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Lymph, Blood, Immune

68WM6 Blood Lymph Immune

QuestionAnswer
According to Humoral Immunity what are the events which take place? B cells initiate response and produce antibodies to antigen 1. T Cells help B cells to proliferate, synthesize, and secrete appropriate antibody 3. Antigens are neutralized by antibodies, form immune complexes, or can be phagocytosed
According to Cellular Immunity what are the events which take place? Antigen is processed by macrophages and recognized by T cells.T cells produce lymphokines Lymphokines attract macrophages and neutrophils to site for phagocytosis or a cytotoxic killer T cell responds directly
What occurs with aging that produces a decline in the immune system? Thymus decreases in size and activity Older individuals with chronic illnesses are at increased risk for infection
What is Immunodeficiency? An abnormal condition of the immune system in which cellular or humoral immunity is inadequate and resistance to infection is decreased
What is a hypersensitivy reaction? An inappropriate and excessive response of the immune system to a sensitizing antigen
Define Hypersensitivity Disorder Inappropriate and excessive response of the immune system to a sensitizing antigen Arise when harmless substances are recognized as foreign (pollens, danders, foods, and chemicals)
Factors That Influence Hypersensitivity Host response to allergen Exposure amount Nature of allergen Route of allergen entry Repeated exposure
What should the assessment of a Hypersensitivity disorder patient include? Should involve the integumentary, gastrointestinal, respiratory, and cardiovascular systems Nurse should be aware of seasonal nature of complaints Subjective data   Objective data
What Diagnostic testing can be done on a hypersensitivy patient? Patient history and physical exam  Laboratory studies Complete Blood Count (CBC) Skin testing Total serum IgE levels RAST (radioallgergosorbent test)
What is the medical management of a patient with hypersensitivity disorder? Symptom management with medications Environmental control Immunotherapy
What patient teaching should be done with a patient with hypersensitivity disorder? Should revolve around the specific diagnosis Inform patient regarding seasonal avoidance of offending allergens Therapeutic medication plan Focus on health promotion and health teaching for self-care management
What is Immunodeficiency Disease? First evidence of immunodeficiency disease is an increased susceptibility to infection Can manifest as recurrent infection or chronic infection Unusually severe infection with complications
Immunodeficiency disease involves an impairment of one or more immune mechanisms? Phagocytosis Humoral response Cell-mediated response Complement Combined humoral and cell-mediated deficiency
Describe what a primary immunodeficiency disease is and why it occurs? Rare and often serious Immune cells are improperly developed or absent Phagocytic defects B-cell deficiency T-cell deficiency Combined B-cell and T-cell deficiency
Describe what a secondary immunodeficiency disease is and why it occurs? More common and less serious Deficiency caused by illness or treatment Drug-induced Stress Hypofunctional state Malnutrition Surgical removal of lymph nodes Hodgkin's disease
Give some examples of conditions thought to be autoimmune? Pernicious anemia Guillain-Barre syndrome Scleroderma Jorgen's syndrome Rheumatoid arthritis Ulcerative colitis Male infertility Myasthenia gravis Multiple sclerosis Systemic lupus erythematosus Type I diabetes mellitus
Fatal reactions in anaphylactic shock are associated with what events? Fall in blood pressure Laryngeal edema Bronchospasm Cardiovascular collapse Myocardial infarction Respiratory failure
How can anaphylaxis be classified as? mild, moderate, and severe
What is the first line treatment for anaphylactic shock? At first sign, 0.5 ml of epinephrine (Adrenalin Chloride) 1:1000 subcutaneously
After Epi what is the treatment for anaphylactic shock? Repeat at 15-minute intervals Benadryl 50-100 mg IM or IV as indicated for allergic signs and symptoms If moderate to severe signs and symptoms occur, IV therapy may be initiated to prevent vascular collapse Intubation to prevent airway obstruction O2
What is Systemic Lupus Erythematosus? Autoimmune disorder characterized by inflammation of almost any body part Chronic and incurable Effects women 9 times more than men; most prevalent in women of childbearing age Occurs when the body produces antibodies against its own cells
Systemic Lupus Erythematosus signs and symptoms? Oral ulcers Arthralgias or arthritis Vasculitis Rash Nephritis Pericarditis Synovitis Organic brain syndromes Peripheral neuropathies Anemia Leukopenia
What are some common complications of Systemic Lupus Erythematosus? Thrombocytopenia Coagulopathies Immunosuppression Dermatitis Anemia is the most common
No single test is considered to be conclusive Positive results on one or more diagnostic test along with at least three other criteria lead to diagnosis what are the diagnostic tests used to diagnose Systemic Lupus Erythematosus? Antinuclear antibody DNA antibody Complement CBC Erythrocyte sedimentation rate Sedimentation rate Coag Rheumatoid factor Rapid plasma reagin Skin and renal biopsy C-reactive protein Coomb's test Lupus erythematosus cell preparation Chest XRAY
Systemic Lupus Erythematosus diagnostic criteria? Erythematous butterfly rash Photosensitivity Oral ulcers Polyarthralgias and polyarthritis Pleuritic pain, pleural effusion, pericarditis, and vasculitis Renal disorders
Systemic Lupus Erythematosus medical management? Relief of symptoms Induce remission Early alleviation of exacerbations Prevention of complications Peritoneal dialysis or hemodialysis
Systemic Lupus Erythematosus drug therapy? Nonsteroidal anti-inflammatory drugs Antimalarial drugs Corticosteroids Antineoplastics Antiinfective drugs
Systemic Lupus Erythematosus patient teaching? Avoidance of sunlight, balancing activity with rest, recognize signs and symptoms of exacerbation signs and symptoms of infection, and proper nutrition (decreased sodium intake). Provide psychosocial, emotional, and spiritual support
Plasmapheresis removal of plasma that contains components causing or thought to cause disease
Plasmapheresis is used to treat autoimmune diseases such as? Systemic lupus erythematosus Glomerulonephritis Myasthenia gravis Thrombocytopenic purpura Rheumatoid arthritis Guillain-Barre syndrome
Plasmapheresis removes pathologic substances present in plasma Antinuclear antibodies (autoantibody) Antigen - antibody complexes Inflammatory mediators (comllement system)
Describe the Plasmapheresis procedure? Removal of whole blood through a needle inserted in 1 arm Removed blood is circulated through a cell separator Needle is inserted into opposite arm for return blood Plasma is replaced by normal saline, LR, FFP, plasma protein fractions or albumin
What are two common complications of Plasmapheresis? Hypotension results from Vasovagal reaction Transient volume changes Citrate toxicity Citrate is used as an anticoagulant and may cause hypocalcemia Signs and symptoms include headache, paresthesias and dizziness
Typing and Cross Matching of Blood Donors Blood typing systems are available to ensure that transfusion products match the recipient's blood as closely as possible Patient's blood type and Rh factor must always be verified to be compatible with the donor transfusion
Selection of Blood Donors Careful selection of blood donors is important in preventing transfusion reactions Donor and recipient numbers are specific and must be thoroughly checked Patient must be identified with an arm band and last 4
Blood Storage Blood and blood components should be refrigerated at specific temperatures until 1/2 hour before administration must be administered within 4 hours of removal from refrigeration must be admin within 6 hours of removal Refrigerator labeled for blood
What size of needle should be used for blood administration? Insert a large gauge IV catheter (14, 16, or 18) for administering blood to an adult patient. This will enhance the flow of blood and prevent hemolysis of the cells
When monitoring for admin reaction how often should you observe vital signs and what should you do if you suspect a reaction? 15 minutes closely Any time an adverse reaction is suspected, immediately stop the blood and infuse normal saline. Notify the charge nurse and physician immediately
What has to be sent to the lab if a blood transfusion reaction occurs? the unused blood and recipient tubing must be sent to the laboratory along with a 10 ml specimen of the patient's venous blood and a post transfusion urine specimen
Function of the blood is to bring oxygen and nutrients to the cells of the body and to remove waste products
The fibrinolytic system is activated when? soon after the clotting cascade to ensure that clotting does not become uncontrolled and to dissolve the clot to reestablish perfusion Blood tends to be more non-thrombogenic than thrombogenic These systems are well-balanced to control hemostasis
Vessel Spasm Contraction of blood vessel immediately after damage to control the loss of blood. Effect lasts for about 30 minutes
Platelet Plug Platelets become activated Controls blood loss if vessel break is small
Clotting Cascade Damage to blood vessels/tissue causes release of substances that activate Dependent on the availability of clotting factors & calcium Intrinsic and extrinsic pathways both end in final common pathway with prothrombin Prothrombin converted to thrombin
Fibrinolysis  Tissue plasminogen activator (t-PA) is present in the lining of all blood vessels, and is released after clot formation t-PA converts plasminogen into plasmin Plasmin dissolves fibrin, thereby dissolving clot Perfusion of blood vessel is reestablished
What are the four steps of Hemostasis? Vessel spasm Platelet plug Clotting cascade Fibrinolysis
Coagulopathies Condition in which a component that is necessary to control bleeding is missing or inadequate Thrombocytopenia Hemophilia Disseminated Intravascular Coagulation (DIC)
Thrombocytopenia  Platelet disorder exhibiting a deficiency of the number of circulating platelets or change in the function of platelets Number of platelets is reduced below 100,000/mm3 (Normal is 150,000 to 450,000/mm3)
Thrombocytopenia Causes Decreased production plts Aplastic anemia  Leukemia  Tumors/chemo Decreased plt survival  Antibody destruction Infection/viral invasion Altered plt function/increased plt consumption DIC  Most common is thrombocytopenia purpura
Thrombocytopenia Petechiae- occur only in platelet disorder  Ecchymoses Severity of signs and symptoms correlates with the platelet count  Significant bleeding can occur with platelet count < 20,000/mm3  Spontaneous bleeding can occur with platelet count < 5,000/mm3
Subjective data for Thrombocytopenia Recent viral infection Current use of medications Extent of alcohol ingestion History of bleeding tendencies
Objective data for Thrombocytopenia Melena, hematuria  Petechiae and ecchymosis  Epistaxis and gingival bleeding  Signs of increased intracranial pressure caused by cerebral hemorrhage Any bleeding tendencies
Thrombocytopenia Diagnostic Complete blood count- shows decreased platelets Peripheral blood smear- to identify abnormalities in all cell lines Bleeding time  Bone marrow aspiration
Thrombocytopenia Medical Management Corticosteroid therapy  Intravenous gamma globulin or immunosuppressive drugs Transfusion of platelets with bleeding (Maintain platelets >50,000/mm3) Plasmapheresis Splenectomy with chronic condition
Thrombocytopenia Nursing Interventions Monitor medications for toxicity Monitor/prevent infection  Meticulous asepsis Gentle handling of patient  Monitor blood, plasma and platelet infusion for reaction and effects on patient's condition
Thrombocytopenia Patient Teaching Instruction on specific signs and symptoms as well as preventive measures Soft toothbrush  Gentle nose blowing  Importance of notifying physician of signs and symptoms of bleeding
Hemophilia A decrease in the formation of prothrombin activators occurs as a result of decreased clotting factors Many hemophiliacs in the 1990s developed HIV due to transfusions
Clinical Manifestations of Hemophilia Internal or external hemorrhage with large ecchymosis into tissues Muscles show deformity and joints become ankylosed (immobile)  Hemarthrosis- ankles, knees, and elbows   Pain, erythema and fever with hemarthrosis Excessive bleeding from small cuts
Subjective and Objective Data of Hemophilia Subjective  Patient and family history of ecchymosis and hemorrhage Pain associated with joint movement  Objective  Presence of blood in subcutaneous tissues, urine, or stool Edematous or immobile joints
Diagnostic testing for Hemophilia Deficiency or absence of factors VIII and/or IX Serum blood tests reveal a normal platelet count, a bleeding time, prothrombin time (PT), and INR Partial thromboplastin time (PTT) is prolonged Hemoglobin/hematocrit may be normal or decreased
What is important to remember regarding Hemophilia? You dont bleed more just longer
What is the medical management of Hemophilia? Minimize bleeding and relieve pain  Transfusion and administration of factors VIII and IX 
What are some nursing interventions for Hemophilia? Control hemorrhage in emergency situations Give reassurance to patient Monitor transfusion of factor VIII concentrate Genetic counseling
What are some patient teaching for Hemophilia? understanding of avoiding injury  (-Avoid ASA) understanding of emergency care  Immobilize/Pressure  Ice  Contract physician  Obtain medical alert avoidance of obesity as weight puts extra pressure on joints with potential for bleeding
Disseminated Intravascular Coagulation Grave coagulopathy resulting from the over stimulation of clotting and anticlotting processes in response to disease or injury. Mortality reaches 80-90%
Describe the process of DIC When thrombosis is stimulated, fibrinolysis is also Microvascular clotting causes decreased perfusion in organs and can lead to end organ damage Consumption of clotting factors &fibrinolysis causes stable clots to degrade with an inability to make clots
What is the cause of DIC? Precipitating causes for DIC  Obstetrical  Neoplastic Trauma Other
What is the subjective signs for DIC? Bleeding complaints (mucous membranes, hematuria, melena, hemoptysis Indications of end organ damage (i.e. dyspnea, chest pain, decreased urine output) Complaints of bone and joint pain Complaint of visual changes
What is the objective signs for DIC? Occult blood or obvious bleeding Purpura on chest and abdomen  Petechiae of skin and mucosa GI bleeding, abdominal tenderness Hematuria Pulmonary embolism or edema Hypotension, tachycardia, decreased or absent peripheral pulses seizures or coma
How is DIC diagnosed? DIC panel- shows prolonged PT/PTT, positive D-dimer (reveals elevated levels of fibrin breakdown products- indicates fibrinolysis)  Decreased fibrinogen and decreased clotting factors
What is the treatment for DIC? Correct the underlying cause, stop the abnormal coagulation and control bleeding  Treat underlying hypoxemia, acidosis  Treat underlying infection Remove inciting trigger
How is volume replaced in DIC? Crystalloids Transfusion (PRBCs, platelets, FFP) and cryoprecipitate (concentrated fibrinogen) Vitamin K  Heparin therapy Aminocaproic acid- fibrinolysis inhibitor  Anti-thrombin III- thrombosis inhibitor
Nursing Interventions for DIC? Monitor for thrombosis and fibrinolysis  Control bleeding and report to physician Monitor for end-organ damage for microvascular thrombi and report Monitor labs Maintain circulating volume Protect from bleeding and trauma 
Medications which may increase Thrombocytopenic Effect? Aspirin  Digitalis derivatives  Furosemide Nonsteroidal anti-inflammatory agents Oral hypoglycemics Penicillins Quinidine  Rifampicin  Sulfonamides Thiazides Rantitidine
Identify the causes of thrombocytopenia, hemophilia and DIC *****? Thrombocytopenia- usually idiopathic Hemophilia- X-linked hereditary trait DIC- secondary process with massive over stimulation of the clotting cascade
Von Willibrand's disease inherited bleeding disorder characterized by abnormally slow coagulation of blood and spontaneous episodes of GI bleeding, epistaxis, and gingival bleeding caused by a mild deficiency of factor VIII. post partum periods, as menorrhagia, and after surgery
Von Willibrand's disease treatment Cryoprecipitate transfusion containing factors VIII, recombinant factor VIII, fibrinogen and/or fresh plasma Desmopressin (DDAVP) is becoming the treatment choice of mild hemophilia
What clotting factor is deficient in vonWillebrand's Disease? Factor 8
Name two nursing diagnosis associated with a patient with a coagulation disorder Altered tissue perfusion, related to hemorrhage Fluid volume deficit, related to hemorrhage Pain, related to thrombosis
AGRANULOCYTOSIS A severe reduction in the number of granulocytes (basophils, eosinophils, and neutrophils) Low white blood count Bone marrow suppression Fatality may result from severe bacterial infections
AGRANULOCYTOSIS Causes Adverse medication reaction or toxicity Neoplastic disease Chemotherapy and radiation therapy Viral and bacterial infections Heredity
AGRANULOCYTOSIS Clinical Manifestations Fever and chills Headache and fatigue Ulcerations of the mucous membranes Bronchial pneumonia and urinary tract infections in later stages
AGRANULOCYTOSIS Subjective and Objective Signs and Symptoms Subjective Fever and extreme fatigue Objective Fever over 100.6 F Erythema and pain from ulcerations Crackles and rhonchi due to exudates
AGRANULOCYTOSIS Diagnosis WBC w/differential- decreased WBC Bone marrow biopsy – suppressed activity Cultures to identify possible infective organism
AGRANULOCYTOSIS Main Medical Managament Goal alleviate bone marrow depression and treat infections Treatment based on organism and drug sensitivity Neutropenic precautions Transfusions as needed
AGRANULOCYTOSIS Nursing Interventions Protect against infection Monitor pt closely Provide high protein, high calorie diet Encourage fluids Handwashing and strict asepsis Observe for s/s of infection Enforce neutropenic precautions Monitor mucous membranes for ulcers
AGRANULOCYTOSIS Patient Teaching S/S of infection Frequent oral hygiene Avoid crowds, infected people, cold or hot environment Medication, diet and rest
LEUKEMIA A malignant disorder of the hematopoietic system which an excess leukocytes accumulates in the bone marrow & lymph nodes WBC replaces bone marrow Abnormal concentration & forms of immature cells found These cells infiltrate lymph nodes, spleen and liver
Leukemia Causes Genetic origins Viruses Exposure to radiation or chemotherapeutic agents
Leukemia Clinical Manifestations Anemia Thrombocytopenia (petechiae, epistaxis, easy bruising) Leukopenia (fever, URI, UTI) Enlarged lymph nodes and painless splenomegaly may be first sign
Leukemia Diagnostic CBC- low, elevated, or severely elevated WBCs Bone marrow biopsy – immature leukocytes Lymph node biopsy – excessive immature WBCs Chest xray mediastinal lymph nodes, lung involvement Peripheral smear – immature WBCs CT/Lumbar puncture
Leukemia Subjective and Objective Data Subjective Pain in bones or joints Fatigue, malaise, and irritability Bleeding abnormalities Objective Infection Occult blood in stools and urine Petechiae, ecchymoses, bleeding of mucous CBC
Leukemia Nursing Interventions Neutropenic prec Pt teaching on the avoidance of infect agents Observe for s/s of infection Monitor for graft vs. host complications non-pharm comfort measures Provide analgesics as order and monitor effects Monitor CBC prtect pt from injury
Leukemia Medical Management Acute- complex combination of chemotherapeutic drugs and total body radiation Chronic –Drug therapy is palliative, not curative; Chlorambucil, Hydroxyurea, Corticosteroids Note: Blood transfusions if severe anemia
What is the goal of medical management of Leukemia? achieve remission or control symptoms Treatment is aimed at eradicating the leukemia with chemotherapy or bone marrow transplant
When caring for a patient with leukemia what nursing interventions can a nurse implement for the emotional state of the patient? Monitor for feelings of abandonment and loneliness Monitor and treat side effects of chemo/rad Obtain thorough knowledge of chemo and prophylactic drugs Encourage pt to verbalize anxiety, fear, anger, helplessness Recommend community support groups
Leukemia Patient Teaching S/S of infection Avoiding infected persons Contact physician for s/s of infection Medication/dietary All procedures and interventions to patient and family
MULTIPLE MYELOMA Malignant neoplastic immunodeficiency disease of the bone marrow The tumor destroys osseous tissue. Plasmas cells proliferate, destroys bone by crowding bone marrow
MULTIPLE MYELOMA Clinical Manifestations Proliferation of malignant plasma cells Development of tumors Bone destruction Bone pain increasing with movement Pathological fractures due to changes Pancytopenia Hypercalcemia with potential renal problems Bence Jones protein primary marker
MULTIPLE MYELOMA Subjective and Objective Data Subjective Pain with movement Assess emotional and spiritual support Objective Expressions of pain Able to perform ADL Fever, s/s of infection esp resp. and urinary Monitor for bleeding
MULTIPLE MYELOMA Diagnosis CBC – pancytopenia Radiographic studies-demineralization of bone, lytic lesions and osteoporosis Bone marrow biopsy – large amt of immature plasma cell Blood and urine- monoclonal protein is marker Protein electrophoresis – Bence Jones protein
MULTIPLE MYELOMA Medical Management Treatment is symptomatic; disease is incurable Radiation and chemotherapy Antineoplastic drugs Monitor CBC Treat hypercalcemia and pain
MULTIPLE MYELOMA Nursing Interventions Maintain neutropenic precautions/clean patient environment. Teach/assess/observe signs/symptoms of infection. Provide high protien, high calorie, high vitamin diet Monitor CBC and report abnomal values Administer antibiotics, as ordered
LYMPHANGITIS Inflammation of one or more lymphatic vessels or channels caused by an acute streptococcal or staphylococcal infection in an extremity
LYMPHANGITIS Clinical Manifestations Fine red streaks from the affected area in the groin or axilla Usually not localized, and edema is diffuse Chills, fever, and local pain accompany headache and myalgiaLymphadenopathy (swollen lymph nodes) Septicemia may occur
LYMPHANGITIS Diagnosis Made by visual inspection and palpitation
LYMPHANGITIS Treatment Administration of penicillin or other antimicrobial drugs controls the infection Hot, moist heat-soaks or packs for comfort
LYMPHANGITIS Nursing Interventions Aseptic technique promotes healing Rest and extremity elevation may relieve the pressure Inspect the area 2-3 times daily and document client’s response to antibiotic therapy
What is the cause of lymphangitis? an acute streptococcal or staphylococcal infection in an extremity
LYMPHEDEMA Primary or secondary disorder characterized by the accumulation of lymph in soft tissue and edema
LYMPHEDEMA Clinical Manifestations Massive edema and tightness cause pressure and pain in the affected extremities Progresses toward the trunk and aggravated by: Pressure, as with pregnancy or premenstruation Obesity Warm, humid environments
LYMPHEDEMA Subjective and Objective Data Subjective data Complaints of pain and pressure Medical history of varicosities, pregnancy, or modified radical mastectomy is important Objective data Observations of the extremities for edema Palpation of distal pulses
LYMPHEDEMA Diagnostic Lymphangiography is used to differentiate lymphedema from venous disorders
LYMPHEDEMA Medical Management Fluid management/ antimicrobials are administered as ordered Diet restrictions include limiting sodium and avoiding spicy foods, which would precipitate thirst
LYMPHEDEMA Complications Mechanical management includes use of compression pumps ad elastic sleeves or stockings on the affected limb
LYMPHEDEMA Nursing Interventions Increase lymphatic drainage Elevation of the extremities while asleep and periodically during the day will facilitate draining the tissues Massage toward the trunk followed by active exercise decreases the edema Avoid constrictive clothing
LYMPHEDEMA Nursing Interventions Monitor/prevent infections Avoid trauma Meticulous skin care Emotional support Body image disturbance secondary to lymphedematous extremities Teach/assess understanding of importance of acceptance and maintaining routine activity
MALIGNANT LYMPHOMA Neoplastic disorder of lymphoid tissue (a neoplasm of the immune system) Cause is unkown herpes-like virus Includes non-Hodgkin’s lymphoma More common in men older than 60 years of age, whites and those of Jewish ancestry Tumors start in lymph nodes
MALIGNANT LYMPHOMA Clinical Manifestations Susceptibility to infection Pressure symptoms in the involved areas Pleural effusion, bone fractures, and paralysis GI malabsorption Bone lesions Painless lymphadenopathy in the cervical area Fever Weight loss Anemia Pruritus
MALIGNANT LYMPHOMA Subjective and Objective Data Subjective Complaints of fatigue, malaise and anorexia Fever and diaphoresis Objective Examination of the abdomen for splenomegaly Lympadenopathy
MALIGNANT LYMPHOMA Diagnostic Bone scan may reveal fractures, lesions, and tumor infiltration CBC-increased RBCs, WBCs, platelets, ESR and anemia Chemistry- increased calcium and alkaline phosphatase Coombs’ test-
MALIGNANT LYMPHOMA Treatment Accurate staging is crucial to determine the treatment regimen Chemotherapy and radiation. Immunotherapy with monoclonal antibodies Bone marrow transplant
MALIGNANT LYMPHOMA Nursing Interventions Supportive care of the patient during radiation and chemotherapy Monitor/prevent infection Maintain strict aseptic technique Maintain neutropenic precautions
MALIGNANT LYMPHOMA Patient Teaching Frequently reassess knowledge Explanations of the extensive diagnostic workup and its importance of staging the disease for determining the treatment plan are an important focus of patient teaching during the diagnostic period support groups
LYMPHOMAS Chemotherapy agents used are: cyclophosphamide (Cytoxan) vincristine (Oncovin) Prednisone doxorubicin (Adriamycin) Bleomycin methotrexate
Radiation LYMPHOMAS Commonly receive radiation to the chest wall, mediastinum, axillae, and neck Some patients will also need radiation to the abdomen; paraaortic area; spleen; and, less commonly, the pelvis
MONOCLONAL ANTIBODY THERAPY- RITUXIMAB Immunotherapy to eliminate malignant cells and induce remission Human cancer cells are injected into laboratory mice Mice make lymphocytes that produce antibodies against the cancer
What is special about MONOCLONAL ANTIBODY THERAPY- RITUXIMAB ? The advantage of this therapy is that it spares normal cells (as opposed to chemotherapy and radiation)
BONE MARROW TRANSPLANT Autologous or allogenic Patients will receive chemotherapy and whole-body radiation. Drugs and radiation dose dependent on type or transplant Allogenic grafts carry the risk of rejection with the development of graft vs. host disease
List three treatments of lymphomas. Radiation Chemo Bone Marrow Transplant
HODGKIN’S DISEASE Malignant disorder characterized by painless, progressive enlargement of lymphoid tissue Affects males twice as frequently as females Two age populations 15-35 years of age and over 50 years of age
HODGKIN’S DISEASE Risk Factors History of mononucleosis (Epstein-Barr virus) Acquired or congenital immune deficiency syndrome Immunosuppressive drugs after organ transplantation History of tonsillectomy or appendectomy History of diminished or delayed exposure to infections
HODGKIN’S DISEASE Clinical Manifestations Anorexia Weight loss Malaise Extreme pruritus Low-grade fever Night sweats Anemia, leukocytosis followed by respiratory infections
HODGKIN’S DISEASE Subjective and Objective Data Malaise Appetite loss Pruritus is often severe Bone pain occurs later in the disease’s course Cervical/supraclavicular lymphadenopathy Splenomegaly, hepatomegaly, and abdominal tenderness Excoriation of skin Edema of face and neck
HODGKIN’S DISEASE Diagnostic CBC-shows anemia, increased WBCs, increased ESR (shows an inflammatory process) Lymph node biopsy that includes laparoscopy for retroperitoneal nodes is performed The presence of Reed-Sternberg Cells remains a hallmark
HODGKIN’S DISEASE Treatment depends on the staging Radiation therapy Stages I and II Chemotherapy and radiation therapy Stages III and IV Advances in treatment enable stage IIIB and stage IV diseases cured with high-dose chemotherapy & bone marrow or peripheral stem cell
HODGKIN’S DISEASE chemotherapy regimens: given in cycles 6 to 12 months, or for at least 2 months after remission Traditional regimen has been MOPP, however patients were developing leukemia Mechlorethamine (Mustargen) Vincristine (Oncovin) Procarbazine (Matulane) Prednisone
Oncologists are now choosing a regimen known as ABVD over MOPP, or replacing mechlorethamine with cyclophosphamide (Cytoxan) to decrease the likelihood of long-term complications doxorubicin (Adriamycin) bleomycin (Blenoxane) vinblastine (Velban) dacarbazine (DTIC-DOME)
Biological response modifier (Neupogen) Stimulates proliferation and differentiation of neutrophils Used to decrease infection in patients receiving antineoplastics that suppress neutrophil production
HODGKIN’S DISEASE Nursing Interventions Knowledge of side effects of radiotherapy or chemotherapy Administer medications as ordered and monitor effect Provide education and emotional support to prepare patients to deal effectively with these side effects
How many stages exist for Hodgkin’s Lymphoma? 4
Oral administration of iron preparations increase the risk of GI bleeding and can lead to alteration in clotting
Ingestion of large amounts of aspirin and other anti-inflammatory medications commonly taken by older adults increase risk of GI bleeding and can lead to alteration in clotting
Blood products should be administered with caution, since older adults are at increased risk of developing congestive heart failure. Careful assessment of cardiopulmonary function and intake and output are essential
What is the current treatment for Hodgkin’s Disease? ABVD over MOPP but depends on the staging
What causes Anemia? Loss of RBCs from hemorrhage Destruction of RBCs Impaired production of RBCs Nutritional deficiencies
What is anemia? condition characterized by reduction of red blood cells, a deficiency of hemoglobin and hematocrit in the blood, or an increased destruction of red blood cells
Hypovolemic Anemia Decreased RBC, hemoglobin, and hematocrit resulting from hemorrhage Blood loss of 1000 ml or more in adult can be severe Blood loss < 500ml can be tolerated
Hypovolemic Anemia Clinical Manifestations Weakness Stupor, irritability Pale, cool, moist skin Poor peripheral pulses Hypotension with increased capillary refill time Tachycardia Hypothermia Decreased hemoglobin and hematocrit
Hypovolemic Anemia Subjective and Objective Data SUBJECTIVE Thirst Weakness, irritability, and restlessness OBJECTIVE Hypotension Rapid, weak, thready pulse Increased respirations Cool clammy skin with pallor Oliguria Mental disorientation
Hypovolemic Anemia Diagnosis CBC show decreased RBC, hemoglobin and hematocrit Caution: lab results may not be accurate indicators until hours after injury
Hypovolemic Anemia Medical Management Control hemorrhage Stop bleeding Replace volume Blood transfusion Plasma Dextran or other volume expanders Crystalloids
Hypovolemic Anemia Nursing Interventions Control bleeding Identify sites of blood loss and report Frequent vital signs, report deterioration Monitor blood and fluid restoration Patient flat and warm Raise knees for acute hypotensive episodes Strict I&Os
Hypovolemic Anemia Patient Teaching Prevent injury to patients Patient teaching Teach/assess understanding for patients with chronic bleeding tendencies Signs/symptoms of bleeding Bleeding occasions Home management When to contact physician
Pernicious Anemia Autoimmune disorder resulting from destruction of parietal cell and gastric mucosa atrophy Parietal cell damage Decreased intrinsic factor production Intrinsic factor is essential for absorption of Vit B12, factor not available to combine w/ Vit B12
Pernicious Anemia Clinical Manifestations Fever Extreme weakness Dyspnea Hypoxia Slight jaundiced Edema of legs Constipation or diarrhea
Pernicious Anemia Subjective Data Palpitations Nausea, dysphagia, flatulence and indigestion Soreness and burning of the tongue Parasthesias (tingling of hands and feet) may develop
Pernicious Anemia Objective Data Observation of smooth and erythematous tongue Infection of teeth and gums Mental disorientation, personality changes and behavior problems Partial or total paralysis due to destruction of the nerve fibers of the spinal cord
Pernicious Anemia Diagnosis Schillings test Megablastic anemia profile Bone marrow aspiration Gastric analysis Peripheral blood smear
Pernicious Anemia Treatment Drug therapy Vit B12 Folic acid and iron supplements Blood transfusion if anemia severe Long term management Life long B12 replacement CBC monitoring every 3-6 months
Pernicious Anemia Nursing Interventions Systematic approach Monitor vital signs every 4 hours Keep patient warm Oral care several times day High protein, vitamin, and mineral diet
Vitamin B 12 is needed for growth and maturation of all body cells B12 deficiency causes? erythrocytes membranes fragile and easy to rupture Nerve myelination – B12 deficiency results in progressive demyelination and degeneration of nerves and white matter
Pernicious Anemia Patient Teaching Teach/assess understanding of medications and diet Patient must understand need for life-long replacement Encourage patient to verbalize feelings Teach/assess understanding of need to space activities and ADLs Encourage frequent rest periods
What is the schillings test and describe the procedure? Stage 1 Digestion of B12, Stage 2 Digestion of Intrinsic Factor Stage 3 After Antibiotics (bacteria) and Stage 4 Pancreatic Enzymes to see if Pancreas affects b12.
Aplastic Anemia Aplasia – failure of the normal process of generation and growth Congenital- chromosomal alterations Cause unknown in 70% of acquired cases Hematopoietic tissue replaced by fatty tissue Depression of erythrocyte production Usually pancytopenic
Aplastic Anemia Causes Viral infections Medications Chemicals Radiation Chemotherapy
Aplastic Anemia Clinical Manifestations Repeated infections with high fever Weakness fatigue, general malaise Dyspnea, palpitations Bleeding tendencies ( petechiae, ecchymoses, GI/GU bleeding) High mortality with complications of infections and hemorrhage
Aplastic Anemia Subjective and Objective Data Subjective History of chemical exposure Level of fatigue with ADLs Objective Pallor Signs of infection Bleeding Dyspnea Tachycardia
Aplastic Anemia Diagnosis Bone marrow biopsy = “dry tap” Hypoplastic or aplastic fatty deposits Decreased cellular elements Decreased hematopoietic activity Peripheral blood smear May not show RBC irregularities
Aplastic Anemia Treatment Identify cause and remove Blood transfusions are avoided, if possible Splenectomy may be required if that is the cause of thrombocytopenia Drug therapy Bone marrow transplant
Aplastic Anemia Nursing Interventions Proper observation and care after bone marrow study Monitor/prevent infections Teach/assess understanding of signs/symptoms of infection and need to report to physician Use protective devices, such as egg crate mattress
Aplastic Anemia Patient Teaching Teach/assess understanding of the signs/symptoms of bleeding and need to report to physician Teach/assess understanding of scheduling activities and avoiding fatigue
Aplastic Anemia is also known as? Bone Marrow Failure
Why are blood transfusions avoided in patients with aplastic anemia? Prevention of iron overloading, prevention of antibody development for transplant candidates, platelet transfusion, as needed – must be HLA typed
Iron Deficiency Anemia RBCs contain decreased levels of hemoglobin Causes Excessive iron loss Chronic bleeding of GI or genitourinary tract
Iron Deficiency Anemia
Iron Deficiency Anemia Clinical Manifestations Pallor – most common Glossitis (inflammation and soreness of the tongue) Fatigue, weakness, shortness of breath Signs and symptoms typical to angina and heart failure may also occur
Iron Deficiency Anemia Subjective or Objective Data Subjective Glossitis and pagophagia (desire to eat ice, clays, or starches) Headache, paresthesias, burning sensation of tongue Objective PallorTachycardia Finger nail fragility with spoon shape and raised border Stomatitis Lips are erythemic
Iron Deficiency Anemia Diagnosis CBC – decreased RBC, hemoglobin, and hematocrit Decreased serum iron levels
Iron Deficiency Anemia Treatment Drug therapy Ferrous sulfate Vitamin C to enhance iron absorption Food sources rich in iron
Iron Deficiency Anemia Nursing Interventions Patient interview is critical to identify cause of anemia Drug therapy Iron replacement as ordered Teach/assess understanding of medications
Iron Deficiency Anemia Patient Teaching Educate patient on nutritional needs to prevent anemia. Foods high in iron include organ meats, white bean, leafy vegetables, raisins, molasses, dry fruits, and egg yolk plan for rest periods when fatigue is present
What is the most common clinical manifestation of iron deficiency anemia? Pallor
Sickle Cell Anemia Most common genetic disorder in U.S. Occurs predominantly in the African-American population A sickled cell is an abnormal, crescent-shape RBC containing hemoglobin S (Hg-S) - a defective hemoglobin molecule. Normal hemoglobin is hemoglobin A (Hg-A)
Sickle Cell Anemia Precipitated by: Dehydration Infection Overexertion Weather changes (cold) Ingestion of alcohol and Smoking Emotional stress
Sickle Cell Anemia Clinical Manifestations Usually asymptomatic for first 10-12 weeks of life Typical patient is anemic but asymptomatic except during painful episodes Loss of appetite and irritability Abdominal enlargement with pooling of blood Joint/back pain Edema of extremities
Sickle Cell Anemia Sujective Data Patient knowledge and feelings about disease process Known precipitating factors Fatigue when anemia is severe Pain description; location, intensity, character, duration
Sickle Cell Anemia Objective Data Abdominal enlargement and jaundice Edema of extremities Signs of hemorrhage Accelerated RBCs breakdown with jaundice and elevated serum bilirubin levels
Sickle Cell Anemia Diagnosis Hemoglobin electrophoresis Peripheral blood smear - shows only anemia CBC -decreased hematocrit and hemoglobin WBCs are increased with infection
Sickle Cell Anemia Treatment Supportive care mainly Drug therapy Rest Blood transfusion used cautiously to treat a crisis Patients should receive pneumovax and flu vaccine annually Research
Sickle Cell Anemia Nursing Interventions Monitor fluid and electrolyte balance Monitor and maintain pain control Genetic counseling as indicated Encourage patient to verbalize feelings/concerns regarding chronic medical condition
What are the two priorities in treating patients with a Sickle Cell Crisis? Fluid management and pain
Polycythemia Primary Vera Myeloproliferative disorder with hyperplasia of bone marrow causing increased circulating erythrocytes, granulocytes and platelets A stem cell abnormality of unknown cause Associated elevated WBC with basophilia
Polycythemia Secondary Caused by hypoxia rather than a defect in the evolution of the RBC Hypoxia stimulates erythropoietein which stimulates erythrocyte production high altitude, pulmonary disease, cardiovascular disease, or tissue hypoxia Physiologic response to hypoxia
Polycythemia Clinical Manifestations Gradual onset with a progressive lengthy course Mainly affects men in middle age Venous distention and platelet dysfunction cause esophageal varices, epistaxis, GI bleeding, and petechiae Hepatomegaly and splenomegaly
Polycythemia Subjective and Objective Data Subjective Sensitivity to hot and cold Pruritus Headaches, vertigo, tinnitus and blurred vision are often present Objective Eczema and dermatological changes, including erythema Hypertension with ventricular hypertrophy and angina
Polycythemia Diagnosis Arterial blood gases CBC Bone marrow examination BMR (Basic Metabolic Rate) is increased without thyroid function alteration
Polycythemia Treatment Directed at decreasing blood volume and viscosity and bone marrow activity Repeated phlebotomy to maintain hematocrit between 45 and 48% Drug therapy - all decrease bone marrow response
Polycythemia Nursing Interventions Secondary polycythemia Maintain adequate oxygenation to prevent secondary polycythemia Control pulmonary disease and avoid high altitudes Polycythemia vera Monitor fluid balance
Polycythemia Patient Teaching Teach/assess understanding of nutritional status Teach/assess understanding of medication regimen Teach/assess understanding of condition Encourage patient to verbalize concerns/feelings regarding condition/prognosis
What is the major complication of polycythemia vera? Thrombosis due to the abnormal increased number of circulating RBCs and platelets
Beliefs of Jehovah's Witnesses Jehovah's Witnesses are opposed to homologous blood transfusions They believe there are eternal consequences to receiving blood products Many agree to certain types of autologous blood transfusion Some agree to the use of various volume expanders
A judgment of the Supreme Court has been that a person of adult majority age has the right to refuse treatment but not to what? withhold treatment from a minor child
Jehovah's Witnesses may accept what types of blood products? Autologous transfusions and certain volume expanders
Active Immunity exists when the body produces specific antibodies to combat infections caused by specific antigens or microbes.
Products inducing Active Immunity Diphtheria and tetanus toxoids Acellular pertussis vaccine Haemophilus influenzae type b conjugate vaccine Hepatitis A vaccine Hepatitis B vaccine Influenza vaccine Measles, mumps, and rubella vaccines Meningococcal polysaccharide vaccine Pneumococ
Artificially Acquired Active Immunity occurs when an individual is given a killed or weakened antigen, which stimulates the formation of antibodies against the antigen.
Humoral Immunity antibody-antigen response.
Cell Mediated Immunity result of the activity of many leukocyte actions, reactions, and interactions that range from simple to complex.
Naturally Acquired Active Immunity occurs when the person is expose to a disease, experiences the disease, and the body manufactures antibodies to provide future immunity to the disease.
Passive Immunity is provided to the person by ready-made antibodies from another human or from an animal source. Immediate immunity to the invading antigen, but only last a short time.
Humoral immunity is mediated by B Cells
What is the use of immunization or vaccines? Immune globulins provide passive immunization to infectious diseases by providing antibodies.
Immunization with vaccines and toxoids containing bacterial or viral antigenic material results in? Examples? endogenous production of antibodies. anthrax vaccine (BioThrax): pre/post exposure and prophylaxis. DTaP diphtheria pertussis vaccine (Certiva, Infanrix, Tripedia): prevent diphtheria, tetanus and pertussis.
hemophilus b conjugate vaccine (Comvax, PedvaxHIB, ActHIB, HibTITER): immunization.
hepatitis A vaccine (Havrix, Vaqta): active immunization against hepatitis A virus (high risk patients, health care workers, food handlers, clotting disorders, travel to endemic areas, chronic liver disease.
hepatitis B vaccine (Engerix-B, Recombivax HB): immunization against all subtypes of hepatitis B virus (high-risk patients, health care workers, all unvaccinated adolescents).
influenza vaccine (Fluzone, FluShield, Fluvirin): prevention of influenza.
measles, mumps, rubella vaccine (MMR II): prevention of measles, mumps, rubella; adults with unreliable history; MMR illness or immunization and occupational exposure.
pneumococcal 7-valent vaccine (Prevnar): immunization against streptococcus pneumonia.
pneumococcal vaccine polyvalent (Pneumovax 23, Pnu-Imune 23): pneumoncoccal immunization. Everyone > 65 yrs, high-risk pts with chronic illnesses including HIV and other high risk pts.
polio vaccine, inactivated (IPV, IPOL, Polio-vax): prevention of polio. tetanus-diphtheria (adult Td): used for prophylaxis treatment of wounds.
varicella vaccine (Varivax): prevention of varicella-zoster (chickenpox), any adult without a hx of chicken pox or herpes zoster.
Contraindications for Vaccines/Immunizations? Hypersensitivity to product Some products contain thimerisol, neomycin, and/or egg protein. RHO(D) immune globulin: RHoD positive patients. hepatitis B immune globulin (Engerix-B, Recombivax HB): coagulation disorders.
influenza vaccine (Fluzone, FluShield, Fluvirin) contraindications? Hypersensitivity to eggs/egg products. Hypersensitivity to thimerosal (injection only). Avoid use in pts with acute neurologic compromise. FluMist should be avoided in pts receiving salicylates.
measles, mumps, rubella vaccine (MMR II)contraindications? Allergy to egg, gelatin or neomycin. Active infection. Immunosuppression. Pregnancy. Avoid becoming pregnant 4 wks after immunization.
Vaccines/Immunization Precautions? Severe bleeding problems (IM injections). Pregnancy and lactation. Renal insufficiency or predisposition to acute renal. Elderly and children. Active Infections.
Side Effects/Adverse Reactions: Immune globulins: Resp: wheezing. CV: hypotension. GI: nausea, vomiting. Derm: flushing. MS: back pain, muscle cramps. Misc: allergic reactions (fever & chills), anaphylaxis.
DTaP diphtheria pertussis vaccine (Certiva, Infanrix, Tripedia) side effects? Redness, tenderness, induration at site. Fever. Malaise. Myalgia. Urticaria. Hypotension. Neurologic reactions. Allergic reactions.
: The nurse monitoring for an anaphylactic reaction in a client who just received a vaccine understands that which of the following medications should be stored nearby? Treatment for anaphylaxis may require the administration of epinephrine. Vasopressors and intermittent positive-pressure breathing oxygen, antihistamines, and corticosteroids may help.
The following are used with corticosteroids for the prevention of transplantation rejection reactions: azathioprine (Imuran). cyclosporine (Neoral, Sandimmune, Gengraf). mycophenolate (CellCept).
Prevention of acute organ rejection (renal transplantation); used with corticosteroids and cyclosporine: basiliximab (Simulect). daclizumab (Zenapax). sirolimus (Rapamune).
Prevention of organ rejection (allogenic liver transplantation); used with corticosteroids: tacrolimus: Oral/IV: Prograf. Topical: Protopic.
Management of selected autoimmune diseases (nephrotic syndrome of childhood and severe rheumatoid arthritis): azathioprine (Imuran). cyclophosphamide (Cytoxan, Neosar). methotrexate (amethopterin, Folex, Trexall).
Immunosuppressants Contraindications? Hypersensitvity to muromonabl-CD3, murine proteins, or polysorbate. Previous muromonab therapy. Fluid volume overload. Fever > 100 degrees F. Chickenpox or recent exposure to chickenpox. Herpes zoster.
Immunosuppressants Side Effects/Adverse Reactions Most common: increased risk of infection. Neuro: trembling or shaking of hands. GI: anorexia, nausea, vomiting. Hemat: megalopblastic anemia, leukopenia, pancytopenia, thrombocytopenia.
Immunosuppressants Nursing Implications Assessment? Monitor for infection (vital signs, sputum, urine, stool, WBC). Neutrophils (normal value): 3000-7000 mm3. Neutropenia: < 1000 mm3.
In Severe neutropenia: < 500 mm3 what should the nurse do? Contact physician First line defense collapes pneumonia/septicemia/infections Protect pt against pathogens VS q4 hr notify if temperature rise NO flowers, plants or fresh fruits and vegetables Hold doses of chemotherapy until neut levels normal
Notify physician immediately if any of the following side effects occur: Unusual tiredness or weakness. Fever or chills. Frequent need to urinate.
Organ Transplant: assess for symptoms of organ rejection throughout therapy. Antigenic determinants on the cells lead to graft rejection via the immune process. Therefore recipient tissue is matched as closely as possible to donor tissue antigenic determinants prior to transplantation. Tissue matching better chance of success
Teach patient of Cyclosporin dose related signs and symptoms: nausea, vomiting, leg cramps, acne or oily skin, hirutism, tremors, nepthrotoxity, gingival hyperplasia and severe hypotension.
Which of the following would not be included by the nurse when teaching a client about the adverse effects associated with the use of azathioprine (Imuran)? Azathioprine’s adverse effects include anorexia, nausea, vomiting, leukopenia, infection, and megaloblastic anemia; increased appetite is not among the possible effects.
The risk to toxicity of methotrexate may be increased by other nephrotoxic drugs, large doses of aspirin, or NSAIDs.
Use of Antineoplastics? Used in the treatment of various solid tumors, lymphomas, and leukemias. Used in some autoimmune disorders such as rheumatoid arthritis (cyclophosphamide, methotrexate). Used in combinations to minimize individual toxicities and increase response.
Contraindications of antineoplastics? Previous bone marrow depression or hypersensitivity. Contraindicated in pregnancy and lactation
Precautions of antineoplastics? Active infections. Decreased bone marrow reserve. Radiation therapy. Other debilitating illnesses. Childbearing potential.
Common side effects of antineoplastics? memory loss tinnituys, ototoxicity cardiotoxicity nausea, vomiting, diarrhea/constipation, malnutrition, weight loss/gain nephrotoxicity pain anemia, hepatotoxicity, depression of immune system, hence infections/sepsis/hemorrhage hair loss
The nurse is aware that classifications of chemotherapy agents include which of the following? Cancer chemotherapy drugs are classified as antimetabolites, alkylating agents, antibiotic antitumor agents, and mitotic inhibitors. Miscellaneous other agents include hormones, antihormones, and corticosteroids.
Allopurinol may be given to decrease uric acid levels.
Assess for cytokine release syndrome CRS? Reactions 30-48 hours and may persist for 6 hrs Acetaminophen/antihistamines treat early reactions Methylprednisolone sodium succinate prevent CRS if given 1-4 hrs 1st dose Hydrocortisone given 30 min after the 1st 2nd dose to control respiratory SE
Created by: alexandra.bell