Gomez - Obstructive vs Restrictive Pulm Disease Flashcards
How is obstructive airway disease defined in terms of FEV1 and FVC
FEV1/FVC is reduced (<0.7)
What are the four classes of emphysema?
Centriacinar/centrilobular (most common)
Panacinar/panlobular
Distal acinar/paraseptal
Irregular/paracicatrical
Describe centriacinar/centrilobular emphysema
Most common form of emphysema, > 95% of cases
Found in smokers
Mainly upper lobes/apices are involved
Describe panacinar/panlobular emphysema
Associated with α-1 antitrypsin deficiency
Smoking will result in earlier onset
Mostly in lower lobes
Describe distal acinar/paraseptal emphysema
Genetic component
Happens in relatively young adults
Associated with formation of subpleural blebs
Blebs can burst and result in pneumothorax
Describe irregular/paracicatrical emphysema
Most common, but most clinically insignificant
Occurs anywhere there has been scarring of lung
Causes relatively few symptoms because of small, localized areas of damage
What is the eitology of emphysema?
Proteolytic digestion of alveolar walls
What causes proteolytic digestion of alveolar walls?
Inflammatory cells like neutrophis secreting neutrophil elastase
What inhibits neutrophil elastase?
α-1 antitrypsin
Deficiency will cause increased and earlier onset of emphysema
How does tobacco contribute to the abundance of neutrophil elastase?
Tobacco induces formation of free radicals
Free radicals inactivates α-1 antitrypsin
This inactivation results in upregulation of neutrophil elastase
Leads to emphysema
What is the clinical picture of emphysema?
Breathing out becomes more difficult
Sx develop after damage to about 1/3 of lung tissue
Low FEV1/FVC, high TLC and RV
Gas exchange is initially adequate
Pts purse their lips to increase back-pressure upon expiration to keep bronchi inflated - “pink puffers”
Why do lungs transplanted into emphysema pts not become emphysematous?
Pt placed on immunosuppresive drugs post transplant
These reduce presence of inflamatory cells
Few to no neutrophils present in lungs to secrete elastase
Therefore it doesn’t matter if pt has α-1 antitrypsin deficiency or not, there are no inflammatory cells to cause destruction
Describe compensatory hyperinflation
Enlarged airspaces due to loss of adjacent tissue
No alveolar damage
Describe obstructive overinflation
Obstruction that allows air in upon inspiration, but occludes airway upon expiration
What is the definition of chronic bronchitis?
3 months of productive cough per year over two consecutive years
What is bronchiolitis obliterans?
Destruction of small airways
Why do pts with chronic bronchitis develop cor pulmonale?
Possible explanation:
Fibrosis due to recurrent infectious processes affects blood vessels, preventing their expansion
This leads to increased pressures which can lead to pulmonary HTN
Eventually causes R heart strain and cor pulmonale
Why do bronchitis pts have hypoxemia?
Increased mucus presence in alveoli impairs gas exchange
Results in pts who are very short of breath and can’t exercise much
Called “blue bloaters” due to cyanosis
What is the Reid index?
Ratio of thickness of glands to the thickness of the wall
Normal should be .4 or less
Describe asthma
Chronic inflammatory airway disorder
Episodic in nature
Partially reversible attacks
What type of hypersensitivity is atopic asthma classified as?
Type I hypersensitivity
What is the role of IL-13 in asthma?
Stimulates submucosal gland hyperplasia
More mucus production
What is a classic cause of drug-induced asthma? What is the mechanism?
Aspirin
Because ASA inhibits COX, but not lipoxygenase, there is a shunt, so more leukotrienes produced
Increased leukotrienes causes bronchoconstriction
What are common morphologic changes observed in pts with Type I asthma?
Airway remodeling resulting in:
Epithelial injury
Fibrosis
Eosinophilic inflammation in bronchial wall
Submucosal gland hyperplasia and increased goblet cells
What are Charcot-Leyden crystals?
Precipitates of galectin-10 containing crystalloid
Galectin-10 comes from eosinophils
What are Curschmann spirals?
Strip of dead epithelial cells that have been shed off
What is bronchiectasis? What causes it?
Permanent dilation of bronchi and bronchioles
Caused by tissue destruction by infection, resulting in large quantities of foul smelling mucus
What conditions are associated with bronchiectasis?
Cystic fibrosis
Obstruction
Infection
Pulmonary sequestration
