1. Bronchial asthma By Dr. Abdelaty Shawky Assistant professor of pathology

2. Bronchial Asthma Asthma is a chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or in the early morning.

3. - These symptoms are usually associated with widespread bronchoconstriction that is reversible, either spontaneously or with treatment. - It is thought that this inflammation is due to an increase in airway responsiveness (bronchospasm) to a variety of stimuli.

4. Some of these stimuli would have little or no effect on non-asthmatics with normal airways. Many cells play a role in the inflammatory response, in particular eosinophils, mast cells, macrophages, T lymphocytes, neutrophils, and epithelial cells.

5. -Classification of bronchial asthma: I. Based on the frequency and severity of symptoms. -Categorization into;  Mild.  Moderate.  Severe persistent asthma.

6. II. Based on response to treatment:  Steroid-dependent.  Steroid-resistant asthma. III. Based on the type of stimulus:  Extrinsic (initiated by exposure to an extrinsic antigen).  intrinsic (initiated by diverse, non-immune mechanisms, including stress, emotions and exercise).

7. IV: Based on the events that trigger bronchoconstriction. -These include;  Seasonal.  drug-induced.  occupational asthma.  asthmatic bronchitis in smokers.

8. Compare extrinsic asthma and intrinsic asthma.

9. Intrinsic asthma Extrinsic asthma 1. Incidence 10%90% 2. Age adults.Children 3. Etiopathognesis - Due to increased vagal reactivity of air ways to various types of stimuli e.g. physical exercise, anxiety, emotions. - No family history of similar cases. - Atopy (type I hyperesensitivity reaction) due to exposure to exogenous non-bacterial antigens e.g. house dust, animal dandruff, pollens, food or spores of fungi. - Positive family history of atopic diseases. 4. Prognosis BadGood

10. * Grossly:  Small bronchi and bronchioles are spastic (thick and narrow).  Trachea & bronchi are hyperaemic and covered by mucus.  Lung tissue shows Acute emphysema (due to partial bronchial obstruction).

11. * Microscopically: The small bronchi and bronchioles show; 1. Thick basement membrane 2. Narrow lumens, contains mucus plugs contain whorls of sheded epithelial cells (curschmann spirals), numerous eosinophils and charcot- leyden crystals (esinophil membranes). 3. The subepithelial tissue show; Hyperplasia of mucous glands. Hypertrophy of the smooth muscle. Inflammatory infiltrate formed mainly of eosinophils.

15. Curschmann spiral Charcot-leyden crystals

16. * Clinical Course: The classic asthmatic attack lasts up to several hours and is followed by prolonged coughing; the raising of copious mucous secretions provides considerable relief of the respiratory difficulty. In some patients, these symptoms persist at a low level all the time.

17. In its most severe form, status asthmaticus, the severe acute paroxysm persists for days and even weeks, and under these circumstances, ventilatory function might be so impaired as to cause severe cyanosis and even death.

18. The clinical diagnosis is aided by the demonstration of an elevated eosinophil count in the peripheral blood and the finding of eosinophils, Curschmann spirals, and Charcot-Leyden crystals in the sputum.

19. In the usual case, with intervals of freedom from respiratory difficulty, the disease is more discouraging and disabling than lethal. With appropriate therapy to relieve the attacks, patients with asthma are able to maintain a productive life. Occasionally, the disease disappears spontaneously.

20. * Complications: 1.Pulmonary hypertension: causing Core pulmonale or heart failure. 2.Emphysema. 3.Bacterial infection causing persistent bronchitis, bronchiectasis or pneumonia. 4.Status asthmaticus: persistent attacks for days or weeks. May lead to respiratory failure.

21. Thanks