Forms of obstructive lung disease
- Emphysema
- Chronic bronchitis
- Asthma
- Bronchiectasis
Chronic bronchitis
Anatomic site: bronchus
Major pathologic changes: mucous gland hyperplasia, hypersecretion
Etiology: tobacco smoke, air pollutants
Signs/symptoms: cough, sputum production
Bronchiectasis
Anatomic site: bronchus
Major pathologic changes: airway dilation and scarring
Etiology: persistent or severe infections
Signs/symptoms: cough, purulent sputum, fever
Asthma
Anatomic site: bronchus
Major pathologic changes: smooth muscle hyperplasia, excess mucus, inflammation
Etiology: immunologic or undefined causes
Signs/symptoms: episodic wheezing, cough, dyspnea
Emphysema
Anatomic site: acinus
Major pathologic changes: airspace enlargement, wall destruction
Etiology: tobacco smoke
Signs/symptoms: dyspnea
Who is more susceptible to developing COPD?
Women and African-Americans
Centriacinar emphysema
- Most common
- Heavy smokers
- Respiratory bronchioles (distal alveoli spared)
- More common in apical segments
Panacinar emphysema
- Acini uniformly enlarged (to alveoli)
- Commonly in lower zones of lung
- Most severe at bases
- associated with alpha-1 antitrypsin deficiency
Paraseptal emphysema
- distal acinus most prominently involved
- along lobular CT septa
- adjacent to areas of fibrosis, scarring, or atelectasis
- is likely the underlying etiology in spontaneous pneumothorax in healthy, young adults
Irregular emphysema
-associated with scarring
Pathogenesis of emphysema
smoke and other irritants cause damage and inflammation»leukotrienes, IL-8, TNF released from resident epithelial cells and macrophages»attract inflammatory cells from circulation»amplify inflammatory process (cytokines)»induce structural changes through growth factors»proteases released from inflammatory and epithelial cells»break down CT»relative deficiency in anti-proteases in some who develop emphysema (alpha-1 antitrypsin)
Alpha-1 antitrypsin deficiency
- Autosomal recessive disorder
- protease inhibitor
- PiMM most common wild-type
- PiZZ abnormal form»accumulate in liver
- damage in liver and lungs
Other pathogenesis
Oxidative stress»tissue damage and inflammation
Infection»exacerbate
Gross morphology with emphysema
- voluminous lungs
- upper 2/3
- blebs and bullae can form
Blebs
air filled space >1 cm
Bullae
air filled space <1 cm
Pink puffers
Overventilate and remain well oxygenated
Other disorders that have emphysema-like changes
Compensatory hyperinflation (dilation of alveoli in response to loss of lung substance elsewhere - surgical removal)
Obstructive overinflation (expands because air is trapped - tumor, foreign object, congenital)
Interstitial emphysema (air enters into SC tissue or mediastinum - alveolar tears in emphysema, chest wounds)
Bullous emphysema
Subpleural blebs or bullae
Often near apex, can be due to old scarring like with TB
Rupture can result in pneumothorax
Pathogenesis of chronic bronchitis
Insult leads to…
- Mucus hypersecretion (hypertrophy/hyperplasia of submucosal glands and, later, goblet cells
- Inflammation (neutrophils, lymphocytes, macrophages)»fibrosis
- Infection»maintains and leads to acute exacerbations
Morphology of chronic bronchitis
Gross: edema of mucous membranes, mucinous purulent secretions, cases of secretions and pus
Microscopic: inflammation of airways, enlargement of mucus-secreting glands, epithelial metaplasia and dysplasia, narrowing of bronchioles caused by mucous plugging, inflammation, and fibrosis
Chronic bronchitis clinical features
- persistent cough
- hypercapnia, hypoxemia, mild cyanosis (blue bloaters)
Asthma morphology
Gross:
- distended lungs
- airways filled with thick mucous plugs
- small areas of atelectasis
Microscopic:
- eosinophils with Carcot-Leyden crystals
- mucous
- airway remodeling (thickening of wall, subbasement membrane fibrosis, increased vascularity, increased size of glands, increased numbers of goblet cells, hypertrophy and hyperplasia of bronchial wall muscle
Allergic bronchopulmonary aspergillosis (ABPA)
- Occurs in patients with asthma and cystic fibrosis
- Results from hypersensitivity reaction to Aspergillus fumigatus
-Can see:
Transient pulmonary infiltrates on imaging
Eosinophilia of blood and sputum
Increased serum IgE
-Get mucous plugs, often see fungal hyphae in mucoinflammatory material
