Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

the most important component is airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

spirometry and peak flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the normal value for FEV1?

A

3,5-4L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the normal value for FVC?

A

5L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the normal value for FEV1/FVC?

A

0,7-0,8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what factors does a predicted FVC rely on?

A

predicted FVC is based on age, sex, height

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the normal value for a peak flow?

A

400-600L/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

80-100% of best value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

50-80% of best value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

<50% of best value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are chronic bronchitis and emphysema better known as?

A

Chronic Obstructive Pulmonary Disease - COPD (COAD or COLD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the main reason for bronchial asthma?

A

type 1 hypersensitivity in the airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why would the mast cells degranulate and cause the inflammation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

is bronchial asthma a reversible airway obstruction?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which deficiency is an extremely rare cause of emphysema?

A

alpha-1-antiprotease (antitrypsin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does chronic bronchitis diagnosis exclude?

A

TB, bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what may chronic bronchitis diagnosis may be confused with?

A

asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is a ‘complicated’ chronic bronchitis?

A

when mucopurulent (acute infective exacerbation) or FEV1 falls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions