Obstructive airway diseases

Question 1

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?

Answer 1

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

Question 2

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

Answer 2

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

Question 3

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

Answer 3

the most important component is airway obstruction

Question 4

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

Answer 4

no

Question 5

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

Answer 5

spirometry and peak flow

Question 6

what is the normal value for FEV1?

Answer 6

3,5-4L

Question 7

what is the normal value for FVC?

Answer 7

5L

Question 8

what is the normal value for FEV1/FVC?

Answer 8

0,7-0,8

Question 9

what factors does a predicted FVC rely on?

Answer 9

predicted FVC is based on age, sex, height

Question 10

what is the normal value for a peak flow?

Answer 10

400-600L/min

Question 11

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

Answer 11

80-100% of best value

Question 12

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

Answer 12

50-80% of best value

Question 13

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

Answer 13

<50% of best value

Question 14

what are the main feature of obstructive lung disease?

Answer 14

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

Question 15

what are chronic bronchitis and emphysema better known as?

Answer 15

Chronic Obstructive Pulmonary Disease - COPD (COAD or COLD)

Question 16

what is the main reason for bronchial asthma?

Answer 16

type 1 hypersensitivity in the airways

Question 17

why would the mast cells degranulate and cause the inflammation?

Answer 17

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

Question 18

how are asthma airways and chronic asthma airways different?

Answer 18

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

Question 19

is bronchial asthma a reversible airway obstruction?

Answer 19

yes

Question 20

how can bronchial asthma be reversed?

Answer 20

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

Question 21

what is the common aetiology of chronic bronchitis and emphysema?

Answer 21

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

Question 22

which deficiency is an extremely rare cause of emphysema?

Answer 22

alpha-1-antiprotease (antitrypsin)

Question 23

what is the clinical definition of chronic bronchitis?

Answer 23

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

Question 24

what does chronic bronchitis diagnosis exclude?

Answer 24

TB, bronchiectasis

Question 25

what may chronic bronchitis diagnosis may be confused with?

Answer 25

asthma

Question 26

what is a 'complicated' chronic bronchitis?

Answer 26

when mucopurulent (acute infective exacerbation) or FEV1 falls

Question 27

what morphological changes are there in large airways?

Answer 27

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

Question 28

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

Answer 28

Goblet cells appear, inflammation and fibrosis in long standing disease

Question 29

what is the pathological definition of emphysema?

Answer 29

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

Question 30

what are the different forms of emphysema?

Answer 30

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

Question 31

what are the steps of centri-acinar emphysema?

Answer 31

begins with bronchiolar dilatation, then alveolar tissue is lost

Question 32

what are the characteristics of centri-acinar?

Answer 32

bigger airways, loss of alveolar tissue

Question 33

what are the characteristics of pan-acinar?

Answer 33

loss of alveolar tissue (less alveoli)

Question 34

what is a periacinar/ scar emphysema/ bullous emphysema?

Answer 34

emphysematous space greater than 1cm

Question 35

what does smoking cause?

Answer 35

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

Question 36

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

Answer 36

anti-elastase

Question 37

what happens when there is too much neutrophils and macrophages?

Answer 37

too much elastase is produced

Question 38

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

Answer 38

tissue destruction and therefore emphysema

Question 39

is airway obstruction in chronic bronchitis and emphysema reversible?

Answer 39

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

Question 40

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

Answer 40

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)

Question 41

what is the normal value of PO2?

Answer 41

10,5-13,5kPa

Question 42

what is the normal value of PCO2?

Answer 42

4,8-6,0kPa

Question 43

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

Answer 43

PO2 < 8 kPa (PCO2 usually normal or low)

Question 44

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

Answer 44

PCO2 > 6,5 kPa (PO2 usually low)

Question 45

what is hypoxaemia?

Answer 45

low concentration of oxygen in the blood

Question 46

what four abnormal states are associated with hypoxaemia?

Answer 46

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

Question 47

why do you get hypoxaemia during COPD?

Answer 47

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

Question 48

why do you get hypoxaemia in pneumonia?

Answer 48

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)

Question 49

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

Answer 49

4L/min

Question 50

what is the normal cardiac output?

Answer 50

5L/min

Question 51

what is the normal V/Q?

Answer 51

4/5 or 0,8

Question 52

what does low V/Q translate as?

Answer 52

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

Question 53

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

Answer 53

due to local alveolar hypoventilation or some focal disease

Question 54

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

Answer 54

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

Question 55

what is a shunt?

Answer 55

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

Question 56

what is the percentage of shunt blood?

Answer 56

2-4%

Question 57

when can there be a pathological shunt?

Answer 57

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

Question 58

how well do large shunts respond to increases in FIO2?

Answer 58

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

Question 59

how are falls in PO2 due to hypoventilation corrected?

Answer 59

raise in FIO2

Question 60

why is shunt a protective mechanism?

Answer 60

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

Question 61

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

Answer 61

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

Question 62

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

Answer 62

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

Question 63

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

Answer 63

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

Question 64

how much does the normal 'free' right ventricle weigh?

Answer 64

<70g

Question 65

how much does the hypertrophied 'free' right ventricle weigh?

Answer 65

more (ex: 165g)

Question 66

why is hypoxic cor pulmonale linked to pulmonary hypertension?

Answer 66

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