Chronic Obstructive Pulmonary Disease (COPD) Flashcards

1
Q

investigations in COPD

A
  • spirometry
  • ABGs
  • plethysmography
  • diffuse capacity of CO
  • CXR (hyperinflation and bullae formation)
  • alpha 1 antitrypsin level
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2
Q

management of COPD

A
  • smoking cessation
  • counselling
  • SABA –> SAMA –> LABA –> LAMA
  • steroids if the patient is Gold D
  • pneumococcal and influenza vaccines
  • theophylline
  • roflumilast
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3
Q

what classification is used for COPD?

A

Gold guidelines

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4
Q

what do the Gold guidelines assess?

A
  • number of exacerbations
  • severity of dyspnoea
  • number of hospitalisations
  • Stage A to D
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5
Q

interventions that reduce mortality

A
  • smoking cessation

- long-term oxygen therapy

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6
Q

characteristics of COPD

A
  • airflow limitation, not fully reversible
  • progressive
  • abnormal inflammatory response
  • no reversibility
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7
Q

definition of chronic bronchitis

A

a persistent productive cough (with sputum) for a minimum of 3 consecutive months for at least 2 successive years

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8
Q

populations at risk for chronic bronchitis

A

middle-aged men who smoke, mainly

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9
Q

emphysema

A

a lung condition characterised by abnormal permanent enlargement of the air spaces distal to the terminal bronchioles with destruction of their walls

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10
Q

people at risk for developing emphysema

A
  • heavy smokers

- if under 40yo, suspect an alpha-1-antitrypsin deficiency

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11
Q

risk factors for COPD

A
  • smoking
  • exposure to irritants (occupational dusts and chemicals)
  • pollutants
  • infection
  • genetic and hyperresponsiveness
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12
Q

effects of smoking on the lung

A
  • interferes with ciliary action
  • direct damage to epithelium
  • inhibits activity of alveolar macrophages to clear bacteria
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13
Q

how do emphysema and bronchitis obstruct air flow?

A

Chronic Bronchitis

  • mucus plugging
  • inflammation and oedema of the bronchioles
  • development of fibrosis
  • co-existent emphysema

Emphysema:
- loss of lung’s elastic recoil which causes small airways to collapse at the beginning of expiration

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14
Q

morphology of chronic bronchitis

A
  • mucopurulent secretions
  • reduced cilia
  • higher number of goblet cells
  • hypertrophic submucous glands
  • congestion
  • oedema
  • squamous metaplasia & dysplasia
  • wall fibrosis
  • smooth muscle hyperplasia
  • inflammation
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15
Q

types of emphysema

A
  • centriacinar
  • panacinar
  • paraseptal (associated with infective diseases)
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16
Q

what is a bulla?

A

a cystically dilated space which is more than 1cm in diameter; these can surround the lesion of interest and if punctured, they can risk pneumothorax

17
Q

where does centriacinar emphysema affect?

A
  • around respiratory bronchioles
  • commonly found in men with chronic bronchitis
  • upper lobes
  • smokers
18
Q

where does panacinar affect?

A
  • across the entire acinus

- lower lobes if there is the congenital kind of emphysema

19
Q

where do bullae appear?

A
  • anterior margins

- apices of the upper lobes

20
Q

histological features of emphysema

A
  • hyperinflation
  • markedly enlarged air spaces
  • destroyed alveolar septa
21
Q

features of bullous emphysema

A
  • young men, smokers

- treated by bullectomy

22
Q

pathogenesis of emphysema

A
  • protease-anti-protease imbalance

- oxidant-anti-oxidant imbalance

23
Q

protease - anti-protease imbalance

A

the increase in proteases cause elastin destruction, leading to emphysema

24
Q

oxidant - anti-oxidant imbalance

A
  • free radicals in tobacco smoke deplete normal lung antioxidants
  • activated neutropils contribute more free radicals
  • oxidative injury inactivates antiproteases –> functional a1AT deficiency
25
Q

complications of COPD

A
  • pulmonary hypertension
  • heart failure
  • cor pulmonale
  • death
  • metaplasia and dysplasia of the respiratory epithelium, causing malignancy
26
Q

effects of smoking

A
  • stimulates release of elastase from neutrophils
  • enhances elastase activity in macrophages
  • causes mast cell activation with release of elastases and NCFs
  • oxidants in cigarette smoke and oxygen free radicals inhibit alpha-1-antitrypsin (antielastase)
  • smokers have neutrophils, macrophages in lungs
  • macrophages release NCFs (neutrophil chemotactic factors)
  • nicotine is also chemotactic for neutrophils
27
Q

what are COPD patients more at risk of?

A
  • cardiovascular diseases (IHD, HF, AF, HTN)
  • osteoporosis
  • anxiety and depression
  • lung cancer
  • infections
  • metabolic syndrome and diabetes
28
Q

what does COPD significantly affect?

A
  • weight loss
  • nutritional abnormalities
  • skeletal muscle dysfunction
29
Q

who should be screened for COPD?

A
  • progressive, persistent dyspnoea
  • chronic cough
  • chronic sputum
  • history of exposure to risk factors (irritants and occupational dust)
  • family history of COPD
30
Q

why is COPD underdiagnosed?

A
  • lack of symptoms which only become diagnosable at later-stages
  • history and examination are non-specific
  • underuse of spirometry which is the gold standard to diagnose COPD
31
Q

which scale is used to assess symptoms?

A

MRC Breathlessness scale

32
Q

things that spirometry does not consider

A
  • the full systemic effects of the disease

- the impact of the disease on the lives of the patients

33
Q

gold spirometry criteria

A

Gold 1: FEV1 >80%
Gold 2: FEV1 50-80%
Gold 3: FEV1 30-50%
Gold 4: FEV1 <30%

34
Q

treatment for COPD

A

Gold A: SAMA/SABA prn (bronchodilators)
Gold B: LABA/LAMA
Gold C & D: ICS + LAMA/LABA