obstructive-lung-diseases

Lung - Pathology Acute Lung Injury Pulmonary edema ARDS (Diffuse alveolar damage) Acute interstitial pneumonia • • • • Pulmonary Edema 1. Hemodynamic disturbances(↑ capillary hydrostatic pressure), MCCLVF, Heart failure cells 2. ↓ oncotic pressure (Hypoalbuminemia)  Renal failure, Malnutrition, Cirrhosis 3. Microvascular injury - ↑ capillary permeability, – Seen in ARDS following a) Infection -viral pneumonia b) Gases, Aspiration, Drugs--heroin, Paraquat (herbicide) c) Shock, Trauma, Sepsis, DIC • • • • ARDS: Also known as ***Diffuse Alveolar Damage (DAD)  pulmonary edema (protein rich)  hyaline membrane disease  hypoxemia (refractory to oxygen Rx ) Mortality in 50% of cases Clinical Manifestations: respiratory insufficiency, Cyanosis, arterial hypoxemia  multi-organ failure Acute interstitial pneumonia Cause is unknown (Unlike ARDS) but Radiographic and Pathologic features, mortality similar to ARDS • Pulmonary Edema Exaggerated lobular structures Pulmonary Edema Thick Alveolar septa pink fluid (Pulmonary Edema) Hemosiderin laden macrophages ARDS (Diffuse alveolar damage) Lung - Pathology Obstructive Pulmonary Diseases Emphysema Chronic bronchitis Asthma Bronchiectasis • Obstructive Pulmonary Diseases • Classical COPDs – Emphysema – Chronic Bronchitis • Obstructive element is also seen in – Bronchial Asthma – Bronchiectasis • Emphysema • • • Panacinar: • • • • • • • Irreversible overinflation of air spaces distal to the terminal bronchioles, with destruction of their walls Types: according to distribution within the acinus Uniform involvement of the acinus Associated with α1-antitrypsin deficiency Enlargement of central parts of the acinus (respiratory bronchioles and alveolar duct), sparing the peripheral alveoli (distal alveoli) More common and more severe in apical segments of upper lobes In heavy smokers and often associated with Chronic bronchitis Enlargement of the distal parts of the acinus (subpleural), sparing the proximal parts (in adjacent to areas of fibrosis, scarring, or Atelectasis) No uniform acinar pattern (seen with scarring) • Centriacinar: • Paraseptal: • Irregular: • Centriacinar vs. Panacinar • Pathogenesis Emphysema• • Protease- Antiprotease Hypothesis (imbalance between proteases and protease-inhibitors) is most important Tobacco Smoking – recruits PMNs, macrophages & Releases the proteases (elastase) – inactivate alpha-1-antitrypsin Common disease • Age: fifth to eighth decades • Clinically: – Dyspnea with prolonged expiration – Cough & expectoration (when associated bronchitis) – barrel shaped Chest (X-ray finding)- ↑AP diameter • Death is due to – Respiratory failure – CHF (Cor pulmonale) – Rupture of bullae  tension Pneumothorax Emphysema - Gross • Bullae if rupture  →tension Pneumothorax (↑ air in pleural space) • Death due to compression great vessels of heart to the point of occlusion • Chronic Bronchitis • Definition : Persistent cough with sputum production for at least 3 • months in at least 2 consecutive years Cause : Initiated by smoking (by causing Chronic irritation of the bronchial mucosa) – infections are secondary • Pathology: Hypertrophy of mucus glands Hyper secretion of mucus • Reid Index = ratio of thickness of mucous gland layer (CD) to the thickness between the epithelium and the cartilage (AB) (normally 0.4). The closer to 1 means there’s an increase in thickness and correlated to progression of disease Normal CD/AB = 0.4 Chronic Bronchitis • Clinical course • • • • • Bronchi & bronchioles are obstructed by mucus plugs bronchiolitis obliterans. In long-standing cases, squamous metaplasia & dysplasia (precancerous) predisposes for squamous cell carcinoma ? ? • • • • • • • Emphysema Slight Cough Blood gas values NORMAL No cyanosis lean forward to breathe easier Diffusing capacity is low Over-distension severe Pink puffers • • • • • Chronic Bronchitis Severe cough Hypercapnia & Severe hypoxemia Cyanotic History of recurrent infections Purulent sputum • Blue bloaters • Bronchial Asthma • • • • Definition :Increased responsiveness of the bronchial tree to various stimuli that results in paroxysms of Bronchospasm reversible bronchospasm  later bronchial inflammation, and obstructive lung disease Types : Extrinsic & Intrinsic Pathology of Extrinsic Asthma Starts within minutes and lasts about 6 hours after exposure to allergen IgE cross-linking  mast cell release of mediators Results in Bronchospasm (have hard time breathing, edema (due to vascular permeability), increased mucus (causes coughing) persist for 12+ hours & Mediators are mainly from leukocytes (Neutrophils, Eosinophils and Basophils) • Acute response • • • Late –phase reaction • Bronchial Asthma Extrinsic Intrinsic • type-I (IgE-mediated) hyper-sensitivity or allergic reaction • Triggered by environmental antigens (dust, pollens, food, ..) • family history of Atopy • Not allergic • triggered by respiratory tract infections &drugs (aspirin). • No family history Bronchial Asthma - Pathophysiology • Bronchial Asthma - Morphology • Occlusion of airways by mucous plugs. • Bronchial walls • • • • • • • Hypertrophy of mucous glands & smooth muscles ↑↑ Eosinophils. Whorled mucous plugs (Curschmann’s spirals) Debris of eosinophils (Charcot-Leyden crystals) Status asthmaticus (severe form of asthma attack) lasts several days  respiratory failure and death disease may disappear spontaneously (atopic) Can lead to chronic bronchitis, emphysema & Cor-pulmonale. • Clinically: Bronchial Asthma • Bronchiectasis • • Infection + permanent dilatation of bronchi Causes: • infections and causes of bronchial obstruction (FB, mucus plugs, tumors, sequestrations, cystic fibrosis) • immotile cilia (Kartagener’s )syndrome (Bronchiectasis, dextrocardia -situs inversus, chronic sinusitis, and infertility) • Clinically: • Chronic cough, productive of purulent sputum • Dyspnea and orthopnea in severe cases • later obstructive respiratory insufficiency & Corpulmonale Bronchiectasis Gross • Distended peripheral bronchi (Due to weakening of wall) Bronchiectasis Gross