COPD/Asthma

Question 1

COPD consists of what two major diseases? how are they different?

Answer 1

chronic bronchitis - mucous gland hyperplasia/hypersecretion

emphysema - airpsace enlargement and wall destruction

Question 2

what is considered to be the “acinus” of the lung?

Answer 2

• acinus = distal bronchiole (respirtatory bronchiole) + alveoli

Question 3

what are the four classifications of emphysema?

Answer 3

• centriacinar
• panacinar
• paraseptal
• irregular

Question 4

centriacinar emphysema

• distribution
• demographics

Answer 4

• distribution:
  
  • effects proximal acinus:
    
    • i.e. –> respiratory bronchioles & proximal alveoli
      
      • ​spares the distal alveoli (which will have normal tissue)
  • m/c in UPPER LOBE APICES
• demographics: heavy smokers

Question 5

panacinar emphysema

• distribution
• demographics

Answer 5

• distriution
  
  • “pan” =throughout acinus:
    
    • i.e., respiratory bronchioles and a_ll of the_ alveoli
  • m/c in lower lung apices/anterior margins
• demographics: alpha-1 antitrypsin deficiency

Question 6

paraseptal emphysema

Answer 6

• distribution
  
  • distal acinus
  • m/c found in:
    
    • areas of fibrosis/atelectasis in upper half of lungs
    • subpleural tissues, just deep to lobule margins
• demographics: associated w/ spontaneous pneumothorax in young adults

Question 7

irrgular emphysema

• distribution
• demographics

Answer 7

clinically insignificant

• distribution - in small foci
• demographics - in pts w/ scarring

Question 8

emphysema pathogenesis

Answer 8

smoke/toxic particles –> induce release of inflammatory mediators (IL-8/TNF) –> which release proteases –> which break down tissue –> oxidative damage –> more inflammation

• reduces elastic recoil (stiffness) of lung parenchyma
• i.e., increases compliance of lung parenchyma
• by t = CR, time constant of lung emptying increases
  
  • –> obstructive disease

Question 9

gross findings of emphysema

Answer 9

• large lungs (upper apices more effected)
  
  • apical blebs, bullae
  • enlarged airspaces

Question 10

emphysema - microscopic morphology

Answer 10

• enlarged alveoli
• thinned septa
  
  • appear “blind ended”

Question 11

bullous emphysema - morphology & sequelae

Answer 11

• blebs/bullae > 1 cm
• may rupture –> pneumothorax

Question 12

chronic bronchitis pathogenesis

Answer 12

• smoking/toxins induce
  
  • mucous hypersecretion (​associated with s_ubmucosal gland hypertrophy_ in trachea/bronchi)
    
    • increases resistance (adds a resistor in sequence) of the airways –> by t = RC –> increases time of emptying

Question 13

what causes acute exacerbations of chronic bronchitis?

Answer 13

infections

Question 14

what is the reid index and its relevance to obstructive airway disease?

Answer 14

ratio of mucous gland layer thickness: normal tissue (between epithelium/cartilage) thickness

• normal = 0.4
• in chronic bronchitis, > 0.4

Question 15

chronic bronchitis - microscopic morphology

Answer 15

• submucosal mucus gland hyperplasia
  
  • ​increased # of goblet cells (bottom pic)
  • reid index > 4
• lymphocyte infintiltration
• t_hickened basement membrane_ (black arrow)

Question 16

asthma pathogenesis

Answer 16

• three types:
  
  • atopic asthma (most common) - characterized overactive IgE & Th2 response to benign antigens
  • drug induced asthma (rare) - due to aspirin (NSAIDS)
  • occupational asthma
• all cause:
  
  • mucous gland hypertrophy (like in chronic bronchitis)
  • basement gland thickening (like in chronic bronchitis)
  • eisonophilia
• which lead to smooth muscle hypertrophy –> increase airway resistance

Question 17

asthma - microscopic morphology

Answer 17

• like chronic bronchitis:
  
  • submucosal mucus gland hyperplasia (inc # goblet cells) - curschmann’s spirals
  • thickened basement membrane
• esionophillic infiltration - ​charcot-layden crystals
• smooth muscle hypertrophy