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 ReactionsAlso called atopic allergy: most common type of

hypersensitivitySome reactions occur only in areas exposed to antigenAllergens 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 IgEExamples: hay 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 RhinitisTriggered by reaction to airborne allergensSeasonal: coincides with timing of environmental

exposure (i.e. spring) & lasts a short timeChronic: 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 responsePrimary: 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

AssessmentHistory: onset & duration symptoms: family historyClinical Manifestations: rhinorrhea, itchy/watery eyes, H/A,

swollen nasal mucosa, post nasal drip, dry/scratchy throat & pharyngitis

Diagnostic studiesCBC: 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 allergenSkin 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 reactionOral food challenge

Used to identify specific allergens when skin testing or food diary fails

IW Table 22-2 p 391

Latex AllergyAllergic reaction to a protein found in

processed natural latexSigns 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

ManagementAsk all clients about use & known reaction to

latex, or specific food allergiesUtilize latex free products in care of client

ManagementHistoryPhysical assessment/clinical manifestationsLaboratory assessmentAllergy testing including skin testing, scratch

testing, intradermal testing, oral food challengeAvoidance therapy, symptomatic therapy,

pharmacotherapyIW Chart 22-1 p 390

PharmacotherapyDecongestant: cause vasoconstriction of inflamed tissue

Examples: Neo-synepherine, AfrinAntihistamines: block histamine from binding to

receptor site, prevents vasodilatation & capillary leakExamples: Benadryl, Chlor-trimeton, Zrytec, Clarinex,

AllegraCorticosteroids: decrease inflammation & immune

responseExamples: Prednisone, Delta-cortef, Beconase, Flonase

Mast cell stabilizers: prevent mast cell membrane from opening when allergen binds to IgEExample: Nasacrom

Leukotriene antagonics: blocks leukotriene receptor & prevents synthesisExamples: Accolate, Zyflo, Singulair

Complementary and alternative therapy(IW Chart 22-3 p 393)

Avoidance and Desensitization Therapy

Avoidance therapyInstruct client to avoid direct or close contact

w/ known allergens

Desensitization therapyUsed when identified allergens can't be easily

avoidedDecrease allergic response by competition

Anaphylaxis Systemic reaction; occurs rapidly after exposure

(in seconds)Initial feelings of uneasiness, apprehension,

weakness & impending doomPruritus & urticariaErythema and sometimes angioedema eyes, lips,

tongueHistamine causes capillary leak

bronchoconstriction, mucosal edema & excess mucus secretion

Congestion, rhinorrhea, dyspnea & increasing respiratory distress with audible wheezing result

Potentially fatalIW Chart 22-2 p 392

Cascade

Itching, urticaria angioedema dyspnea, increased salivation, audible wheezing laryngeal edema, stridor, hypoxia hypotension, dysrhythmias, shock cardiopulmonary arrest

InterventionsInitially assess respiratory function; must

always establish and maintain an airway Prepare for emergency intubation or tracheostomyOxygen 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: bronchodilatorInhaled beta-adrenergic agonist via small volume (high

flow) nebulizer Q2-4 hrs; bronchodilatorCorticosteroids; decrease inflammationDopamine, 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

ManagementD/C medication or blood productHemolytic crisis or renal failure can occurTreatment usually symptomatic

May require plasmapheresis

Type III: Immune Complex ReactionsExcess 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 ReactionsReactive cell T-lymphocyte (T-cell)Antibodies & complement not involvedLocal 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

ManagementInterventionIdentification and removal of allergenClient preparationProcedureFollow-up careReaction 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 hyperthyroidismIW Table 22-3 p 396

ManagementOne organ: removal of enough tissue to return

function to normalWidespread involvement: decrease autoantibody

production with immunosupression

Sjögren’s SyndromeGroup of problems often appear with other

autoimmune disordersDry eyes, dry mucous membranes of

nose/mouth (xerostomia) & vaginal drynessInsufficient tears causing inflammation &

ulceration of corneaTreatment: immunomodulation &

symptomatic therapy

Goodpasture’s Syndrome

Autoimmune disorder in which autoantibodies made against glomerular basement membrane & neutrophils

Lungs and kidneysShortness of breath, hemoptysis, decreased

urine output, weight gain, edema, hypertension & tachycardia

Treatment: high-dose corticosteroids

TherapiesPharmacotherapy:

Rheumatrex (methotrexate)Cytoxan (cyclophosphamide)CorticosteroidsSandimmune (cyclosporine)Plaquenil (hydroxchloroquine)

SymptomaticArtificial tears, salivaLubricantsPain control

Renal support: hemodialysis, peritoneal dialysisOther

Plasmapheresis (filter plasma, remove proteins)