Obstructive vs Restrictive Pulmonary Diseases PDF

OBSTRUCTIVE VERSUS RESTRICTIVE PULMONARY DISEASES Dereje G(MD) Introduction Obstructive Airway Disease Resistance to airflow Restrictive Lung Disease Limited lung Expansion Obstructive Airway Diseases Forced vital capacity (FVC) is either normal or sl...

OBSTRUCTIVE VERSUS RESTRICTIVE PULMONARY DISEASES Dereje G(MD) Introduction Obstructive Airway Disease Resistance to airflow Restrictive Lung Disease Limited lung Expansion Obstructive Airway Diseases Forced vital capacity (FVC) is either normal or slightly decreased. Forced expiratory volume at 1 second (FEV1), is significantly decreased. The ratio of FEV to FVC is characteristically decreased. Expiratory obstruction may result from anatomic airway narrowing as in Asthma or from loss of elastic recoil, characteristic of emphysema.  The major diffuse obstructive disorders are:- Emphysema chronic bronchitis bronchiectasis asthma. Each with distinct clinical and anatomic characteristics but overlaps between emphysema, chronic bronchitis, and asthma are common. Chronic Bronchitis and Emphysema constitutes COPD Restrictive Lung Diseases FVC is reduced Expiratory flow rate is normal or reduced proportionately. ratio of FEV to FVC is near normal. Restrictive defects occur in two general conditions: (1) chest wall disorders in the presence of normal lungs. (2) acute or chronic interstitial lung diseases. The classic acute restrictive disease is ARDS. pneumoconioses, interstitial fibrosis of unknown etiology. infiltrative conditions such as sarcoidosis. Obstructive Airway Diseases Emphysema Emphysema is characterized by permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without significant fibrosis. Has four major types of emphysema: (1) centriacinar (2) panacinar (3) distal acinar (4) irregular. Only the first two types cause significant airway obstruction, with centriacinar emphysema being about 20 times more common than panacinar disease.  Centriacinar (centrilobular) emphysema. proximal parts of the acini are affected, distal alveoli are spared. The lesions are more common and severe in the upper lobes, particularly in the apical segments. Common in cigarette smokers, often in association with chronic bronchitis.  Panacinar emphysema. the acini are uniformly enlarged. occurs more commonly in the lower lung zones associated with α1-anti-trypsin deficiency. Distal acinar (paraseptal) emphysema. distal acini is primarily involved. The emphysema is more striking adjacent to the pleura, and at the margins of the lobules.  Irregular emphysema;- acinus is irregularly involved, is almost invariably associated with scarring. such as that resulting from healed inflammatory diseases. Pathogenesis noxious particles cause lung damage and inflammation, which, particularly in patients with a genetic predisposition, result in parenchymal destruction. Factors that influence the development of emphysema include the following;- Protease–anti-protease imbalance Oxidative stress Airway infection Inflammatory cells and mediators Morphology Typical panacinar emphysema produces pale, voluminous lungs that often obscure the heart when the anterior chest wall is removed at autopsy. centriacinar emphysema. deeper pink than in panacinar emphysema less voluminous, and the upper two-thirds of the lungs are more severely affected than the lower lungs.  destruction of alveolar walls without fibrosis, leading to enlarged air spaces. the number of alveolar capillaries is diminished. Terminal and respiratory bronchioles deformed. Bronchiolar inflammation and submucosal fibrosis are consistently present in advanced disease. Clinical Features Dyspnea cough wheezing Weight loss  The classic presentation of emphysema with no “bronchitic” component;- Air space enlargement is severe and diffusing capacity is low. Barrel-chested and dyspneic, with obviously prolonged expiration, sitting forward in a hunched-over position. Dyspnea and hyperventilation are prominent. Gas exchange is adequate and blood gas values are relatively normal. pink puffers.”  Emphysema-chronic bronchitis Dyspnea is less prominent No increment in respiratory drive The patient retains carbon dioxide, hypoxic and often cyanotic. Blue bloaters In most patients with COPD the symptoms fall in between these two extremes.  Hypoxia-induced pulmonary vascular spasm and loss of pulmonary capillary surface area from alveolar destruction causes the gradual development of secondary pulmonary hypertension, which in 20% to 30% of patients leads to right-sided congestive heart failure Death from emphysema is related to either respiratory failure or right-sided heart failure. Chronic Bronchitis Defined clinically. A persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. asthmatic bronchitis COPD Pathogenesis The distinctive feature of chronic bronchitis is hypersecretion of mucus, beginning in the large airways. Cigarette Smoking, Sulfur Dioxide… Environmental irritants induce hypertrophy of mucous glands. These irritants also cause inflammation marked by the infiltration of macrophages, neutrophils, and lymphocytes.  The airflow obstruction in chronic bronchitis results from (1) small airway disease, (2) coexistent emphysema. Small airway disease (chronic bronchiolitis) is an important component of early, mild airflow obstruction, chronic bronchitis with significant airflow obstruction almost always is complicated by emphysema. Morphology The mucosal lining of the larger airways usually is hyperemic and swollen by edema fluid and is covered by a layer of mucinous or mucopurulent secretions. enlargement of the mucussecreting glands. Variable numbers of inflammatory cells, largely lymphocytes and macrophages but sometimes also admixed neutrophils, are frequently seen in the bronchial mucosa.  Chronic bronchiolitis (small airway disease), characterized by goblet cell metaplasia, mucous plugging, inflammation, and fibrosis, also is seen. In severe cases, there may be complete obliteration of the lumen as a consequence of fibrosis. It is the submucosal fibrosis that leads to luminal narrowing and airway obstruction. Emphysematous changes often coexist. Clinical Features Cough Sputum Patients with chronic bronchitis and COPD have frequent exacerbations, more rapid disease progression, and poorer outcomes than those with emphysema alone. References Robbins Basic Pathology