Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Nursing Management of Clients with Stressors of Immune Function NUR133 Lecture # 7 K. Burger, MSEd, MSN, RN, CNE Immune Response FUNCTIONS Defense against invading pathogens Removal of “worn-out” cells Immune surveillance Immune Response COMPONENTS LEUKOCYTES Neutrophils Eosinophils Basophils Lymphocytes: B-lymphocytes/ T-lymphocytes Monocytes Immune Response COMPONENTS OTHER Bone marrow / stem cells Lymph nodes Spleen Thymus Tonsils/adenoids Appendix GALT Immune Response Innate Non-specific First line of defense Immediate Inflammatory process Adaptive Specific Sustained Antibody mediated or Cell mediated Adaptive Immune System Acquired Immunity Antibody Mediated B-Lymphocytes react to extracellular antigens Sensitization occurs Division into Plasma and Memory Cell Antibody response Immediate and Long-term Cell Mediated T-Lymphocytes react to intracellular antigens Sensitization occurs Proliferation of T-cell subsets: Cytotoxic Helper Suppressor Classifications of Adaptive Immunity Adaptive immunity Natural active – most effective/ longest lasting Artificial active – vaccination / immunization Natural passive – maternal/fetus transmission Artificial passive – injection of antibodies Immune Function Excess Auto-immune Disease Failure of body to recognize it’s own HLA Antibody production against self SLE, Rheumatoid arthritis, Scleroderma +++ Hypersensitivity / Allergic Response Excessive response to an antigen Type I – Type V Hypersensitivity / Allergic Response Type I Type II Type III Type IV Type V Immediate: atopic reaction rhinitis/ anaphylaxis Cytotoxic: transfusion reaction Mediated: Immune complex Rheumatoid arthritis Delayed: Poison ivy, PPD Stimulated: Graves disease Type I Immediate Hypersensitivity Triggered by allergens: Pollen, mold, dust, certain foods or meds etc. B cells synthesize IgE antibodies to allergen IgE antibodies attach to mast cells/basophils Result = retained sensitivity Localized and/or systemic (anaphylactic) Hypersensitivity Assessment History: family hx, exposures, symptoms Physical: headache, rhinorrhea, tearing eyes Labs: elevated eosinophils elevated ESR Skin testing: scratch / intradermal Food challenge Hypersensitivity Nursing Diagnoses Ineffective health maintenance r/t deficient knowledge regarding allergies Latex allergy r/t hypersensitivity to natural rubber latex Risk for latex allergy r/t repeated exposure to products containing latex Hypersensitivity Interventions Avoidance therapy Desensitization therapy Drug therapy Decongestants Antihistamines Corticosteroids Mast Cell Stabilizers Leukotriene Antagonists Anaphylaxis Emergency Interventions Establish and maintain open airway O2 @ high flow ( 4-6 L/min) Establish IV access with NS or RL Epinephrine 1:1000 0.3 – 0.5 ml sc Benadryl 25-100 mg IV Suction prn Elevate HOB ( unless severe hypotension) Theophylline, Beta agonists, Corticosteroids to stabilize Immunodeficiency Absence or inadequate production of immune bodies Primary ( congenital ) Secondary ( acquired) Induced ( related to external stressors ) Acquired Immunodeficiency AIDS Pathophysiology HIV virus docks with CD4 (helper T-cells) Enters CD4 cell’s DNA Creates more virus Virus buds off original host CD4 to attack more cells CD4 cell no longer working as immune cell Acquired Immunodeficiency AIDS Classifications A – HIV positive B - Infected with HIV C – AIDs Progression Months – Years Dependent on: Means of acquisition Personal factors Acquired Immunodeficiency HIV / AIDS Assessment History Physical exam Testing ELISA Western Blot Viral load CBC with differential CD4 / CD8 count Additional Resource Testing Guidelines NYS DEPARTMENT OF HEALTH HIV / AIDS Web Resource http://www.health.state.ny.us/diseases/aids/index.htm Stages of HIV Infection Stage I: 3wks-3mos prior to seroconversion. Mild illness S/S or asymptomatic Stage II: 1-10 yrs after seroconversion Low rate of replication CD4 normal Stage III: Persistent lymphadenopathy Stage IV: Rapid replication of HIV virus Multiple opportunistic infections Very low CD4 counts Stage V: “Full Blown AIDS” CD4 very low HIV / AIDS Clinical Manifestations Opportunistic Infections Protozoal - Pneumocystis carinii (PCP) Fungal Candida albicans Bacterial - Mycobacterium avium (MAC) Mycobacterium tuberculosis Viral Cytomegalovirus (CMV) Herpes simplex (HSV) Malignancies Kaposi’s Sarcoma HIV / AIDs Clinical Manifestations (cont) Endocrine complications Aids Dementia Complex Wasting Syndrome Skin Changes HIV / AIDS Nursing Diagnoses Risk for infection Impaired skin integrity Diarrhea Imbalanced nutrition Acute/ Chronic pain Impaired gas exchange Disturbed thought processes Social isolation AIDS/ HIV Interventions Prevention and early detection of infection Maintenance of adequate respiratory function Pain management Maintenance of skin integrity Promotion of nutrition and IBW maintenance Maintenance of self-esteem Maintenance of orientation AIDS / HIV Interventions Drug Therapy Anti-retroviral agents in “cocktail” HAART ( Highly active anti-retroviral therapy) Nucleoside Reverse Transcriptase Inhibitors: Retrovir AZT Non-nucleoside RTI: Viramune Protease Inhibitors : Invirase Fusion Inhibitors: Fuzeon Immune enhancers: BRMs Antibiotics: Bactrim, Pentam, Flagyl Antituberculars: INH