ALLERGYDR. MA. TERESA S. FAJARDOPEDIATRICSHEMATOLOGY / ONCOLOGY

IMMUNOLOGIC BASISOF ALLERGIC DISEASETO DETECT AND ELIMINATE ANYTHING FOREIGNTO THE BODYBENEFICIAL (IMMUNITY) OR HARMFUL (ALLERGY)

COMPONENTS IN HOST'S RESPONSE TO THE ALLERGEN ENVIRONMENT

TARGET CELLS

B AND T LYMPHOCYTES

IMMUNOLOGIC CAPABILITIES OF THE HOSTPRIMARY ( NON- SPECIFIC )SECONDARY (SPECIFIC)TERTIARY ( TISSUE DAMAGING RESPONSE)

PRIMARY RESPONSE

MOST PRIMITIVE

PHAGOCYTOSIS / INFLAMMATION

SECONDARY RESPONSESPECIFIC RESPONSEMECHANISMS : B CELL / T CELL RESPONSECOMPLEMENT SYSTEMCOAGULATIPON SYSTEM

TERTIARY RESPONSE

TISSUE – DAMAGING RESPONSES ( TYPES I, II, III, IV )PROPOSED BY GELL AND COOMBS

MEDIATORS OF ALLERGYPREFORMED MAST CELL MEDIATORSRAPIDLY FORMED MAST CELL MEDIATORS

PREFORMED MAST CELLMEDIATORSVASOACTIVE MEDIATORSCHEMOTACTIC MEDIATORSENZYMESPROTEOGLYCANS

PREFORMED MAST CELLMEDIATORS ( VASOACTIVE MEDIATORS)1. HISTAMINE BRONCHOSPASM AND

VASCULAR PERMEABILITY2. ADENOSINE INHIBIT PLATELET

AGGREGATION STIMULATE IRRITANT

RECEPTORS

PREFORMED MAST CELLMEDIATOR (CHEMOTACTIC MEDIATORS ) 1. NEUTROPHIL FACTOR RECRUITMENT /

ACTIVATION OF NEUTROPHIL2. EOSINOPHIL FACTOR RECRUITMENT /ACTIVATION

OF EOSINOPHIL

PREFORMED MAST CELLMEDIATOR ( ENZYMES)1. NEUTRAL PROTEASES

( TRYPTASE , CHYMASE ) COMPLEMENT/ KININ

ACTIVATION2. ACID HYDROLASES ( BETA-

GLUCORONIDASE) INFLAMMATION

PREFORMED MAST CELLMEDIATOR (PROTEOGLYCANS)HEPARIN ANTICOAGULANT ANTICOMPLEMENT ACTIVITY

RAPIDLY FORMED MAST CELL MEDIATORSPLATELET- ACTIVATING FACTORPROSTAGLANDINLEUKOTRIENES

RAPIDLY FORMED MASTCELL MEDIATORSBIOLOGIC ACTIVITY : VASODILATATION VASCULAR LEAKAGE SMOOTH MUSCLE CONTRACTION GLANDULAR SECRETION STIMULATION OF THE IRRITANT ( ITCH / SNEEZE ) RECEPTORS PRO –ANTI-INFLAMMATORY MEDIATOR

CYTOKINESNEWLY SYNTHESIZED PROTEINS THAT REGULATE IMMUNE RESPONSEPOTENT PRO- INFLAMMATORY MEDIATORSGROWTH / DIFFERENTIATION OF EOSINOPHILS AND MAST CELLS

CYTOKINES AND ALLERGYIgE REGULATIONEOSINOPHILIAMAST CELL DEV ‘T AND ACTIVATIONINFLAMMATION

IMMUNOLOGIC MECHANISM IN ALLERGIC INFLAMMATION

ALLERGEN EXPOSURE ----MAST CELL ACTIVATION----

VASOACTIVE AMINE ACTIVATION ---- IMMEDIATE REACTIONS ( VASODILATATION, EDEMA, SM

CONTRACTION, MUCUS SECRETION) ------------ 3 -8 HRS

LATE PHASE RESPONSE (INFILTRATION OF EOSINOPHILS

MONONUCLEARS AND NEUTROPHILS) ----------- AFTER 24 -48 HRS ------

T- CELL ACTIVATION --------- CHEMOTACTIC MEDIATORS -------- CELLULAR INFILTRATION ------

INFLAMMATORY MEDIATORS ------------ EDEMA, DESQUAMATION, CELLULAR INFI;LTRATION AND MUCUS

SECRETION

ALLERGIC RHINITISSYMPTOMS: “ SNEEZERS AND RUNNERS” -- PAROXYSMAL SNEEZING -- WATERY RHINORRHEA -- ITCHY NOSE ---NASAL BLOCKAGE (VARIABLE) -- DIURNAL RHYTHM (WORST DAYTIME IMPROVES AT NIGHT -- OFTEN ASSOCIATED WITHJ CONJUNCTIVITIS

ALLERGIC RHINITISSYMPTOMS: BLOCKERS -- LITTLE OR NO SNEEZING -- THICK NASAL MUCUS (CATARRH) MORE OFTEN POSTERIOR (POST NASAL DRIP) -- NO ITCH -- NASAL BLOCKAGE OFTEN SEVERE -- CONSTANT BUT MAYBE WORST AT NIGHT

RHINITIS DEFINITIONNASAL DISCHARGEBLOCKAGESNEEZE/ ITCH

TWO OR MORE SYMPTOMS FOR MORE THAN ONE HOUR ON MOST DAYS

ALLERGIC RHINITIS

TREATMENT ENVIRONMENTAL CONTROL IMMUNOTHERAPY PHARMACOTHERAPY PARENT/PATIENT EDUCATION

ASTHMA

CHRONIC, RECURRENT , OCCASIONALLY FATALCHRONIC INFLAMMATORY DISORDER OF THE AIRWAYS IN WHICH CELLS PLAY A ROLE, INCLUDING M MAST CELLS AND EOSINOPHILSWIDESPREAD BUT VARIABLE AIRFLOW OBSTRUCTION THAT IS OFTEN REVERSIBLE EITHER SPONTANEOUSLYOR WITH TREATMENT ASSSOCIATED WITH AIRWAYRESPONSIVENESS

PRECIPITANT OF ASTHMA

RESPIRATORY INFECTION (VIRAL)ALLERGENSFOODHOUSEHOLD INHALANTSOUTDOOR INHALANTSIRRITANTSEXERCISEEMOTIONAL FACTORS

PATHOPHYSIOLOGY OFASTHMA ,SEVEREASTHMA -- MUCUS SECRETION , BRONCHOSPASM ,EDEMA ---INCREASED RESISTANCE TO AIRFLOW---HYPERINFLATION, ATELECTASIS , CNS DEPRESSION--PULMONARY VASOCONSTRICTION--CARDIAC FAILURE AND COMA

ASTHMA

CLINICAL MS: WHEEZING , A HIGH- PITCHED OR SQUEAKING EXPIRATORY SOUND ONSET , ACUTE /INSIDIOUS COUGH , TACHYPNEA , DYSPNEA HYPERINFLATION OF THE CHEST, TACHYCARDIS ABDOMINAL PAIN WITH VOMITING LOW GRADE FEVER HUNCHED- OVER SITTING POSITIUON

MANAGEMENT OFASTHMAACHIEVE AND MAINTAIN CONTROL OF SYMPTOMSPREVENT ASTHMA EXACERBATIONSMAINTAIN PULMONARY FUNCTIONS AS CLOSE TO NORMAL LEVELSAVOID ADVERSE EFFECTS FROM ASTHMA MEDICATIONSPREVENT IRREVERSIBLE AIRWAY OBSTRUCTIONPREVENT ASTHMA MORBIDITY

MANAGEMENT PROGRAMS FOR ASTHMA

EDUCATE PATIENTS/PARENTS ASSESS AND MONITOR SEVERITYAVOID OR CONTROL TRIGGERSMEDICATION PLANS FOR CHRONIC ASTHMAPLANS FOR EXACERBATIONSPROVIDE REGULAR FOLLOW-UP

STATUS ASTHMATICUS

SEVERE ACUTE ASTHMALIFE-THREATENING EPISODEUNRESPONSIVE TO THE USUAL APPROPRIATE THERAPY WITH ADRENERGIC AGENT AND THEOPHYLINELEADS TO ACUTE RESPIRATORY INSUFFICIENCY

ATOPIC DERMATITISCHRONIC ,HERITABLE, DISTINCTIVE CUTANEOUS INFLAMMATORY DISEASE CHARACTERIZED BYEARLY AGE OF ONSET AND INTENSE PRURITUSSKIN LESION: DRY, IRRITATED, WEEPING, EXCORIATEDLICHENIFIED LESIONS ON THE FLEXURAL AREASIN LATE CHILDHOOD AND ADOLESCENSEWIIH GENETIC PREDISPOSITIONRELAPSING CAN DEVELOP ALLERGIC RHINITIS AND ASTHMA

STAGES OF ATOPIC DERMATITISINFANTILE STAGE 4TH -6TH MONTH OF AGE ERYTHEMATOUS, PRURITIC, WEEPING DERMATITIS IN THE CHEEKS WHICH SPREADS TO THE FOREHEAD AND EXTENSOR SURFACES OF THE ARMS AND LEGS CIRCUMORAL AREA AND EYELIDS ARE USUALLY SPARED

STAGES OF ATOPIC DERMATITISCHILDHOOD STAGE: 2-4 YRS OF AGE PRURITIC, EXCORIATED PAPULESON THE FLEXURAL SURFACES OF EXTREMITIES AND FACE LICHENIFICATION IN THE POPLITEAL AND ANTECUBITAL FOSSAE AND ANKLES MAY DISAPPEAR BEFORE 10 YRS

STAGES OF ATOPIC DERMATITISADULT STAGE : HIGHLY PRURITIC , CONFLUENT PAPULES ON THE DORSAL ASPECT OF THE HANDS, UPPER EYELIDS AND FLEXURAL AREAS OF THE EXTREMITIES

STIGMAS OF ATOPICDERMATITISLICHENIFICATION DENNIE ‘S LINEATOPIC PALMSBUFFED NAILSWHITE DERMOGRAPHISMDELAYED BLANCHED PHENOMENONDRYNESS XEROSISATOPIC PERSONALITYHOUSEWIFE’S ECZEMAATOPIC FOOTALLERGIC SHINERS

CRITERIA FOR THE DIAGNOSISOF ATOPIC DERMATITISMUST HAVE 3 OR MORE BASIC FEATURES :1.PRURITUS2.TYPICAL MORPHOLOGY

/DISTRIBUTION3.TENDENCY TO RECURRENCES4.PERSONAL OR FAMILY HISTORY

CRITERIA FOR THE DIAGNOSIS OF ATOPIC DERMATITISPLUS ANY THREE OR MORE OF THE FF FEATURES: ICHTHYOSIS, ELEVATED SERUM IgE , EARLY AGE ONSET CUTANEOUS INFECTION, IMPAIRED T- CELL IMMUNITY HAND/FOOT DERMATITIS , NIPPLE ECZEMA, , CHEILITIS, RECURRENT CONJUNCTIVITIS, DENNIE MORGAN INFRAORBITAL FOLD CATARACT, ORBITAL DARKENING, PITYRIASIS ALBA FOOD HYPERSENSITIVITY

ATOPIC DERMATITISTREATMENT AVOID ENVIRONMENTAL FACTORS GOOD HYDRATION OF THE AFFECTED AREAS MOISTURIZERS CORTICOSTEROIDS IN THE SUBACUTE PHASE

URTICARIA ( HIVES)RAISED ERYTHEMATOUS SKIN LESIONS ASSOCIATEDWITH MARKED PRURITUSDUE TO VASODILATATION OF SMALL VENULESAND CAPILLARIES AND EXUDATION OF FLUIDINTO THE SUPERFICIAL DERMISANGIOEDEMA IS URTICARIA INVOLVING THE DEEPER SUBCUTANEOUS TISSUES

CLASSIFICATION OF URTICARIAIMMUNOLOGIC ANAPHYLACTIC / CYTOTOXIC/ IMMUNE COMPLEXANAPHYLACTOID HEREDITARY ANGIOEDEMA/ CHEMICAL/ ASPIRIN SENSITIVITY PHYSICAL DERMATODRAPHIA/ COLD/ CHOLINERGIC/ SOLAR/PRESSUREMISC INFECTION/ PIGMENTOSA/ PSYCHOGENIC/IDIOPATHIC

URTICARIA

TREATMENT SYMPATHOMIMETIC AGENTS : EPINEPHRINE ANTIHISTAMINICS CORTICOSTEROIDS

ALLERGIC CONTACT DERMATITISCOMMON DISORDER IN CHILDHOODERYTHEMA, PAPULES, VESICLES, SWELLINGWEEPING ANG ITCHING24 -48 HRS AFTER EXPOSURETYPE IV

CAUSES OF CONTACTDERMATITISIRRITANTS ANIMALSPLANTS CLOTHINGNICKEL DRUGSCHROMATEMERCURYCOSMETICS

ADVERSE FOOD REACTIONIMMUNOLOGIC REACTION RESULTING FROM INGESTION OF FOOD PRODUCTSAND ADDITIVES

I

FOOD ALLERGY(HYPERSENSITIVITY)IMMUNOLOGIC REACTION RESULTING FROM INGESTION OF FOOD ADDITIVE , IgE MEDIATED

FOOD ANAPHYLAXISCLASSIC ALLERGIC HYPERSENSITIVITY REACTION TO FOOD OR FOOD ADDITIVES INVOLVING IgE AND THE RELEASE OF CHEMICAL MEDIATORS

FOOD INTOLERANCEABNORMAL NON-IMMUNOLOGIC PHYSIOLOGIC RESPONSE TO FOOD OR FOOD ADDITIVES

FOOD IDIOSYNCRASYHYPERSENSITIVITY WITHOUT IMMUNE RESPONSE

FOOD TOXICITYADVERSE REACTION CAUSED BY DIRECT ACTION OF FOOD ADDITIVE/ FOOD ON THE HOST RECIPIENT WITHOUT IMMUNE MECHANISM FOUND NATURALLY IN FOOD OR SECONDARY TO CONTAMINATION BY MICROORGANISM OR PARASITES

RISK OF MANIFESTINGATOPY BASED ON FAMILYHISTORY OF ATOPYFAMILY HISTORY OF ATOPY RISK OF ATOPY

BIPARENTAL( SAME ALLERGY) 50-80 %BIPARENTAL OR UNIPARENTAL 40-60% PLUS ONE SIBLINGUNIPARENTAL OR SIBLING 20-49%NEGATIVE 5-15 %

MANIFESTATIONS OFFOOD ALLERGYGASTROINTESTINAL:: VOMITING, ENTEROCOLITIS,MALABSORPTION, BLEEDING RESPIRATORY : RHINITIS, ASTHMA, OTITIS MEDIADERMATOLOGY : URTICARIA, ATOPIC DERMATITIS,ALOPECIANEUROLOGIC : SEIZURE, LETHARGYHEMATOLOGY : ANEMIAANAPHYLACTIC SHOCK

ADVERSE DRUG REACTION“ AN EFFECT WHICH IS UNINTENDED AND OCCURSAT DOSES NORMALLY USED IN MAN FOR PROPHYLAXISDIAGNOSIS AND THERAPY “ OCCURS WITHIN A REASONABLE TIME FOLLOWING ADMINISTRATION OF THE DRUGREACTIONS : INTOLERANCE, IDIOSYNCRASY, HYPERSENSITIVITY ,PSYCHOGENIC

CLASSIC ANTIHISTAMINICSETHANOLAMINES EXAMPLES : DIPHENHYDRAMINE , CARBINOXAMINE CLEMASTINE, DIMENHYDRINATE GENERAL COMMENTS: SEDATIVE EFFECT HIGH, MODERATE ANTICHOLINERGIC EFFECTS, RELATIVE LOW GIT EFFECTS

CLASSIC ANTIHISTAMINICSALKYLAMINES : CHLORPHENIRAMINE , TRIPROLIDINE, BROMPHENIRAMINE, PHENIRAMINEGENERAL COMMENTS : LOW SEDATIVE , ANTICHOLINERGIC AND GI EFFECTS , BEST GROUPFOR DAYTIME USE

CLASSIC ANTIHISTAMINICSETHYLENEDIAMINES: ANTAZOLINE TRIPELENNAMINEGENERAL COMMENTS :LOW SEDATIVE , ANTICHOLINERGIC EFFECTS , GI EFFECTS COMMON

CLASSIC ANTIHISTAMINICSPIPERAZINES : HYDROXYZINE , MECLIZINE , CHLORCYCLIZINEGENERAL COMMENTS : DROWSINESS IS FREQUENT ,DRY MOUTH A USUAL CHOLINERGIC EFFECT

CLASSIC ANTIHISTAMINICSPHENOTHAZINE : METHDILAZINE , PROMETHAZINETRIMEPRAZINEGENERAL COMMENTS : MARKED SEDATIVE EFFECT( USEFUL TREATMENT OF PRURITUS )

CLASSIC ANTIHISTAMINICSPIPERIDINES : CYPROHEPTADINE , BENZOCYCLOHEPTATHIPINEAZATADINEGENERAL COMMENTS : DROWSINESS IS COMMONUSEFUL IN THE TREATMENT OF URTICARIA