Sie sind auf Seite 1von 4

Chronic Obstructive Pulmonary Disease (COPD) Lung Diseases Obstructive Resistance to airflow (partial/ complete obstruction) Any level

from trachea, large bronchi to terminal, respiratory bronchioles Major diseases y Emphysema (COPD) y Chronic bronchitis (COPD) y Bronchiectasis y Asthma y Bronchiolitis Emphysema Condition of lung, characterized by y Abnormal permanent enlargement of airspaces distal to terminal bronchiole y Destruction of walls (without obvious fibrosis) Associated with smoking Normal Acinus

Restrictive Expansion of lung parenchyma Total lung capacity

Emphysema Centriacinar/ Centrilobular

Panacinar

Paraseptal/ Distal Acinar

Irregular

Commonest type (95%) In heavy smokers Assoc. w. chronic bronchitis Affect central/ proximal parts of acini (distal alveoli are spared)

Acini uniformly enlarged Commonly in y Lower zones of lung y Anterior margins of lung Severe in base of lung Assoc. w. 1-antitrypsin deficiency

Distal part of acini Occurs adjacent to areas of y Fibrosis y Scarring y Atelectasis Severe in upper half of lungs (multiple continuous enlarged airspaces forming cysts) Cause of spontaneous pneumothorax (young adults)

Acinus irregularly involved Invariable associated with scarring Asymptomatic, clinically insignificant

Centriacinar Emphysema Dilated airspaces Loss of respiratory bronchioles in proximal part of acinus (sparing of distal alveoli) Upper lobes (apical segments) y More common y More severe Walls contain black pigment Inflammation (around bronchi, bronchioles)

Panacinar Emphysema All parts of alveoli Emphysema

Emphysema Loss of alveolar walls Remaining airspaces dilated

Centriacinar Emphysema Enlarged air spaces around small airway Respiratory epithelium (arrow) Peripheral alveoli are normal

Panacinar Emphysema Air spaces of entire acinus, lobule enlarged (occasional remaining intact alveoli) Inflammation, fibrosis minimal

Bullous Emphysema Large bullae on surface of lungs Loss of lung parenchyma (by destruction of alveoli) Permanent dilatation of airspaces Bullae large dilated airspaces that bulge out from beneath pleura

Pathogenesis (Emphysema) Proteases-Antiprotease Imbalance Homozygous patients with genetic deficiency of 1-antitrypsin ( chance of developing emphysema) Intratracheal installation of proteolytic enzyme papain degrades elastin (induce emphysema) 1-Antitrypsin Synthesized in liver Present in serum, tissues Neutrophils in lungs (release elastase in response to inflammation) Deficiency of 1-antitrypsin Development of emphysema Causes of 1-antitrypsin deficiency PiZZ phenotype (assoc. w. deficiency) Smoking y Accumulation of neutrophils & macrophages in lungs (Due to chemo attraction) Elastase production in y macrophages (elastase can digest 1-antitrypsin)

Differences Normal, Emphysema, Chronic Bronchitis Oxidant-Antioxidant Imbalance Tobacco smoke Plenty of Free Radicals Activated Neutrophils Deplete antioxidants Incite tissue damage

Clinical Features (Emphysema) Pink Puffers Puff through pursed lips Well oxygenated (hence, pink) Emphysema Compliance of lung (above normal) y Easy to distend y Empty slowly Chronically over inflated lung y TLC (total lung capacity) y Functional residual capacity y Residual volume Lessens curvature of diaphragm ( efficient in generating small swings in pleural pressure for breathing) Pulmonary Function Test Compromised expiratory flow (due to lung recoil) FEV1 FVC FEV1/ FVC ratio Other Types Compensatory hyperinflation Obstructive over inflation Interstitial emphysema

Chronic Bronchitis Persistent cough with sputum 3 months in at least 2 consecutive years Absence of any identifiable cause Simple Bronchitis Chronic Asthmatic Bronchitis Productive cough Intermittent bronchospasm present No airflow obstruction Epidemiology (Chronic Bronchitis) Smokers (90% of patients) Middle aged men (commonly) Pathogenesis (Chronic Bronchitis) Hyper secretion of mucous Goblet cells of small airways (small bronchi, bronchioles) Alterations in small airways y Goblet cell metaplasia (with mucous plugs in lumen) y Clustering of pigmented macrophages y Inflammatory cell infiltrate y Fibrosis of bronchiolar wall Role of infection is secondary y Does not initiate bronchitis y Maintain bronchitis Infections may lead to acute exacerbations Cigarette smoke Interferes with ciliary action of respiratory epithelium y y Causes direct damage to epithelia y Inhibits ability of alveolar leukocytes to clear bacteria

Reid Index Ratio of bronchial mucous gland layer to bronchial wall thickness (perichondrium to basement membrane) Indicator of mucous gland hypertrophy Reid Index 0.4 Mucous gland hypertrophy

Clinical Features (Chronic Bronchitis) Blue Bloaters Exhibit relatively poor oxygenation Blue, bloated in appearance Due to y Withdrawn from physical activity y Overweight (may be) y Poor muscle tone

Chronic Bronchitis Chronic inflammatory cells in submucosa (Chronic bronchitis does not have characteristic pathologic findings)

Bronchiectasis Permanent dilatation of bronchi & bronchioles Caused by destruction of muscle & elastic tissue Results from (associated with) chronic necrotizing infection Etiology (Bronchiectasis) Cystic fibrosis Intralobular sequestration of lung Immunodeficiency states Post infectious conditions necrotizing pneumonia Primary ciliary dyskinesia y Autosomal recessive syndrome y Poorly functioning cilia of airway walls y Recurrent infections occur y Lead to bronchiectasis Allergic bronchopulmonary aspergillosis y Results from hypersensitivity reaction to fungus Pathogenesis (Bronchiectasis) Obstruction Due to y Mucous impaction y Tumours y Foreign bodies Impairment of normal clearing mech. Pooling of secretions (distal to obstruction) Inflammation Morphology (Bronchiectasis)

Asthma Chronic inflammatory disorder of airways Triad of Reversible airway obstruction y y Chronic bronchial inflammation with eosinophils y Bronchial smooth muscle hypertrophy, hyperreactivity Classification (Asthma) Atopic (Extrinsic) 70% of cases Due to IgE & TH2-mediated immune response to environmental antigens

Non-Atopic (Intrinsic) 30% of cases Triggered by non-immune stimuli y Pulmonary infections y Stress y Exercise

Infection Lead to y Inflammation y Destruction of airways Permanent dilatation (due to destruction of airways)

Morphology (Asthma) Over distended lungs Occlusion of bronchi, bronchioles (by thick tenacious mucous plugs) Mucous plugs (contain whorls of shed epithelium curschmann spirals) Numerous eosinophils & crystalloids (made up of eosinophil proteins charcot-leyden crystals) Airway remodelling

Bronchiectasis

Asthma Occlusion of bronchi, bronchioles Thick mucous plugs Airway remodelling

Bronchiectasis Permanent dilatation (of bronchi, bronchioles)

Bronchiectasis Asthma Curschmann spirals Whorls of shed epithelium Airway Remodelling (Asthma) Normal Asthma Charcot-leyden crystals Eosinophil proteins

Bronchial Asthma

Bronchiectasis Dilated bronchus Mucosa & wall not clearly seen Necrotizing inflammation with destruction

Accumulation of mucous (bronchial lumen) Goblet cells (secrete mucous) Hypertrophy mucous glands Chronic inflammation (recruitment of eosinophils, macrophages, TH2 cells)