immune system alterations
TRANSCRIPT
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Immune System Alterations:Hypersensitivities
Chapter 14
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Hypersensitivity ReactionsHypersensitivity reactions
Overreaction of immune systemagainst foreign antigens; or
reaction against its own tissueleading to tissue damageClassified according to
source of antigen, time sequence(immediate or delayed) or basicimmunologic mechanisms causinginjury
Autoimmune diseasesBody fails to recognize self-proteinsand reacts against self-antigens
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Allergic Reaction
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Type I: IgE Mediated ReactionALLERGIC REACTIONSANAPHYLACTIC reactionsOccurs to susceptible people who are highlysensitized to specific allergenAntigen: exogenous pollen, food, dust, drugsAntibody produced: IgE : produced on 1 st
exposure to allergen & (bind to mast cells &basophils)Chemical mediators released
Histamine, mast cells, leukotrienes,prostaglandinsWhen released attack target tissue= allergic symptoms
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Type I: AllergensDrugs
PCN, Sulfa, Insulin, ASA, Tetracyclines, Local anesthetics, Chemoagents, Cephalosporins, NSAIDS
Insect venomsWASPS, Hornets, yellow jackets, bumblebees, antsFoods
Nuts, peanuts, eggs, milk, shellfish, fish, chocolate, strawberries, wheat,soybeans, food additives
Animal seraTetanus, rabies, diptheria & snake venom antitoxin
Treatment measuresBlood products (whole blood & components), iodine contrast media forIVP, Scans or angiograms .allergic extracts
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Type I
Clinical manifestations: Anaphylactic rxnWheal & flare reaction : Localized mediatorresponse
Characterized by pale wheal containingedematous fld. surrounded by red flare fromhyperema
Classic example : Mosquito biteServes as diagnostic purpose as means ofdemonstrating allergic reactions to specific
allergies during skin tests
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Anaphylaxis
OverviewSudden severe allergic rxn from massivehistamine release from cells-Life threateningCommon causes: foods: nuts, shellfish;drugs, latex, insect bites & stingsCan lead to shock & or death if untreated
Onset: within minutes to an hour; severeepisode: more rapid onset
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Anaphylaxis: Manifestations/NsgAssessment
Initial : angioedema (face, lips, tongue & orneck), urticaria (hives) w/pruritis @ site ofexposure
Dyspnea, wheezing, respiratory obstructionDysphagiaSkin erythema, flushing
Weak, rapid pulse, hypotension, dilatedpupilsSyncope, shockCirculatory shock; death (untreated)
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Systemic Anaphylaxis
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Anaphylaxis: TherapeuticMgmt: Emergency
INITIAL:Ensure/maintain patent AIRWAYHigh-flow O2 via non-rebreather mask
Remove causative agent (i.e. insect stinger, if present) Establish I.V. access EPINEPHRINE 1:1000 OF 0.01 Ml/KG(0.3-0.5 mL)
IM midanterior lateral thigh, Repeat q5-15 minutesNebulizer tx: albuterol (Proventil)Antihistamine: diphenhydramine (Benadryl) IM orIV
Steroids: methylprednisolone (Solumedrol)
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Anaphylaxis: TherapeuticMgmt: Emergency
HypotensionPosition: recumbent &elevate legs [modified
Trendelenberg] EPINEPHRINE 1:1000 OF 0.1 mL/kg IV q2-5 minutes
Maintain BP w/fluids,volume expanders,vasopressors: i.e.dopamine (Intropin)
ONGOING MonitoringVS, respiratory effort,cardiac rhythm
O2 saturation LOC Anticipate intubation w/severe distress
Anticipate cricothyrotomy or tracheostomy w/severe laryngeal spasm
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Patient Teaching
Avoid future contact w/allergenWear Medic-alert identification listing allergy
Notify all caregiversLearn how to use Epinephrine auto-injectorpens. Teach others how to use Epi pen.
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Type I: Atopic Reactions
Inherited tendency to become sensitized toenvironmental allergensAtopic diseases
Allergic rhinitisAsthmaAtopic dermatitisUrticariaangioedema
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Atopic dermatitis
EczemaChronic, inherited skin disorderCharacterized by exacerbations & remissions
Cause: several environmental allergens, often difficult toidentifyIgE: elevated; Skin test: +Skin lesions: generalized, vasodilation of blood vesselsleading to interstitial edema w/vesicle formation
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Urticaria
HivesTransient wheals :pink,raised, edematous,pruriticareas bodyLocal vasodilation(erythema), wheal & flaring:
due to histamine releasePruritis and lesions(WELTS): due to histamine
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Angioedema
Localized cutaneous lesions involving deeperlayers of skin & submucosaPrincipal areas of involvement : eyelids, lips,tongue, larynx, hands, feet, GI tract, genitalsManifestation:
Swelling : starting in face, progressing to airways &other body areasNo welts; outer skin may be normal or have reddishhueLesions may burn or itch; abdominal pain if in GI tract
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Type II:Cytotoxic & CytotoxicRxns
Involves activation of complement by antigen-antibodyInvolve direct binding of IgG or IgM antibodies to anantigen on cell surface
Production of autoantibodies that destroy own cells ortissuesTarget cells destroyed: RBCs, PLTs, WBCAntigens involved: ABO blood group, Rh factor & drugs
Disorders : ABO incompatibility transfusion rxn , Rhincompatibility transfusion rx, autoimmune and drugrelated hemolytic anemia, leukopenia,thrombocytopenia, erythroblastosis fetalis (hemolytic
disease of newborn, Good Pasture syndrome
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Type II: Hemolytic TransfusionReaction
Receiving ABO incompatible blood from adonorMISMATCHED BLOOD TRANSFUSION :Transfused with incompatible blood,antibodies immediately coat foreign RBCcausing agglutination (clumping).
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Type II: Good PastureSyndrome
Anti-glomerular basement antibody diseaseDisorder involving lungs and kidneys
Autoimmune reaction involving glomerularand alveolar basement membranes.Deposits of IgG from complement activation,resulting in pulmonary hemorrhage andglomerulonephritis
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Type III: Immune ComplexReactions
Formation of antibody-antigen complexes (binding ofantibody & antigen together)
Antibodies mostly being IgG and IgM.
Lead to activation of serum factors causing inflammationand lead to activation of complement cascadeCommon sites for deposit: kidneys, skin, joints, bloodvessels and lungs
Example of type IIIRheumatoid arthritis & Systemic Lupus Erythematosus (SLE),acute glomerulonephritis
Serum sickness
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Type IV: DelayedHypersensitivity Reactions
Cell-mediated response involving TlymphocytesInvolve recognition and response of Tlymphocytes to foreign substancesManifestations
Contact dermatitisHypersensitivity reactions to bacterial, fungal andviral infections; transplant rejection s
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Contact Dermatitis
Allergic contact dermatitisDelayed hypersensitivity reaction involving the skin Eczematous lesions develop within 48 hMost common antigenic substancesencountered:
Metal compounds (nickel containing),rubbercompounds, catechols present in poison ivy,poison oak,poison sumac, cosmetics & somedyes.
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Contact Dermatitis
Acute dermatitisSkin lesions: erythematous, edematous, coveredw/papules, vesicles and bullae.Pruritis, burning or stingingChronic contact dermatitis: lesions become thick,scaly and lichenified
Main difference b/w contact dermatitis and atopicdermatitis:CD: localized and restricted to area exposed toallergens;
Atopic: widespread
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Latex AllergiesAllergy as a result of exposure to latex productMore frequent & prolonged exposure, thegreater the likelihood of developing allergy
Latex proteins become aerosolized throughpowder on gloves and can result in seriousreaction when inhaled by sensitized individuals
Recommendation : USE OF POWDER FREEGLOVES IN HEALTHCARE FACILITIES to avoidrespiratory exposure to latex proteins
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Latex Allergies:Who is atRisk?
Healthcare workers: HIGHEST RISKFood handlers
HairdressersIndustrial workersHousekeepers
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Types of Latex Allergies
Type IV contact dermatitisDue to chemicals used in manufacturing processof glovesDelayed reaction: occurs within 6-48 hours
Manifestations:Initially : dryness, pruritis, fissuring and cracking
of skin followed byRedness & crusting at 24 to 48hChronic exposure: lichenification, scaly,hyperpigmentation
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Types of Latex Allergies
Type I allergic reactionResponse to natural rubber latex proteinsOccurs within minutes of contact w/proteins
ManifestationsRash, pruritis, flushing, redness, urticaria, rhinitis,conjunctivitis
Asthma due to full blown anaphylactic shockSystemic reactions from exposure to latexproteins via various routes: skin, mucousmembranes, inhalation, blood
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Latex Food Syndrome
Foods: may cause an allergic rxn in peoplewho are allergic to latex due to proteins inrubber being similar to food proteins-Latexfood syndromeMost common foods:
BANANAAVOCADOKIWICHESTNUTWATER CHESTNUT
GUAVAHAZELNUTSPOTATOESPEACHESGRAPES
APRICOTS
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Nursing and CollaborativeManagement: Latex Allergies
Identification of patients and HCW at riskThorough health hxThorough allergy hxGreatest risk factor
Long term multiple exposures to latex products: HCW
Patients w/multiple surgeries Rubber industry workers
Additional: hx hay fever, asthma, allergies tocertain foods
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Nursing and CollaborativeManagement: Latex Allergies
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Nursing and CollaborativeManagement: Latex Allergies
Latex protection protocols for latex + allergicpatients or hx s/s related to latex exposureLatex-free productsTeach patients to avoid certain foodsMedic-alert braceletEpi pen at all times
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Assessment
Complete health and allergy hxNote past & present hx
Note allergen and type of reaction to allergenFood allergy: maintain daily food dairyScreen for medication allergy
Comprehensive head to toe exam
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Diagnostic Studies
CBC w/diff, absolute lymphocyte count and esosinophilcountEsosinophil count: elevated w/type involving IgE
immunoglobulinSerum IgE: elevate d w/type I: diagnostic indicator ofatopic diseasesRadioallergosobent test [RAST]: invitro test for IgE
antibodies to specific allergensSputum, nasal, bronchial secretions tested foreosinophilsPFTS: if asthma suspected
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Skin Test
Used to identify specific allergens that arecausing allergic symptoms3 different methods
Scratch or prick testIntradermal test
Patch test
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Skin TestResults
Positive reactions: hypersensitive to test withinminutes after insertion in the skin and may
last for 8-12 hours.Positive reaction manifested: local wheal andflare response . Means person is sensitized tothat allergen
PrecautionsHighly sensitive person is always at risk fordeveloping anaphylactic reaction to skin tests.NEVER LEAVE PT ALONE DURING TESTINGPERIOD.
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Skin TestPrecautions
Highly sensitive person is always at risk foranaphylactic reaction to skin test
Never leave patient alone during testingperiodIf skin testing contraindicated, use RAST test
If severe reaction: remove extract immediatelyapply anti-inflammatory cream to siteIntradermal testing: arm is used so that atourniquet can be applied during a severereaction. EPI injection may be necessary
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Drug Therapy
AntihistaminesAllergic rhinitis, urticaria
Sympathomimetic/Decongestants
EPINEPHRINE[ADRENALIN]: DOC FORANAPHYLAXIS IV/IMPO: Phenylephrine [Neo-synephrine].Pseudoephedrine [Sudafed]: allergic rhinitis
Corticosteroids:Nasal sprays: allergic rhinitisAntipruritics: topical agentsMast cell stabilizers: intal [Cromolyn]Leukotriene receptor antagonists:montelukast [Singular]
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Autoimmune diseasesGrouped according to organ specific andsystemic diseases.SLE: systemic lupus erythematosusLyme diseaseApheresis
Platepheresis: remove plts
Leukocytapheresis: remove WBCLymphocytapheresis: used to decrease highlymphocyte counts
Plasmapheresis
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Transplant Rejection
Major problem following organ transplantationWill occur as a normal immune response toforeign tissue.Controlled by immunosuppressive therapy,ABO, HLA matching and ensuring thatcrossmatching is negative.Prevention, early diagnosis and tx of rejectionare essential for long-term graft function
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Hyperacute Rejection
Antibody mediated humoralOccurs in minutes to hours after transplant
Vessels are rapidly destroyedOccurs due to person having preexistingantibodies against transplanted tissue ororgan.No treatment and transplanted organ must beremovedMost susceptible organ is kidney.
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Acute Rejection
Most commonManifested in first six months post transplant
Mediated by recipients lymphocytes whichhave been activated against donated [foreign]tissue or organPT will require LIFE LONGIMMUNOSUPPRESSIVE THERAPY.
High risk for INFECTION
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Chronic RejectionOccurs over months or years\ IrreversibleOccurs for unknown reasons or from repeated
episodes from acute rejectionTransplanted organ is infiltrated with largenumbers of T and B cellsChronic rejection results in fibrosis and scarringNo definitive therapyTx is supportiveTransplant list for retransplant
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Immunosuppressive therapy
Corticosteroids-prednisone,methylprednisolone [Solumedrol]Calcineurin inhibitors
Cyclosporine [Sandimmune,Neoral, Gengraf]Tacrolimus [Prograf]
CytotoxicCyclophosphamide [Cytoxan]Azathiopine [Imuran]Sirolimus [Rapamune]
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Immunosuppressive therapy
Monoclonal antibodiesPolyclonal antibody
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Immunosuppressive therapy
Calcineurin inhibitorsCyclosporine [Sandimunne], tacrolimus[Prograf}
PO, IVA/E: Nephrotoxicity, increase risk for infection,neurotoxic: tremors, seizures, liver toxicity,
lymphoma, HTN, hirsutism, leukopenia, gingivalhyperplasia
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Immunosuppressive therapyCytotoxicCyclophosphamide [Cytoxan]
HEMORRHAGIC CYSTITIS, NEUTROPENIA
Nsg: FORCE FLUIDSAzathiopine [Imuran]
Bone marrow suppression, thrombocytopenia,anemia, neutropenia
Sirolimus [Rapamune]: renal transplant ptsHigh cholesterol, leuko/thrombopenia, anemia,diarrhea, althralgia. Not used in liver or lung.
Increases incidence of malignancies
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Immunosuppressive therapy
Mycophenolate mofetil [Cellcept]Lymphocyte specific inhibitor of purinesynthesis with suppressive effects on both Tand B lymphocytresMost effective when used in combow/tacrolimus and cyclosporine
Many GI toxicities making it a major limitation
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Graft versus host disease
Immunoincompetent patient is transfused withimmunocompetent cells.Host or recipient rejects tissue
Onset: 7 to 30 days post transplantTarget organs: skin, liver, GI tractBiggest problem: InfectionBacterial and fungal infections: predominate immediately
after transplant when granulocytopenia existsInterstitial pneumonitis: primary concern later in diseaseCorticosteroids, immunosuppressive drugs used aspreventive rather than tx measure. Radiation.