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    Allergy new Allergy new Presentation Transcript

    • ALLERGY
      DR. MA. TERESA S. FAJARDO
      PEDIATRICS
      HEMATOLOGY / ONCOLOGY
    • IMMUNOLOGIC BASISOF ALLERGIC DISEASE
      TO DETECT AND ELIMINATE ANYTHING FOREIGN
      TO THE BODY
      BENEFICIAL (IMMUNITY) OR HARMFUL (ALLERGY)
    • COMPONENTS IN HOST'S RESPONSE TO THE ALLERGEN
      ENVIRONMENT
      TARGET CELLS
      B AND T LYMPHOCYTES
    • IMMUNOLOGIC CAPABILITIES OF THE HOST
      PRIMARY ( NON- SPECIFIC )
      SECONDARY (SPECIFIC)
      TERTIARY ( TISSUE DAMAGING
      RESPONSE)
    • PRIMARY RESPONSE
      MOST PRIMITIVE
      PHAGOCYTOSIS / INFLAMMATION
    • SECONDARY RESPONSE
      SPECIFIC RESPONSE
      MECHANISMS :
      B CELL / T CELL RESPONSE
      COMPLEMENT SYSTEM
      COAGULATIPON SYSTEM
    • TERTIARY RESPONSE
      TISSUE – DAMAGING RESPONSES
      ( TYPES I, II, III, IV )
      PROPOSED BY GELL AND COOMBS
    • MEDIATORS OF ALLERGY
      PREFORMED MAST CELL MEDIATORS
      RAPIDLY FORMED MAST CELL MEDIATORS
    • PREFORMED MAST CELLMEDIATORS
      VASOACTIVE MEDIATORS
      CHEMOTACTIC MEDIATORS
      ENZYMES
      PROTEOGLYCANS
    • PREFORMED MAST CELLMEDIATORS ( VASOACTIVE MEDIATORS)
      HISTAMINE
      BRONCHOSPASM AND VASCULAR PERMEABILITY
      ADENOSINE
      INHIBIT PLATELET AGGREGATION
      STIMULATE IRRITANT RECEPTORS
    • PREFORMED MAST CELLMEDIATOR (CHEMOTACTIC MEDIATORS )
      1. NEUTROPHIL FACTOR
      RECRUITMENT / ACTIVATION OF NEUTROPHIL
      2. EOSINOPHIL FACTOR
      RECRUITMENT /ACTIVATION OF EOSINOPHIL
    • PREFORMED MAST CELLMEDIATOR ( ENZYMES)
      1. NEUTRAL PROTEASES ( TRYPTASE , CHYMASE )
      COMPLEMENT/ KININ ACTIVATION
      2. ACID HYDROLASES ( BETA- GLUCORONIDASE)
      INFLAMMATION
    • PREFORMED MAST CELLMEDIATOR (PROTEOGLYCANS)
      HEPARIN
      ANTICOAGULANT
      ANTICOMPLEMENT ACTIVITY
    • RAPIDLY FORMED MAST CELL MEDIATORS
      PLATELET- ACTIVATING FACTOR
      PROSTAGLANDIN
      LEUKOTRIENES
    • RAPIDLY FORMED MASTCELL MEDIATORS
      BIOLOGIC ACTIVITY :
      VASODILATATION
      VASCULAR LEAKAGE
      SMOOTH MUSCLE CONTRACTION
      GLANDULAR SECRETION
      STIMULATION OF THE IRRITANT ( ITCH / SNEEZE )
      RECEPTORS
      PRO –ANTI-INFLAMMATORY MEDIATOR
    • CYTOKINES
      NEWLY SYNTHESIZED PROTEINS THAT REGULATE
      IMMUNE RESPONSE
      POTENT PRO- INFLAMMATORY MEDIATORS
      GROWTH / DIFFERENTIATION OF EOSINOPHILS
      AND MAST CELLS
    • CYTOKINES AND ALLERGY
      IgE REGULATION
      EOSINOPHILIA
      MAST CELL DEV ‘T AND ACTIVATION
      INFLAMMATION
    • 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 RHINITIS
      SYMPTOMS:
      “ SNEEZERS AND RUNNERS”
      -- PAROXYSMAL SNEEZING
      -- WATERY RHINORRHEA
      -- ITCHY NOSE
      ---NASAL BLOCKAGE (VARIABLE)
      -- DIURNAL RHYTHM (WORST DAYTIME IMPROVES
      AT NIGHT
      -- OFTEN ASSOCIATED WITHJ CONJUNCTIVITIS
    • ALLERGIC RHINITIS
      SYMPTOMS:
      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 DEFINITION
      NASAL DISCHARGE
      BLOCKAGE
      SNEEZE/ 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 FATAL
      CHRONIC INFLAMMATORY DISORDER OF THE
      AIRWAYS IN WHICH CELLS PLAY A ROLE, INCLUDING M
      MAST CELLS AND EOSINOPHILS
      WIDESPREAD BUT VARIABLE AIRFLOW OBSTRUCTION
      THAT IS OFTEN REVERSIBLE EITHER SPONTANEOUSLY
      OR WITH TREATMENT ASSSOCIATED WITH AIRWAY
      RESPONSIVENESS
    • PRECIPITANT OF ASTHMA
      RESPIRATORY INFECTION (VIRAL)
      ALLERGENS
      FOOD
      HOUSEHOLD INHALANTS
      OUTDOOR INHALANTS
      IRRITANTS
      EXERCISE
      EMOTIONAL FACTORS
    • PATHOPHYSIOLOGY OFASTHMA ,SEVERE
      ASTHMA -- 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 OFASTHMA
      ACHIEVE AND MAINTAIN CONTROL OF SYMPTOMS
      PREVENT ASTHMA EXACERBATIONS
      MAINTAIN PULMONARY FUNCTIONS AS CLOSE
      TO NORMAL LEVELS
      AVOID ADVERSE EFFECTS FROM ASTHMA MEDICATIONS
      PREVENT IRREVERSIBLE AIRWAY OBSTRUCTION
      PREVENT ASTHMA MORBIDITY
    • MANAGEMENT PROGRAMS FOR ASTHMA
      EDUCATE PATIENTS/PARENTS
      ASSESS AND MONITOR SEVERITY
      AVOID OR CONTROL TRIGGERS
      MEDICATION PLANS FOR CHRONIC ASTHMA
      PLANS FOR EXACERBATIONS
      PROVIDE REGULAR FOLLOW-UP
    • STATUS ASTHMATICUS
      SEVERE ACUTE ASTHMA
      LIFE-THREATENING EPISODE
      UNRESPONSIVE TO THE USUAL APPROPRIATE THERAPY
      WITH ADRENERGIC AGENT AND THEOPHYLINE
      LEADS TO ACUTE RESPIRATORY INSUFFICIENCY
    • ATOPIC DERMATITIS
      CHRONIC ,HERITABLE, DISTINCTIVE CUTANEOUS INFLAMMATORY DISEASE CHARACTERIZED BY
      EARLY AGE OF ONSET AND INTENSE PRURITUS
      SKIN LESION: DRY, IRRITATED, WEEPING, EXCORIATED
      LICHENIFIED LESIONS ON THE FLEXURAL AREAS
      IN LATE CHILDHOOD AND ADOLESCENSE
      WIIH GENETIC PREDISPOSITION
      RELAPSING
      CAN DEVELOP ALLERGIC RHINITIS AND ASTHMA
    • STAGES OF ATOPIC DERMATITIS
      INFANTILE 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 DERMATITIS
      CHILDHOOD 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 DERMATITIS
      ADULT STAGE :
      HIGHLY PRURITIC , CONFLUENT PAPULES ON THE
      DORSAL ASPECT OF THE HANDS, UPPER EYELIDS AND
      FLEXURAL AREAS OF THE EXTREMITIES
    • STIGMAS OF ATOPICDERMATITIS
      LICHENIFICATION
      DENNIE ‘S LINE
      ATOPIC PALMS
      BUFFED NAILS
      WHITE DERMOGRAPHISM
      DELAYED BLANCHED PHENOMENON
      DRYNESS XEROSIS
      ATOPIC PERSONALITY
      HOUSEWIFE’S ECZEMA
      ATOPIC FOOT
      ALLERGIC SHINERS
    • CRITERIA FOR THE DIAGNOSISOF ATOPIC DERMATITIS
      MUST HAVE 3 OR MORE BASIC FEATURES :
      1.PRURITUS
      2.TYPICAL MORPHOLOGY /DISTRIBUTION
      3.TENDENCY TO RECURRENCES
      4.PERSONAL OR FAMILY HISTORY
    • CRITERIA FOR THE DIAGNOSIS OF ATOPIC DERMATITIS
      PLUS 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 DERMATITIS
      TREATMENT
      AVOID ENVIRONMENTAL FACTORS
      GOOD HYDRATION OF THE AFFECTED AREAS
      MOISTURIZERS
      CORTICOSTEROIDS IN THE SUBACUTE PHASE
    • URTICARIA ( HIVES)
      RAISED ERYTHEMATOUS SKIN LESIONS ASSOCIATED
      WITH MARKED PRURITUS
      DUE TO VASODILATATION OF SMALL VENULES
      AND CAPILLARIES AND EXUDATION OF FLUID
      INTO THE SUPERFICIAL DERMIS
      ANGIOEDEMA IS URTICARIA INVOLVING THE DEEPER SUBCUTANEOUS TISSUES
    • CLASSIFICATION OF URTICARIA
      IMMUNOLOGIC
      ANAPHYLACTIC / CYTOTOXIC/ IMMUNE COMPLEX
      ANAPHYLACTOID
      HEREDITARY ANGIOEDEMA/ CHEMICAL/ ASPIRIN SENSITIVITY
      PHYSICAL
      DERMATODRAPHIA/ COLD/ CHOLINERGIC/ SOLAR/PRESSURE
      MISC
      INFECTION/ PIGMENTOSA/ PSYCHOGENIC/IDIOPATHIC
    • URTICARIA
      TREATMENT
      SYMPATHOMIMETIC AGENTS : EPINEPHRINE
      ANTIHISTAMINICS
      CORTICOSTEROIDS
    • ALLERGIC CONTACT DERMATITIS
      COMMON DISORDER IN CHILDHOOD
      ERYTHEMA, PAPULES, VESICLES, SWELLING
      WEEPING ANG ITCHING
      24 -48 HRS AFTER EXPOSURE
      TYPE IV
    • CAUSES OF CONTACTDERMATITIS
      IRRITANTS ANIMALS
      PLANTS CLOTHING
      NICKEL DRUGS
      CHROMATE
      MERCURY
      COSMETICS
    • ADVERSE FOOD REACTION
      IMMUNOLOGIC REACTION RESULTING FROM INGESTION OF FOOD PRODUCTS
      AND ADDITIVES
      I
    • FOOD ALLERGY(HYPERSENSITIVITY)
      IMMUNOLOGIC REACTION RESULTING FROM
      INGESTION OF FOOD ADDITIVE , IgE MEDIATED
    • FOOD ANAPHYLAXIS
      CLASSIC ALLERGIC HYPERSENSITIVITY REACTION
      TO FOOD OR FOOD ADDITIVES INVOLVING IgE AND THE
      RELEASE OF CHEMICAL MEDIATORS
    • FOOD INTOLERANCE
      ABNORMAL NON-IMMUNOLOGIC PHYSIOLOGIC RESPONSE TO FOOD OR FOOD ADDITIVES
    • FOOD IDIOSYNCRASY
      HYPERSENSITIVITY WITHOUT IMMUNE RESPONSE
    • FOOD TOXICITY
      ADVERSE 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 ATOPY
      FAMILY HISTORY OF ATOPY RISK OF
      ATOPY
      BIPARENTAL( SAME ALLERGY) 50-80 %
      BIPARENTAL OR UNIPARENTAL 40-60%
      PLUS ONE SIBLING
      UNIPARENTAL OR SIBLING 20-49%
      NEGATIVE 5-15 %
    • MANIFESTATIONS OFFOOD ALLERGY
      GASTROINTESTINAL:: VOMITING, ENTEROCOLITIS,MALABSORPTION, BLEEDING
      RESPIRATORY : RHINITIS, ASTHMA, OTITIS MEDIA
      DERMATOLOGY : URTICARIA, ATOPIC DERMATITIS,
      ALOPECIA
      NEUROLOGIC : SEIZURE, LETHARGY
      HEMATOLOGY : ANEMIA
      ANAPHYLACTIC SHOCK
    • ADVERSE DRUG REACTION
      “ AN EFFECT WHICH IS UNINTENDED AND OCCURS
      AT DOSES NORMALLY USED IN MAN FOR PROPHYLAXIS
      DIAGNOSIS AND THERAPY “
      OCCURS WITHIN A REASONABLE TIME FOLLOWING ADMINISTRATION OF THE DRUG
      REACTIONS : INTOLERANCE, IDIOSYNCRASY, HYPERSENSITIVITY ,PSYCHOGENIC
    • CLASSIC ANTIHISTAMINICS
      ETHANOLAMINES
      EXAMPLES : DIPHENHYDRAMINE , CARBINOXAMINE
      CLEMASTINE, DIMENHYDRINATE
      GENERAL COMMENTS: SEDATIVE EFFECT HIGH,
      MODERATE ANTICHOLINERGIC EFFECTS, RELATIVE LOW
      GIT EFFECTS
    • CLASSIC ANTIHISTAMINICS
      ALKYLAMINES : CHLORPHENIRAMINE , TRIPROLIDINE,
      BROMPHENIRAMINE, PHENIRAMINE
      GENERAL COMMENTS : LOW SEDATIVE , ANTICHOLINERGIC AND GI EFFECTS , BEST GROUP
      FOR DAYTIME USE
    • CLASSIC ANTIHISTAMINICS
      ETHYLENEDIAMINES: ANTAZOLINE TRIPELENNAMINE
      GENERAL COMMENTS :LOW SEDATIVE , ANTICHOLINERGIC EFFECTS , GI EFFECTS COMMON
    • CLASSIC ANTIHISTAMINICS
      PIPERAZINES : HYDROXYZINE , MECLIZINE , CHLORCYCLIZINE
      GENERAL COMMENTS : DROWSINESS IS FREQUENT ,DRY
      MOUTH A USUAL CHOLINERGIC EFFECT
    • CLASSIC ANTIHISTAMINICS
      PHENOTHAZINE : METHDILAZINE , PROMETHAZINE
      TRIMEPRAZINE
      GENERAL COMMENTS : MARKED SEDATIVE EFFECT
      ( USEFUL TREATMENT OF PRURITUS )
    • CLASSIC ANTIHISTAMINICS
      PIPERIDINES : CYPROHEPTADINE , BENZOCYCLOHEPTATHIPINE
      AZATADINE
      GENERAL COMMENTS : DROWSINESS IS COMMON
      USEFUL IN THE TREATMENT OF URTICARIA