COPD/Asthma/ILD (8/27-9/4) Flashcards
What part of the airway is the most susceptible to significant airflow obstruction?
Bronchioles - not supported by cartilage - lack submucosal glands - contain circumferential smooth muscles
What type of lung defect is COPD?
obstructive (air intake is limited)
What two diseases fall under COPD?
chronic bronchitis emphysema
What is the main symptoms of COPD?
dyspnea
Bronchitis has what type of lung defect?
obstructive (air intake is limited)
What is the pathogenesis of/causes bronchitis?
1) hypertrophy of the mucus-secreting glands in the bronchi leads to:
a) hypersecretion -> mucus plugging
b) thickening of the bronchial wall
2) (recurrent) infections due to altered epithelium, cilia, and mucus production (inadequate clearance) -> inflammation/formation of lymphoid follicles
3) intermittent bronchospasms of smooth muscle surrounding airways
all impedes air flow
What are pathological findings of bronchitis? (4)
1) inflammatory cells (macrophage, neutrophils) and lymphoid follicles
2) thickening of bronchiole wall due to hypertrophy of mucus glands (reid index >50%)
3) luminal mucus plugging
How is chronic bronchitis diagnosed?
productive cough >3 months for 2 consecutive years
What are some general characteristics of emphysema in terms of: type of defect? histological finding? elastic recoil? compliance? fibrosis?
- obstructive lung defect
- permanent enlargement of airspaces distal to the terminal bronchioles + destruction of alveolar walls/decrease in airway tethering
- loss of elastic recoil
- increased compliance
- NO FIBROSIS
What are the 2 main patterns of emphysema? Where are they located? What are they caused by?
1) centriacinar - focal destruction of respiratory bronchioles due to cigarette smoking 2) panacinar - destruction of alveoli distal to the terminal bronchioles due to A1AT deficiency
What is the role of A1AT? How does it protect against smoke?
Alpha-1-antitrypsin - blocks elastase Smoke recruits inflammatory cells, which increase elastase production to destroy lung parenchyma, thus reducing elastic recoil
How does smoking cause emphysema?
Smoke does 2 things: 1) it recruits inflammatory cells, which increase elastase production to destroy lung parenchyma, thus reducing elastic recoil. 2) it inactivates A1AT, which causes results in increased elastase activity, thus resulting in an increased lung parenchyma destruction and ultimately reduction of elastic recoil.
What type of lung defect is asthma?
obstructive defect (air can’t get in)
What is asthma?
hyper-responsiveness of the tracheobronchial tree to stimuli, which leads to repeated episodes of reversible bronchoconstriction
What are the two main types of Asthma?
EXtrinsic
- allergic/Type I hypersensitivity
- atopy/genetic predisposition to producing IgE to allergens
- may be due to increased Th2 production, which secrete IL’s to stimulate B cells to produce IgE and activate eosinophils to produce major basic protein.
INtrinsic
- non-allergic - non-hereditary
Which T cell is a key player in the extrinsic pathway of asthma?
Th2 - secrete IL’s to stimulate B cells to produce IgE, which stimulates mast cells - activate eosinophils to produce major basic protein both result in damage to the epithelium and airway constriction
What are the pathological findings of asthma? 93)
1) thick mucus plugs
2) thickened epithelial basement membranes
3) eosinophils
4) inflammation
5) edema
6) hypertrophied smooth muscle + submucosal gland proliferation
What is bronchiectasis?
permanent airway DILATION due to the sequelae of continued airway damage (repeat infections, aspirations of drugs and chemicals, obstruction)
What is the pathology of bronchiectasis?
loss of cilia increased mucus destruction of alveolar wall due to inflammation w. or w.o microabscesses, squamous metaplasia, peribronchial fibrosis
What inflammatory cells predominate in COPD lungs?
macrophages, CD8, and neutrophils, which promote inflammation that ultimately lead to small airway narrowing and alveolar destruction.
What is the difference betwen reversible and irreversible airflow limitation in COPD lungs?
Reversible: airway inflammation + airway remodeling
Irreversible: parenchymal destruction, loss of elastic recoil
What are 5 mechanisms of airflow obstruction?
- mucus hypersecretion -> luminal obstruction
- disruputed alveolar attachments -> easier for airway to collapse (ie emphysema)
- mucosal inflammation/fibrosis -> thickened alveolar walls (ie bronchitis)
- reduced elastic recoil -> reduced airflow (emphysema)
- smooth muscle contraction -> narrowing of the airways (ie bronchitis)
How are the symptoms of chronic bronchitis different than that of emphysema, even though they both fall under the umbrella term of COPD?
Chronic bronchitis:
1) productive cough
2) hypoxemia
3) pulmonary HTN
Emphysema
1) breathlessness
2) adequate oxygen saturation
3) cachexia (wasting disease - loss of weight, muscle atrophy, fatigue, weakness)
What is the elastase hypothesis?
A1AT is a major inhibitor of serine proteases in the lungs, and it antagonizes the effects of the neutrophils in the lungs.
Deficiency is caused by a recessive mutation, where the liver (site of A1AT production) does not synthesize it or release it.
Thus, a smoker with A1AT deficiency is at high risk of developing COPD at an earlier age (30-50) compared to the usual onset (50-60)
