Emphysema

• abnormal permanent enlargement of airways distal to terminal bronchioles with destruction of their walls

characteristics:

• hallmark is progressive destruction of alveoli
• loss of “bunch of grapes” morphology
• alveoli often coalesce into larger, dilated airspaces
  • in severe cases, formation of bullae (may rupture ? pneumothorax)
• alveolar dilation
  • loss of surface area for gas exchange
    • may result in chronic hypoxemia (decreased O2) and/or hypercarbia ( increased CO2)
  • loss of elastic fibres (loss of elastic recoil)
    • lungs become less elastic or more compliant (“floppy”)
    • leads to air trapping and hyperinflated lungs
• air trapping occurs because of:
  • loss of alveolar elasticity
    • elastic recoil of alveoli during expiration is what makes quiet expirations passive
    • helps “push” air out of alveoli and splint open terminal bronchioles
  • loss of alveolar interdependence
    • adjacent alveoli and bronchioles “pull” each other open
    • relies on properties of elastic recoil
    • destruction of elastic fibres between small airways predisposes them to collapse

   

Why do alveoli become damaged?

• release of lytic enzymes
  • chronic irritation (e.g. cigarette smoke) attracts neutrophils
  • neutrophils secrete enzymes (proteases, elastases) which break down alveoli
• presence of certain bacteria
  • in COPD, lungs often colonized with bacteria
  • bacteria may contribute to inflammatory and/or destructive process
• ongoing damage in the presence of ongoing irritation
  • never too late to quit smoking!
• alpha1-Antitrypsin deficiency
  • genetic disorder
    • deficient or absent levels of ?1-antitrypsin
    • also affects the liver (cirrhosis)
    • suspect alpha1-antitrypsin deficiency if emphysema develops at an early age or in a non-smoker
  • antitrypsin normally attenuates the actions of a protease (trypsin)
    • trypsin contributes to breakdown and damage of alveoli and bronchioles
  • cigarette smoking decreases the effects of alpha1-antitrypsin