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
what is an exacerbation
= an acute change in a patients baseline dyspnoea, cough and/or sputum
26
what causes an exacerbation of COPD?
- changes in weather, e.g. cold or damp - viral upper resp tract infection - viral of bacterial bronchitis
27
what are signs of mild COPD?
- there are few signs | - just quiet wheezes throughout the chest
28
what are signs of severe COPD?
- tachypnoeic (rapid breathing) - prolonged expiration - accessory muscles of respiration are used - chest expansion is poor - lungs hyperinflated - pursing on the lips on expiration
29
what are later stages of COPD associated with? How could this respiratory failure be treated?
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
what is pulmonary hypertension?
HIGH blood pressure
31
what causes pulmonary hypertension?
- chronic alveolar hypoxia and hypercapnia | - leads to constriction of pulmonary arterioles
32
how is COPD usually diagnosed?
- usually clinical, based on history of breathless & sputum production in a CHRONIC SMOKER.
33
if a patient has the symptoms of COPD but isn't a smoker, what is the explanation most likely to be?
asthma | UNLESS, there is a family history of alpha 1 antitrypsin deficiency
34
what is alpha 1 antitrypsin?
= 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
what happens if there is an alpha 1 deficiency?
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
how can the diagnosis of COPD be confirmed? | what would lung function pattern be?
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
in patients with COPD, what sit the FEV1 usually?
< 80% | - if the FEV1 is > or equal to 80%, a diagnosis of COPD is only made if there are respiratory signs of COPD
38
what is the ratio of FEV1/FVC that would show COPD?
< 70%
39
What would a chest X-ray show in a patient with COPD?
- 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
what is the single most useful measure to help manage COPD?
tell them to stop smoking
41
give 3 examples of bronchodilators?
1) B-adrenoceptor agonists 2) theophylline 3) anti-muscarinic drugs
42
give an example of short acting B-adrenoceptor agonists (SABA)? what do short acting B-adrenoceptor agonists do?
- e.g. salbutamol | - feel less breathless after inhaling one
43
in more severe COPD, what sort of b-adreneoceptor should be used?
= a LABA | = long acting beta-2 adrenoceptor agonists
44
give 3 examples of a LABA?
1) formoterol - 12microgram powder inhaler, twice daily 2) salmeterol - 50micrograms twice daily or 3) indacaterol - 150 to 130 mcirograms once daily
45
what do theophylline do?
- they are of little benefit in COPD | - but they may help control symptoms of dysponae & wheeze
46
what do anti-muscarinic drugs do?
they give more prolonged & greater bronchodilator
47
give examples of 2 long acting agents?
1) tiotropium (18micrograms daily) | 2) aclidinium (375micrograms daily)
48
what are the drugs tiotropium and aclidnium preferred over?
they are prefered over ipratropium or oxitropium
49
what is tiotropiums effect?
- improves quality of life but doesn't effect decline of FEV1
50
what drugs could be given to reduce sputum viscosity and reduce the number of exacerbations?
= ANTI-MUCOLYTIC AGENTS e.g. carbocisteine 2.25g daily
51
when should corticosteroids be used?
- in symptomatic patients with moderate/severe COPD
52
what corticosteroid drug should always initially be given?
PREDNISOLONE, 30mg | - with measurements of lung function before and after the treatment period
53
if there is evidence of substantial improvement in airflow limitation (FEV1 increase of > 15%), what change should be made to the drugs?
- prednisolone should be discontinued | - replaced by INHALED CORTICOSTEROID (beclometasone, 40micrograms twice daily)
54
what effect do combinations of corticosteroids and B2 agonists have?
- protect against lung function decline | - don't improve overall mortality
55
when should antibiotics be given?
- promptly in an exacerbation | - should always be given in acute episodes
56
why should they be given during exacerbations and acute episodes?
= prevent hospital admissions & further lung damage
57
what PaO2 value should long term oxygen therapy be offered to?
patients with PaO2 < 7.3 kPa (when breathing air)
58
what medical conditions allows long term oxygen therapy to given to people with a PaO2 of 7.3-8kPa?
people with; - pulmonary hypertension - secondary polycythaemia - nocturnal hyperaemia - peripheral oedema - evidence of pulmonary hypertension
59
what value might the PaO2 drop to in patients with COPD during the night?
2.5kPa | = profound nocturnal hypoxaemia
60
what is pulmonary rehabilitation and how can it help patients with COPD?
= exercise training that. can modestly increase exercise capacity - diminished sense of breathlessness - improved general wellbeing
61
what other measures can be done for people with COPD?
1) regular vaccines 2) alpha 1 anti-trypsin replacement - (weekly or monthly infusions) 3) surgery - lung transplantaion - surgical bullectomy