Allergy and Immunology Board Review November 8, 2012 - PowerPoint PPT Presentation

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Allergy and Immunology Board Review November 8, 2012
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Allergy and Immunology Board Review November 8, 2012

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  1. Allergy and Immunology Board ReviewNovember 8, 2012

  2. Test Question True or False. I love daylight savings. • True • False

  3. introduction

  4. General Facts • Atopy represents the genetic predisposition to develop allergic diseases • Atopic dermatitis • Allergic rhinitis • Asthma • Food allergy • A child with one component of atopy syndrome has a 3x greater risk of developing a second component

  5. Influential Factors • History of atopy in a first-degree relative or parent is the greatest risk factor for atopy • Neither parent: 10-15% risk • One parent: 20-40% risk • Both parents: 30-60% risk • Early childcare exposure reduces the risk for development of asthma…“hygiene hypothesis” • Non-genetic risk factors • Aeroallergen sensitivity • Environmental exposures • Diet (mom’s and baby’s)

  6. Environmental exposure • Early exposure to tobacco smoke, especially the mother’s, increases the frequency of asthma in children!!! • This is even true for babies whose mom smokes during pregnancy • Passive exposure to cigarette smoke may exacerbate asthma and allergic rhinitis! • 1-800-QUIT-NOW 

  7. Question #1 You are seeing an 8yo female with atopy syndrome back in clinic after referring her to Allergy/Immunology for some help. Skin prick testing was positive for various indoor allergens, including dog and cat. The family has a dog that has been around since your patient was 3yo. How should you counsel this family regarding their pet? • Nothing. The dog is not affecting her symptoms. • Tell the parents that they must sell the dog or find someone take her. • Tell the parents that they must sell the child or find someone to take her. • Keep the dog from the bedroom and decrease her exposure to pillows, carpeted areas, and stuffed animals. • Bathe the dog once a week and things should be fine.

  8. Environmental exposure • Identification of indoor allergens is important • Dust mites among most common • Animal dander from indoor pets…cat, dog, rodents • Cockroach, especially in inner-city areas • Mold • Avoidance • Pet removal • May not always be correct answer because of attachment • Removal/isolation from patient’s bedroom more likely!! • Impermeable covers, HEPA filters, vacuuming frequently • Removal of carpet and stuffed animals • No single intervention alone is likely to have a significant overall effect

  9. diet • Maternal diet during pregnancy and/or breastfeeding has NOT been shown to significantly alter the incidence of atopy • Restricting the mother’s diet will not be the correct answer!!! • Breastfeeding for the first 3-6 months after birth reduces the risk of atopic dermatitis in “at risk” babies • The AAP recommends exclusive breastfeeding for at least 4 months with supplementation of hypoallergenic formula if needed in “high risk” newborns (both parents or one parent and one sibling have atopy)

  10. Allergic rhinitis

  11. Rhinitis • Rhinitis: Inflammation of the membrane lining the nose and/or postnasal drainage • Chronic rhinitis can be either allergic or non-allergic • Stimuli (allergens, medications, hormones) cause mast cells and basophils to degranulate • Chemical mediators are releasedcausing rhinorrhea and nasal congestion • Histamine release causes sneezing and itching • Allergic rhinitis: IgE-mediated hypersensitivity reaction to specific allergens

  12. Allergic rhinitis • History • Nasal congestion: mouth breathing, snoring, nasal voice • Nasal irritation: sneezing, nasal pruritis, nose blowing, sniffing, snorting, coughing • Itchy eyes and postnasal drip • Impact on quality of life, seasonality, triggers, alleviating factors, and medication use are also important • Comorbidities…sinusitis and otitis media • Physical exam • Pale, edematous turbinates • Cobblestoning of posterior OP from lymphoid hyperplasia • “Allergic shiners” from venous engorgement • Dennie lines from edema • Allergic salute: transverse nasal crease

  13. Question #2 What is the MOST common cause of perennial (persistent) allergic rhinitis? • Using Afrin (a nasal decongestant) for longer than a week. • Cold weather or change in temperatures. • Eggs, wheat, milk, peanuts, and soy. • Outdoor allergens…different pollens and grasses. • Indoor allergens like animal dander, molds, and dust mites.

  14. Allergic rhinitis • Triggers • Seasonal rhinitis: outdoor plant allergens or specific molds that vary depending on the time of year • Perennial rhinitis: indoor allergens such as dust mites and animal dander • Testing to identify allergen hypersensitivity • Percutaneous (prick or puncture) skin testing remains the most specific and cost-effective diagnostic modality • RAST testing (for IgE) in blood can also be used • Nasal eosinophilia (nasal smear >4% eosinophils)

  15. Question #3 A 12yo girl presents with recurrent rhinorrhea, sneezing, ocular pruritis, and nasal congestion each spring and fall. On PE, she has bilateral conjunctivalerythema, enlarged and pale nasal turbinates, and a transverse nasal crease. Which medication will be your BEST first choice medication for symptom improvement? • Intranasal decongestant • Intranasal corticosteroid • Ocular antihistamine • Oral decongestant • Oral leukotriene antagonist

  16. treatment • Allergen avoidance = initial management • Intermittent symptoms: indoors during high pollen times, AC during spring and fall pollen seasons • Indoor allergens: decrease humidity (<50%), bed/pillow covers; remove pets from home OR decrease exposure by eliminating from bedroom and areas with rugs/pillows/heavy upholstery • Intranasal corticosteroids: first-line pharmacotherapy • Regular use can reduce nasal blockage, rhinorrhea, sneezing, and nasal itching • Most common adverse effect = epistaxis • Antihistamines (H1 or H2) • Decreased sneezing, itching, and rhinorrhea • NOT effective at treating congestion

  17. Asthma…get excited!!Only 29 Content Specs 

  18. Pathophysiology • Disease of airway inflammation mediated by a variety of cell types, resulting in hyper-responsive airways

  19. Question #4 What is the primary mediator during the early phase of an asthma exacerbation? • Cytokines and chemokines • Eosinophils • IgE • IgA • T-lymphocytes

  20. Pathophysiology • Early phase • IgE mediated • Mast cells and basophils degranulate causing bronchospasm • Short-acting beta agonists!! • Late phase • Inflammatory • Increased bronchial hyperresponsiveness • 4-12 hours after exposure to environmental insult • STEROIDS!!!

  21. Predisposing conditions • Family history of asthma • Atopy syndrome: allergic rhinitis and eczema • Most children with asthma (60-80%) are sensitized to at least 1 aeroallergen • Common indoor allergens: house dust mite, mold, cockroach, and animal dander • Skin testing should be considered for any child with persistent asthma • Exposure to tobacco smoke • Potent airway irritant • More likely to have mod-severe asthma with decreased lung function

  22. Question #5 16-year-old boy who runs on his high school cross-country team has been having trouble with coughing and wheezing during exercise. He has a history of intermittent asthma that is well controlled when he is not running. His coach is worried that he may have exercise-induced asthma (EIA). Which of the following is NOT characteristic of this diagnosis?? • EIA is sometimes the only presentation of asthma. • The symptoms often resolve with or without medication once the exercise is stopped. • Long acting beta agonists are the preferred treatment and the effect will continue even with long-term use. • The onset of wheezing 5 minutes after exercise starts with resolution within 20-30 minutes after stopping. • Is often a sign of poorly controlled/more severe asthma.

  23. Triggers • Exercise induced asthma: Coughing and wheezing after 5-6 minutes of exercise, gradual improvement after 20-30 minutes of rest (with or without med); smog increases severity!! • Can be the only presentation OR a sign of underlying, poorly controlled/more severe asthma Medications Aspirin NSAIDS Beta Blockers

  24. Early wheezing • Transient wheezers cease to wheeze after age 3 • Often associated with a LRTI, especially RSV • RSV and future development of asthma… • Exact data varies • Risk increases with severe infection (ie. hospitalization) • More than 80% of infants with a history of wheezing in the first postnatal year (especially with URIs) do not wheeze after age 3 • Atopic wheezers are most likely to develop persistent asthma • Kids with early onset asthma (<3y) with a parental history of asthma, confirmed atopic dermatitis, or sensitization to aeroallergens are least likely to outgrow asthma.

  25. Clinical manifestations • Cough (may be the only symptom) • Nighttime symptoms are common! • Wheezing • Difficulty breathing • “Chest tightness” • Symptoms often worsen in presence of triggers • Be sure discharge planning includes a full assessment of potential triggers in the home, school, or neighborhood! • Other signs of atopy

  26. Asthma Classification • Severity is initially best determined at time of diagnosis, before starting therapy • Determined by the most severe level of symptoms • Exercise-induced symptoms do not count towards severity • Four categories: intermittent, mild/moderate/severe persistent • The most important distinction is between intermittent and persistent asthma because all individuals with persistent asthma should be started on long-term controller medication (inhaled corticosteroids) • 2007 Guidelines breaks down into 3 age categories

  27. Question #6 You are rounding on Purple team with Dr. Hescock. You are presenting a 7yo male patient to the team who is here with status asthmaticus. Dr. Hescock asks you to classify his asthma at baseline. Per mom, he usually coughs one night per week and uses his albuterol at home 4-5 days/week. He saw a pulmonologist last month for PFTs, and his FEV1 was 75%. How would you BEST classify his asthma? • Intermittent • Mild Persistent • Moderate Persistent • Severe Persistent

  28. Major risk factors (one required): parental history of asthma, eczema, aeroallergen sensitivity • Minor risk factors (2 required): sensitization to foods, more the 4% eosinophilia, wheezing apart from colds

  29. PFTs should be performed at the initial time of asthma diagnosis (if old enough…5-6 years) • PFTs should also be assessed every 6-12 month in ALL patients with persistent asthma!

  30. Question #7 You have determined that a 4yo patient you are seeing in clinic today has mild persistent asthma. You have given mom a prescription for her albuterol MDI. What is the other MOST important prescription you need to write? • Inhaled corticosteroid • Long acting beta agonist • Nasonex • Leukotriene receptor antagonist (Montelukast) • Theophylline

  31. Outpatient Treatment • Short-acting beta agonists (rescue med)…work on the early (bronchospasm) phase • Treatment of ANY persistent asthma should include a long-term controller medication for prevention. • First-line = inhaled corticosteroids • Decreases bronchial inflammation and hyper-responsiveness • Block the late response to allergen (inflammatory phase) • Most effective anti-inflammatory medication for asthma • Reduce asthma symptoms • Improve lung function • Reduce acute exacerbations • Reduce the risk of death from asthma

  32. Outpatient Treatment • Inhaled Corticosteroids • Side effects: oral candidiasis, dysphonia (hoarseness), reflex cough, bronchospasm • Can be reduced by using a “spacer” with MDI, slowing the rate of inhalation, as well as rinsing the mouth with water after use High dose ICS may have an initial early affect on growth velocity, but no data suggests effect on final adult height; no known decrease in bone mineral density

  33. Alternative Medications • Leukotriene receptor antagonists (montelukast and zafirlukast) • Interfere with the action of leukotrienes…potent inflammatory mediators that are released from mast cells, eosinophils, and basophils • Alternative (not preferred) therapy for patients with mild persistent asthma • “Add-on” therapy for patients who do not achieve good control with medium-dose ICS • Theophylline • Omalizumab • Cromolyn sodium and nedocromil

  34. Alternative Medications • Long acting beta agonists (LABA) • 12 hours of bronchodilation by stimulation beta-2 receptors in the airway  Increased cAMP  Relaxation of smooth muscle • Available as dry powder inhaler (formoterol) or in combination with ICS (salmeterol/formoterol) • NOT • To be used to treat acute exacerbations • Anti-inflammatory…so do NOT use as monotherapy • Prevent exercise-induced bronchospasm, but effect deteriorates with long-term administration • Preferred “add-on” medication in kids > 12 years

  35. Question #8 You are in the ER seeing a patient with asthma for increased WOB that started with the weather change yesterday. His last admission was during the winter last year. He is afebrile and other than his wheezing and increased WOB with a dry cough, ROS is negative. On PE, you hear diffusely decreased breath sounds, wheezes, and no crackles. His CXR is shown. What other medication would you start besides Albuterol and Steroids? • Rocephin • Azithromycin • Both Rocephin and Azithromycin • Augmentin • None of the above

  36. Exacerbations • Patients who have any degree of asthma severity can have a severe exacerbation. • Symptoms of severe obstruction • Dyspnea at rest, inability to speak whole phrases • Cyanosis, accessory muscle use (retractions) • Quiet breath sounds (NO wheeze = bad) • Peak flow less than 40% predicted or personal best • Failure to respond to initial treatments • Patients with exacerbations uncontrolled by home medications should present to the ER! • Atelectasis on CXR is common • Antibiotics are NOT indicated unless there is true evidence of bacterial infection • CPT is not helpful

  37. Exacerbation Treatment • An inhaled short-acting beta agonist is first-line (albuterol, levalbuterol) • Relax smooth muscle within minutes, peak effect at15-30 minutes, wears off at 4-6 hours • Often patients will need a continuous treatment • Side effects: tachycardia, tremulousness, irritability, hypokalemia • Oxygen if increased WOB or with low O2 Saturations • Consider MIVFs • Patients are prone to increased HR because of chest hyper-expansion that impedes venous return • Albuterol increases HR even further • Ipratropium bromide (anticholinergic) in ER can decrease admission rates

  38. Exacerbation Treatment • For severe exacerbations that are unresponsive to SABAs alone…systemic corticosteroids to treat late phase • Improve airway responsiveness to SABAs, improve lung function (FEV1) and oxygenation, and decrease the risk of relapse from acute exacerbation • 2mg/kg/day (3-10 days depending on severity) • NO difference between IV/PO steroids in terms of efficacy • IF a patient is having a moderate to severe exacerbation with increased WOB, IV steroids should be ordered • Can give higher doses…varies but 1mg/kg q6h and possibly up to 2mg/kg q6h! • Magnesium sulfate IV and MORE…but no content specs on this 

  39. Risks of Severity • Risk factors for ICU admission OR higher rate of death • One or more life-threatening exacerbations of asthma • Severe asthma requiring chronic oral steroids • Abnormal FEV1 • Poor adherence • Poor control of daily asthma symptoms • Frequent daily short-acting beta agonist use • Excessive use (>2 days/week) has been associated with poorly controlled asthma and an increased risk of hospitalization and death! • Low socioeconomic status, family dysfunction • Patient psychological problems…depression/stress

  40. Self Assessment • Teaching the patient and/or family ways to recognize exacerbations is extremely important to patient outcome! • Counseling the family at EVERY visit regarding proper use of daily controller medications and rescue medications is essential to good control! • Be sure your patients know when an ER visit is necessary!

  41. Urticaria, Angioedema, & Anaphylaxis

  42. Anaphylaxis • Immediate and potentially life-threatening reaction to an allergen • Symptoms typically develop within minutes up to 2 hours • Rare cases of delayed reactions >2hrs after exposure • Most common symptoms = cutaneous • Pruritus, flushing, urticaria, angioedema • Occur in up to 90% of patients

  43. Anaphylaxis

  44. Anaphylaxis - triggers • Foods • Most common: milk, egg, soy, wheat, peanut/tree nut, seafood • Drugs • Most common: Penicillin • Low-risk of cephalosporin cross-reactivity • Other antibiotics (sulfa, etc), aspirin, NSAIDs, chemo • Insects • Hymenoptera (vespids, bees, stinging ants) • Large local reactions increase risk for anaphylaxis • Latex • Rubber tree antigens

  45. Anaphylaxis - triggers • Vaccines • Egg: influenza, yellow fever • Gelatin, Neomycin: MMR • Perioperative • Muscle relaxants, latex, antibiotics, opioids, blood products • Exercise • Can be food-dependent • Immunotherapy • Idiopathic

  46. Question #9 The parents of a 10-year-old boy who has a peanut allergy ask your advice on treatment of food allergy reactions at school. Last year, their son started itching diffusely and had difficulty breathing during lunchtime after accidentally eating some of his friend's chocolate candy bar that contained peanuts. The child is allowed to carry his own self-injectable epinephrine at school. His current weight is 90 lb (41 kg).Of the following, the BEST advice for the child, if a similar situation occurs, is to • Have the school call emergency services (911), who should evaluate and administer epinephrine if needed • Have the school nurse observe the child for 10 to 15 minutes while calling his parents • Immediately administer 0.15 mg of self-injectable epinephrine • Immediately administer 0.30 mg of self-injectable epinephrine • Take an oral antihistamine immediately

  47. Anaphylaxis - Treatment • Most important = recognize symptoms!! • Early administration of epinephrine • Best route = IM (lateral thigh) • Dose = 0.01mg/kg (max. 0.5mg) • EpiPen • 0.15mg for <30kg • 0.30mg for >30kg • Corticosteroids to help prevent the late-phase or biphasic reaction • 20% will have symptoms 4-24hrs after initial reaction • +/- H1-antihistamines