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PATHOLOGY OF BRONCHIAL ASTHMA

PATHOLOGY OF BRONCHIAL ASTHMA. Bronchial Asthma. Define bronchial asthma. o Describe types of bronchial asthma. o Discuss etiopathogenesis of asthma. o Describe morphological features. Obstructive and restrictive lung diseases. Obstructive lung diseases

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PATHOLOGY OF BRONCHIAL ASTHMA

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  1. PATHOLOGY OF BRONCHIAL ASTHMA

  2. Bronchial Asthma • Define bronchial asthma. • o Describe types of bronchial asthma. • o Discuss etiopathogenesis of asthma. • o Describe morphological features.

  3. Obstructive and restrictive lung diseases • Obstructive lung diseases • (i.e. increased resistance to air flow) include:- • 1. BronchialAsthma. • 2. Emphysema. • 3. Chronic bronchitis. • 4. Bronchiectasis. • 5. Cystic fibrosis and bronchiolitis. • Why should we care about asthma?

  4. What is Asthma? • Definition: • Asthma is a chronic inflammatory disorder of the airways that causes recurrentspasmodic episodes, due to increased hyperirritability or responsiveness of the bronchial tree to various stimuli. • This associated with these clinical manifestations: • 1. Wheezing. • 2. Breathlessness. • 3. Chest tightness. • 4. Cough, particularly at night and/or in the early morning. • It is manifested physiologically by a widespread narrowing of the air passages, which may be relieved spontaneously or as a result of therapy. Can not cure but can controlled. • Life threatening disease • How long this episodes taking place? (Mild, severe) (Min\hr)

  5. Bronchial asthma risk factors • 1- Atopy(allergic asthma- largest risk factor- genetic). • _______________________________ 2 – Environmental factors( viruses, occupational exposures, allergens, cold air, dust, smoking ,others… ). ____________________________________ 3- family history. ________________________________________________________________________________________________ 4- others……………..

  6. Common triggers for asthma Disease characteristics

  7. Bronchial asthma Classifications Asthma may be categorized into types • ____________________________________________ _______________________________________________ 3- Bronchoconstriction triggering agents - include ( a) Seasonal asthma ( b) Exercise-induced asthma. (c) Drug-induced asthma (e.g., aspirin & NSAID). (d) Occupationalasthma (e) Eemotional asthma . (f ) Asthmaticbronchitis in smokers. _________________________________________ 4-Recent studies added three subphenotypes of Asthma , based on Airway inflammation pattern.

  8. Asthma Types • 1- Atopic asthma (allergicsensitization, Extrinsic) : • Classic example of type I IgE-mediated hypersensitivity reaction. • Usually encountered in patient known case of rhinitis, eczema. • Genetic predisposition. • A positive family history of asthma is common. • Begins in childhood. • Triggered by environmental allergens, such as dusts, pollens, roach or animal dander, and certain types of foods., etc… • Diagnosis: clinical diagnosis is essential +……………………………. • (a) Skin test : Using the offending antigen  immediate wheal-and-flare reaction. • (b) Serum radioallergosorbent tests (called RAST): TO identify the presence of IgE specific for a panel of allergens.

  9. Asthma Types 2. Non-atopic asthma: - Non allergic. - Triggered commonly  by Respiratory infection due to viruses (e.g., rhinovirus, parainfluenza virus). - Family history: less common. - Skin test: reveals negative reaction. - Mechanism: It is thought thatvirus-induced inflammation of the respiratory mucosa  lowers the threshold of the subepithelialvagal receptorsto irritants.

  10. Asthma Types 3- Bronchoconstriction triggering agents • (a) Drug-Induced Asthma. • - Aspirin-sensitive asthma + NSAID occurring with recurrent rhinitis and nasal polyps. • -Others examples: adrenergic antagonists, coloring agents . • Commonly occurs in adult. • Mechanism: • Aspirin inhibiting the cyclooxygenase pathway of arachidonicacid metabolism without affecting the lipoxygenase route, thus tipping the balance toward elaboration of the bronchoconstrictorleukotrienes.

  11. Asthma Types • (b) Occupational Asthma. • Caused or worsened by breathing in irritants on the job.  • Triggered\stimulated by: • 1) Fumes (epoxy resins, plastics) • 2) Metal and dusts (platinum, wood, cotton) • 3) Chemicals and Gases (formaldehyde, penicillin products, toluene, enzymes). • 4) Animal substances (5) Plants • - Minute quantities & Repeated exposure. • - Mechanisms: • According to stimulus include:- • Type I hypersensitivity reactions . • Liberation of bronchoconstrictor substances. • Hypersensitivity responses of unknown origin.

  12. Bronchial asthma • 4- Pattern of the Airway inflammation : • 1) Eosinophilic asthma. • 2) Neutrophilic asthma. • 3) Mixed inflammatory asthma. • 4) Pauci-granulocytic asthma. • These subgroups may differ in their: • (a) Etiology. • (b) Immunopathology. • (c ) Response to treatment.

  13. Asthma Pathogenesis-1 • GENETIC CONSIDERATIONS • Genetic predisposition • In case of Atopic asthma- type I hypersensitivity • Inheritance of susceptibility genes (postulation) that makes individuals prone to develop strong TH2 reactions against environmental antigens (allergens)

  14. Asthma Pathogenesis-2 • 1. The airway epithelium and submucosa contain dendritic cells that capture &process antigen \allergens. • Initial sensitization stimulate induction of TH2 cells. • 2. TH2 cells secrete cytokines e.g.(IL-4, IL-5,IL-13) that promote allergic inflammation and stimulate B cells to produce IgE and other antibodies. • 3. Action of Cytokins • (a) IL-4 Production of IgE by B cells. • (b)IL-5  Activates recruited eosinophils. • (c ) IL-13 Mucus secretion(bronchial submucosal glands)  also Promotes IgE production by B cells.

  15. Asthma Pathogenesis-3 (Early & Late reaction) • 3. IgE coats submucosal mast cells. • 4. Repeat exposure triggers the mast cells to release granule contents and produce cytokines and other mediators induce the early-phase (immediate hypersensitivity) reaction and the late-phase reaction

  16. Asthma Pathogenesis-4 (Early reaction- Minutes) - AntigensTh2+ IgEproductionIgEbinding to mast cells leads to Eosp. recruitment& release of primary mediators= (Histamine, chemotactic factors, and secondary mediators i.e. leukotriens, prostaglandins, cytokines and neuropeptides). This results in: • (A) Bronchospasm- triggered by direct stimulation of subepithelialvagal (parasympathetic) receptors through both central and local reflexes . • (B) Secretion of mucus. • (C) Variable degree of vasodilatation& increase permeability. • (D) Accumulation of leukocytes.

  17. Asthma Pathogenesis-5 (Late reaction- Hours) • - 6- 10 hr later, produces a continued state of airway hyperresponsiveness with eosinophilic and neutrophilic infiltration. (steroid helpful to treat this stage) Components: consists largely of inflammation with recruitment of leukocytes= ( Eosinophils, neutrophils, and more T cells). - Leukocyte recruitment is stimulated by chemokines produced by mast cells, Epithelial cells (eotaxin ) and T cells, and by other cytokines. - Outcome: persistent bronchospasm, edema, and necrosis of epithelialcells by The major basic protein of eosinophils.

  18. Cellular sources of inflammatory mediators& their effects

  19. Atopic asthma Epithelial cell injury Allergen IgE Mucus secretion Muscle contraction Mucus secretion Mast cell Muscle contraction Release of inflammatory mediators Recruitment of leukocytes Acute phase Late-phase

  20. Morphology of Asthma • - Gross appearance: - Done in lungs necropsy-study • 1. Over-inflated and failure to collapse with patchy atelectasis (pt. dying with Status asthmaticus). • 2. Occlusion of airways by gelatinous mucous & exudate • plugs (the bronchial branches up to terminal bronchioles) Microscopic appearance: • Edema, hyperemia, and inflammatory infiltrate (with excess eosinophils) in the bronchial walls. • Increase in the size of submucosal glands (hypertrophy\ hyperplasia) • Patchy necrosis and shedding of epithelial cells. • Over time – features of airway remodeling. -

  21. Airway remodeling. • Overall thickening of airway wall . Reduction of diameter • Basement membrane fibrosis(BM thickening). • Increases muscle mass (Hypertrophy and/or hyperplasia). • Increased in size and number of blood vessels. • Increase number of the submucosal glands. • Mucus metaplasia of epithelium. • Increased fibrogenic factors collagen type I,II “scar” • Irreversible Airflow obstruction.

  22. Epithelial remodeling CONTROL • Epithelium is damaged • New blood vessels • New muscle • New mucosal cells • Collagen deposition

  23. Bronchial asthma, microscopic

  24. Investigating asthma used to monitor a person's ability to breathe out air. Reduced when airways are constricted. • 1. Elevated eosinophil count in the peripheral blood &CBC. • 2. Sputum smear- Whorled mucous plugs = Curschmann spirals. • 3. Sputum smear- Charcot-Leyden crystals in the sputum (Specially in atopic asthma). (Sputum). • 4. Sputum -Creola bodies (desquamated epithelial cells) • 5. Skin Test • 6. RAST test.

  25. Curschman’s spirals

  26. Charcot-Leyden crystals

  27. THE END

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