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Allergies and Children

Allergies and Children. Richard E. Freeman MD MPH Korin Trumpie , PA-C Lock Haven University 2013. Includes Asthma Food allergies Atopic dermatitis (eczema) Allergic rhinitis Urticaria. Allergic Diseases. Allergies: ( allos =other & ergon =reaction)

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Allergies and Children

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  1. Allergies and Children Richard E. Freeman MD MPH KorinTrumpie, PA-C Lock Haven University 2013

  2. Includes • Asthma • Food allergies • Atopic dermatitis (eczema) • Allergic rhinitis • Urticaria Allergic Diseases

  3. Allergies: • (allos=other & ergon=reaction) • Used the term when referring to his patients who expressed an “altered state of reactivity” to common environmental antigens • Clements von Pirquet- Austrian Pediatrician 1906 • 1960’s discovered that most patients with allergy problems produced IgE in response to antigens Allergy

  4. ALLERGEN: • a type of antigen that produces an abnormally vigorous immune response in which the immune system fights off a perceived threat that would otherwise be harmless to most persons • by stimulating a type-I hypersensitivity reaction in atopic individuals through Immunoglobulin E (IgE) responses

  5. ATOPY: • /ˈætəpi/; Greek ἀτοπία - placelessness, out of place, special, unusual, extraordinary) • Hereditary (familial) predisposition in which a individual responds to several or many common environmental allergens but only after sensitization. • BUT NOT ALL Allergic REACTIONS ARE ATOPIC

  6. Not all allergic reactions are IgE mediated • Non IgE mediated • More poorly understood • T-cell mediated (Th1) • Usually delayed in onset 4-28 hours after exposure • Non-allergic rhinitis

  7. THE ALLERGIC PATHWAY

  8. Antigen-presenting cells • Dendritic cell, Landerhan cells, macrophages • Induce allergic inflammation by “presenting” allergens to T- cells • Dendritic and Langerhan cells can “prime” naïve T-cells • Dendritic cells in skin, intestine and lung are immature • Actively phagocytize antigens • Cells migrate to area lymph nodes • Antigens are fully processed & converted • Causing T-cells to proliferate and differentiate Antigen Presenting Cells-Step1

  9. T helper cells Type 2 (TH2) • Atopic persons respond by activation of TH2 helper cells • Secrete cytokines that favor IgE mediated responses • Also secrete interleukins which • Switch immunoglobulin isotypes to IgE • Enhance IgE synthesis • Differentiate and develop eosinophils (from stem cells) • Contribute to mast cell development • Th2 thought to play big role in development of asthma and allergies T helper Cell Type 2 (TH2) Step 2

  10. T helper cells Type 1 (TH1) • Non-atopic person: • responds to exposure to potential allergens by making TH1 cells • Secrete cytokines that stimulate IgG responses

  11. IgE • Derived from Plasma cells (activated Lymphocytes) • memory • Acute allergic response is dependent on IgE and its ability to bind to allergen • Binding initiates intracellular cascade IgE – it’s role: STEP 3

  12. Eosinophils • Help defend against parasites • Found in peripheral blood and tissue • Accumulate where allergic rxns take place • Contain intracellular granules that are sources of inflammatory proteins • These proteins • Damage epithelial cells • Induce airway hyper-responsiveness • Degranulate basophils and mast cells EOSINOPHILS- Step 4

  13. Eosinophils

  14. Mast cells • Derived from cells in bone marrow • Enter circulation and travel to peripheral tissues where they undergo tissue specific maturation • Mature mast cells do not circulate • Located throughout connective tissue and lie next to vessels • Mast cell and basophil degranulate • Releasing mediators of allergenic inflammation: histamine,serine proteases and proteolytics, lipids, cytokines, and chemokines = Allergic Response MAST CELLS-

  15. Three patterns of inflammatory reactions • EARLY PHASE RESPONSE • LATE PHASE RESPONSE • CHRONIC RESPONSE Mechanisms of Allergic Inflammation

  16. IMMEDIATE (from mast cell degranulation) • Occurs within minutes of allergen exposure • Resolves within 1 to 3 hours • Associated with increased local vascular permeability • Tissue swelling Sneezing • Increased blood flow Wheezing • Itching Abdominal cramps Early Phase Response

  17. Occur within hours of exposure • Reach peak at 6 to 12 hours • Resolve by 24 hours • Associated with infiltration of neutrophils and eosinophils, then basophils, monocytes,macrophages and TH2 cells • Skin – redness, edema, induration • Nose - sustained nasal blockage • Lungs - wheezing Late Phase Response

  18. Persist for days to years • Seen in patients with chronic allergic diseases • Contributing factors • Recurrent exposure to allergens and microbial agents • Tissue remodeling leading to irreversible changes in target organs • TH2 cytokines can maintain active inflammation Chronic Response

  19. Familial pre-disposition seen • Environment plays a big role • ie. Hygiene hypothesis • Genetic basis • Controversial • Genetic coding controls • systemic expressions of atopy, • increased IgE synthesis and • eosinophilia • Control local inflammatory response, asthma and atopic dermatitis Genetic Basis for Atopy

  20. THE CLEANER OR MORE STERILE THE ENVIRONMENT THE HIGHER THE RISK OF ALLERGIC DISORDERS. • MORE CHILDREN in house – LESS ALLERGIES • PLAYING IN DIRT/OUTSIDE EARLIER- LESS ALLERGIES • FREQUENT BATHING/ANTIBACTERIAL SOAPS- • MORE ALLERGIES HYGIENE HYPOTHESIS

  21. HISTORY • A careful History and P/E remain the most effective diagnostic means of diagnosis. • Description of symptoms- severity • Triggers- inhaled, food, pets, • Place-home, school, outside, bedroom,daycare • Age at presentation • Infants and young children-- food, environment • Older children-- seasonal • Timing-Seasonal vs Perennial, night-time, morning, activity • - How long do the symptoms last? Diagnosis of Allergic Disease

  22. DESCRIPTION OF SYMPTOMS • HEENT: • Congestion, rhinorrhea, type of nasal discharge,, sneezing or pruritus of nose or eyes • Lungs: • Wheezing, Cough, Shortness of Breath • Skin: • Rash, (eczema, contact dermatitis, uricaria) • GI tract: • nausea, diarrhea, abdominal pain • Other complaints: • headache, fatigue, lethargy, impaired concentration, and difficulty in learning. • ?

  23. MEDICATIONS: • Meds used and how he/she responds to them • PAST MEDICAL HISTORY • atopic conditions,( i.e. eczema), drug allergy, food allergy, recurrent infections such as sinusitis and otitis media • FAMILY HISTORY • 50% risk with one positive parent • 66% risk if both parents have positive history ALLERGY HISTORY -cont

  24. Behaviors • Allergic salute – rubs nose upward with palm of hand • Allergic click – tongue against roof of mouth to scratch soft palate • Rubbing of eyes History

  25. PE: TOROUGH • ALLERGIC FACIES • Allergic shiner – gray purple color to lower lids • Found in 60% allergic patients • Found in 40% of non-allergic patients • Dennie-Morgan lines- creases from inner canthus parallel and underneath rim of lower lid • Allergic transverse nasal crease • Elongated facial structures- • mouth breathing PE

  26. Denne-Morgan lines Allergic shiners &Dennie-Morgan lines

  27. Nasal crease Transverse Nasal crease- Prolonged nasal salute

  28. Allergic Facies

  29. Physical Exam • Allergic facies • Skin – dry, urticaria, eczema • Eyes - ropy discharge, cobblestoning of conjunctivae • Ears - check for serous fluid • Nose – Turbinates- boggy, pale to purple rather than beefy red • Mouth-High arched palate from chronic mouth breathing, and tongue thrusting • Dental malocclusion • Lungs – wheezing PE

  30. The Snotty Nose

  31. Eosinophilia; • peripheral smear and mucous of nose (Hensel Stain) • Parasites/allergies • Total serum IgE: • Sometimes elevated (neither sensitive or specific) • RAST – Radioallergosorbent test, • documents allergen specific IgE (less sensitive than skin tests) • ELISA • Skin Allergy Testing – • inject allergen subq. Some patients have late phase response • Methacholine Challenge Test- • bronchial provocation. Non-asthmatics do not constrict. Requires 20% decrease in FEV-1 Diagnostic Testing

  32. Environmental Control • Majority of our time spent indoors • Improved building causes • increase humidity and • concentration of indoor allergens • Dust mite • In bedding, carpet, upholstered furniture • Fecal pellets are source of allergen • Do not survive in humidity <50% • Emphasize control in bedroom Treatment

  33. Environment • PETS • Cats more sensitizing than dogs • Hair, dander, saliva main sources of allergens • Remove pet – still takes 6 months to clear allergens • Keep one room pet free • Insects and pests • Mice, cockroaches • Limit access to home and food Treatment

  34. Environment • Irritants • Tobacco smoke • Wood burning stove • Kerosene heaters • Fungi • Aspergillis and Penicillium • Keep humidity < 50% • Wipe down walls and floors Treatment

  35. PHARMACOLOGIC • Adrenergic agents- • 2 adrenergic receptor sites • Alpha-adrenergics • Constriction of small blood vessels in the bronchial mucosa • Used for nasal congestion: pseudoephedrine (CAUTION) • Beta-adrenergics- short and long action • Used in treatment of asthma • B-2 produces bronchodilation • Epinephrine has alpha and beta effects • DRUG OF CHOICE FOR ANAPHYLAXIS Treatment

  36. Pharmacologic • Anticholinergic agents • Diphenhydramine (Benadryl) • Use: Skin manifestations- urticaria, itching • Sedating, • Avoid in asthma • Ipratroprium bromide (atrovent) – atropine-like • Inhibits vagally mediated responses • MDI or nebulized for asthma • Nasal spray, • limited to severe cases, • does not alleviate sneezing, congestion or pruritis Treatment

  37. Pharmacologic • Antihistamines • Most frequently used • H-1 receptor causes allergic inflammation, pain, pruritis, vasodilation, increased mucous production • 1st generation H-1 antihistamines cause somnolence and impaired cognition – benadryl, phenergan • 2nd generation negligible side effects and once a day dosing- loratadine Treatment

  38. Pharmacologic • Chromones (chromoglycates) • Inhibit mast cell degranulation/ mediator release • Safe • Usually require multiple dosing (short half life) • Better for prophylaxis • Cromolyn sodium • Nedocromil sodium Treatment

  39. Pharmacologic • Glucocorticoids- • Widely used • Block more mediators • Topical • Ophthalmic drops • Nasal sprays • Inhaled • Oral or IV Treatment

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