Pathology of Bronchial Asthma PDF 2024

Bronchial Asthma -2024 Khadiga Ali Pathology of Bronchial Asthma Khadiga M. Ali Assistant Professor of Pathology Outlines Definition....

Bronchial Asthma -2024 Khadiga Ali Pathology of Bronchial Asthma Khadiga M. Ali Assistant Professor of Pathology Outlines Definition. Etiology/Types. Pathogenesis. Phases. Airway remodeling Sputum Examination Definition Chronic inflammatory disease of airways that is characterized by recurrent attacks of widespread broncho-constriction (Airway hyper-responsiveness) in response to various stimuli. It is an Obstructive pulmonary disease Etiology/Types (1) Extrinsic (immunological, atopic, allergic) asthma: (2) Intrinsic (non-immunological, non-atopic, non allergic) asthma: Extrinsic Asthma Intrinsic Asthma Incidence More common Less common Age children and young Any age, mainly in late individuals Adult Family history of asthma Present Absent or atopic disease Preceding allergic illness Present Absent (atopy) Associated nasal polyp, Absent Present chronic bronchitis Pathogenesis Type I hypersensitivity Hyperirritability of bronchial reaction tree Exact mechanism is unclear IgE level in the serum Elevated Normal 1 Bronchial Asthma -2024 Khadiga Ali Allergen inhaled allergens such as infection, exposure to cold, house dust, animal dandruffs, physical exercise, anxiety, plant pollens, fungi emotions, aspirin and inhaled irritants Prognosis Good Bad Pathogenesis of type 1 hypersensitivity reaction Exposure to allergen for first time: Presented by macrophages in association with class II MHC to CD4T cells → It differentiates into CD4 T2 → Stimulates B lymphocytes to matures into plasma cells Plasma cells secretes IgE specfic to allergen IgE binds to mast cells. Mast cells contain granules of histamin, and other mediators. On subsequent exposure The allergen binds directly to IgE on surface of mast cells These cells degranulate resulting in release of histamine and other mediators causing manifestations of early phase These cells also synthesize other mediators that cause late phase Phases of Asthma Early phase Late phase Starts within 30-60 min after Starts hours (5 -6hrs) after exposure exposure to allergen Mediators includes Mediators are: 1-Histamin 1- IL4, IL5, IL13 2-Leukotriens 2- Major basic protein 3- Platelet activating factor These mediators cause : These mediators cause : 1-VD 1- Attraction of eosinophils 2-Edema(due to increased vascular 2-Attraction of mast cells permeability) 3-Damage of surface epithelium (caused by 3-Bronchospasm major basic protein secreted by 4-Increased mucous secretion eosinophils) 4- Exposure of vagal nerve endings 5- Easy passage of inhaled allergen to mast 2 Bronchial Asthma -2024 Khadiga Ali cells in the subepithelium. LEADING TO : Recurrent attacks Microscopic Examination All these changes are known as Airway remodeling 1. Increased mucous in the airways: small airways may have Luminal mucous plug. 2. Surface epithelium: Goblet cell hyperplasia and thickened basement membrane 3. In the wall: Smooth muscle hypertrophy and hyperplasia Mucous gland hyperplasia 4. Abundant eosinophils and eosinophilic derived substances such as Curschman spirals. Charcot- leyden crystals 5. Increased vascular permeability & Eventually fibrosis Sputum Examination Sputum: It is viscous and yellow and is rich in eosinophils. Microscopy shows: 3 Cs 1-Curschman spirals Corkscrew-shaped twist of condensed mucus. 2-Charcot- leyden crystals Mainly in atopic asthma. They have the shape of a pair of long, narrow, pyramids placed base-to-base. Derived from an eosinophil lysophospholipase binding protein called galectin-10. 3-Creola bodies Compact clusters or strips of columnar epithelial cells shed from the bronchus. Best wishes 3