Hypersensitivity SLE PDF

Hypersensitivity Systemic Lupus Erythematous  Body's natural or induced response to foreign agent The Immunocompromised patients Concep Ineffective immune system Hypersensitivity t of Overreaction of immune...

Hypersensitivity Systemic Lupus Erythematous  Body's natural or induced response to foreign agent The Immunocompromised patients Concep Ineffective immune system Hypersensitivity t of Overreaction of immune system Immuni Autoimmune disorders Immune system attacks own ty body Immunodeficiency Incompetent immune system  Hypersensitivity or Hyper-responses – Four types of allergic reactions Alterations Type I: immediate and hypersensitivity Manifestatio Type II: cytotoxic ns hypersensitivity Type III: immune complex reaction Type IV: delayed-type hypersensitivity  Type I: localized or systemic – Antibodies bind to cells – releases substances – inflammation – Asthma, allergic rhinitis, food allergies Type II: tissue-specific reaction – Antibodies activates system that causes tissue damage – Transfusion reaction, hemolytic Types of disease of newborn, ABO incompatibility Hypersensitiv Type III: Immune-complex-mediated ity Reactions reaction – Immune complexes deposited in tissues – inflammatory reaction – Serum sickness, acute glomerulonephritis Type IV: Delayed reactions – Cell-mediated immune response – Antigen stimulates T-cells – Contact dermatitis, TB test, GVH  Pathophysiology and Etiology Type I (IgE- mediated) hypersensitivity Common hypersensitivity reactions Triggered when allergen interacts with free IgE IgE binds to mast cells and basophils – release histamines Allergens can be ingested in foods,  Type I (IgE-mediated) hypersensitivity – Anaphylaxis: acute systemic response Pathophysiol Histamine and other mediators released ogy and – Localized response is more Etiology common Hay fever, Asthma, Atopic dermatitis (eczema), bee stings, food allergies  Can occur within minutes IgE triggers histamine releases Hypersensitivi Sign/Symptoms ty Type 1 – swelling, redness, itching skin sensitivity – runny nose – bronchi constrict and spasm – wheezing/crackles  Pharmacotherapy Collaborative Non-steroidal anti-inflammatory Antihistamines block histamine Treatment for receptors Steroids impair inflammatory response Type I Theophylline OR Epinephrine – keeps mast cells intact reducing signs/symptoms of bronchospasms Collaborative Treatment for Type I Immunotherapy Desensitization (Goal to create hypo- sensitization) Repeated injections of allergen to reduce the allergic response – Allergy injections  -Refer clients with allergic rhinitis, asthma, atopic dermatitis to Collaborati allergist on -For children, help parents design action plan for school  Lifespan and Cultural Considerations May outgrow certain allergies as client ages – Uncommon to outgrow peanut allergy Individuals who develop allergies in adulthood typically have them for rest of their lives  Client will avoid known substances that provoke hypersensitivity Plannin response g Client will describe self-care to reduce symptoms of seasonal allergies  Patient exhibits decreased symptoms and decreased Evaluati frequency of on hypersensitivity responses  Pathophysiology and Etiology Type II (cytotoxic) hypersensitivity – Binding of IgG- or IgM-type with antigen activates a complex cascade of a hypersensitivity response – Destruction of target cell – Stimulated by antigen Blood transfusion ABO blood types Collaborative Treatment for Type II Prevention of Transfusion Reaction Prior to blood administration blood is checked by 2 RN’s Blood transfusion reaction Stop transfusion of ABO incompatible blood will stop hemolysis Keep IV infusing with NS Call Provider if mild reaction – Rash/itching » Antihistamine Call Rapid Response if major reaction – Bloody urine/pain - Discuss in future semester  Type III (immune complex– mediated) hypersensitivity Results from formation of antibody–antigen immune complexes in circulatory system – Pathophysiol IgG or IgM Deposited in capillaries or ogy and joints Etiology Antibody-Antigen immune complexes are deposited in organs, activate complement cascade, and cause inflammatory damage.  Pathophysiology and Etiology Type III (immune complex– mediated) hypersensitivity – Systemic Immune complex deposited in small blood vessels of organs and tissues Serum sickness – response to some medications TYPE III Localized disease Immun Deposited in joints = Arthritis. e Deposited in kidneys = Comple Glomerulonephritis x Deposit in connective tissue = SLE Diseas e Type III Hypersensitivity Reaction Immune Complex Auto Immune Systemic Lupus Erythematosus (SLE)  Overview Systemic lupus erythematosus (SLE) – Chronic, inflammatory connective tissue disease – Affects almost all body systems – Manifestations (signs and symptoms) vary widely – Autoantibodies created – Caused by deposition of autoantibody- antigen complexes in connective tissues Damages cells and tissues Autoantibodie s Autoimmune diseases -Immune system loses ability to distinguish self from others -Attacks own body -Results from hyper- activity of B cells -Most cases diagnosed in teen, early adult years  SLE autoantibodies react with corresponding antigen – Form immune complexes – Deposited into connective Pathophysiolo tissue – Deposits trigger gy and inflammatory response Etiology – Local tissues damaged – Sites of deposition kidney, musculoskeletal system, brain, heart, spleen, lung, GI tract, skin, peritoneum  Women of childbearing age – 90% of diagnoses Risk More common: – African American Factors – Hispanic – Native Americans – Asians  Course – Mild in most patients – Periods of remission Clinical and exacerbation Manifestatio – Number, severity of ns exacerbations tend to decrease with time  Early manifestations – joint pain (mimic those of Rheumatoid Arthritis) Red butterfly rash Clinical Manifestatio across cheeks, bridge ns of nose Diffuse, maculopapular rash on skin exposed to sun Red Butterf ly Rash Maculopapular Rash  Diagnostic Tests Anti-DNA antibody testing – specific indicator of SLE: antibodies are rarely found in any other disorder Erythrocyte sedimentation rate (ESR)– increased due to inflammation 100 mm/hr – (normal range15 - 30 mm/hr) CBC – anemia and/or leukopenia Urinalysis – Proteinuria during exacerbation of SLE when kidneys are involved  Drug Therapy Skin, arthritic manifestations -Antimalarial drugs (Hydroxychloroquine) -treats rash -Corticosteroids Severe, life-threatening manifestations -High-dose corticosteroid therapy Initially 40–60 mg/day prednisone Tapered as soon as clinically possibly  Immunosuppressive agents – Cyclophosphamide or Drug azathioprine Alone or in combination Therap with corticosteroids y – Increased risk for: Infection Malignancy Bone marrow depression  Drug Therapy Immunosuppressive agents Teaching points for patient Avoid large crowds, exposure to infection Report signs of infection to physician Plan pregnancy for best outcome (mother and infant) Women may not experience menstruation while taking cyclophosphamide Consult with healthcare provider prior to receiving immunizations – immunosuppressive medications Consult healthcare provider before adding herb, vitamin, or supplement to diet Avoid sun exposure: Use sunscreen  Nutritional status Skin Respiratory Nursing assessment Musculoskeletal Process: Neurological Assessme assessment nt GI assessment Psychosocial assessment Pain  Risk for Infection Risk for Ineffective Tissue Perfusion Chronic Pain Diagno Risk for Activity sis Intolerance Risk for Disturbed Body Image Compromised Family Coping  Steroid treatment can impact Implementat nutrition ion: Promote – Increase appetite Adequate Nutrition – Risk for weight gain – Taper dose to discontinue Implementation: Promote Skin Integrity Provide patient education Include possible effects on skin Discuss relationship between sun exposure, disease activity Teach strategies to limit sun exposure Implementation: Promote Rest and Comfort Encourage frequent rest periods Physical therapist – program to encourage mobility, increase muscle strength  Patient maintains weight within standardized range Patient maintains healthy skin Patient maintains balance of rest and activity to Evaluati promote health Patient maintains on medication regimen to promote health, prevent side effects Patient develops or maintains positive body image  Pathophysiology and Etiology Type IV (delayed) hypersensitivity Type IV (delayed) hypersensitivity – Cell-mediated immune responses. Does not involve antibodies – Results from exaggerated interaction between antigen and T-cells – Purified Protein Derivative/PPD/ TB skin test Administer subdermal Read in 48 – 72 hours 10mm swelling = positive Delayed Type IV Hypersensitivity Response is from: – macrophages causing inflammation and tissue damage – Continued macrophage activation can cause chronic inflammation resulting in tissue lesions, scarring, and granuloma formation Delayed response arise 48-72 hours after exposure rather than within minutes What is your clinical decision? Questions?