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Stage 2: Supporting Life > COPD - Clinical Features and Pathophysiology > Flashcards

COPD - Clinical Features and Pathophysiology Flashcards

1
Q

What is COPD?

A

A common, preventable and treatable disease that is characterised by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles of gases

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2
Q

What % of smokers develop COPD?

A

15%

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3
Q

What are the most common respiratory symptoms of COPD?

A

Dyspnoea, cough and/or sputum production

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4
Q

What are causes of COPD?

A

1) Tobacco smoking (active and passive) → even if it was a long time ago, appears later bc it needs time for normal decline of respiratory system to develop the symptoms
2) Biomass fuel exposure → poorly ventilated dwellings
3) Occupational exposures → organic and inorganic dusts, chemical agents, fumes

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5
Q

What is the pathogenesis of COPD?

A

Cigarette smoke and environmental particles (trigger) and host factor amplifying mechanisms → lung inflammation and antioxidants/antiproteases not working → oxidative stress and impaired repair mechanisms → pathological changes of COPD

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6
Q

What are inhibitory factors to oxidative stress?

A

Antioxidants and antiproteases

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7
Q

What happens in inflammation in COPD?

A

Increased neutrophils, macrophages and T cells (CD8 > CD4) in the lungs

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8
Q

What is the extent of the inflammation related to?

A

The degree of airflow obstruction

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9
Q

Why is the inflammatory pattern of COPD markedly different from asthma?

A

Asthma involves eosinophilic inflammation

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10
Q

What are the inflammatory mediators in COPD?

A

1) Leukotriene B4 → neutrophil and T cell chemoattractant
2) Chemotactic factors e.g. IL-8 and growth related oncogene alpha → amplify pro-inflammatory responses
3) Pro-inflammatory cytokines TNF-alpha, IL-1beta and IL-6
4) Growth factors e.g. TGF- beta → cause fibrosis in the airways

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11
Q

What is the inflammatory mechanism in COPD?

A

1) Cigarette smoke and other environmental noxious agents activate macrophages and epithelial factors to release chemotactic factors that recruit neutrophils and CD8 cells from the circulation
2) This leads to alveolar wall destruction and mucous hypersecretion
3) Fibroblasts are also activated, leading to abnormal tissue repair

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12
Q

What are sources of oxidants leading to oxidative stress in COPD?

A
  • Cigarette smoke

- Reactive oxygen and nitrogen species from inflammatory cells

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13
Q

What happens to markers of oxidative stress in stable and exacerbated COPD?

A

They increase (even more in exacerbations)

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14
Q

What are the actions of oxidative stress?

A

1) Inactivates antiproteases
2) Stimulates mucus production
3) Amplifies inflammation by enhancing transcription factor activation (e.g. NF kappaB) and gene expression of pro-inflammatory mediators

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15
Q

What happens to the airways in COPD (pathophysiology)?

A

1) Hypertrophy and hyperplasia of bronchial submucosal glands and increased number of goblet cells → mucus hypersecretion
2) Destruction of cilia → difficulty coughing (expectorating)
3) Narrowing of airways due to remodelling
4) Increased airways resistance

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16
Q

Where does the narrowing process of airways start and why?

A

In smaller airways (<2mm) bc small particles from tobacco smoke can go down these

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17
Q

What happens to the lung parenchyma in COPD (pathophysiology)?

A

1) Proteolytic enzymes destroy alveolar tissue (air spaces)
2) Elastin and collagen are destroyed → reduced elasticity and structural integrity of the lungs
3) This leads to loss of elastic recoil (increased compliance) → worse chest expansion

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18
Q

What are the main clinical features of COPD?

A
  • Dyspnoea (normally main problem)
  • Exercise limitation
  • Wheeze
  • Sputum
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19
Q

What are other clinical features of COPD?

A
  • Increased RR
  • Accessory muscle use
  • Wheeze
  • Reduced chest expansion
  • Barrel chest (lung hyperinflation from gas trapping) → reaches equilibrium at more positive pressures
  • Reduced breath sounds
  • Asterixis
  • Cyanosis
  • Cor pulmonale
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20
Q

Why are there reduced breath sounds in COPD?

A

Bc there is air space between where the sound is happening and the stehoscope

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21
Q

What are the 4 main pathological features of COPD?

A

1) Airflow obstruction
2) Loss of lung elasticity
3) Loss of alveoli
4) Airway inflammation

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22
Q

What are the 5 main features of COPD?

A

1) Expiratory flow limitation
2) Decreased elastic recoil of lungs
3) Gas exchange
4) Hyperinflation
5) Sputum production

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23
Q

What are some extra-pulmonary features of COPD?

A
  • Weight loss
  • Muscle wasting
  • Cardiovascular co-morbidities
  • Depression
  • Osteoporosis
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24
Q

How do you diagnose COPD?

A

Symptoms + spirometry (to diagnose obstruction) → v important not to misdiagnose COPD

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25
Q

What happens to FEV1 and therefore FEV/FVC ratio in COPD?

A

Both decrease (FVC is the same)

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26
Q

What will be the post-bronchodilator FEV1/FVC in all levels of COPD?

A

<0.7

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27
Q

What are the 4 stages of COPD?

A

1) Mild
2) Moderate
3) Severe
4) Very severe

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28
Q

What is %FEV1 predicted in mild COPD?

A

≥ 80%

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29
Q

What is %FEV1 predicted in moderate COPD?

A

50-79%

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30
Q

What is %FEV1 predicted in severe COPD?

A

30-49%

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31
Q

What is %FEV1 predicted in very severe COPD?

A

< 30%

32
Q

Why are patients with COPD breathless on exertion?

A

Bc the flow volume envelope is limited (look at diagram) → COPD affects normal breathing

33
Q

What are the physiological features of COPD?

A

1) Static hyperinflation (affected by compliance)
2) Gas trapping and the equal pressure point (EPP)
3) Dynamic hyperinflation

34
Q

What compliance do stiff lungs have e.g. fibrosis

A

Low (high elastic resistance)

35
Q

What compliance in lungs with emphysema?

A

High (tissue destruction, floppy)

36
Q

What is the effect of asthma on compliance?

A

Asthma does not usually affect compliance

37
Q

What does the stiffness (compliance?) of lungs affect?

A

1) The ease with which the lungs can be inflated
2) FRC (the volume in the lungs when the muscles are relaxed → bc FRC occurs when inward recoil of lungs exactly balances outward recoil of the chest wall

38
Q

What happens to FRC in a stiff lung (fibrosis)?

A

Increasing lug recoil → reduced FRC

39
Q

What happens to FRC in floppy lungs (emphysema)

A

Reduced recoil → increased FRC (barrel chest)

40
Q

What happens to FRC in respiratory muscle weakness?

A

FRC is normal bc the two recoils are normal

41
Q

What happens in static hyperinflation in COPD?

A

1) At rest, the lungs of a patient with COPD are likely to be hyperinflated
2) FRC and RV are increased
3) Furthermore, gas trapping occurs in expiration

42
Q

What happens normally to pressure during expiration?

A

1) Ppl +30
2) Alveolar pressure > Ppl due to elastic recoil
3) Hence, trans airway pressure is positive and the airways stay open until EPP during forced expiration → at EPP, small airways close, preventing alveoli from closing

43
Q

When do small airways collapse?

A

No cartilage so whether they are open depends on pressure → so when pressure on outside > inside, airway will collapse

44
Q

What happens to airways in disease (COPD)?

A

1) More airways close at EPP and this can happen in tidal breathing
2) This leads to gas trapping in airways
3) Also, due to reduced elasticity, the pressure inside the airways is lower, so you reach EPP sooner

45
Q

What does dynamic hyperinflation occur (in alveoli?) in COPD?

A
  • Reduced recoil (alveoli is stretched)
  • Reduced tethering
  • Increased airways resistance
  • Small airways closes sooner due to airway narrowing, so ventilation decreases
46
Q

What is the pressure pulling inwards on the alveoli?

A

Transpulmonary pressure (PL)

47
Q

What happens to Vmax of flow (max capacity) in COPD and what does this mean?

A

Vmax decreases, meaning in COPD the flow volume loop has no ‘space’ to go into exercise breathing

48
Q

When does expiratory flow limitation (EFL) occur?

A

When flow ceases to increase with increasing expiratory effort bc small airways close

49
Q

When can EFL occur in COPD and what is the effect of this?

A

In tidal breathing → since max expiratory flow is reached during tidal breathing, the minimum time of lung emptying is fixed i.e. can’t empty lungs faster by pushing harder in expiration

50
Q

What is the effect of EFL in tidal breathing on IC and IRV?

A

EFL in tidal breathing → increased RR during exercise → increased EELV despite expiratory muscle activity → decreased inspiratory capacity (IC) and inspiratory reserve volume (IRV)

51
Q

What happens to the ‘shape’ of tidal breathing in COPD?

A

It loses its circle shape

52
Q

Why can’t COPD patients increase their tidal volume by v much?

A

Bc they breathe much closer to TLC → IC is smaller

53
Q

What happens to IRV in COPD?

A

It is lower

54
Q

What causes exercise limitation in COPD?

A

1) Once IRV is within 0.5L of TLC, TV can’t increase anymore despite continued increases in contractile respiratory effort
2) This causes dyspnoea to increase to intolerable levels
3) This leads to exercise limitation

55
Q

Why does it get harder to breathe when your lungs hyperinflate?

A

Dynamic hyperinflation forces COPD patients to breathe at higher lung volumes where…

1) Lung compliance is lower
2) Work of breathing (PxV) is higher)
3) There is limitation to tidal volume expansion

56
Q

What is another consequence of dynamic hyperinflation?

A

Threshold load

57
Q

What causes functional diaphragm weakness in COPD?

A

Hyperinflation

58
Q

Why do patients with COPD tend to use accessory muscles?

A

Due to the functional diaphragm weakness, the diaphragm contracts parallel to the ground so it doesn’t increase volume (no anatomical weakness of diaphragm)

59
Q

What are the increased loads on the respiratory system as a result of COPD?

A
  • Resistive

- Dynamic hyperinflation → threshold, elastic

60
Q

What leads to reduced muscle pump capacity as a result of COPD?

A

1) Functional weakness of the diaphragm

2) Limitation of tidal volume expansion (hyperinflation)

61
Q

How does the load-capacity imbalance (high load, low capacity) in COPD manifest?

A

As an increase in the drive to breathe → breathlessness

62
Q

Why does the load-capacity imbalance lead to breathlessness?

A

1) Signal from brain to breathe goes to the periphery, however bc of increased load this signal goes back to the brain
2) Bc the desired outcome wasn’t achieved, there is the sensation of breathlessness
3) Increased neural drive → increased dyspnoea

63
Q

What else can develop in COPD?

A

Pulmonary hypertension

64
Q

Why does pulmonary hypertension develop in COPD?

A

1) Chronic hypoxia, leading to pulmonary vasoconstriction

2) Muscularisation, intimal hyperplasia, fibrosis and obliteration

65
Q

What are the effects of pulmonary hypertension?

A

Cor pulmonale → oedema, death

66
Q

What is exercise limitation in COPD due to?

A

Lung mechanics and peripheral muscle performance

67
Q

What is peripheral muscle fatigue in COPD?

A

A reversible decrease in force-generating ability of a muscle resulting from recent activity

68
Q

What are causes of peripheral muscle fatigue?

A

1) Lower limb atrophy
2) Reduced muscle metabolism
3) Morphological muscle changes

69
Q

What is the effect of lower limb atrophy?

A

1) Muscle weakness
2) Increased susceptibility to fatigue
3) Poor resistance to exercise

70
Q

What muscle morphological changes occur in COPD?

A

1) Decreased type 1 fibres
2) Decreased CSA for type 1 and type 2 fibres
3) Decreased myosin heavy chain I and decreased oxidative enzyme activity (strong determinants of muscle endurance)
4) Increased anaerobic metabolism

71
Q

What is evidence for significance of peripheral muscle fatigue in exercise limitation?

A

1) Persistent exercise limitation after full restoration of lung function after lung transplantation
2) Bronchodilators in quadriceps of pre-fatigued patients failed to improve exercise tolerance
3) Patients reporting leg fatigue as exercise-limiting symptoms less likely to improve exercise tolerance with bronchodilators

72
Q

What is used as a biomarker of peripheral muscle fatigue and can predict survival in severe COPD?

A

Quadriceps muscle strength

73
Q

What features in a patient should make you consider a diagnosis of COPD?

A
  • Over 35
  • Progressive, persistent dyspnoea, usually worse with exercise
  • Chronic cough (may be intermittent and unproductive)
  • Chronic sputum
  • Frequent ‘winter bronchitis’
  • Exposure to cigarette smoke (active or passive), occupational dusts and chemicals, smoke from home cooking/heating fuels
74
Q

What test should you perform on someone to diagnose COPD?

A

Spirometry

75
Q

What predicts levels of hospitalisation and death in COPD patients independent of disease severity/lung function?

A

Physical activity levels

Stage 2: Supporting Life (30 decks)

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