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Flashcards in Path: COPD Deck (9)
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1
Q

Types of emphysema

A
  • 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)
2
Q

Panacinar emphysema

A
  • 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
3
Q

Centriacinar emphysema

A
  • 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
4
Q

Paraseptal emphysema

A
  • 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
5
Q

Pathogenesis of emphysema

A
  • 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
6
Q

Chronic bronchitis 1

A
  • 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)
7
Q

Chronic bronchitis 2

A
  • 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
8
Q

Asthma

A
  • 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
9
Q

Bronchiectasis

A
  • 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