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Respiratory system > Obstructive Airway Disease > Flashcards

Obstructive Airway Disease Flashcards

1
Q

name three obstructive airway diseases

A

asthma, emphysema, chronic bronchitis

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2
Q

what two diseases make up copd?

A

emphysema and bronchitis

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3
Q

what is the normal ration of FEV1/FVC?

A

70%-80%

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4
Q

how is peak expiratory flow measured?

A

with a peak expiratory flow meter, it is measured during forced expiration

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5
Q

how hoes obstructive lung disease affect spirometry readings?

A

FEV1 : volume of air exiting the lung in the first second is reduced
FVC: total amount expired may be reduced
the ratio FEV1/FVC is less than 70%

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6
Q

what would an asthmatics spirometry readings look like?

A

they would look normal unless they were having an attack when the readings took place

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7
Q

what causes the hypersensitivity in airways?

A

mast cell degranulation caused by many factors such as drugs, chemicals, stress, colds e.c.t

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8
Q

what chemotactic factors create bronchial hyperreactivity?

A 
> histamine
> lysosomal enzymes
> microthrombi
> complement prostaglandins
>major basic proteins
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9
Q

what causes smooth muscle contraction in asthma?

A

inflammation caused by mast cell degranulation

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10
Q

what is the aetiology of chronic bronchitis and emphysema?

A 
> smoking
> atmospheric pollution
> occupation (dust)
> alpha-1-antiprotease deficiency (only for emphysema)
> age
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11
Q

over what sort of time span would a cough suggest COPD?

A

most days in 3 consecutive months for 2 or more consecutive years.

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12
Q

describe the morphological changes in large airways in COPD?

A

> hyperplasia of mucous glands
hyperplasia of goblet cells
increased number of goblet cells

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13
Q

what are the morphological changes in small airways in COPD?

A

> goblet cells appear

> inflammation and fibrosis (in long standing disease)

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14
Q

what is the terminal bronchi?

A

this is the last conducting airway and is a sub millimetre in diameter

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15
Q

what does emphysema do to the lung?

A

this destroys the walls in the alveoli, increasing the size of airspace distal to the terminal bronchiole therefore decreasing the surface area for which diffusion can occur.

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16
Q

describe the pattern of centriacinar emphysema

A

the alveolar walls immediately surrounding the terminal bronchioles are degraded. this is seen at the apex of the upper lobes due to decreased blood flow leading to ineffective clearing.

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17
Q

what areas of the lungs does panacinar emphysema affect?

A

the lower regions of the lungs, here huge areas of lung tissue are destroyed

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18
Q

a patient has a emphysemas space greater than a centimetre at the edge of their lung. how is this described and what sort f emphysema is this?

A

this space is a bleb or a bulla and is found in periacinar emphysema

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19
Q

how does alpha-1-antitrypsin deficiency lead to emphysema?

A

in alpha-1-antitrypsin deficiency the anti-proteases are absent leading to an increase in elastase (proteases), produced by neutrophils, which causes tissue destruction = emphysema

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20
Q

how does smoking lead to emphysema?

A

smoking decreases anti-elastases (anti-proteases), increases neutrophils, increases elastases (proteases) and decreases the work of the repair mechanism elastin system. this all leads to tissue destruction = emphysema.

21
Q

why in emphysema patients do they often only breath with half their lung?

A

since the alveoli are collapsing the body retains air in the lungs so small airways do not collapse on expiration.

22
Q

what, roughly, is the total prevalence of COPD in the UK?

A

1.5-2 million

23
Q

what social factors affect COPD?

A

education and household income:

higher education and household income decrease the prevalence of COPD.

24
Q

how many people in the uk die of COPD a year?

A

30,000 people

25
Q

is COPD higher in men or women?

A

men

26
Q

give some examples of jobs that could lead to COPD

A

coal mining, hard rock mining, baker, farming, plastics, leather, rubber, tunnel working

27
Q

what is the troublesome genotype in alpha-1-antitripsin?

A

PiZZ, it is found in 0.03% of the population

28
Q

what percentage of smokers develop airflow obstruction?

A

20% develop clinically significant COPD
30% develop significant but subclinical airflow obstruction
50% never develop airflow obstruction

29
Q

does the total tobacco consumption affect the rate at which COPD is developed?

A

yup, and by stopping smoking the damage is not reversed but it can be stopped

30
Q

describe breathlessness in COPD

A

there is a gradual onset with little variation starts with just exertion like stair and hills then worsens to walking on the flat with contemporaries then at rest.

31
Q

what sort of cough would you expect in someone with COPD?

A

there would be a long history of cough that brings up clear/mucoid sputum. it is present all day or year with little variability.

32
Q

what might be seen in the past medical history of a patient with COPD?

A

> asthma as a child
respiratory diseases
ischaemic heart disease

33
Q

what signs of COPD would you expect to see on examination of the hands?

A

> peripheral cyanosis (white nail beds)

> tremor or CO2 flap

34
Q

what signs of COPD would be seen on examination of the chest and head?

A 
> pursed lip breathing
> use of accessory muscles
> hyperexpanded barrel chest
> paradoxical movement of the ribs and abdomen
> prolonged expiration
35
Q

on percussion and auscultation of the chest what would you hear if the patient had COPD?

A

> decrease cardiac dullness to percussion
decrease in breath sounds
no crackles

36
Q

what signs would suggest a Cor Pulmonale?

A

> an elevated JVP (jugular venous pressure)
hepatomegaly (enlargement of the liver)
ascites (build up of fluids between the two layers of the peritoneum, membrane that lines the abdomen)
oedema

37
Q

what essential investigations would you carry out on a patient that you suspect has COPD?

A

> spirometry to demonstrate airflow obstruction (FEV1/FVC ratio is less than 70%)
full pulmonary function test
gas trapping, to look at the lung volumes
carbon monoxide gas transfer

38
Q

if the patient has COPD how would you expect the CO gas transfer test to go?

A

there would be decreased gas transfer, decreased tissue destruction and decreased transfer factor of the lung for carbon monoxide

39
Q

what would the results of a gas trapping test be if the patient had COPD?

A

there should be an increased residual volume and total lung capacity

40
Q

what drugs would you use to show that there was fixed airflow with spirometry?

A

> bronchodilator: 15 minutes post neb 2.5-2mg salbutamol. 30 minutes post neb 2.5-5mg salbutamol + 500ug ipratropium
oral corticosteroids: 30-40mg prednisolone daily for 2 weeks.

41
Q

what would you expect a chest radiograph of a COPD patient to look like?

A

> hyperinflated lung fields
flattened diaphragms
bullae

42
Q

what can precipitate an exacerbation of COPD?

A

> viral/ bacterial infection
sedative drugs
pneumothorax
trauma

43
Q

describe some non-respiratory problems that arise form COPD

A

> COPD can cause separation of various protein factors.
there is loss of muscle mass as not enough energy goes to muscles which become deconditioned.
patients are prone to cardiac conditions especially if they are hypoxic.
weight loss occurs
depression and anxiety

44
Q

what non-pharmacological management could you provide to a patient with COPD?

A

> smoking cessation
nutritional support
psychological support
pulmonary rehabilitation - exercise

45
Q

name some short acting bronchodilators

A

> SABA, salbutamol

> SAMA, ipratropium

46
Q

name some long lasting bronchodilators

A

> LAMA (long acting anti-muscarinic agents), umeclidium and tioptropium
LABA (long acting beta 2 agonists), salmeterol

47
Q

name some high dose inhaled corticosteriods

A

ICS and LABA, fluticasone/vilanterol

48
Q

when is long term oxygen given to COPD patients?

A

> in patients with Pa02 less than 7.3kPa
where their PaO2 is between 7.3kPa and 8kPa and there is; polycythaemia, nocturnal hypoxia, peripheral hypoxia, peripheral oedema or pulmonary hypertension.

49
Q

what management would you consider for an exacerbation of a COPD patient?

A

> short acting bronchodilators (salbutamol)
steroids (prednisolone 40mg a day for 5-7 days)
antibiotics, if there is evidence of infection
hospital admission if there is: tachypneoa, low o2 saturation, hypotension

Respiratory system (19 decks)

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