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Systems: Resp. WK > 12. Pathology of Obstructive Lung Disease > Flashcards

12. Pathology of Obstructive Lung Disease Flashcards

1
Q

Does localised or generalised obstruction have a wider variety of causes?

A

Generalised obstruction (includes many rare disease which can obstruct even small bronchial airways)

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2
Q

What does localised obstruction include?

A
  • lung cancer and tumours
  • inhaled foreign bodies
  • chronic scarring diseases e.g. bronchiectasis and secondary fibrocaseous TB
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3
Q

What are the 3 main obstructive airway diseases?

A
  1. chronic bronchitis
  2. emphysema
  3. asthma
    (all have airway obstruction. airflow limitation)
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4
Q

Is mechanism for obstruction the same or different in 3 main obstructive diseases; chronic bronchitis, emphysema and asthma

A

it’s different for each

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5
Q

What are chronic bronchtitis and emphysema better known as?

A

COPD (chronic obstructive pulmonary disease), COAD (chronic pulmonary airway disease) or COLD (chronic pulmonary lung disease)

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6
Q

Do chronic bronchitis and emphysema almost always go together?

A

Yes, vast majority of patients have both (only a small minority have one and not the other)

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7
Q

What is FEV1?

A

forced expiratory volume of air exiting the lung in the 1st second

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8
Q

What is FVC?

A

forced vital capacity; final total amount of air expired (max you can physically breathe out before you collapse)

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9
Q

What is the usual ratio of FEV1: FVC

A

70-80%

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10
Q

What is the usual VOLUME for FEV1 and FVC?

A

FEV1: 3.5-4L
FVC: 5L
Normal ratio= FEV1/FVC= 70-80%

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11
Q

What does the ratio of FEV1:FVC tell us?

A

the limitation of airway obstruction (healthy person will have around 80%)

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12
Q

What factors are taken into account when predicting FVC? (3)

A
  1. age
  2. sex
  3. height
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13
Q

Except from FEV1:FVC ratio, what other method is used to measure obstruction?

A

Peak Expiratory Flow Rate (PEFR) - often used for asthmatics

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14
Q

What does peak expiratory flow rate measure?

A

measures peak flow rate during forced expiratory effort

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15
Q

What is the normal peak expiratory flow rate value?

A

400-600litres/minute

normal range is 80-100% of best value

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16
Q

What value marks a moderate fall in peak expiratory flow rate?

A

50-80%

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17
Q

What value marks a marked fall in peak expiratory flow rate (e.g. in obstruction cases)?

A

<50%

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18
Q

What happens to FEV1 and FVC in obstructive lung disease (when there is airflow limitation)?

A

FEV1 is REDUCED
FVC may be reduced but not always
( FEV1 is less than 70% of FVC and PEFR is overall reduced)

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19
Q

Will an asthmatic, who is not having an asthma attack and is feeling well demonstrate a low FEV1:FVC ratio?

A

No, their FEV1:FVC ratio will be normal (only when they are having asthmatic symptoms will they have a lower ratio)

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20
Q

What type of hypersensitivity in the airways leads to asthma?

A

Type 1 hypersensitivity: can be triggered by specific IgE, drugs, chemicals. stress or cold

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21
Q

Is asthma reversible?

A

YES (reversed with drugs or time/spontaneously)

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22
Q

What occurs in the airways as a result of chemotectic factors that contributes to asthmatic symptoms? (5)

A
  • smooth muscle contraction
  • inflammation
  • oedema
  • mucus
  • plasma exudation
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23
Q

What is the aetiology/cause of chronic bronchitis and emphysema? (5)

A
  1. SMOKING
  2. atmospheric pollution
  3. occupation (dust e.g. mill workers)
  4. age
  5. susceptibility (in genes, some people cannot detoxify their bodies as well)
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24
Q

What inherited deficiency is an extremely rare cause of emphysema but NOT chronic bronchitis?

A

alpha-1-antiprotease (antitrypsin) deficiency

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25
Q

Are chronic bronchitis and emphysema on the rise in developing countries?

A

Yes; because of increase in tobacco companies and their profit

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26
Q

Why are men more likely to develop chronic bronchitis and emphysema?

A

More likely to work in work environments that exposes them to toxic agents and more likely to smoke

27
Q

Is the damage done by smoking to cause emphysema, reversible?

A

No, it’s not reversible

28
Q

What happens if someone stops smoking at age 45 (middle age)?

A

Their lung function has already declined which is irreversible but the remaining lung function that is left over is improved and its decline is slowed down compared to smoker’s lung

29
Q

What happens if someone stops smoking at age 65? (late)

A

Their lung function has severely declined to very low levels and will not restore much of the lung function (only a little bit will be restored). Smoker’s FEV declines MUCH faster than non-smoker’s

30
Q

What symptom is used to define chronic bronchitis CLINICALLY?

A

cough productive of sputum on most days in at least 3 consecutive months for 2 or more consecutive years (excluded TB and bronchiectasis etc)

31
Q

What is chronic bronchitis clinically often confused with?

A

chronic bronchial asthma (which is poorly treated)

32
Q

When is COMPLICATED chronic bronchitis diagnosed? (2)

A
  1. when mucopurulent (acute infective exacerbation) and sputum is yellow/green colour
  2. when FEV1 falls
33
Q

What are common morphological changes in chronic bronchitis which appear in large airways? (3)

A
  1. mucous gland hyperplasia
  2. goblet cell hyperplasia
  3. inflammation and fibrosis is a minor component
34
Q

What is meant by hyperplasia?

A

increase in tissue or organ due to increase in reproduction rate of its cells

35
Q

Where are mucous glands found in large airways? (1)

A

between cartilage plates and linings (mucus production in response to irritation)

36
Q

What are common morphological changes in chronic bronchitis which appear in small airways? (2)

A
  1. goblet cells appear (which are not normally there; it’s a defence mechanism)
  2. inflammation and fibrosis in long standing disease
37
Q

Define pathologically emphysema (no functional definition exists)

A

Pathological definition: increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilation or from destruction of their walls and without obvious fibrosis

38
Q

What is the terminal bronchiole?

A

last conducting airway completely lined with respiratory epithelium

39
Q

What is an acinus?

A

many alveolar sacs (1-2cm in diameter) which contains respiratory bronchioles

40
Q

What are 3 forms of emphysema? (loss of alveolar walls can occurs in different places in acinus)

A
  1. centriacinar (emphysema located in the middle of lobule)
  2. panacinar (emphysema located across the lobules)
  3. periacinar/paraseptal (emphysema located on the peripheral edges of lobule)
41
Q

Which region of the acinus is the region where most of the “action” takes place?

A

In centriacinar; irritation, inflammation is at its maximum when something is inhaled (it’s destroyed the most in the middle causing loss of tissue and dilatation of airways)

42
Q

What are the 2 steps when centriacinar emphysema begins to develop?

A
  1. begins with bronchiolar dilatation

2. alveolar tissue is lost

43
Q

What is bullous emphysema?

A

Characterised by damaged alveoli that distend to form exceptionally large airspaces especially in the uppermost parts of the lung

44
Q

Where does the tissue damage in centriacinar emphysema is at its maximal?

A

At the apex (apex is less efficient at clearance of infection)

45
Q

Where does the tissue damage in panacinar emphysema at its maximal?

A

in the lower region

46
Q

What is a “bulla”?

A

Emphysematous space greater than 1cm

47
Q

What is a “bleb”?

A

Often used to describe bulla spaces just underneath the pleura

48
Q

When can bullas cause problems?

A

When they burst and can lead to pneumothorax as air gets into pleural space

49
Q

What does emphysema look like on a chest x ray?

A

hyperinflated chest (looks like person constantly has a half-in breath inhaled which stays in the lungs) to achieve some ventilation in the body

50
Q

What can smoking lead to malfunction of?

A

alpha-1 antitrypsin (which causes emphysema and inflammation to lung tissue)

51
Q

What other enzyme imbalance occurs in emphysema?

A

protease-antiprotease imbalance

52
Q

Once alveolar network is lost, can it be repaired?

A

No, it can’t

53
Q

In a healthy individual, what counter balancing system exists which includes what 2 enzymes?

A
  1. elastase (protease)

2. anti-elastase (anti-protease)

54
Q

In healthy individuals, what 3 other mechanisms exist which uphold the elastin framework in alveolar tissue?

A
  1. repair mechanisms
  2. elastin synthesis
  3. immune mechanism (neutrophils and macrophages)
55
Q

What enzyme is absent in alpha 1-antitrypsin deficiency which takes away a protective mechanism?

A

anti-elastase (anti-protease)

56
Q

What occurs in alpha-1-antitrypsin deficiency in terms of elastase?

A

Everything sways to elastase function as anti-elastase is removed from the equation leading to tissue damage and fault in repair mechanism = emphysema

57
Q

What occurs in smokers in terms of protective enzymes?

A
  • damages function of protective enzymes; anti-elastase
  • has negative effect on repair mechanism
  • leads to tissue destruction and ultimately emphysema
58
Q

What is the most important feature of emphysema?

A

loss of alveolar attachments which causes most of airflow limitations (like snapping strings that keep a tent standing up)

59
Q

Does emphysema mainly affect large or small airways? (4)

A

SMALL AIRWAYS:

  • smooth muscle tone
  • inflammation
  • fibrosis
  • partial collapse of airway wall on expiration
60
Q

Do large airways have any contribution to COPD?

A

little contribution by glands and mucous

61
Q

Do patients with COPD ever get back to their normal spirometry reading?

A

No, never

62
Q

What 2 features that are affected by COPD in the small airways can respond to pharmacological intervention?

A
  1. smooth muscle tone

2. inflammation

63
Q

Why do the alveoli not collapse on expiration every time we breathe out?

A

due to alveolar network (if it’s cut, then alveoli will collapse)

Systems: Resp. WK (40 decks)

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