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S2 Respiratory System > Obstructive airway diseases > Flashcards

Obstructive airway diseases Flashcards

1
Q

what characteristic is shared by lung cancer, other tumours, inhaled foreign bodies, chronic scarring diseases like bronchiectasis and secondary tuberculosis associated with obstruction of large airway?

A

they are localised obstruction of the airways (most likely the large airways)

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2
Q

is it possible to have generalised obstruction of the airways? which part of the airway do they affect?

A

yes, but they are rare, they affect the small airways (bronchiolar)

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3
Q

what is the most component of chronic bronchitis, emphysema and asthma?

A

the most important component is airway obstruction

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4
Q

do chronic bronchitis, emphysema, asthma have the same mechanism for obstruction?

A

no

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5
Q

what 2 test can be used to demonstrate obstructive lung disease?

A

spirometry and peak flow

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6
Q

what is the normal value for FEV1?

A

3,5-4L

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7
Q

what is the normal value for FVC?

A

5L

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8
Q

what is the normal value for FEV1/FVC?

A

0,7-0,8

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9
Q

what factors does a predicted FVC rely on?

A

predicted FVC is based on age, sex, height

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10
Q

what is the normal value for a peak flow?

A

400-600L/min

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11
Q

what is the normal range for peak expiratory flow rate (PEFR)?

A

80-100% of best value

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12
Q

what is the value of a moderate fall for peak expiratory flow rate (PEFR)?

A

50-80% of best value

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13
Q

what is the value of a marked fall for peak expiratory flow rate (PEFR)?

A

<50% of best value

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14
Q

what are the main feature of obstructive lung disease?

A

airflow limitation, PEFR reduced, FEV1 reduced, FVC possibly reduced, FEV1 less than 70% of FVC

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15
Q

what are chronic bronchitis and emphysema better known as?

A

Chronic Obstructive Pulmonary Disease - COPD (COAD or COLD)

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16
Q

what is the main reason for bronchial asthma?

A

type 1 hypersensitivity in the airways

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17
Q

why would the mast cells degranulate and cause the inflammation?

A

because of specific IgE, drugs, chemicals, ‘stress’, cold

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18
Q

how are asthma airways and chronic asthma airways different?

A

chronic asthma airways have mucus, plasma exudation, epithelial shedding/damage, more inflammation, all of which makes it even more difficult for the air to pass

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19
Q

is bronchial asthma a reversible airway obstruction?

A

yes

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20
Q

how can bronchial asthma be reversed?

A

by drugs, medical intervention or spontaneously (bronchial smooth muscle contraction and inflammation can be modified by drugs)

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21
Q

what is the common aetiology of chronic bronchitis and emphysema?

A

smoking, atmospheric pollution, dust, effect of age and susceptibility, prevalence (men > women but.. increasing in developing countries)

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22
Q

which deficiency is an extremely rare cause of emphysema?

A

alpha-1-antiprotease (antitrypsin)

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23
Q

what is the clinical definition of chronic bronchitis?

A

cough productive sputum most days in at least 3 consecutive months for 2 or more consecutive years

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24
Q

what does chronic bronchitis diagnosis exclude?

A

TB, bronchiectasis

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25
Q

what may chronic bronchitis diagnosis may be confused with?

A

asthma

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26
Q

what is a ‘complicated’ chronic bronchitis?

A

when mucopurulent (acute infective exacerbation) or FEV1 falls

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27
Q

what morphological changes are there in large airways?

A

mucous gland hyperplasia, Goblet cell hyperplasia, (inflammation and fibrosis is a minor component)

28
Q

what morphological changes are there in small airways? (when chronic bronchitis takes place)

A

Goblet cells appear, inflammation and fibrosis in long standing disease

29
Q

what is the pathological definition of emphysema?

A

increase beyond the normal in the size of airspaces distal to the terminal bronchial arising either from dilatation or from destruction of their walls and without obvious fibrosis

30
Q

what are the different forms of emphysema?

A

centriacinar, panacinar, periacinar - scar (irregular, bullous emphysema)

31
Q

what are the steps of centri-acinar emphysema?

A

begins with bronchiolar dilatation, then alveolar tissue is lost

32
Q

what are the characteristics of centri-acinar?

A

bigger airways, loss of alveolar tissue

33
Q

what are the characteristics of pan-acinar?

A

loss of alveolar tissue (less alveoli)

34
Q

what is a periacinar/ scar emphysema/ bullous emphysema?

A

emphysematous space greater than 1cm

35
Q

what does smoking cause?

A

protease-antiprotease imbalance (lack of anti-elastase, production of elastase, production of neutrophils and macrophages, lack of repair mechanisms and elastin synthesis)

36
Q

which protein is no longer produced in case of alpha-1-antitrypsin deficiency?

A

anti-elastase

37
Q

what happens when there is too much neutrophils and macrophages?

A

too much elastase is produced

38
Q

what happens when there is too much elastase, no anti-elastase to regulate it, too little repair mechanisms and too much elastin synthesis ?

A

tissue destruction and therefore emphysema

39
Q

is airway obstruction in chronic bronchitis and emphysema reversible?

A

traditional considered as no, there actually may be a reversible component

40
Q

does emphysema pathogenesis include partial collapse of airway wall on expiration?

A

yes, the loss of alveolar attachment (alveolar to main small airway) is most important and causes the airway wall to collapse (as it is held by the alveoli like a tent, the alveoli being it’s pegs)

41
Q

what is the normal value of PO2?

A

10,5-13,5kPa

42
Q

what is the normal value of PCO2?

A

4,8-6,0kPa

43
Q

what is the value of PO2 for a type 1 respiratory failure?

A

PO2 < 8 kPa (PCO2 usually normal or low)

44
Q

what is the value of PCO2 for a type 2 respiratory failure?

A

PCO2 > 6,5 kPa (PO2 usually low)

45
Q

what is hypoxaemia?

A

low concentration of oxygen in the blood

46
Q

what four abnormal states are associated with hypoxaemia?

A

ventilation/perfusion imbalance, diffusion impairment, alveolar hypoventilation, shunt

47
Q

why do you get hypoxaemia during COPD?

A

because all four abnormal states are present:

  • airway obstruction causes VENTILATION AND PERFUSION ABNORMALITY (MISMATCH)
  • reduced respiratory drive causes ALVEOLAR HYPOVENTILATION
  • loss of alveolar surface area causes DIFFUSION IMPAIRMENT
  • only during acute infective exacerbating causes SHUNT
48
Q

why do you get hypoxaemia in pneumonia?

A

2 abnormal states are present:

  • bronchitis/ bronchopneumonia cause MISMATCH (some ventilation of abnormal alveoli, just not enough)
  • severe bronchopneumonia and lobar pattern with large areas of consolidation cause SHUNT (no ventilation of abnormal alveoli)
49
Q

what is the normal volume of air breathed in during a minute?

A

4L/min

50
Q

what is the normal cardiac output?

A

5L/min

51
Q

what is the normal V/Q?

A

4/5 or 0,8

52
Q

what does low V/Q translate as?

A

hypoxaemia (low V/Q is the commonest cause of it)

53
Q

how could there be low V/Q in just some alveoli?

A

due to local alveolar hypoventilation or some focal disease

54
Q

how do you that hyoxaemia due to low V/Q?

A

slightly increase the fraction of inspired O2 (FIO2), the fraction of O2 which comes from an oxygen device

55
Q

what is a shunt?

A

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

56
Q

what is the percentage of shunt blood?

A

2-4%

57
Q

when can there be a pathological shunt?

A

when there is alveolar malformations, congenital heart disease and pulmonary disease

58
Q

how well do large shunts respond to increases in FIO2?

A

poorly, the blood leaving normal lung is already 98% saturated

59
Q

how are falls in PO2 due to hypoventilation corrected?

A

raise in FIO2

60
Q

why is shunt a protective mechanism?

A

the body does not want to send blood to alveoli short of oxygen

61
Q

how does the pulmonary circulation react to hypoxia? when is this localised? when does this concern all vessels?

A

vasoconstriction, can be localised except when there is hypoxaemia (then all vessels constrict)

62
Q

what disease results in hypertrophy of the right ventricle? what does this disease affect?

A

chronic (hypoxic) cor pulmonale, affects the function and/or the structure of the lung

63
Q

when is cor pulmonale not responsible for hypertrophy of the right ventricle?

A

when pulmonary alterations are the result of diseases primarily affecting the left side of the heart or congenital heart disease

64
Q

how much does the normal ‘free’ right ventricle weigh?

A

<70g

65
Q

how much does the hypertrophied ‘free’ right ventricle weigh?

A

more (ex: 165g)

66
Q

why is hypoxic cor pulmonale linked to pulmonary hypertension?

A

because there is pulmonary vasoconstriction, hypertrophy in pulmonary arterioles, loss of capillary bed, secondary polycythaemia (production of RBC) and bronchopulmonary arterial anastamoses

S2 Respiratory System (43 decks)

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