Lec 11 COPD Flashcards
What is the major risk factor for developing COPD?
cigarette smoking
What is the definition of COPD?
persistent limited expiratory airflow that is not fully reversible
What happens to lung volumes in obstructive lung disease?
increased RV
decrease FVC
very decreased FEV1
–> low FEV1/FVC ratio < 0.7
What happens to FEV1/FVC in COPD? with bronchodilator?
decreased < 0.7
not fully improved by bronchodilator
What is chronic bronchitis?
a clinical definition
- chronic productive cough for > 3 months per year for 2 or more consecutive years
What is clinical course of chronic bronchitis?
- periods of exacerbations of chronic productive cough often precipitated by resp tract infection
residual clinical disease even between exacerbations
What is pathology in chronic bronchitis?
- hyperplasia of mucus-secreting glands
- high reid index > 50%
- bronchial wall thickening [from gland enlargement, edema, basement membrane thickening, increased smooht muscle]
What is Reid index? Normal? abnormal?
thickness of bronchial mucous gland / total thickness of broncial wall
normal ~ 33%
in chronic bronchitis > 50%
What is emphysema?
pathologic diagnosis
destruction of lung parenchyma and enlargement of air spaces distal to the terminal bronchiole
What is centrolobular [centricacinar] emphysema?
involves mostly respiratory bronchiole
happens mostly in upper lung zone
most common in smokers
Which type of emphysema typically seen in smokers?
centrilobular [centriacinar]
What is panlobular [panacinar] emphysema?
uniformly/diffusely involves acinus
happens mostly in lower lung zones
What type of emphysema typically associated with a1-antitrypsin deficiency?
step1
panlobular/panacinar
What type of emphysema usually in upper lung area?
usually centriacinar = smoking associated
What is protease-antiprotease theory of emphysema?
elastin = structural protein in walls of alveoli
neutrophils supply elastase; a1 antitrypsin inhibits elastase
too much elastase/not enough antitrypsin –> destruction of elastin in alveoli wall –> increased compliance
What type of disease should you think if breathing through pursed lips? why?
step1
emphysema
pursed lips = increase airway pressure and prevent collapse during respiration
What is mech of smoking in emphysema?
- inactivates a1-antitrypsin
- recruits neutrophils that release elastase
- causes functional a-1 antitrypsin deficiency
What is z variant of a1-antitrypsin?
Glu342–> Lys 342
have normal transcription/translation but protein folding problem + can’t form internal salt bridge causes Z molecule aggregates in hepatocytes
can’t be secreted
What is s variant of a1-antitrypsin?
more common than Z but less important
makes protein more suscpetibl to intracellular proteolysis
What variants of a1 antitrypsin have highest COPD risk?
null homozygous, Z-null het, ZZ hom have highest risk
SS does not really have increased risk
How is lung compliance altered in emphysema?
more compliant = for given volume have lower pressure
What are breathing mechanics in emphysema?
alvoelar P = P alverolar wall + P pleura
in distal airway right next to alveolus Pbr > Ppl
then reaches equal pressure point where Pbr = Ppl
in emphysema –> there is less alveolar wall pressure so less pressure in alveoli/bronchi meaning that the equal pressure point is more distal in airspaces where there is not cartilage to prevent collapse
How is airway tethering altered in emphysema?
decreased
What are 3 mechs of airways obstruction?
- lots of mucus in space
- increased smooth muscle mass
- decreased tehtering
What happens to lung volumes in emphysema?
- increased total lung capacity and FRC because lungs are more compliant
What is dynamic hyperinflation? How is it changed in COPD?
normal = when you exercise, minute ventilation goes up and tidal volume goes up while inspiratory reserve volume goes down and end expiratory volume is the same
COPD = when you exercise, increase inspiratory/expiratory rate but not you have less time to expire –> you expire less air –> expiratory lung volume goes up = expiratory flow limitation and you feel dyspnea
What happens to V/Q in chronic bronchitis?
have decreased ventilation and preserved perfusion
What happens to V/Q in emphysema?
have no V/Q mismatch because you are destroying everything
hyperinflated alveoli compressing capillary
What is DLco?
measurment of rate of transfer of gas from alveolus to hemoglobin within capillary
What happens to DLco in emphysema?
decreased b/c loss of internal surface area and of capillary bed in lung
What happens to DLco in pure asthma?
not changed
What are symptoms of COPD?
- dyspnea
- cough [w/ sputum]
- acute exacerbations triggered by resp infeciton, air pollution, bronchospasm
What do you see on physical exam in chronic bronchitis?
- prolonged expiratory phase
- decreased breath sounds
- wheezing
- ronchi = from profuse airway secretions
- severe COPD –> barrel shaped chest, purse lipped breathing, emaciation
What mech of COPD cause increased risk of pulmonary HTN?
- increased risk for thromboembolism
- hypoxia/inflammation causing vasoconstriction
- hyperinflation of alveoli compress capillary –> increase pressure
- LV dysfunction backup of pressure into lungs
What is relationship in #s smoking and COPD?
- 80 % of people who have COPD are smokers
- symptomatic COPD in 20% of smokers
What are effects of smoking that specifically lead to chronic bronchitis?
- cause bronchial mucous gland hypertrophy + hyperplasia
- bronchial wall inflammation
- impaired mucociliary clearance
What are effects of smoking that specifically lead to emphysema?
- increased number of neutrophils –> more elastase
- oxidation of a1 antitrypsin decrease function
How do packyears correlate to lung function? What happens if you stop smoking
- more pack years = worse lung function
if you stop smoking –> go back to normal rate of lung aging but starting at a worse place; can’t reverse damage already done
What are other risk factors for COPD besides smoking?
- occupational exposure [miner, agriculture]
- indoor pollution from cooking with biomass fuels
What is “Blue bloater”?
chronic bronchitis
- elevated hemoglobin from hypoxemia
- overweight and cyanotic
- peripheral edema
- ronchi and wheezing
What is “pink puffer”?
emphysema
- older and thin
- severe dyspnea
- quiet chest from parenchymal destruction
- X ray shows hyperinflation with flattened diaphragm
What treatment for COPD has survival benefit?
- stop smoking
- give supplemental O2 for hypoxemic patients
What treatment for COPD symptoms?
- bronchodilators
- corticosteroids
What is lung volume reduction surgery? who does it benefit?
reduce lung volume by removing emphysematous tissue = cuts out dead space so less wasted ventilation + increases elastic recoil / mechanical function of diaphragm
benefits pts with upper lung zone emphysema
