Immune System Alterations

8/2/2019 Immune System Alterations

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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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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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Monoclonal antibodiesPolyclonal antibody


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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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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.

Immune System Alterations

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