Lec 11 COPD Flashcards

1
Q

What is the major risk factor for developing COPD?

A

cigarette smoking

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2
Q

What is the definition of COPD?

A

persistent limited expiratory airflow that is not fully reversible

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3
Q

What happens to lung volumes in obstructive lung disease?

A

increased RV
decrease FVC
very decreased FEV1
–> low FEV1/FVC ratio < 0.7

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4
Q

What happens to FEV1/FVC in COPD? with bronchodilator?

A

decreased < 0.7

not fully improved by bronchodilator

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5
Q

What is chronic bronchitis?

A

a clinical definition

- chronic productive cough for > 3 months per year for 2 or more consecutive years

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6
Q

What is clinical course of chronic bronchitis?

A
  • periods of exacerbations of chronic productive cough often precipitated by resp tract infection

residual clinical disease even between exacerbations

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7
Q

What is pathology in chronic bronchitis?

A
  • hyperplasia of mucus-secreting glands
  • high reid index > 50%
  • bronchial wall thickening [from gland enlargement, edema, basement membrane thickening, increased smooht muscle]
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8
Q

What is Reid index? Normal? abnormal?

A

thickness of bronchial mucous gland / total thickness of broncial wall

normal ~ 33%
in chronic bronchitis > 50%

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9
Q

What is emphysema?

A

pathologic diagnosis

destruction of lung parenchyma and enlargement of air spaces distal to the terminal bronchiole

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10
Q

What is centrolobular [centricacinar] emphysema?

A

involves mostly respiratory bronchiole

happens mostly in upper lung zone

most common in smokers

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11
Q

Which type of emphysema typically seen in smokers?

A

centrilobular [centriacinar]

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12
Q

What is panlobular [panacinar] emphysema?

A

uniformly/diffusely involves acinus

happens mostly in lower lung zones

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13
Q

What type of emphysema typically associated with a1-antitrypsin deficiency?

step1

A

panlobular/panacinar

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14
Q

What type of emphysema usually in upper lung area?

A

usually centriacinar = smoking associated

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15
Q

What is protease-antiprotease theory of emphysema?

A

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

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16
Q

What type of disease should you think if breathing through pursed lips? why?

step1

A

emphysema

pursed lips = increase airway pressure and prevent collapse during respiration

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17
Q

What is mech of smoking in emphysema?

A
  • inactivates a1-antitrypsin
  • recruits neutrophils that release elastase
  • causes functional a-1 antitrypsin deficiency
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18
Q

What is z variant of a1-antitrypsin?

A

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

19
Q

What is s variant of a1-antitrypsin?

A

more common than Z but less important

makes protein more suscpetibl to intracellular proteolysis

20
Q

What variants of a1 antitrypsin have highest COPD risk?

A

null homozygous, Z-null het, ZZ hom have highest risk

SS does not really have increased risk

21
Q

How is lung compliance altered in emphysema?

A

more compliant = for given volume have lower pressure

22
Q

What are breathing mechanics in emphysema?

A

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

23
Q

How is airway tethering altered in emphysema?

A

decreased

24
Q

What are 3 mechs of airways obstruction?

A
  • lots of mucus in space
  • increased smooth muscle mass
  • decreased tehtering
25
Q

What happens to lung volumes in emphysema?

A
  • increased total lung capacity and FRC because lungs are more compliant
26
Q

What is dynamic hyperinflation? How is it changed in COPD?

A

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

27
Q

What happens to V/Q in chronic bronchitis?

A

have decreased ventilation and preserved perfusion

28
Q

What happens to V/Q in emphysema?

A

have no V/Q mismatch because you are destroying everything

hyperinflated alveoli compressing capillary

29
Q

What is DLco?

A

measurment of rate of transfer of gas from alveolus to hemoglobin within capillary

30
Q

What happens to DLco in emphysema?

A

decreased b/c loss of internal surface area and of capillary bed in lung

31
Q

What happens to DLco in pure asthma?

A

not changed

32
Q

What are symptoms of COPD?

A
  • dyspnea
  • cough [w/ sputum]
  • acute exacerbations triggered by resp infeciton, air pollution, bronchospasm
33
Q

What do you see on physical exam in chronic bronchitis?

A
  • prolonged expiratory phase
  • decreased breath sounds
  • wheezing
  • ronchi = from profuse airway secretions
  • severe COPD –> barrel shaped chest, purse lipped breathing, emaciation
34
Q

What mech of COPD cause increased risk of pulmonary HTN?

A
  • increased risk for thromboembolism
  • hypoxia/inflammation causing vasoconstriction
  • hyperinflation of alveoli compress capillary –> increase pressure
  • LV dysfunction backup of pressure into lungs
35
Q

What is relationship in #s smoking and COPD?

A
  • 80 % of people who have COPD are smokers

- symptomatic COPD in 20% of smokers

36
Q

What are effects of smoking that specifically lead to chronic bronchitis?

A
  • cause bronchial mucous gland hypertrophy + hyperplasia
  • bronchial wall inflammation
  • impaired mucociliary clearance
37
Q

What are effects of smoking that specifically lead to emphysema?

A
  • increased number of neutrophils –> more elastase

- oxidation of a1 antitrypsin decrease function

38
Q

How do packyears correlate to lung function? What happens if you stop smoking

A
  • 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

39
Q

What are other risk factors for COPD besides smoking?

A
  • occupational exposure [miner, agriculture]

- indoor pollution from cooking with biomass fuels

40
Q

What is “Blue bloater”?

A

chronic bronchitis

  • elevated hemoglobin from hypoxemia
  • overweight and cyanotic
  • peripheral edema
  • ronchi and wheezing
41
Q

What is “pink puffer”?

A

emphysema

  • older and thin
  • severe dyspnea
  • quiet chest from parenchymal destruction
  • X ray shows hyperinflation with flattened diaphragm
42
Q

What treatment for COPD has survival benefit?

A
  • stop smoking

- give supplemental O2 for hypoxemic patients

43
Q

What treatment for COPD symptoms?

A
  • bronchodilators

- corticosteroids

44
Q

What is lung volume reduction surgery? who does it benefit?

A

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