Path: COPD

Question 1

Types of emphysema

Answer 1

• COPD: persistent airflow limitation w/ enhanced chronic inflammation due to noxious particles or gases
• Emphysema: permanent enlargement of airspace distal to terminal bronchiole w/ destruction of airspace walls (pathologic Dx)
• Panacinar (associated w/ alpha1 AT deficiency)
• Centriacinar (most common, associated w/ smoking)
• Paraseptal (associated w/ bullae and pneumothorax)

Question 2

Panacinar emphysema

Answer 2

• Dilation and destruction initially of acinar structures distal to respiratory bronchioles (i.e. alveolar destruction)
• Grossly there are multiple small cystic spaces giving the lung a fishnet appearance, usually affects lower lobes more
• There will be very few normal looking alveoli
• There is dilation, fenestration, and derangement of acinic structures w/ breaks in the alveolar walls
• Associated w/ alpha1 antitrypsin (AT) deficiency

Question 3

Centriacinar emphysema

Answer 3

• Dilation and destruction in the proximal portion of the acinus (respiratory bronchioles)
• There is spotty multifocal cystic spaces w/ interstitial deposits of “anthracotic” pigment
• Tends to effect upper lobes more
• Cystic spaces represent dilation and destruction of respiratory bronchioles
• There will be normal alveoli, surrounded by lots of scar tissue
• Associated w/ smoking

Question 4

Paraseptal emphysema

Answer 4

• Changes in distal alveolar ducts and sacs, more common in the apices or upper lobes
• Can manifest as bullae (extreme) and is associated w/ pneumothorax due to shearing forces

Question 5

Pathogenesis of emphysema

Answer 5

• Alveolar wall destruction (septal rupture) is due to a complex imbalance btwn proteases (elastases) and antiproteases (anti-elastases)
• Major anti-elastase is alpha1 AT
• Elastases are released by PMNs and macs in the lungs (A1 AT inactivates PMN elastases but not mac elastases)
• O2 radicals and mac elastases can inactivate A1 AT, and smoking causes O2 generation, lymphocyte infiltration and lymphocyte release of elastases
• Loss of lung elastic tissue, along w/ alveolar destruction, creates the Sx seen in emphysema

Question 6

Chronic bronchitis 1

Answer 6

• Clinical Dx, based on if the pt had a chronic productive fought over a 3 mo period for 2 successive years
• Earliest changes seen are hypertrophy of submucosal glands and increased # of goblet cells in the trachea and bronchi
• There is hyper secretion of mucus, w/ a Reid index (indicating the thickness of submucosal glands) of >.5 (normal is ≤.4)

Question 7

Chronic bronchitis 2

Answer 7

• Additionally, there is goblet cell metaplasia, mucous plugging, inflammation and fibrosis causing bronchiolar narrowing
• Severe cases can see complete obstruction of bronchioles (bronchiolitis obliterans)
• Can also see squamous metaplasia and dysplasia
• Cause is multifactorial, but is associated w/ tobacco smoke

Question 8

Asthma

Answer 8

• Dysfunction of airway mast cell, eosinophils, and T cells (hypersensitivity type 1)
• Grossly the lungs are over-inflated w/ small areas of atelectasis
• There is bronchial and bronchiolar occlusion by thick mucus plugs
• The plugs contain whorls of shed respiratory epithelium forming Curschmann spirals, aggregates of columnar cells (Creole bodies) and sloughed ciliated cells
• The bronchiolar wall shows eosinophil and CD4 cell infiltration (eosinophil infiltration is hallmark)
• Elevated IgE levels
• There is some hypertrophy and hyperplasia of mucous and submucosal glands w/ increased mucus production

Question 9

Bronchiectasis

Answer 9

• Permanent abnormal dilation of bronchi and bronchioles associated w/ chronic necrotizing infections (mostly terminal bronchioles)
• Infectious agents include: TB, S Aureus, H Influenzae, HIV, influenze virus
• Hereditary etiologies include CF, Kartagener-immotile cilia disease
• Can also be due to bronchial/bronchiolar obstruction such as aspiration