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RESP - 1 > Obstructive Airway Disease > Flashcards

Obstructive Airway Disease Flashcards

1
Q

What diseases or conditions may be mistaken for obstructive airway diseases?

A

Tumours, FBs, chronic scarring, bronchiectasis, TB etc are associated with obstruction of a large airway = local obstruction. These are not primarily obstructive diseases.

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2
Q

What are the three big OADs?

A

Chronic bronchitis
Emphysema
Asthma

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3
Q

What is COPD?

A

Chronic bronchitis and emphysema.
(chronic obstructive pulmonary disease)

CB and E almost always go together. Few genetic conditions where only E.

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4
Q

What are FEV1 and FVC and how can they be used to test lung function?

A

FEV1 - forced expiratory volume of air exiting lungs in first second after taking deep breath in and trying to blow as much air out as quickly as possible.

FVC = forced vital capacity.

FEV/FVC normally = 70-80%.

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5
Q

What are the norm values for FEV1, FVC and FEV1/FVC?

A

FEV1 = 3.5-4L
FVC = 5L
FEV1:FVC - 0.7/0.8

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6
Q

How can spirometry be used to measure lung function?

A

Can determine FEV1, FVC and compare to predicted.

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7
Q

What are your predicted values based on?

A

Age, sex, height.

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8
Q

Obstructive lung disease may also be demonstrated by PEFR, what is this?

A 
Peak expiratory flow rate (PEFR). 
50-80% of best is moderate fall. 
<50% of best is marked fall.
80-100% of best best value = normal. 
Normal 400-600 L/min
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9
Q

What is the key thing about obstructive lung disease?

A

There is airflow limitation.

Meaning PEFR and FEV1 are 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 hypersensivity in the airways.
Airways obstructed by inflammation (degranulation of mast cells). Constriction of smooth muscle around airways, overproduction of mucus –> narrowing of airways and airway irritation.
Reverses in time and as a result of medication. (inflammation also modified by drugs)

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11
Q

What are the aetiologies of COPD?

A

Smoking, atmospheric pollution, dust.
As age increases susceptibility increases.
More prevalent in men.
Increasing prevalence in developing countries.

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12
Q

What is a rare cause of emphysema?

A

Alpha-1-antiprotease (antitrypsin) deficiency is an extremely rare genetic cause.

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13
Q

Describe the effect of age and smoking on lung function.

A

In 20s have optimum lung function, as age increases lung function decreases. Non-smoker/not susceptible to smoke lung function decreases at a very slow rate, and they should never really experience lung problems.

Smoker’s lung function will decrease v. rapidly, and they will experience lung problems at a younger age.

If you manage to stop smoking in mid 40s then rate of decline returns to normal, damage will not be repaired but lung function will not deteriorate as quickly.

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14
Q

Define chronic bronchitis clinically?

A

Cough productive of sputum most days, in at least 3 consecutive months for 2 or more consecutive years.
EXCLUDES TB, bronchiectasis etc.

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15
Q

What is complicated chronic bronchitis?

A

When mucopurulent (yellow/green mucus) (acute infective exacerbation) or FEV1 falls.

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16
Q

Describe the morphological changes in the large airways in chronic bronchitis.

A

Mucous gland hyperplasia.
Goblet cell hyperplasia.
Inflammation and fibrosis is a minor component.

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17
Q

Describe the morphological changes in the small airways in chronic bronchitis.

A

Goblet cells appear.
Inflammation and fibrosis in long standing disease.
= airways narrower, lumen smaller –> airflow limitation.

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18
Q

What is the pathological definition of emphysema?

A

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

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19
Q

What is an acinus?

A

Respiratory bronchioles and alveoli.

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20
Q

What are the different forms of emphysema?

A 
Centriacinar
Panacinar
Periacinar
Scar - irregular
Bullous emphysema
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21
Q

Which area is most susceptible to emphysema and why?

A

Centriacinar - this is where material is deposited as it’s where laminar flow changes to gas exchange - the region where inflammation and irritation is max

22
Q

What part of the lung is most affected in centriacinar emphysema?

A

Apex of upper lobe or whole lobe. Clearance mechanisms better in lower lobe as better blood supply. Clearance dependent on alveolar macrophages.

23
Q

Where does panacinar emphysema affect?

A

The whole lung, lower regions mostly. Gas exchange area destroyed and just left with vessels suspended in middle of space.

24
Q

Where does periacinar emphysema affect?

A

Loss of tissue at edge of acinus. Particular in acini that are up against the pleura (end up with spaces under the pleura). Generally don’t cause anything until they burst = pneumothorax.

25
Q

What is a bulla?

A

Emphysematous space greater than 1cm.

26
Q

What is a bleb?

A

Space just under the pleura.

27
Q

What are the aetiologies of emphysema?

A

Smoking –> protease-antiprotenase imbalance.
Ageing
Alpha-1-antitrypsin deficiency.

28
Q

Describe results from damage in a normal individual.

A

Inflammation results in release of elastase from neutrophils and macrophages which are supposed to kill bacteria/FB but also start to dissolve own tissue so obv want to stop that. System of anti-elastase and anti-proteases balances this. Repair mechanisms aren’t great once we’ve already lost the alveolar frame work. Normally this is all kept in check though.

29
Q

Describe what happens in alpha-1-antitrypsin deficiency.

A

Anti-elastases aren’t produced as needed and so elastase not kept in check and this leads to tissue destruction which can’t be fixed by the repair mechanisms in the lung –> emphysema.

30
Q

How does smoking lead to emphysema?

A

Smoking leads to decreased repair mechanisms, increased neutrophils and macrophages leading to increase elastase production. It also decreases anti-elastase production. Overall leading to lots of tissue destruction and emphysema.

31
Q

Is airway obstruction in COPD reversible?

A

Traditionally considered irreversible. But not entirely true. There may be a reversible component. May be an element of airflow limitation (in CB) that can be reversed by same drugs used to treat asthma. Most obstruction not reversible.

32
Q

What parts of the airway obstruction in COPD respond to pharmacological intervention?

A

Smooth muscle tone and inflammation.

33
Q

Why is their partial collapse of the airway wall on expiration?

A

Loss of alveolar attachments due to emphysema.

34
Q

Why do patients with emphysema take half breaths?

A

The radial pull of the attached alveolar walls around the thin floppy airways act like guy ropes pulling it open. If you lose these walls (as in centriacinar emphysema), the alveoli collapse. Small airways become floppy and can’t stop open enough for a normal breath.
Half breaths keep the airways open.

35
Q

What are the two types of respiratory failure?

A

Type 1 - PaO2 <8kPa (PaCO2 normal or low)

Type 2 PaCO2 >6.5kPa (PaO2 usually low).

36
Q

What are the four abnormal states associated with hypoxaemia?

A

Ventilation/perfusion imbalance (V/Q), e.g. airway obstruction
Diffusion impairment, e.g. loss of alveolar surface
Alveolar hypoventilation, e.g. reduced respiratory drive
Shunt, e.g. only during AIE, 0 ventilation in area of tissue.

37
Q

Give an example of when you might get a ventilation/perfusion abnormality (mismatch).

A

Bronchitis

Bronchopneumonia.

38
Q

Give an example of when you may get shunt.

A

Severe bronchopneumonia

Lobar pattern with large areas of consolidation.

39
Q

What is normal V/Q?

A

Normally breath about 4L/min, CO about 5L/min so V/Q = 4/5 or 0.8.

40
Q

What is the commonest cause of hypoxaemia encountered clinically?

A

Low V/Q.

41
Q

How do you treat hypoxia associated with low V/Q?

A

It responds v well to even small increases in FIO2.

42
Q

How do V/Q mismatch and shunt differ?

A

Some ventilation of abnormal alveoli, just not enough in V/Q mismatch, in shunt no ventilation of abnormal alveoli.

43
Q

What is shunt?

A

Blood passing from the R to L side of heart without contacting ventilated alveoli. Normally 2-4% shunt.
Pathological shunt in AV malformations, congenital heart disease and pulmonary disease.

44
Q

Do you give oxygen with shunt?

A

Might give oxygen to make them feel better, but it won’t actually help the shunt as blood leaving normal lung is already 98% saturated.

45
Q

What does alveolar hypoventilation do?

A

Increases PACO2 and thus increases PaCO2. Increase in PACO2 decreases PAO2 which causes PaO2 to fall.

46
Q

How do you correct alveolar hypoventilation?

A

Corrected by raising FIO2.

47
Q

What patients commonly get alveolar hypoventilation?

A

COPD patients as they are used to chronically high levels of CO2 and they just become used to this and rely on hypoxic drive to breathe. So if you treat them with oxygen will lose drive to breath.

48
Q

What happens to pulmonary vessels during hypoxia?

A

Physiological pulmonary arteriolar vasoconstriction when alveolar oxygen tension falls, can be localised effect. All vessels constrict if there is hypoxaemia.

49
Q

What is the purpose of vasoconstriction of pulmonary vessels during hypoxia?

A

Protective mechanism. Don’t send blood to alveoli short of oxygen.

50
Q

What is chronic (hypoxic) Cor pulmonale?

A

Hypertrophy of the right ventricle resulting from disease affecting the function and/or structure of the lung, except where pulmonary alterations are the result of diseases primarily affecting the left side of the heart or congenital heart disease.

RESP - 1 (27 decks)

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