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Allergies: Review, Relief, Prevention, Patient Education

Allergies: Review, Relief, Prevention, Patient Education. Kara Parker, MD Oct 15, 2009. Objectives. To present a larger picture of the factors that create and prevent allergies.

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Allergies: Review, Relief, Prevention, Patient Education

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  1. Allergies:Review, Relief, Prevention,Patient Education Kara Parker, MD Oct 15, 2009

  2. Objectives • To present a larger picture of the factors that create and prevent allergies. • To review the components of allergic disease – genetics, immune reaction, environmental triggers, and physical response. • To present the pharmaceutical, vaccination, and nutraceutical therapies for allergies • To offer resources for environmental control and prevention of allergy development and triggers

  3. Goals • To help prepare you for boards – all material taken from AAFP reviews, and residency guidelines are followed. • To help you be a clinician with a broader understanding of development and triggers of allergies and ways to prevent and control symptoms.

  4. Overview Review the epidemiology of allergic disease, and pre and post-natal contributors Review allergic rhinitis and conjunctivitis Review anaphylaxis and drug allergy Review allergy testing Review immunotherapy (antigen vaccination) Review food allergy, both IgE, and IgG Review pharma and nutraceuticals for prevention/ relief Review environmental control and patient education

  5. Breathe!

  6. Toxins vs allergens • Toxins: Potentially injurious to any one, depending on dose. • Allergens: Only injurious to predisposed individuals.

  7. Burden of disease • Allergies are increasing in the Industrialized world. • In America over 50 million people report allergic symptoms, 20% have atopic disease • Allergies are the 6th most common chronic disease in the US • 14 million visits yearly for hay fever symptoms • Peanut allergy has doubled in the past 5 years

  8. The Hygiene Hypothesis • The decreasing incidence of early infections due to sanitization, vaccination, and antibiotics lead to underdevelopment of TH1 • And thus disproportionate TH2 activity • T cells are programmed in infancy, and perpetuate what they have learned.

  9. Th1/Th2 Imbalance and Inflammatory Disease • Th1: Intracellular defense • T cell-mediated activation of macrophages and neutrophils • Th2 : Humoral defense. • B cell-mediated activation of mast cells, eos, basos, ↑ IgE, IgG4

  10. TH1/TH2 Imbalance • TH1 predominance leads to organ specific autoimmune disease (Rheumatoid arthritis,Multiple sclerosis,Thyroiditis,Lyme arthritis,Crohn’s disease, IDDM ) • TH2 predominance leads to atopic and allergic disease.(Allergic diseases, asthma, contact dermatitis,Scleroderma,Ulcerative colitis, Systemic lupus erythematosus )

  11. Allergies are more common in: • Nonwhite populations • People who live in high pollution areas • Higher socioeconomic classes • People with a FH of allergy • People born during peak allergy season • Firstborn children • Children exposed to cigarettes • Children given formula and food before 4 mo.

  12. Allergies are less common In people who: • Come from a large family • Attended a daycare center at an early age • Were exposed to common early infections • Did NOT get antibiotics for treatment of early childhood illnesses • Have high intakes of vitamin D, vitamin C, bioflavonoids and, probiotics, omega-3 FA.

  13. Genetic links • Allergies run in families and have genetic predisposition • One major allergy gene has a 24% incidence, but a low penetrance. • Genetic links alone do not account for the sharp rise in allergies in the past 30 years.

  14. Gene Links to Allergies

  15. Mold

  16. Early Exposures - Mold • Early exposure of infants to certain airborn molds increases the risk of allergies to molds, pets, pollen, dust mites, and foods. • Penicillum, aspergillis, and alternaria were worst. • Other mold exposures seem to be protective and beneficial.

  17. Early Exposures - Tobacco. • Early Exposure to tobacco smoke is linked to development of allergic rhinitis • Infants exposed to 20 or more cigs/ day had a 3 –fold increase in incidence of AR • 43% of American infants are exposed to tobacco smoke daily.

  18. In Utero Exposures • At 22 weeks gestation the fetus can make IgE Ab to egg, milk, and dust mites. • 23% of homes have beds with levels of dust mites high enough to trigger atopy. • What is Mom exposed to that triggers a fetal allergic response?

  19. The Allergic Process: • Initial exposure: Sensitization stage where IL-4 is produced from antigen presentation, • developing TH2, • Signaling IgE production to the antigen • Recruiting eosinophils, growing mast cells, differentiating B cells to secrete IgE antibodies

  20. Second exposure • Antigen is identified and bound by the IgE antibodies on the surface of sensitized mast cells and basophils. • Allergen/Antibody complex activates and degranulates the cells. • Histamine, protease, chemotaxins, leukotrienes, prostaglandins enter blood. • Localized inflammation is induced in diverse areas of the body leading to allergic symptoms.

  21. Allergic Inflammation: • Acute: Rejection of a stressor (allergen) • Chronic: Persistence of the acute phase response. • Maladaptive – more detrimental than beneficial • Self perpetuating • Disrupts homeostasis • Alters cellular physiology • Destroys tissue • Systemic response

  22. Allergic symptoms • Recurrent Sneezing • Nasal pruritis • Nasal congestion • Eye, throat, and ear tingling and pruritis • Headache • Sleep disturbance • Concentration difficulties

  23. Allergic Rhinitis

  24. Allergic Rhinitis • Can be seasonal, perennial, or occupational • Is a systemic illness with constitutional symptoms • Fatigue • Malaise • HA

  25. Associated Symptoms • Excessive mucus production • Congestion • Sneezing paroxysm • Watery eyes • Nasal and ocular pruritis

  26. Allergic Rhinitis • Shares a co-morbidity with asthma, eczema, and chronic sinusitis • Determining allergic rhinitis (IgE mediated) from other types is important as therapies are different

  27. Allergic vs. non-allergic rhinitis • Non- allergic includes: • Vasomotor • Hormonal • Drug induced • Structural • Occupational (irritant) • Eosinophilia syndrome • Emotional rhinitis

  28. New Classification of AR • Instead of seasonal (pollens molds) and perennial (indoor exposures) • Use intermittent, persistent, mild, moderate, severe for allergic rhinitis

  29. PE suggestive of AR • Gen: fatigue, lack of concentration • Eyes: Allergic shiners, conjunctivitis • Ears: Air fluid levels – chronic congestion • Nose: Deviated septum, pale boggy mucosa, and polyps • Mouth: Enlarged tonsils, clear postnasal dc • Chest: wheezing, Skin: atopic dermatitis

  30. Medical History • FH: allergies, asthma, eczema • PMH: any of the above • Age: 80% of illness starts before age 20 • Success of past and current TX • Environmental factors: Got a cat, new job with exposure, basement flooding, etc. • Stress – often mind body plays a part

  31. Diagnosing AR • If nasal and constitutional symptoms are chronic, or last longer than 1 week after a viral cold and PE and story likely for AR: • Check for sinusitis • If negative, do a trial of antihistamines • If a positive response, Dx allergic rhinitis

  32. Allergy Testing • No clear guidelines for when to do allergy testing. • If Diagnosis is unclear • If case is severe • If patient is a potential candidate for immunotherapy • If testing will change treatment outcomes

  33. Allergy Testing • Not routinely recommended • Usually done by allergists or specialized dermatologists • Will be covered in detail later.

  34. Conventional treatment • 1) Allergen avoidance • 2) Pharmacologic treatment • 3) Allergen Immunotherapy

  35. Allergen Avoidance • Stay indoors during peak allergy season • Keep windows closed and air cond. on • HEPA filter for purifying airborne allergies • Wash hair before bed • Keep home dusted • Dust mite covers if needed • Removal of mold • Special precaution with pets

  36. Rx: Antihistamines Antagonization of H1 receptor sites can reduce histamine symptoms: sneezing, rhinorrhea, nasal itching, lacrimation. First generation OTC remedies produce sedation (diphenhydramine, promethazine most; chlorpheniramine, brompheniramine least SE’s are dry mucous membranes, urinary retention, blurred vision are common.

  37. Second Generation Antihistamines • Have minimal or no anti-cholinergic SE’s • Do not readily cross the BBB • Cardiotoxity from astimizole and terfenidine – both removed from market

  38. Nasal Decongestants • Activate alpha adrenergic receptors in the vascular smooth muscle of the resp. mucosa • Oral formulations (sudafed) cause insomnia, restlessness, tachycardia, BP elevation • Topical decongestants can only be used for a 3-5 day period, as they cause rebound SX’s

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