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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

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  • 1. ALLERGY DR. MA. TERESA S. FAJARDO PEDIATRICS HEMATOLOGY / ONCOLOGY
  • 2. IMMUNOLOGIC BASISOF ALLERGIC DISEASE TO DETECT AND ELIMINATE ANYTHING FOREIGN TO THE BODY BENEFICIAL (IMMUNITY) OR HARMFUL (ALLERGY)
  • 3. COMPONENTS IN HOST'S RESPONSE TO THE ALLERGEN ENVIRONMENT TARGET CELLS B AND T LYMPHOCYTES
  • 4. IMMUNOLOGIC CAPABILITIES OF THE HOST PRIMARY ( NON- SPECIFIC ) SECONDARY (SPECIFIC) TERTIARY ( TISSUE DAMAGING RESPONSE)
  • 5. PRIMARY RESPONSE MOST PRIMITIVE PHAGOCYTOSIS / INFLAMMATION
  • 6. SECONDARY RESPONSE SPECIFIC RESPONSE MECHANISMS : B CELL / T CELL RESPONSE COMPLEMENT SYSTEM COAGULATIPON SYSTEM
  • 7. TERTIARY RESPONSE TISSUE – DAMAGING RESPONSES ( TYPES I, II, III, IV ) PROPOSED BY GELL AND COOMBS
  • 8. MEDIATORS OF ALLERGY PREFORMED MAST CELL MEDIATORS RAPIDLY FORMED MAST CELL MEDIATORS
  • 9. PREFORMED MAST CELLMEDIATORS VASOACTIVE MEDIATORS CHEMOTACTIC MEDIATORS ENZYMES PROTEOGLYCANS
  • 10. PREFORMED MAST CELLMEDIATORS ( VASOACTIVE MEDIATORS) HISTAMINE BRONCHOSPASM AND VASCULAR PERMEABILITY ADENOSINE INHIBIT PLATELET AGGREGATION STIMULATE IRRITANT RECEPTORS
  • 11. PREFORMED MAST CELLMEDIATOR (CHEMOTACTIC MEDIATORS ) 1. NEUTROPHIL FACTOR RECRUITMENT / ACTIVATION OF NEUTROPHIL 2. EOSINOPHIL FACTOR RECRUITMENT /ACTIVATION OF EOSINOPHIL
  • 12. PREFORMED MAST CELLMEDIATOR ( ENZYMES) 1. NEUTRAL PROTEASES ( TRYPTASE , CHYMASE ) COMPLEMENT/ KININ ACTIVATION 2. ACID HYDROLASES ( BETA- GLUCORONIDASE) INFLAMMATION
  • 13. PREFORMED MAST CELLMEDIATOR (PROTEOGLYCANS) HEPARIN ANTICOAGULANT ANTICOMPLEMENT ACTIVITY
  • 14. RAPIDLY FORMED MAST CELL MEDIATORS PLATELET- ACTIVATING FACTOR PROSTAGLANDIN LEUKOTRIENES
  • 15. 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
  • 16. CYTOKINES NEWLY SYNTHESIZED PROTEINS THAT REGULATE IMMUNE RESPONSE POTENT PRO- INFLAMMATORY MEDIATORS GROWTH / DIFFERENTIATION OF EOSINOPHILS AND MAST CELLS
  • 17. CYTOKINES AND ALLERGY IgE REGULATION EOSINOPHILIA MAST CELL DEV ‘T AND ACTIVATION INFLAMMATION
  • 18. 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
  • 19. 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
  • 20. 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
  • 21. RHINITIS DEFINITION NASAL DISCHARGE BLOCKAGE SNEEZE/ ITCH TWO OR MORE SYMPTOMS FOR MORE THAN ONE HOUR ON MOST DAYS
  • 22. ALLERGIC RHINITIS TREATMENT ENVIRONMENTAL CONTROL IMMUNOTHERAPY PHARMACOTHERAPY PARENT/PATIENT EDUCATION
  • 23. 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
  • 24. PRECIPITANT OF ASTHMA RESPIRATORY INFECTION (VIRAL) ALLERGENS FOOD HOUSEHOLD INHALANTS OUTDOOR INHALANTS IRRITANTS EXERCISE EMOTIONAL FACTORS
  • 25. PATHOPHYSIOLOGY OFASTHMA ,SEVERE ASTHMA -- MUCUS SECRETION , BRONCHOSPASM ,EDEMA ---INCREASED RESISTANCE TO AIRFLOW---HYPERINFLATION, ATELECTASIS , CNS DEPRESSION-- PULMONARY VASOCONSTRICTION--CARDIAC FAILURE AND COMA
  • 26. 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
  • 27. 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
  • 28. 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
  • 29. STATUS ASTHMATICUS SEVERE ACUTE ASTHMA LIFE-THREATENING EPISODE UNRESPONSIVE TO THE USUAL APPROPRIATE THERAPY WITH ADRENERGIC AGENT AND THEOPHYLINE LEADS TO ACUTE RESPIRATORY INSUFFICIENCY
  • 30. 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
  • 31. 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
  • 32. 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
  • 33. 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
  • 34. 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
  • 35. 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
  • 36. 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
  • 37. ATOPIC DERMATITIS TREATMENT AVOID ENVIRONMENTAL FACTORS GOOD HYDRATION OF THE AFFECTED AREAS MOISTURIZERS CORTICOSTEROIDS IN THE SUBACUTE PHASE
  • 38. 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
  • 39. 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
  • 40. URTICARIA TREATMENT SYMPATHOMIMETIC AGENTS : EPINEPHRINE ANTIHISTAMINICS CORTICOSTEROIDS
  • 41. ALLERGIC CONTACT DERMATITIS COMMON DISORDER IN CHILDHOOD ERYTHEMA, PAPULES, VESICLES, SWELLING WEEPING ANG ITCHING 24 -48 HRS AFTER EXPOSURE TYPE IV
  • 42. CAUSES OF CONTACTDERMATITIS IRRITANTS ANIMALS PLANTS CLOTHING NICKEL DRUGS CHROMATE MERCURY COSMETICS
  • 43. ADVERSE FOOD REACTION IMMUNOLOGIC REACTION RESULTING FROM INGESTION OF FOOD PRODUCTS AND ADDITIVES I
  • 44. FOOD ALLERGY(HYPERSENSITIVITY) IMMUNOLOGIC REACTION RESULTING FROM INGESTION OF FOOD ADDITIVE , IgE MEDIATED
  • 45. FOOD ANAPHYLAXIS CLASSIC ALLERGIC HYPERSENSITIVITY REACTION TO FOOD OR FOOD ADDITIVES INVOLVING IgE AND THE RELEASE OF CHEMICAL MEDIATORS
  • 46. FOOD INTOLERANCE ABNORMAL NON-IMMUNOLOGIC PHYSIOLOGIC RESPONSE TO FOOD OR FOOD ADDITIVES
  • 47. FOOD IDIOSYNCRASY HYPERSENSITIVITY WITHOUT IMMUNE RESPONSE
  • 48. 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
  • 49. 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 %
  • 50. 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
  • 51. 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
  • 52. CLASSIC ANTIHISTAMINICS ETHANOLAMINES EXAMPLES : DIPHENHYDRAMINE , CARBINOXAMINE CLEMASTINE, DIMENHYDRINATE GENERAL COMMENTS: SEDATIVE EFFECT HIGH, MODERATE ANTICHOLINERGIC EFFECTS, RELATIVE LOW GIT EFFECTS
  • 53. CLASSIC ANTIHISTAMINICS ALKYLAMINES : CHLORPHENIRAMINE , TRIPROLIDINE, BROMPHENIRAMINE, PHENIRAMINE GENERAL COMMENTS : LOW SEDATIVE , ANTICHOLINERGIC AND GI EFFECTS , BEST GROUP FOR DAYTIME USE
  • 54. CLASSIC ANTIHISTAMINICS ETHYLENEDIAMINES: ANTAZOLINE TRIPELENNAMINE GENERAL COMMENTS :LOW SEDATIVE , ANTICHOLINERGIC EFFECTS , GI EFFECTS COMMON
  • 55. CLASSIC ANTIHISTAMINICS PIPERAZINES : HYDROXYZINE , MECLIZINE , CHLORCYCLIZINE GENERAL COMMENTS : DROWSINESS IS FREQUENT ,DRY MOUTH A USUAL CHOLINERGIC EFFECT
  • 56. CLASSIC ANTIHISTAMINICS PHENOTHAZINE : METHDILAZINE , PROMETHAZINE TRIMEPRAZINE GENERAL COMMENTS : MARKED SEDATIVE EFFECT ( USEFUL TREATMENT OF PRURITUS )
  • 57. CLASSIC ANTIHISTAMINICS PIPERIDINES : CYPROHEPTADINE , BENZOCYCLOHEPTATHIPINE AZATADINE GENERAL COMMENTS : DROWSINESS IS COMMON USEFUL IN THE TREATMENT OF URTICARIA