There is a narrow window of time for these drugs to be successful in dissolving thrombi during emergent events. Therefore, prompt initiation of the emergency system is essential. Bleeding is the most common adverse reaction, along with dysrhythmias, hypotension, polyneuropathy, cholesterol embolism, pulmonary embolism, and drug hypersensitivity. If administered with other anticoagulants in the patient’s system, there is increased risk of bleeding. What should the LPN/LVN consider when assisting with the administration of these drugs? What patient and family teaching should occur? Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Antiplatelet Agents Action Inhibit platelet aggregation (clumping)
Reduce thrombus formation Uses Salicylic acid (aspirin) Reduces incidence of myocardial infarction-related deaths in men over 50 Drug of choice in ischemic stroke Platelet aggregation or clumping is essential for a blood clot (thrombus) to develop. Aspirin continues to be one of the leading antiplatelet agents. Many drugs, especially OTC preparations, contain aspirin compounds; patients should be made aware that these will increase the risk of bleeding. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Antiplatelet Agents (cont.)
Uses (cont.) Dipyridamole (Persantine), ticlopidine (Ticlid), clopidogrel (Plavix) Myocardial prophylaxis for men Adjunctive therapy with thrombolytics to prevent an infarction or stroke Abciximab (ReoPro), anagrelide (Agrylin) During cardiac catheterization and cardiac procedures Bleeding is the most common adverse reaction to antiplatelet agents. Other adverse reactions include diarrhea, nausea, dyspepsia, rash, GI pain, neutropenia, purpura, vomiting, flatulence, pruritus, dizziness, and anorexia. Antiplatelets have variable reactions when given with antacids, cimetidine, digoxin, and theophylline. During an emergent situation, close patient monitoring is crucial. What patient and family teaching should occur? Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Question ? Which is the anticoagulant of choice when an immediate effect is needed? Warfarin Plavix (clopidogrel bisulfate) Heparin Aspirin Correct Answer: 3 Rationale: Heparin, which is only effective when given IV or subcutaneously, is the anticoagulant of choice when an immediate effect is needed. Warfarin, Plavix, and aspirin are oral agents used for long-term anticoagulant therapy. Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

Chapter 7 Care of the Patient with a Blood or Lymphatic Disorder

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