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Respiratory (Annie) > Lower respiratory tract diseases - COPD > Flashcards

Lower respiratory tract diseases - COPD Flashcards

1
Q

what does COPD stand for?

A

chronic OBSTRUCTIVE pulmonary disease

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2
Q

what is COPD?

A

= airflow limitation that is not fully reversible

  • airflow limitation is progressive & associated with an abnormal inflammatory response of the lungs to noxious particles or gases
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3
Q

what causes COPD?

A

long term exposure to toxic particles or gases

= SMOKING

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4
Q

is COPD referring to one singular condition or is it an overarching diagnosis?

A

it is an OVERARCHING DIAGNOSIS, brining together a variety of clinical syndromes associated with airflow limitation and destruction of lung parenchyma

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5
Q

what is the most consistent pathological finding in COPD?

A
  • increased numbers of mucus-secreting goblet cells in bronchial mucosa
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6
Q

what happens to the bronchi & lumen in more advanced cases of COPD?

A
  • bronchi becomes inflamed

- pus is seen in the lumen

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7
Q

what is seen microscopically to the walls of the bronchi and bronchioles?

A
  • walls of bronchi & bronchioles are infiltrated with acute & chronic INFLAMMATORY CELLS; e.g. lymphoid follicles
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8
Q

what follows inflammation?

IMPORTANT

A
  • scarring and thickening of the walls which narrows the airways
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9
Q

explain the balance between proteases and antiproteases?

A
  • noxious particles increase the number of proteinases
  • these are normally neutralised by anti-proteinase
  • but this increase in proteinase upsets the protienase-antiprotienase balance allowing proteinases to digest the lung tissue
  • effectively causing emphysema
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10
Q

what are the 3 main features of COPD?

A

1) hypersecretion of mucus
2) small airway obstruction
3) alveolar destruction

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11
Q

what are the 2 diseases that comprise COPD?

A

1) chronic bronchitis

2) emphysema

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12
Q

what is emphysema?

A

abnormal permanent ENLARGEMENT OF AIR SPACES, accompanied by DESTRUCTION of their WALLS & without obvious fibrosis

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13
Q

what is enlargement of the air spaces trough to be a secondary cause of?

A

small airway inflammation and destruction

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14
Q

how is emphysema classified?

A
  • classified according to the site of damage;
    1) CENTRI-ACINAR emphysema
    2) PAN-ACINAR emphysema
    3) IRREGULAR emphysema
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15
Q

where is the centri-acinar emphysema located?

A
  • usually involves the upper part of the lungs

- changes spreading outwards, starting from the bronchioles

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16
Q

what is centri-acinar emphysema associated with?

A

substation airflow limitation

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17
Q

where is pan-acinar emphysema located?

A
  • usually seen in lower part of the lungs

- alveoli are completely destroyed

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18
Q

in what people is pan-acinar seen in?

A

people with alpha 1 ant-itrypsin deficiency

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19
Q

what is pan-acinar associated with?

A
  • severe airflow limitation

- Va/Q mismatch

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20
Q

what does emphysema result in?

A
  • expiratory airflow limitation
  • air trapping
  • impaired gas exchange
  • Va/Q mismatch
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21
Q

how do people with COPD cope with respiratory infections?

A
  • they cope badly

- the infections are often the cause of an exacerbation of COPD

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22
Q

symptoms of COPD

A
  • productive chronic cough, white or clear sputum
  • wheeze
  • breathlessness
    (could be as severe as breathless after getting dressed)
  • colds settle on the chest

systemic effects;

  • hypertension
  • osteoporosis
  • depression
  • decreased muscle mass with general weakness
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23
Q

who is most likely to get COPD?

A
  • mainly diagnosed in middle aged-elderly

- smokers of many years

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24
Q

are symptoms of COPD chronic or acute?

A

chronic

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25
Q

what is an exacerbation

A

= an acute change in a patients baseline dyspnoea, cough and/or sputum

26
Q

what causes an exacerbation of COPD?

A
  • changes in weather, e.g. cold or damp
  • viral upper resp tract infection
  • viral of bacterial bronchitis
27
Q

what are signs of mild COPD?

A
  • there are few signs

- just quiet wheezes throughout the chest

28
Q

what are signs of severe COPD?

A
  • tachypnoeic (rapid breathing)
  • prolonged expiration
  • accessory muscles of respiration are used
  • chest expansion is poor
  • lungs hyperinflated
  • pursing on the lips on expiration
29
Q

what are later stages of COPD associated with?

How could this respiratory failure be treated?

A

respiratory failure
- PaO2 < 8kPa
OR
- PaCO2 > 7kPa

  • removal of retained secretions (cough up secretions)
  • respiratory support (non-invasive ventilatory techniques)
  • respiratory stimulants (e.g. doxapram)
  • corticosteroids, antibiotici and bronchodilators can be used
30
Q

what is pulmonary hypertension?

A

HIGH blood pressure

31
Q

what causes pulmonary hypertension?

A
  • chronic alveolar hypoxia and hypercapnia

- leads to constriction of pulmonary arterioles

32
Q

how is COPD usually diagnosed?

A
  • usually clinical, based on history of breathless & sputum production in a CHRONIC SMOKER.
33
Q

if a patient has the symptoms of COPD but isn’t a smoker, what is the explanation most likely to be?

A

asthma

UNLESS, there is a family history of alpha 1 antitrypsin deficiency

34
Q

what is alpha 1 antitrypsin?

A

= a proteinase inhibitor produced in the liver
- secreted into the blood and diffuses into the lungs

  • it inhibits proteinases that are capable of destroying alveolar wall connective tissue
35
Q

what happens if there is an alpha 1 deficiency?

A

the alpha 1 anti-trypsin accumulates in the liver, leading to low levels in the lungs

  • so the proteinase isn’t being inhibited
  • therefore it can destroy the alveolar walls & connective tissue
  • leading to symptoms of COPD
36
Q

how can the diagnosis of COPD be confirmed?

what would lung function pattern be?

A

by spirometry results that show IRREVERSIBLE AIRFLOW OBSTRUCTION

  • PEFR reduced
  • reduced FEV1
  • reduced FVC
  • FEV1/FVC ratio REDUCED
  • FEV1 response to B2 agonists < 15%
37
Q

in patients with COPD, what sit the FEV1 usually?

A

< 80%

- if the FEV1 is > or equal to 80%, a diagnosis of COPD is only made if there are respiratory signs of COPD

38
Q

what is the ratio of FEV1/FVC that would show COPD?

A

< 70%

39
Q

What would a chest X-ray show in a patient with COPD?

A
  • relatively normal
  • overinflation of lungs
  • low, flattened diaphragm
  • presence of large bullae
  • blood vessels may be pruned
  • large proximal vessels & relatively little blood visible in peripheral lung fields
40
Q

what is the single most useful measure to help manage COPD?

A

tell them to stop smoking

41
Q

give 3 examples of bronchodilators?

A

1) B-adrenoceptor agonists
2) theophylline
3) anti-muscarinic drugs

42
Q

give an example of short acting B-adrenoceptor agonists (SABA)?
what do short acting B-adrenoceptor agonists do?

A
  • e.g. salbutamol

- feel less breathless after inhaling one

43
Q

in more severe COPD, what sort of b-adreneoceptor should be used?

A

= a LABA

= long acting beta-2 adrenoceptor agonists

44
Q

give 3 examples of a LABA?

A

1) formoterol
- 12microgram powder inhaler, twice daily

2) salmeterol
- 50micrograms twice daily

or

3) indacaterol
- 150 to 130 mcirograms once daily

45
Q

what do theophylline do?

A
  • they are of little benefit in COPD

- but they may help control symptoms of dysponae & wheeze

46
Q

what do anti-muscarinic drugs do?

A

they give more prolonged & greater bronchodilator

47
Q

give examples of 2 long acting agents?

A

1) tiotropium (18micrograms daily)

2) aclidinium (375micrograms daily)

48
Q

what are the drugs tiotropium and aclidnium preferred over?

A

they are prefered over ipratropium or oxitropium

49
Q

what is tiotropiums effect?

A
  • improves quality of life but doesn’t effect decline of FEV1
50
Q

what drugs could be given to reduce sputum viscosity and reduce the number of exacerbations?

A

= ANTI-MUCOLYTIC AGENTS

e.g. carbocisteine 2.25g daily

51
Q

when should corticosteroids be used?

A
  • in symptomatic patients with moderate/severe COPD
52
Q

what corticosteroid drug should always initially be given?

A

PREDNISOLONE, 30mg

- with measurements of lung function before and after the treatment period

53
Q

if there is evidence of substantial improvement in airflow limitation (FEV1 increase of > 15%), what change should be made to the drugs?

A
  • prednisolone should be discontinued

- replaced by INHALED CORTICOSTEROID (beclometasone, 40micrograms twice daily)

54
Q

what effect do combinations of corticosteroids and B2 agonists have?

A
  • protect against lung function decline

- don’t improve overall mortality

55
Q

when should antibiotics be given?

A
  • promptly in an exacerbation

- should always be given in acute episodes

56
Q

why should they be given during exacerbations and acute episodes?

A

= prevent hospital admissions & further lung damage

57
Q

what PaO2 value should long term oxygen therapy be offered to?

A

patients with PaO2 < 7.3 kPa (when breathing air)

58
Q

what medical conditions allows long term oxygen therapy to given to people with a PaO2 of 7.3-8kPa?

A

people with;

  • pulmonary hypertension
  • secondary polycythaemia
  • nocturnal hyperaemia
  • peripheral oedema
  • evidence of pulmonary hypertension
59
Q

what value might the PaO2 drop to in patients with COPD during the night?

A

2.5kPa

= profound nocturnal hypoxaemia

60
Q

what is pulmonary rehabilitation and how can it help patients with COPD?

A

= exercise training that. can modestly increase exercise capacity

  • diminished sense of breathlessness
  • improved general wellbeing
61
Q

what other measures can be done for people with COPD?

A

1) regular vaccines

2) alpha 1 anti-trypsin replacement
- (weekly or monthly infusions)

3) surgery
- lung transplantaion
- surgical bullectomy

Respiratory (Annie) (47 decks)

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