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Flashcards in Lec 11 COPD Deck (44):

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?




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?


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?



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"?

- 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