bronchial asthma for mbbs students and pgs students.pptx

Bronchial asthma

1. Bronchial asthma By Dr. Pravalika

2. Introduction Asthma is a disease characterized by episodic airway obstruction and airway hyperresponsiveness usually accompanied by airway inflammation. Airway hyperresponsiveness is a hallmark of asthma. It is defined as an acute narrowing response of the airways in reaction to agents that do not elicit airway responses in nonaffected individuals or an excess narrowing response to inhaled agents as compared to that which would occur in nonaffected individuals. Primarily targets the bronchi and its subdivisions and nonrespiratory bronchioles. More common in children than adults and a Majority (50%-80%) develop symptoms before 5 years of age In most cases, the airway obstruction is reversible, but in some , a component of the obstruction may become irreversible. In a large proportion of patients, the airway inflammation is eosinophilic, but some patients may present with differing types of airway inflammation, and in some cases, there is no obvious evidence of airway inflammation.

3. Extrinsic asthma Type I HSR with exposure to extrinsic allergens - Typically develops in children with an atopic family history to allergies Initial sensitization to an inhaled allergen Stimulate induction of subset 2 helper T cells (CD4 TH2) that release interleukin (IL)-4 and IL-5 IL-4 stimulates isotype switching to IgE production. IL-5 stimulates production and activation of eosinophils. IL-13 stimulates mucus secretion from bronchial submucosal glands also promotes IgE production by B cells. The T cells and epithelial secrete chemokines that recruit more T cells and eosinophils thus exacerbating the reaction.

4. lgE binds to the Fc receptors on submucosal mast cells, and repeat exposure to the allergen triggers the mast cells to release granule contents and produce cytokines and other mediators, which collectively induce the early-phase (immediate hypersensitivity) reaction and the late-phase reaction. The early-phase reaction is dominated by bronchoconstriction , increased mucus production, variable degrees of vasodilation, and increased vascular permeability. Late phase reaction (4-8 hours later) Eotaxin is produced - Chemotactic for eosinophils and activates eosinophils Eosinophils release major basic protein (MBP) and cationi c protein . Damage epithelial cells and produce airway constriction Other mediators involved Leukotrienes LTC-D-E, causes prolonged bronchoconstriction . Acetylcholine causes airway muscle contraction.

5. Histologic changes In bronchi Thickening of the basement membrane Edema and a mixed inflammatory infiltrate Hypertrophy of submucosal glands Hypertrophy/hyperplasia of smooth muscle cells Histologic changes in the bronchioles Formation of spiral-shaped mucus plugs Contain shed epithelial cells called Curschmann spirals Pathologic effect of MBP and cationic protein Crystalline granules in eosinophils coalesce to form Charcot-Leyden crystals. Patchy loss of epithelial cells, goblet cell metaplasia Thick basement membrane Smooth muscle cell hypertrophy and hyperplasia

6. Intrinsic asthma Nonimmune Causes Virus-induced respiratory infection Examples-rhinovirus, parainfluenza virus, respiratory syncytial virus Air pollutants . Aspirin or nonsteroidal drug sensitivity . The above drugs block cyclooxygenase activity and therefore inhibit formation of prostaglandins and thromboxanes . This leaves the lipoxygenase pathway open for production of leukotrienes ( bronchoconstrictors ). Stress, exercise, and cigarette smoke