1. M.A.Zohal pulmonologist

2. Chronic inflammatory disease of airways, characterized by increased responsiveness of the tracheobronchial tree to stimuli Manifested physiologically by a widespread narrowing of the air passages and clinically by paroxysms of dyspnea, cough, and wheezing Episodic disease, with acute exacerbations interspersed with symptom-free periods Most attacks are short-lived, lasting minutes to hours.

3. Prevalence  Increasing in many parts of the world  4–5% of the adult population of the U.S. is affected. Age  All ages affected, but more predominant in early life  ~50% of cases develop before 10 years of age.  Another one-third of cases occur before 40 years of age. Sex  2:1 male-to-female ratio in childhood  Sex ratio equalizes by 30 years of age.

7. Epithelial damage may contribute to AHR in a number of ways, including:  loss of its barrier function to allow penetration of allergens;  loss of enzymes (such as neutral endopeptidase) that normally degrade inflammatory mediators;  loss of a relaxant factor  exposure of sensory nerves, which may lead to reflex neural effects on the airway

8. First-degree relative with a history of asthma Personal or family history of atopy History of multiple respiratory infections during childhood Receiving breast milk appears to reduce the risk of developing asthma.

9.  Associated with a personal and/or family history of allergic diseases, such as rhinitis, urticaria, and eczema  Immunoglobulin E mediated Allergen:  Dust mites (often found in pillows, mattresses, carpets and drapes)  Cockroaches  Animal dander, especially cats  Seasonal pollens

10.  No defined immunologic mechanism  Precipitants  Upper respiratory infections  Exercise  Gastroesophageal reflux  Exposure to cold air  Tobacco smoke  Pollutants: ozone, nitrogen dioxide  Sulfites in food  Emotional stress  Pharmacologic agents  Aspirin  Nonsteroidal anti-inflammatory drugs  Tartrazine dyes  β-Adrenergic antagonists

11. Classic symptom triad  Wheezing  Dyspnea  Cough Typical acute attack  Often occurs at night  Patients experience a sense of constriction in the chest, often with a nonproductive cough.  Respiration becomes audibly harsh.  Wheezing first during expiration and then in both phases of respiration  Expiration becomes prolonged.

12.  Patients with allergic asthma  Exposure to antigen typically produces an immediate response.  Airway obstruction develops in minutes and then resolves.  30–50% of patients have a second wave of bronchoconstriction, a "late reaction," 6-10 hours later.  In a minority, only a late reaction occurs.

13.  Respiratory rate Increases with severity  Heart rate Increases with severity Relative bradycardia with impending respiratory failure  Use of accessory respiratory muscles Increases with severity Paradoxical thoracoabdominal movement with impending respiratory failure  Pulsus paradoxus (normally < 10 mmHg) 10-25 mmHg in moderate episode >25 mmHg in severe episode  Ear, nose, and throat examination  Nasal polyps in patients with allergic asthma, cystic fibrosis,asprin sensitivity  Skin  Eczema and atopic dermatitis in allergic patients

14.  Recurrent pulmonary emboli  Upper airway obstruction by tumor or laryngeal edema  Glottic dysfunction  Endobronchial disease  Carcinoid tumors Carcinoid tumors  Chronic bronchitis or emphysemabronchitis or emphysema  Eosinophilic pneumonia  Congestive heart failure  Systemic vasculitis with pulmonary involvement Systemic vasculitis  Vocal cord dysfunction

15.  history  physical examination  pulmonary function tests

16. First-degree relative with a history of asthma Personal or family history of atopy History of multiple respiratory infections during childhood Receiving breast milk appears to reduce the risk of developing asthma.

17. If occupational exposure is suspected ask about:  workplace and work history in detail.  Specific contaminants?  Availability and use of protective devices?  Do coworkers have similar complaints?  Ask about every job; short-term exposures may be significant.

18.  Physical examination  Presence of wheezing, especially expiratory  Assessment of airflow obstruction severity  Pulmonary function tests  Bronchoprovocation test may be required if wheezing or airflow obstruction is not initially demonstrated.  Shows initial airflow obstruction and reversibility with bronchodilator inhalation

19.  Complete blood count may show eosinophilia.  Serum immunoglobulin E level  o Elevated in allergic asthma  o Normal in idiosyncratic asthma  o Marked elevations may suggest allergic bronchopulmonary  aspergillosis.  Sputum examination  o Eosinophilia  o Curschmann’s spirals (casts of small airways)  o Charcot–Leyden crystals  o Presence of large numbers of neutrophils suggests bronchial infection.

20.  Arterial blood gas  Shows hypoxemia during attacks  Usually, hypocarbia and respiratory alkalosis are present.  Normal or elevated arterial partial pressure of carbon dioxide suggests severe respiratory muscle fatigue or airways obstruction and impending respiratory failure.

21.  o Findings  Forced vital capacity (FVC); FEV1; maximum, mid-, and peak  expiratory flow rate; and FEV1/FVC ratio are decreased.  Residual volume and total lung capacity are increased.  Diffusing capacity of the lung for carbon dioxide is usually  normal or slightly increased.  Reduction of FEV1 to < 25% predicted or < 0.75 L after  administration of a bronchodilator indicates severe disease.  Bronchoprovocation test  o May be required when spirometry results are normal and no wheezing  is present  o Heightened airway

22.  Establish diagnosis by demonstrating reversible airway obstruction.  Reversibility is defined as a ≥ 12% increase in (FEV1) after 2 puffs of a β-adrenergic agonist.  Helpful in judging severity of airway obstruction and for following response to treatment  More reliable than clinical examination or patient’s subjective symptoms

23.  Mortality  Only 0.09–0.25% of admissions to hospital are at risk of an untoward event.  Particularly good prognosis for those whose disease is mild and develops in childhood  The proportion of children who still have asthma 7–10 years after the initial diagnosis varies from 26–78% (average, 46%).  Only 6–19% continue to have severe disease.  Even when untreated, persons with asthma do not continuously move from mild to severe disease with time.  Clinical course is characterized by exacerbations and remissions.  Some studies suggest:  Spontaneous remissions occur in approximately 20% of those who develop the disease as adults.  ~40% can be expected to experience improvement, with less frequent and severe attacks, as they grow older.