Loss of alveolar surface area & capillary bed & elastic connective tissue-> ↓elastic recoil and ↑compliance.

Primary pathology defect : not in the airways, rather in the respiratory unit walls, where the loss of elastic tissue results in a loss of appropriate recoil tension to support airways during expiration. Oxidants : Cigarette smoke Endogenous oxidantsĪntielastases : alpha 1 antiprotease alpha 2 macroglobulin Bronchial mucus inhibitorĪctivation is represented by solid lines Inhibition by dashed lines The latter is responsible in large part for the more significant resting hypoxemia seen in chronic bronchitis compared with emphysema. Altered ventilation/perfusion relationships include areas of high and low V/Q ratios. Obstruction with prolonged expiratory time produces hyperinflation. The nonuniform airway obstruction of chronic bronchitis has substantial effects on ventilation and gas exchange.Bronchioles : infiltrated with inflammatory cells and are distorted, with associated peribronchial fibrosis.Bronchial smooth muscle hypertrophy and hyperresponsiveness to nonspesific bronchoconstrictor stimuli (histamine & methacholine).Hypertrophy and hyperplasia of submucosal glands : glands often comprising over 50 % of the bronchial wall thickness.

Chronic inflammation : Normal Normal ciliated ciliated pseudos pseudostrat tratifie ified d columnar columnar epitheli epithelium um -> -> patchy patchy squa squamo mous us meta metapl plas asia ia : abse absenc nce e of norm normal al bron bronch chia iall epit epithe heli lium um -> -> Mucociliary clearance function severely diminished or completely abolished.

Airway mucosa : infiltrated infiltrated with inflammatory inflammatory cells : PMN leukocytes leukocytes & lymphocytes.

Inflammation of airways, particularly small airways.

(Sylvia A.Price, Pathophysiology, 4 edition page:693,EGC) CHRONIC BRONCHITIS An inflammatory inflammatory process in the airways + mucosal thickening thickening and mucus hypersecretion -> diffuse obstruction. Panacinar empysema asym asympt ptom omat atic ic in old age Small airways collaps when Expiration Centriacinar emphysema pred predom omin inan anttĬentriacinar emphysema chronic bronchiolitisĬentriacinar & panacinar emph emphys ysem ema a Weaken of bronchioli’s bronchioli’s wall and rupture of the alveoli Risk factor genetic (deficiency alpha 1-antitrypsin) 1-antitrypsin)Ĭlearance function Of the lung disturbance PATHOPHYSIOLOGY Tobacco smoke Air polution

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