18. Obstructive and restrictive lung disease Flashcards Preview

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Flashcards in 18. Obstructive and restrictive lung disease Deck (39):
1

What is the 'tidal volume'?

This is the amount of air that enters the lung during normal inhalation at rest
The same amount leaves the lung during exhalation

2

What is the normal value for tidal volume?

500ml

3

What are the inspiratory and expiratory reserve volumes and how do these differ to one another?

'Inspiratory reserve volume' - maximum level of air that can be drawn into the lungs upon force

Expiratory reserve volume - the addition level of air that can be forced from the lungs

The expiratory reserve volume is less than the inspiratory reserve volume

4

What is the 'vital capacity'?

The greatest volume of air that can be expelled from the lungs after taking the deepest possible breath

Vital capacity = tidal volume + inspiratory reserve volume + expiratory reserve volume

5

What is the 'functional residual capacity'?

The volume of air present in the lungs at the end of passive expiration

This consists of the expiratory reserve volume and the residual volume

6

What is the 'residual volume'?

The volume of air still in the lungs after the most forcible expiration possible i.e. referring to the anatomical dead space

This occurs because of the trachea which has cartilage meaning that it will not collapse and hence will maintain some air within

7

What is the total lung capacity?

Tidal volume + inspiratory reserve volume + expiratory reserve volume + residual volume OR

Vital capacity + residual volume

8

How can you analyse an obstructive disease?

The best way is via peak flow
Peak expiratory flow rate (PEFR) - person's maximum speed of expiration as measured with a peak flow metre

9

How does the peak flow rate vary during the day and why is this useful?

Varies between morning and evening - lowest in the morning and highest in the evening

The worse someone's asthma is, the greater the change is between the morning and the evening peak flow rate

10

What is a vitalograph and why is it used? (NEED TO KNOW)

This is an electric peak flow metre - as well as measuring the peak flow, also measures the flow as a function of time and provides you with a volume

SO provides you with someone's forced expiratory volume (FEV1)

11

What is FEV1?

Forced expiratory volume - the total volume of air that can be exhaled from the lungs after taking the deepest breath possible i.e. FEV1 + FEV2 + FEV3

FEV2 - in the second second

FEV 3 - in the third second

12

What is FVC?

Forced vital capacity - the volume of air that a person can breath out during a forced breath in the first second

13

What is the relevance of the FEV1/FVC ratio and why is this particularly useful and used ?

Using a vitalograph, can calculate the ratio between how much you breath out in the first second compared to the forced vital capacity
This is useful because it allows patients to be compared against each other regardless of whether they are small/big/male/female etc.

14

What is the difference between obstructive and restrictive diseases?

Obstructive - the lungs can still inflate as much as they ought to but there is an obstruction of the airways

Restrictive - the lungs cannot inflate as much as they ought to

15

How can the FEV1/FVC ratio signify the presence of an obstructive disease?

In an obstructive disease, the FEV1/FVC ratio will be reduced - FVC normal but FEV1 value reduced

SO takes longer to expel this same volume of air due to e.g. narrowed airways

16

How can the FEV1/FVC ratio signify the presence of a restrictive disease?

The FEV1 value and the FVC value will both be reduced SO the FEV1/FVC ratio in total will not be decreased and is normal OR can even be slightly increased

17

SO how can you recognise a restrictive lung disease from investigations?

A key feature of restrictive lung diseases will be a reduced vital capacity

18

What are the main obstructive diseases?

Asthma and COPD

19

What is asthma?

REVERSIBLE airway obstruction often arising from atopic stimuli (allergens)

20

Briefly describe asthma

Asthma patients have smaller airways
Have hyper-responsiveness - airways will constrict to many more stimuli compared to other individuals
Can lead to other allergic conditions such as skin inflammatory reactions - get skin reactions to irritants much more vigorously

21

What are the main features of asthma?

Bronchoconstriction
Secretion of mucous
Airway inflammation

22

What is the pathophysiologicaly of the immediate response to allergens in asthma?

In asthma, there are oversupplied IgE receptors which hence provoke a response where it would not in an non-asthmatic
So the inhaled allergens bind to IgE on mast cells
The mast cells then degranulate and release inflammatory mediators e.g. histamines
The histamine mediates immediate bronchoconstriction which stimulates mucous secretion - this repeatedly happens in asthmatics and encourages eosinophils to invade into the blood

23

What is the pathophysiology of the delayed response to allergens in asthma?

There are many eosinophils presnet in the lungs - these are activated by the mast cells
These discharge proteins that cause damage to the epithelial cells i.e. the lining of the bronchioles and these damaged cells release factors which stimulate afferent nerves for pain
These afferent nerves reflexively stimulate bronchoconstriction

SO there is direct bronchoconstriction from the histamines and then also bronchoconstriction from the reflex SO there is a much more powerful bronchoconstrictor respone

24

Why do asthmatics have an excess mucous level causing increased coughing?

Due to the damaged epithelium, there are less cells with cilia and so the mucous cannot be transported as efficiently and accumulates in the bronchioles - SO much more stagnant mucous which decreases the lumen of the airways
This mucous often contains bacteria - increased presence of bacteria will mean that there are more chances of a lung infection

25

What substances can trigger asthma?

Air pollutants e.g. dusts, smoke, mists, fumes
Pollens, mites, molds
Animal fur
Medications
Foods

26

What are the symptoms of asthma?

Troublesome cough - particularly at night or after physical activity
Breathing problems during particular seasons
Coughing, wheezing, chest tightness following exposure to allergen
Colds that last more than 10 days

27

What are the signs of asthma?

Wheezing sounds during normal breathing
Hyperexpansion of the thorax
Atopic dermatitis, eczema or other allergic skin conditions

28

How can asthma be diagnosed?

Spirometry is key - particularly the peak flow and FEV1/FVC ratio

29

What long term medication can be taken to treat asthma?

Inhaled corticosteroids
Long acting beta 2 agonists
Leukotriene modifiers

30

What short term medication can be used to treat asthma?

Short acting beta 2 agonists to be used in acute episodes

31

What is the action of beta 2 agonists?

Relaxes the bronchial smooth muscle e.g. salbutamol

32

What are the roles of spacers and nebulisers to treat asthma?

Puffers can be very hard to use efficiently - the powder can gets stuck at the back of the throat SO spacers are more commonly used - increase the quantity of the drug that enters the lungs and hence reduces the amount that is lost

Nebulisers - machines that produce an inhaled mist of children - for small children or for severe asthma attacks

33

What is COPD composed of?

COPD is a combination of chronic bronchitis and emphysema

34

What is chronic bronchitis?

Inflammation of the bronchi or the bronchioles causing damaged epithelium and proliferation of squamous cells - resulting the in the production of excess mucous and a chronic cough

After a while, this inflammation results in hypertrophy of the bronchiole mucous secreting glands

There is an increased level of bacteria containing mucous and this can result in increased infections

35

What is emphysema?

Destruction of the walls of the alveoli leading to enlargement of the alveolar air spaces to form bullae
Particular occurs due to cigarette smoking

36

Give the pathophysiology of emphysema

Cigarette smoke stimulates neutrophils
The neutrophils release enzymes which breakdown elastin - serum elastase
The enzyme destruction leads to loss of the wall fo the alveoli
Action of elastase is usually controlled by alpha-1-anti-tripsin which generally protects the walls against elastase but the cigarette smoke inativates the inhibitor

SO cigarette smoke both stimulates the release of elastase AND inhibits the action of the inhibitor - much greater level of damage to the alveolar walls

37

What is the normal role of serum elastase?

Serum elastase is usually used to break down the wall of the alveoli if require to remove a pocket of infection

38

What different restrictive disorders are there and why?

Pneumonia, pneumothorax, pulmonary fibrosis - loss of volume for air to fill so cannot take up as much O2

Pleural thickening or neuromuscular weakness - cannot expand or contract the lung so the lung cannot inflate as effectively

39

What is a flow volume loop?

Shows flow against volume rather than against time
Shows PEF - peak expiratory flow

RECOGNISE THE DIFFERENT TYPES OF THESE - YEAR 1