Anatomic Site: Bronchus

Major Pathologic changes: Mucous gland hyperpalasia, Hypersecretion

Etiology: Tobacco Smoke, Air polutants

SxS - Cough, sputum production

Anatomic Site: Acinus

Major changes: Airspace enlargement; wall destruction

Etiology: Tobacco Smoke

SxS: Dyspnea

• Centiacinar: 95% of cases
• Panacinar
• Paraseptal and irregular. Only first 2 cause clinically significant airflow

• Central or proximal parts are effected.
• More common and severe in upper lobes
• Occurs mostly in heavy smokers

• The acini are uniformly enlarged
• More common in lower zones
• Most severe at bases
• Associate with Alpha1-antitrypsin Deficiency

• Affect distal part of acinus
• Severe in upper lobes, enlarged airspaces
• Cause of pneumothorax in young adults

• Associates with scarring, likely the most common form
• is asymptomatic and clinically insignificant

• Macrophages, Neutrophils and both T-lymphocytes
• Inflam cells release proteases and mediators
• LKT b4, IL-8, TNF, etc that damange lung structures

• Environmental: 

Functional deficiency of alpha1-antitrypsin, CIG SMOKING, AIR POLLUTION

• Genetic (1 in 3000)

Congenital deficiency of alpha1-antitrypsin, polymorphism in proteinase inhib on chrom 14.

Emphysema: Mechanism of obstruction

(3)

• Loss of elastic tissue/recoil CARDINAL FEATURE

1. decreased radial traction. 2. alveoli distention with trapped air

• Goblet cell metaplasia - mucus plugging lumen

• Thickening of Bronchiolar wall

Smooth muscle hypertrophy, Neutro, macro, B&T

• Dyspnea
• Cough/wheezing/weight loss/barrel-chested
• sits forward in hunched position
• expiratory airflow limitation (diagnostic key)

Eventually Emphysema patients develop

• cor pulmonale and CHF due to secondary pulmonary vascular hypertension

• Respiratory acidosis and Coma
• RIght sided heart failure
• massive collpase of the lungs secondary to pneumothorax

• Tobacco smoke (90%), dust from grain, cotton, silica

• Hypertrophy of submucosal glands
• Hypersecretion of mucus
• Activation of neutrophils that inturn stimulate mucus hypersecretion

• Goblet cell hyperplasia

Leading to excessive mucus production (cardinal feature) and airway obstruction

• Direct damage to airway epi
• interferes with ciliary action
• inhibits bronchial and alveolar leukocytes to clear bacteria

• Cardinal symptom: Persistent n productive cough
• later on: hypercapnia, hypoxemia, mild cyanosis
• over the years: Cor pulmonale and heart failure, cancer

• Older, severe and early dyspnea
• Late coughing, low sputum
• Occasional infections, terminal respiratory insuff
• rare cor pulmonale, but terminal
• normal or slightly increased airway resistance
• low elastic recoil
• Hyperinflation; small radiograph