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Medicine 1 Respiratory > Pathology of Obstructive Lung Disease > Flashcards

Pathology of Obstructive Lung Disease Flashcards

1
Q

What is localised obstruction?

A

Obstruction of a large airway

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2
Q

What can localised obstruction be caused by?

A

Lung cancer

Inhaled foreign bodies

Chronic scarring diseases like bronchiectasis and secondary tuberculosis

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3
Q

What is generalised small airway obstruction?

A

Bronchiolar obstruction

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4
Q

Other names for COPD include

A
  • Chronic Obstructive Airways Disease
  • Chronic Obstructive Lung Disease
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5
Q

How rare is it for patients to have only chronic bronchitis or only emphysema?

A

Very rare

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6
Q

Aside from spirometry, what can obstructive lung disease be demonstrated by?

A

Peak expiratory flow rate (PEFR)

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7
Q

What is the normal peak expiratory flow rate?

A

400-600L/min

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8
Q

What is the normal range, moderate fail and marked fail of PEFR?

A

80-100% of best value is normal 50-80% is moderate fail <50% is marked fail

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9
Q

How does obstructive lung disease affect spirometry and peak expiratory flow rate?

A

Always airflow limitations

Peak expiratory flow rate is reduced

FEV1 is reduced

FVC may be reduced

FEV1 is less than 70% of FVC

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10
Q

What is bronchial asthma?

A

Type 1 hypersensitivity in the airways

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11
Q

What is bronchial asthma mediated by?

A

Immunologically mediated, leading to the degranulation of mast cells that releases a number of chemical factors

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12
Q

What are the 2 main effects of the chemical factors released by mast cell granules?

A
  • induce inflammation by attracting a number of inflammatory cell types into the airway leading to swelling and edema within the bronchial mucosa
  • chemicals which have a direct effect on the bronchial smooth muscle leads to airway inflammation and constriction
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13
Q

What is important about bronchial asthma?

A

Reversible airway obstruction either spontaneously or as a result of medical intervention

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14
Q

What can bronchial smooth muscle contraction and inflammation be modified by?

A

Drugs

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15
Q

Do asthmatics have airflow limitations all the time?

A

No, only during an asthma attack

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16
Q

What is the aetiology of chronic bronchitis and emphysema?

A

Smoking

Atmospheric pollution

Occupational dust

Alpha-1-antitrypsin deficiency

Effects of age and susceptibility

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17
Q

What is Alpha-1-antiprotease(antitrypsin) deficiency?

A

A rare inherited disease where the patient suffers from a deficiency in antitrypsin or antiprotease enzymes causing emphysema alone

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18
Q

Do more men or woman have COPD and why?

A

Men because they smoke more

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19
Q

What is chronic bronchitis?

A

Cough production of sputum most days in at least 3 consecutive months for 2 or more consecutive years (excludes TB, bronchiectasis)

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20
Q

What is chronic bronchitis easily confused with?

A

Chronic bronchial asthma

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21
Q

Complicated chronic bronchitis refers to

A

when sputum becomes infected, mucopurulent, yellow or green during an acute infection

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22
Q

What is morphological?

A

Size, shape and structure of a given organ

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23
Q

What are morphological changes in the large airways due to chronic bronchitis?

A

Mucous gland hyperplasia

Goblet cell hyperplasia

Inflammation and fibrosis is a minor component

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24
Q

What is hyperplasia?

A

Enlargement of an organ or tissue caused by an increase in the reproductive rate of its cells

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25
Q

What are morphological changes in the small airways due to chronic bronchitis?

A

Goblet cells appear

Inflammation and fibrosis in long-standing disease

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26
Q

What is emphysema?

A

Increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilation of from destruction of their walls and without obvious fibrosis

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27
Q

What is an acinus?

A

gas exchange tissue part of the lung defined by everything distal to the terminal bronchiole

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28
Q

What is the size of the normal acinus duct?

A

1-2cm, cannot see where one ends and where another begins

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29
Q

What are the different forms of emphysema?

A

Centriacinar

Panacinar

Periacinar

Scar ‘irregular’

Bullous emphysema

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30
Q

What is the most common kind of emphysema?

A

Centriacinar, where tissue is lost in the middle of the acinus

31
Q

What is the process of centriacinar emphysema?

A

1) Begins with bronchiolar dilation
2) Then alveolar tissue is lost

32
Q

What is panacinar emphysema?

A

Whole tissue is wiped out, so huge areas of tissue are lost

33
Q

What is a bulla?

A

Emphysematous space greater than 1cm

34
Q

What term is often used to describe bullas just underneath the pleura?

35
Q

What is periacinar emphysema?

A

Holes against the pleura, where if they burst they cause a pneumothorax

36
Q

What happens if a periacinar emphysema bursts?

A

Pneumothorax

37
Q

Centriacinar emphysema predominates
in

A

the upper parts of the lungs (we find the holes in
the lungs in the apical parts of the upper lobe and the apical
parts of the lower lobe)

38
Q

Panacinar emphysema predominates

A

large areas of the lung

39
Q

Where do you expect to see panacinar emphysema?

A
  • Alpha-1-antitrypsin deficiency
  • very heavy cigarette smokers
  • people who have slightly
    poorer functioning anti enzymes
40
Q

Scar emphysema have no clinical significance and it simply refers to

A

development of emphysema to
spaces around scars in the lung

41
Q

What is the difference in an X-ray between someone with emphysema and someone who is healthy?

A

With emphysema can see all of the ribs. whereas can only see 10 posterior ribs in someone who is healthy

42
Q

What are elastases?

A

Enzymes released by macrophages

43
Q

What are anti-elastases?

A

Enzymes that get rid of elastases to stop them from dissolving our own tissue

44
Q

Why do patients with emphysema have hyperinflated lungs?

A

Because it is the only way they can keep their small airways from collapsing.

45
Q

Why do elastases not dissolve a lot of our own tissue?

A

They are balanced with anti-elastases that remove them

46
Q

How does smoking change the elastase balance?

A

Inhibits anti-elastase and repair mechanisms

47
Q

What leads to an anti-elastase deficiency?

A

Smoking and alpha-1-antitrypsin deficiency

48
Q

What is the reversible component of COPD?

A

Smooth muscle tone and inflammation

49
Q

What disease is the main cause of COPD?

A

Emphysema (loss of alveolar walls) which is irreversible

50
Q

Why is the loss of alveolar walls irreversible?

A

We cannot grow new lung tissue

51
Q

What keeps bronchioles open?

A

There attachment to alveolar walls, so when the walls are lost they close during the process of breathing out

52
Q

When do bronchioles close once alveolar walls are lost?

A

During expiration

53
Q

What are the 2 kinds of respiratory failure?

A

Type 1 (PaO2 < 8kPa)

Type 2 (PaCO2 > 6.5kPa)

54
Q

What are the 4 abnormal states associated with hypoxia?

A

Ventilation/perfusion imbalance (V/Q, airway obstruction)

Diffusion impairment (lost of alveolar surface area)

Alveolar hypoventilation (reduced respiratory drive)

Shunt (only during acute infective exacerbation)

55
Q

What cause ventilation/perfusion imbalance?

A

Airway obstruction

56
Q

What causes diffusion impairment?

A

Loss of alveolar surface area

57
Q

What causes alveolar hypoventilation?

A

Reduced respiratory drive

58
Q

What is hypoxia during pneumonia caused due to?

A

Ventilation/perfusion mismatch (some ventilation but not enough from abnormal alveoli)

Shunt (no ventilation of abnormal alveoli)

59
Q

What kinds of pneumonia is hypoxaemia caused by ventilation/perfusion mismatch?

A

Bronchitis/bronchopneumonia

60
Q

What kinds of pneumonia is hypoxaemia caused by shunt?

A

Severe bronchopneumonia

Lobar patterns with large areas of consolidation

61
Q

What is the most common cause of hypoaemia?

A

Low ventilation/perfusion ratio

62
Q

What does hypoxaemia due to low V/Q respond well to?

A

Increasing FIO2

63
Q

What is shunt?

A

Blood passing from right to the left of the heart without contacting ventilated alveoli

64
Q

How do large shunts respond to increasing FIO2?

A

Poorly because the blood leaving the normal lung is already 98% saturated

65
Q

How does alveolar hypoventilation affect PA and Pa of O2 and CO2?

A

Increases PACO2 and so increases PaCO2

An increase in PACO2 decreased PAO2, which causes PaO2 to fall

Fall in PaO2 corrected by increasing FIO2

66
Q

What does FIO2 stand for?

A

Fraction of inspired air which is oxygen

67
Q

What are some pulmonary vascular changes in hypoxia?

A

Physiological: pulmonary arteriolar vasocontriction (when oxygen tension falls, can be localised effect, all vessels constrict if there is hypoxaemia)

Protective mechanism: (do not send blood to alveoli short of oxygen)

68
Q

What happens to all vessels during hypoxaemia?

A

They all constrict

69
Q

What is chronic cor pulmonale?

A

Hypertrophy of the right ventricle resulting from disease affecting the function and/or the structure of the lung (except where pulmonary alterations are the result of disease primary affecting the left side of the heart or congenital heart disease)

70
Q

What should a normal right ventricle weigh?

A

Less than 70g

71
Q

Why does the right ventricle weigh more than normal in cor pulmonale?

A

Due to having to work harder to pump blood to the rest of the body against greater resistance

72
Q

What does cor pulmonale lead to?

A

pulmonary hypertension

73
Q

Why does cor pulmonale lead to pulmonary hypertension?

A

Pulmonary vasocontriction

Muscle hypertrophy and intimal fibrosis of pulmonary arterioles

Loss of capillary bed

Secondary polycythaemia

Medicine 1 Respiratory (20 decks)

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