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Hypersensitivity Concepts Vo
 

Hypersensitivity Concepts Vo

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    Hypersensitivity Concepts Vo Hypersensitivity Concepts Vo Presentation Transcript

    • Peggy D. Johndrow 2009
    • Hypersensitivities/Allergies
      • Increased or excessive response to presence of antigen to which client has been exposed
      • Degree of reaction ranging from uncomfortable to life threatening
      • Terms hypersensitivity and allergy used interchangeably
    • Type I: Rapid Hypersensitivity Reactions
      • Also called atopic allergy: most common type of hypersensitivity
      • Some reactions occur only in areas exposed to antigen
      • Allergens contacted:
        • Inhaled (plant pollens, fungal spores, animal dander, house dust, grass, ragweed)
        • Ingested (foods, food additives, drugs)
        • Injected (bee venom, drugs, biologic substances)
        • Contacted (pollens, foods, environmental proteins)
      • Related to increased production of IgE
      • Examples: h ay fever, allergic rhinitis, allergic asthma, anaphylaxis, & allergies to certain foods &/or medications
      • Anaphylaxis : severe reaction, involve all blood vessels and bronchiolar smooth muscle, causing widespread blood vessel dilation, decreased cardiac output, and bronchoconstriction
      • IW Table 22-1 p 388
    • Allergic Rhinitis
      • Triggered by reaction to airborne allergens
      • Seasonal: coincides with timing of environmental exposure (i.e. spring) & lasts a short time
      • Chronic: occurs intermittently without seasonal pattern or continuously when exposed to certain allergens
      • Pathophysiology: initial exposure body responds by making antigen specific IgE which bind to surface of basophils & mast cells
      • Repeat exposure to allergen results in two phase response
        • Primary: allergen binds to IgE molecules; cell degranulates, histamine released resulting in capillary leak, mucous secretion, pruritis, & erythema
        • Secondary: additional proteins released, increased WBC’s; more generalized reaction occurs
    • Assessment
      • History: onset & duration symptoms: family history
      • Clinical Manifestations: rhinorrhea, itchy/watery eyes, H/A, swollen nasal mucosa, post nasal drip, dry/scratchy throat & pharyngitis
      • Diagnostic studies
        • CBC: increased eosinophil count (1-2%)
          • IgE indicates tendency to have allergic responses (>100 IU/mL)
        • RAST: determines specific allergies by determining blood level of IgE against certain allergen
        • Skin testing
          • Immediate hypersensitivity reaction occurs in 15 min’ positive = redness & wheal
          • Instruct client to stop systemic glucocorticoids & antihistamines 5 days prior to procedure
          • Emergency equipment available
        • Intradermal testing
          • Performed if a specific allergen did not produce a reaction
        • Oral food challenge
          • Used to identify specific allergens when skin testing or food diary fails
      • IW Table 22-2 p 391
    • Latex Allergy
      • Allergic reaction to a protein found in processed natural latex
      • Signs and symptoms vary in range (immediate to delayed)
      • Increased risk for allergy seen with high exposure to latex, spina bifida, allergy to bananas or avocados
      • Management
        • Ask all clients about use & known reaction to latex, or specific food allergies
        • Utilize latex free products in care of client
    • Management
      • History
      • Physical assessment/clinical manifestations
      • Laboratory assessment
      • Allergy testing including skin testing, scratch testing, intradermal testing, oral food challenge
      • Avoidance therapy, symptomatic therapy, pharmacotherapy
      • IW Chart 22-1 p 390
    • Pharmacotherapy
      • Decongestant: cause vasoconstriction of inflamed tissue
        • Examples: Neo-synepherine, Afrin
      • Antihistamines: block histamine from binding to receptor site, prevents vasodilatation & capillary leak
        • Examples: Benadryl, Chlor-trimeton, Zrytec, Clarinex, Allegra
      • Corticosteroids: decrease inflammation & immune response
        • Examples: Prednisone, Delta-cortef, Beconase, Flonase
      • Mast cell stabilizers: prevent mast cell membrane from opening when allergen binds to IgE
        • Example: Nasacrom
      • Leukotriene antagonics: blocks leukotriene receptor & prevents synthesis
        • Examples: Accolate, Zyflo, Singulair
      • Complementary and alternative therapy
      • (IW Chart 22-3 p 393)
    • Avoidance and Desensitization Therapy
      • Avoidance therapy
        • Instruct client to avoid direct or close contact w/ known allergens
      • Desensitization therapy
        • Used when identified allergens can't be easily avoided
        • Decrease allergic response by competition
    • Anaphylaxis
      • Systemic reaction; occurs rapidly after exposure (in seconds)
      • Initial feelings of uneasiness, apprehension, weakness & impending doom
      • Pruritus & urticaria
      • Erythema and sometimes angioedema eyes, lips, tongue
      • Histamine causes capillary leak bronchoconstriction, mucosal edema & excess mucus secretion
      • Congestion, rhinorrhea, dyspnea & increasing respiratory distress with audible wheezing result
      • Potentially fatal
      • IW Chart 22-2 p 392
    • Cascade
      • Itching, urticaria  angioedema  dyspnea, increased salivation, audible wheezing  laryngeal edema, stridor, hypoxia  hypotension, dysrhythmias, shock  cardiopulmonary arrest
    • Interventions
      • Initially assess respiratory function; must always establish and maintain an airway
      • Prepare for emergency intubation or tracheostomy
      • Oxygen reduces hypoxemia: O2 via NC 2 2-6L/min to maintain SAO2 >90%
      • Pharmacotherapy: (IW Chart 22-3 p 393)
        • Epinephrine (1:1000) .03-0.5 mL SQ; with initial symptoms
        • Antihistamines (25-100mg) IM, IV or PO; treat angioedema & urticaria
        • Theophylline (6mg/kg) IV over 20-30 min: bronchodilator
        • Inhaled beta-adrenergic agonist via small volume (high flow) nebulizer Q2-4 hrs; bronchodilator
        • Corticosteroids; decrease inflammation
        • Dopamine, Levophed; increase B/P
      • May require CPR
    • Type II: Cytotoxic Reactions
      • Body makes special autoantibodies directed against self cells that have some form of foreign protein attached
      • Clinical examples include hemolytic anemias, thrombocytopenic purpura, hemolytic transfusion reactions, Goodpasture’s syndrome, and drug-induced hemolytic anemia
      • Management
        • D/C medication or blood product
        • Hemolytic crisis or renal failure can occur
        • Treatment usually symptomatic
          • May require plasmapheresis
    • Type III: Immune Complex Reactions
      • Excess antigens cause immune complexes to form in blood; these circulating complexes usually lodge in small blood vessels
      • Usual sites include kidneys, skin, joints & small blood vessels
        • Lodge in the small vessel walls, trigger inflammation & cause tissue or vessel damage
      • Deposited complexes trigger inflammation, resulting in tissue or vessel damage
      • Examples: rheumatoid arthritis, systemic lupus erythematosus & serum sickness
      • IW Table 22-3 & Women Health p 396
    • Type IV: Delayed Hypersensitivity Reactions
      • Reactive cell T-lymphocyte (T-cell)
      • Antibodies & complement not involved
      • Local collection of lymphocytes & macrophages causes edema, induration, ischemia & tissue damage at site within hours to days after exposure
      • Examples: Tb test (positive purified protein derivative), contact dermatitis, poison ivy skin rashes, insect stings, tissue transplant rejection & sarcoidosis
    • Management
      • Intervention
      • Identification and removal of allergen
      • Client preparation
      • Procedure
      • Follow-up care
      • Reaction self-limiting & treated symptomatically
    • Type V: Stimulatory Reactions
      • Inappropriate stimulation of a normal cell surface receptor by an autoantibody, resulting in a continuous “turned-on” state for the cell
      • Example: Graves’ disease, form of hyperthyroidism
        • IW Table 22-3 p 396
      • Management
        • One organ: removal of enough tissue to return function to normal
        • Widespread involvement: decrease autoantibody production with immunosupression
    • Sjögren’s Syndrome
      • Group of problems often appear with other autoimmune disorders
      • Dry eyes, dry mucous membranes of nose/mouth (xerostomia) & vaginal dryness
      • Insufficient tears causing inflammation & ulceration of cornea
      • Treatment: immunomodulation & symptomatic therapy
    • Goodpasture’s Syndrome
      • Autoimmune disorder in which autoantibodies made against glomerular basement membrane & neutrophils
      • Lungs and kidneys
      • Shortness of breath, hemoptysis, decreased urine output, weight gain, edema, hypertension & tachycardia
      • Treatment: high-dose corticosteroids
    • Therapies
      • Pharmacotherapy:
        • Rheumatrex (methotrexate)
        • Cytoxan (cyclophosphamide)
        • Corticosteroids
        • Sandimmune (cyclosporine)
        • Plaquenil (hydroxchloroquine)
      • Symptomatic
        • Artificial tears, saliva
        • Lubricants
        • Pain control
      • Renal support: hemodialysis, peritoneal dialysis
      • Other
        • Plasmapheresis (filter plasma, remove proteins)