Empfohlen
Weitere Àhnliche Inhalte
Was ist angesagt?
Was ist angesagt? (20)
Ăhnlich wie Asthma
Ăhnlich wie Asthma (20)
Mehr von Dr. Arun Mathai Mani
Mehr von Dr. Arun Mathai Mani (20)
KĂŒrzlich hochgeladen
KĂŒrzlich hochgeladen (20)
Asthma
- 1. ASTHMA
- 2. DEFINITION Chronic inflammatory disorder of the airways Widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment Bronchial hyperresponsiveness to a variety of stimuli
- 3. affects 300 million people world-wide socio-economic impact is enormous, poor control leads to days lost from school or work, unscheduled health-care visits and hospital admissions
- 4. Adult Asthma Facts 14.5 million workdays lost due to asthma, a 2.3 fold increase from the early 80s to the mid 90s Adults accounted for over 1.3 million ED visits and 288,000 hospitalizations due to asthma One third of asthma related deaths occur in patients 35-44 years old Over 50% of asthma related deaths occur in patients 65 years and older Morb Mortal Wkly Rep. 2002 March 29; 51:1-13.
- 6. Atopy major risk factor for asthma genetically determined production of specific IgE antibody suffer from other atopic diseases, particularly allergic rhinitis and atopic dermatitis (eczema) most common allergens are - house dust mites, cat and dog fur, cockroaches, grass and tree pollens
- 7. Most Patients with Asthma Have Allergic Rhinitis Approximately 80% of asthmatics have allergic rhinitis Asthma alone Allergic rhinitis alone Allergic rhinitis + asthma Adapted from The Workshop Expert Panel. Management of Allergic Rhinitis and its Impact on Asthma (ARIA) Pocket Guide. A Pocket Guide for Physicians and Nurses. 2001; Bousquet J and the ARIA Workshop Group J Allergy Clin Immunol 2001;108(5):S147-S334; Sibbald B, Rink E Thorax 1991;46:895-901; Leynaert B et al Am J Respir Crit Care Med 2000;162:1391-1396.
- 8. IgE and Asthma in Adults Asthma Serum IgE (IU/mL) Odds ratio N = 2657 0.32 1 3.2 10 32 100 320 1000 3200 4400 2200 1100 55 22..55 11 Burrows B, et al. New Engl J Med. 1989;320:271-277.
- 9. Intrinsic Asthma negative skin tests to common inhalant allergens and normal serum concentrations of IgE later onset of disease (adult-onset asthma), commonly have concomitant nasal polyps, and may be aspirin-sensitive
- 11. AIR POLLUTION sulfur dioxide, ozone, and diesel particulates, may trigger asthma symptoms Indoor air pollution may be more important with exposure to nitrogen oxides from cooking stoves and exposure to passive cigarette smoke
- 12. OCCUPATIONAL EXPOSURE relatively common and may affect up to 10% of young adults Chemicals such as toluene diisocyanate and trimellitic anhydride, fungal amylase in wheat flour in bakers suspected when symptoms improve during weekends and holidays
- 15. DENDRITIC CELL WITH AN ALLERGEN
- 16. DENDRITIC CELL CAPTURES THE ALLERGEN AND RUNS WITH IT TO THE LYMPH NODE
- 18. T CELL CAPTURES THE ALLERGEN
- 19. CELL RECRUITMENT
- 21. TISSUE DAMAG E
- 23. IgE-dependent Release of Inflammatory Mediators IgE Allergens FceRI Over Minutes Lipid mediators: Prostaglandins Leukotrienes Wheezing Bronchoconstriction Over Hours Cytokine production: Specifically IL-4, IL-13 Mucus production Eosinophil recruitment Immediate Release Granule contents: Histamine, TNF-a, Proteases, Heparin Sneezing Nasal congestion Itchy, runny nose Watery eyes
- 24. Bronchoconstriction Before 10 Minutes After Allergen Challenge
- 25. Mechanisms of Airway Obstruction Smooth Muscle Contraction Mucus Hypersecretion Loss of Elastic Recoil ? Peribronchial Fibrosis Airway Wall Edema Vascular dilatation
- 26. Airway Inflammation in Asthma
- 27. Impact of IInnffllaammmmaattiioonn oonn SSmmaallll AAiirrwwaayyss Normal Acute Fatal Asthma Chronic Severe Asthma
- 28. CLINICAL FEATURES AND DIAGNOSIS
- 29. SYMPTOMS Recurrent episodes of: Shortness of breath Wheezing Chest tightness Cough, particularly at night and early in the morning
- 30. PATTERN OF SYMPTOMS Perennial, seasonal or both Continual, episodic or both Diurnal variations, especially nocturnal and on awakening early in the morning
- 31. PRECIPITATING AND/OR AGGRAVATING FACTORS Viral respiratory infections Environmental allergens Exercise Occupational chemicals or allergens Irritants Changes in weather Endocrine factors GERD Sinusitis
- 32. PHYSICAL EXAM Normal physical exam - asthma is under control Expiratory wheezing with normal or decreased air movement Accessory respiratory muscle use Ominous sign- no wheezing with decreased air movement
- 33. Cough may be the dominant symptom in some patients, and the lack of wheeze or breathlessness may lead to a delay in reaching the diagnosis of so-called âcough-variant asthma
- 34. EVALUATION CLINICAL HISTORY SPIROMETRY METHACHOLLINE CHALLENGE TEST ALLERGY SKIN TESTS
- 35. Spirometry: A Simple, Basic Measurement Essential to initial evaluation Helps assess severity of airflow obstruction Aids in differential diagnosis Obstructive versus restrictive airway disease Reversibility of airflow obstruction Confirms periodic home PEFR measurements in selected patients
- 36. Spirometry in asthma reduced FEV1, FEV1/FVC ratio, and PEF Improvement in FEV1>12% with bronchodilator therapy Measurements of PEF twice daily may confirm the diurnal variations in airflow obstruction â more than 20% is considered diagnostic
- 41. Spirometry: Flow-Volume FFllooww ((ll//ss)) VVoolluummee ((ll)) 55 44 33 22 11 00 --22 --44 1 2 3 4 5 --66 Pre-albuterol Post-albuterol Predicted Loops in Asthma
- 42. Bronchoprovocation Challenges methacholine or histamine challenge calculation of the provocative concentration that reduces FEV1 by 20% (PC20) Measures the increased AHR exercise testing is done to demonstrate the postexercise bronchoconstriction if there is anpredominant history of EIA
- 43. Reasons for Performing Bronchoprovocation Challenges in Clinical Practice To quantify the severity of the airway hyperresponsiveness(AHR) Clarify a clinical diagnosis of asthma when a reasonable degree of doubt exists To determine the presence of bronchial hyperresponsiveness in patients with chronic cough
- 45. INHALANT ALLERGENS Animal allergens House-dust mites Cockroach allergens Indoor fungi (molds) Outdoor allergens
- 46. ALLERGEN SKIN TESTS Eugene Braunwald, Atlas of Internal Medicine, 2nd edition
- 47. EVALUATION CBC with differential ( eosinophilia often seen in asthma, ABPA and CS vasculitis) Total igE specific IgE to inhaled allergens [radioallergosorbent test(RAST)] CXR CT of the chest ABG in status asthmaticus
- 48. Exhaled NO is now being used as a noninvasive test to measure eosinophilic airway inflammation The typically elevated levels in asthma are reduced by ICS, so this may be a test of compliance with therapy
- 49. ASTHMA CLASSIFICATION AND THERAPY
- 50. Classification of Asthma sx frequency less than 2 times / week sx frequency 2 times / week or more Intermittent Asthma Persistent Asthma MILD sx frequency >2/days per week, not daily FEV1>80% MODERATE sx frequency daily FEV1=60-80% SEVERE sx frequency throughout the day FEV1<60%
- 51. Goals of Therapy: Asthma Control â Minimal or no chronic symptoms day or night â Minimal or no exacerbations â No limitations on activities; no school/work missed â Maintain (near) normal pulmonary function â Minimal use of short-acting inhaled beta2- agonist â Minimal or no adverse effects from medications
- 52. Avoidance of aggravating factors particularly important occupational asthma relevant to atopic patients where removing or reducing exposure to relevant antigens, e.g. a pet animal, may effect improvement
- 53. House dust mite exposure may be minimised by replacing carpets with floorboards and using mite impermeable bedding Measures to reduce fungal exposure and eliminate cockroaches Medications known to precipitate or aggravate asthma should be avoided
- 55. BRONCHODILATOR THERAPIES beta2-adrenergic agonists, anticholinergics, and theophylline Short-acting beta2-agonists (SABAs) such as albuterol and terbutaline â doa 3-6 hrs Long-acting 2-agonists (LABAs) include salmeterol and formoterola doa >12 hours
- 56. CONTROLLER THERAPIES Inhaled Corticosteroids - most effective controllers for asthma Systemic Corticosteroids Antileukotrienes - montelukast and zafirlukast Cromones - Cromolyn sodium and nedocromil sodium Anti-IgE -Omalizumab
- 57. MANAGEMENT OF CHRONIC ASTHMA
Hinweis der Redaktion
- Slide 4 Allergic rhinitis and asthma frequently coexist. Most patients with asthma have allergic rhinitis (up to 80%).15-18 Among participants from two French centers in the European Community Respiratory Health Survey (ECRHS), 79% (77/98) of patients with asthma had concurrent rhinitis, and 20% (77/378) with allergic rhinitis had concurrent asthma. Asthma was defined as one or more asthma attacks in the preceding 12 months or positive response to metachloline challenge. Patients were considered to have allergic rhinitis if they responded positively to one or two questions regarding rhinitis symptoms.18 Epidemiologic studies support the suggestion that allergic rhinitis should be suspected as a comorbid condition in most patients with asthma.
- IgE is a key component of asthma in most asthma patients, as shown by Burrows and colleagues who investigated the relationship between IgE levels and the risk of developing asthma in adults. As the graph shows, the higher the total serum IgE concentration, the higher were the odds of having asthma. Burrows et al studied the association of self-reported asthma and serum IgE levels in 2657 subjects in a general population. They found that, regardless of the subjectsâ allergy status or age group, the prevalence of asthma was closely related to the serum IgE level (P&lt;0.0001). The figure in this slide shows the odds ratio of having asthma at seven levels of total IgE concentrations after correction for age, sex, smoking habits, and skin-test index in a logistic analysis. The solid green line represents the risk of asthma. Vertical lines are 95% confidence intervals around the regression for each odds ratio corresponding to a given log IgE level. The log odds ratio of having asthma increases linearly with the serum IgE level. Burrows B, Martinez FD, Halonen M, Barbee RA, Cline MG. Association of asthma with serum IgE levels and skin-test reactivity to allergens. N Engl J Med. 1989;320:271-277.
- The high levels of TH2-type cytokines that are found at sites of allergic inflammation are consistent with a TH2-cell-based aetiology of atopic disease. Furthermore, studies in mouse models of asthma have shown that allergic airway inflammation is dependent on CD4+ T cells and, more specifically, is seen when T-cell receptor-transgenic TH2, but not TH1, cells are adoptively transferred to mice. Finally, the absolute requirement for TH2 cells in directing allergic airway inflammation has been shown by the use of interleukin-4 (IL-4)-deficient mice. In these studies, defective priming of TH2 cells in the absence of IL-4 resulted in a failure to generate allergic inflammatory responses after subsequent airway challenge. Of note, if IL-4 was blocked only during inhaled antigen challenge, airway inflammatory responses were intact, indicating that once TH2-cell priming has occurred, IL-4 is no longer necessary for airway inflammation. This has also been confirmed by studies in which effective TH2-cell sensitization was achieved despite the absence of IL-4. Specifically, we have shown that IL-4-independent TH2-cell responses with high levels of IL-5 and IL-13 production can be generated in IL-4-deficient mice by epicutaneous exposure to soluble protein. In this system, mice showed no deficit in airway eosinophilia or mucus secretion following inhaled antigen challenge. So, the main role of IL-4 in allergic airway inflammation is during the initial priming of TH2-effector cells, whereas IL-5 and IL-13 have been shown, in numerous studies in both mice and humans, to be more directly responsible for the characteristic eosinophil infiltrates and mucus hypersecretion.
- IgE binds to high- and low-affinity receptors (Fcï„RI or Fcï„RII) on effector cells. The inflammatory cascade is initiated when IgE bound to effector cells is cross-linked by allergen. This results in the degranulation of effector cells and the release of a comprehensive array of mediators that are linked to the pathophysiology of asthma.
- This slide shows autopsy specimens from the small airways of a patient with chronic severe asthma, a patient with acute fatal asthma, and a normal individual. In the healthy individual, the epithelium is not highly folded and the lumen remains open. In contrast, the airway wall of the patient with acute fatal asthma shows marked thickening and is completely occluded by the highly folded epithelium and mucous plug. Interestingly, the airway of the patient with chronic severe asthma is less acutely constricted, but the airway wall is still much thicker than normal, and the airway is partially obstructed by a cellular plug.