L5, Resp Pathology - COPD PDF

pathology - respiratory COPD LECTURE (5) COPD Dr. M. Shalaby pathology - respiratory COPD  Group of pulmonary diseases characterized by : DEFINITION :...

pathology - respiratory COPD LECTURE (5) COPD Dr. M. Shalaby pathology - respiratory COPD  Group of pulmonary diseases characterized by : DEFINITION :  Resistance to air flow due to partial or complete obstruction at any level. ① Chronic bronchitis. ③ Emphysema. TYPES : ② Bronchial asthma. ④ Bronchiectasis  It is persistent productive cough (cough of sputum) for at least 3 DEFINITION: consecutive months in at least 2 consecutive years.  Due to chronic irritation of the bronchial mucosa by: 1. Cigarette smoking. CAUSES: 2. Atmospheric pollution 3. Chronic inflammation of upper resp. tract, tonsils or mouth. PATHOLOGY:  Occur in middle-aged men  Bronchial mucosa appears thick, opaque and covered by excess mucous. N/E  Mucous gland hyperplasia and decreased number of ciliated cells. M/E  Squamous metaplasia "BRONCHI"  Chronic inflammatory cell infiltrations. Dr. M. Shalaby pathology - respiratory COPD ① Centrilobular emphysema. ② Bronchopneumonia. ③ Bronchogenic carcinoma. COMPLICATION ④ Chronic hypoxaemia resulting in persistent pulmonary VC , pulmonary hypertension ⑤ Cardiac failure. Dr. M. Shalaby  pathology - respiratory COPD  Permanent dilatation of air spaces distal to the terminal bronchioles accompanied by damage of their walls. i.e. respiratory bronchioles, alveolar ducts and alveoli (respiratory acinus).  Commonest chronic lung disease & more in males 40-60 years. Dr. M. Shalaby pathology - respiratory COPD A. CENTRIACINAR (CENTRILOBULAR): B. PANACINAR (PANLOBULAR):  Respiratory bronchiole (central part of  The whole acinus INVOLVE acinus).  More in old females.  Related to cigarette smoking & explained by:  Related to inherited ① Elastase - Antielastase Imbalance Theory: deficiency of antielastase  Smoking weakens walls of air spaces by ↑↑ (α1 antitrypsin) in elastase and ↓↓ antielastase patient's blood. ② Direct Damage Theory:  Therefore the action of  The walls of air spaces are directly injured elastase secreted from PATHOGENESIS by toxic substances of cigarette smoking neutrophils and ③ Chronic Bronchitis Theory: macrophages becomes  Smoking recruits neutrophils & unopposed. macrophages and stimulates the release of elastase from them  It increases mucus secretion → mucus plugs → partially obstruct bronchi & terminal bronchioles. During expiration the air is entrapped and increases gradually the intraluminal pressure. Dr. M. Shalaby pathology - respiratory COPD A- CENTRIACINAR EMPHYSEMA:  Upper zones of lung lobes are first affected.  The lungs are moderately enlarged.  C/S: Enlarged air spaces. B- PANACINAR EMPHYSEMA: ① Barrel shaped chest: The chest wall takes a fixed exaggerated inspiration position: a- The anteroposterior diameter increases to equal the transverse. The sternum is pushed forward. b- Ribs, costal cartilages & intercostal spaces are horizontal. N/E ② Lungs: Lower zones of lung lobes are first affected.  The lungs are voluminous and very light.  They are pale and dry.  The surface is smooth and presents the indentations of ribs.  Lungs have a feathery feeling and pit on pressure (due to loss of elastic tissue).  Large bullae project on the surface in the poorly supported parts (along apices, anterior margin and free edge of base).  A bulla is an emphysematous space of more than 1 cm in diameter, it is semitranslucent with paper – thinned walls. Dr. M. Shalaby pathology - respiratory COPD A) Centrilobular emphysema  Dilated respiratory bronchioles with normal A.D. and alveoli. B) Panacinar emphysema Alveoli  Few in number, ↑↑ in size, distorted in shape.  Thin & in advanced stages, alveolar septa rupture. Interalveolar  Interalveolar capillaries are compressed by dilated air septa spaces. M/E Dr. M. Shalaby pathology - respiratory COPD Respiratory system C. V. S ① Ch. bronchitis.  Pulmonary hypertension ② Interstitial emphysema.  Right sided heart failure. ③ Spontaneous pneumothorax ④ Respiratory failure. Other types of emphysema 1. Obstructive Hyperinflation 2. Compensatory Hyperinflation 3. Senile (Atrophic) hyperintlation 4. Interstitial Emphysema: It is the escape of alveolar air into the interstitial tissue of the lung. Dr. M. Shalaby pathology - respiratory COPD  Permanent (irreversible) dilatation of medium sized bronchi and DEFINITION: bronchioles.  Chronic suppurative inflammation in their walls and surrounding lung CAUSE : tissue.  Frequent before the age of 20 years C/P:  Males more than females.  It can occur in adults.  Weak bronchial wall (Chronic pyogenic infection)  Forces for dilatation which may be: a- Pushing forces from inside ( bronchial obstruction) b- Pulling forces from outside. PATHOGENESIS Dr. M. Shalaby pathology - respiratory COPD  Bilateral and basal.  Dilated medium and smaller sized bronchi and bronchioles that are filled with pus.  Their lining are thick  Their walls show fibrosis. N/E ① The affected bronchi show chronic suppurative inflammation. a- Lumen: reveals shedded epithelial cells, inflammatory cells & RBCs b- Mucosa: Extensive ulceration c- Wall: is infilterated by inflammatory cells. M/E ② Lungs:  Areas of collapse and fibrosis  Areas of compensatory emphysema Dr. M. Shalaby