Lung pathology 2


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Lung pathology 2

  1. 1. Obstructive Lung Diseases Dr.G.Bhanu prakash ,,
  2. 2. 1.Chronic Bronchitis• It is defined clinically as the presence of productive cough for At least 3 months in at least 2 consecutive yrs in absence of any other identifiable cause.• The most important initiating agent is smoking resulting in airways irritation leading to mucus hypersecretion, the latter may cause airways obstruction. Infection plays a secondary role particularly in maintaining chronic bronchitis and are also responsible for the acute exacerbations. Dr.G.Bhanu prakash , www.gims-,
  3. 3. • Histologic features Include chronic lymphocytic infiltration of the airways and submucosal gland hypertrophy. There is also increase in Reid index (it is the ratio of the thickness of the mucus gland layer to the thickness of the wall. The bronchial epithelium may also have squamous metaplasia and dysplasia.• clinical features: Late onset of dyspnea with productive cough(copious sputum), recurrent infections, hypoxemia and mild cyanosis (BLUE BLOATERS). Long standing chronic bronchitis can cause cor pulmonale (right sided heart failure due to pulmonary hypertension). Dr.G.Bhanu prakash , www.gims-,
  4. 4. 2.EmphysemaIt is abnormal permanent enlargement of the air space distal to terminal bronchioles and is associated with destruction of their walls.• Most imporant etiological agent for emphysema is smoking which causes inflammation in airways resulting in increased neutrophils and macrophages. These inflammatory cells release elastase responsible for destruction of lung tissue resulting in emphysema. Dr.G.Bhanu prakash , www.gims-,
  5. 5. • Normally, the pulmonary tissue destruction by elastase is prevented by the presence of anti- elastase activity which is primarily due to α1- AT (with minor contribution from secretory leukoprptease inhibitor in bronchial mucus and α serum 1- macroglobulin). So any increase in neutrophils (usually in smokers) or deficiency of α1-AT would contribute to development of emphysema. Characteristically, there is loss or reduction of elastic recoil of the lung. Dr.G.Bhanu prakash , www.gims-,
  6. 6. • α1-AT is synthrsized in the liver. The normal α1-AT phenotype is PiMM. The abnormal phenotype is PiZZ which is associated with α1- AT deficiency and development of emphysema at earlier age and greater severity.+ Dr.G.Bhanu prakash , www.gims-,
  7. 7. EmphysemaCentriacinar Panacinar Distal acinar Irregular Dr.G.Bhanu prakash , www.gims-,
  8. 8. ntriacinar Panacinar Distal acinarement of •Involvement of the •Distal part of acinus ispart of acinus entire acinus affected with sparing ofaring of alveoli . proximal part of acinus •Seen with α1-ATn smokers . deficiency • Seen in smokers .y more sever in •Occurs more •Involvement of lungobes (due to severely in lower adjacent to pleura deficiency of lobes at base of lung •Associated with the 1-AT to this less (due to lower lung Dr.G.Bhanu prakash , www.gims- development ofd region). distribution of,
  9. 9. • Clinical features: progressively increasing dyspnea, weight loss, late onset of cough with scanty sputum. The patient is non- cyanotic, uses accessory muscle of respiration and shows pursed lip breathing.(PINK PUFFERS)• Management: Cessation of smoking and use of bronchodilators is the mainstay of the management.Mnemonic: emPhysema had letter P (and not B). So Pink Puffer.Chronic Bronchitis has letter B(and not P) so blue Bloater. Dr.G.Bhanu prakash , www.gims-,
  10. 10. 3.AsthmaHyperactivity of the airways resulting in reversible bronchoconstriction and air flow obstruction on exposure to some external stimuli is called asthma. ASTHMA Extrinsic asthma Intrinsic asthma Dr.G.Bhanu prakash , www.gims-,
  11. 11. Extrinsic asthma Intrinsic asthmaype I hypersensitivity •Viral pulmonary infectionaction • Cold • Inhaled irritantsCommoner type of asthma • StressPositive family history • Exercise erum IgE levels are • Drug induced (mostevated commonly by aspirin ingestion) • Negative family history • Serum IgE levels are norma Dr.G.Bhanu prakash , www.gims-,
  12. 12. • Pathogenesis: Primary exposure of an allergen causes T H2 cell dominated inflammatory response resulting in IgE production and eosinophil recruitment (called sensitization). Exposure to the same allergen causes cross linking of IgE bound to IgE receptors on mast cells in the airways which cause opening up of epithelial cells due to released mediators.• Antigens then cause activation of mucosal mast cells and eosinophils and this along with neruonal reflexes (subepithelial vagal receptors)cause bronchospasm, increased vascular permeability and mucus production (Acute or immediate response). Dr.G.Bhanu prakash , www.gims-,
  13. 13. • Later on, leukocytic infiltration causes release of more mediators and damage to the epithelium (late Phase Reaction). Eosinophils in airways release major basic protein which causes epithelial damage and more airways constriction.• Leukotrienes C4, D4, E4 and acetylocholine have definite role in bronchoconstriction whereas agents like histamine, PGD2 and platelet activating factor (PAF) may also role in the features of the disease. Dr.G.Bhanu prakash , www.gims-,
  14. 14. • In intrinsic asthma, aspirin causes shift of the arachidonic acid metabolism towards the lipoygenase pathway resulting in formation of the bronchoconstrictor leukotrienes.• Virus induced inflammation lowers the threshold of the subepithelial vagal receptors to irritants.• Exercise causes loss of water and heat from the respiratory tract. The water loss causes mucosal hyperosmolarity which stimulates release from the mast cells. This explains the pahtogenesis of exercise induced asthma. Dr.G.Bhanu prakash , www.gims-,
  15. 15. • Important fact: IL- 13 gene polymorphism is strongly associated with bronchial asthma. ADAM-33 is another gene causing proliferation of smooth muscle cells and fibroblasts in bronchi resulting in bronchial hyperreactivity and subepithelial fibrosis. Dr.G.Bhanu prakash , www.gims-,
  16. 16. • Clinical features:Acute asthmatic attack is characterized wheezing, cough and severe dyspnea.• Morphology: The most stroking macroscopic finding is occlusion of the bronchi and bronchioles by mucus plugs.Histologically, there are numerous eosiphils, Charcot leyden crystalsQ (composed of eosinophil membrane protein called as galectin-10) and Curschmann spirals Q (whorls of shed airways epithelium). Dr.G.Bhanu prakash , www.gims-,
  17. 17.  Structural changes in the bronchial wall called “airway remodelling” is characterized by presence of eosiphilic inflammation and edema of bronchial walls, increased size of submucosal glands, hypertrophy of bronchial wall smooth muscle and deposition of subepithelial collagen in the bronchial wall. Individual epithelial cells presents in the sputum of the patients are called Creola bodies. Management is done with bronchodilators and corticosteroids (for details, refer to the review of pharmacology by the same authors. Dr.G.Bhanu prakash , www.gims-,
  18. 18. 4. Bronchiectasis• Abnormal permanent airways dilation resulting from chronic necrotizing infection is called bronchiectasis. Cause Bronchial Necrotizing Congenital Miscellaneous Obstruction pneumonias Tumor Cystic fibrosis Mycobactrium SLE Kartagener syndrome Staph. aureus Rheumatoid Foreign body arthritis (triad of Bronchiectasis+ Aspergillus Situs inversus+ sinusitis) Post Influenza virus trasplanation Dr.G.Bhanu prakash , www.gims-,
  19. 19. • Obstruction and infection are the chief contributors to the damages of airways wall associated with destruction of smooth muscle and elastic tissue fibrosis and further dilation of bronchi. Dr.G.Bhanu prakash , www.gims-,
  20. 20. • Clinical features:Chronic cough, fever, foul smelling sputum production, recurrent pulmonary infection, sinusitis and immune deficiencies.It usually affects vertical air passages of the lower bilaterally with involvement of left side more frequent than right.The dilated bronchi can be followed directly out to the pleural surfaces. There is usually presence of inflammatory cell in the walls of bronchi and bronchioles which may also exhibit squamous metaplasia. Dr.G.Bhanu prakash , www.gims-,
  21. 21. • Complications include massive hemoptysis, amyloidosis, visceral abscess and cor pulmonale.• Management is done by chest physiotherapy, natural drainage, bronchilators and antibiotics. High Resolution CT scan (HRCT) is the best investigation for the detection of bronchiectasis. Dr.G.Bhanu prakash , www.gims-,
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