103 - COPD Flashcards

1
Q

What happens to the lungs in emphysema?

A

The alveolar membranes break down

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2
Q

What happens to the lungs in chronic bronchitis?

A

The airways (bronchioles) narrow due to inflammation and excess mucus

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3
Q

Define forced vital capacity

A

Deepest breath in followed by deepest breath out

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4
Q

Define FEV1

A

How much air can be expired in 1 second

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5
Q

Impact of COPD on FEV1 - why?

A

FEV1 is reduced in COPD due to gas trapping, OBSTRUCTIVE lung disease.

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6
Q

What is the dead space of a lung?

A

Area of lung which does not participate in gas exchange

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7
Q

How to test physiological dead space?

A

Bohr equation

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8
Q

How to test anatomical dead space

A

Nitrogen washout/Fowler’s method

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9
Q

How to test functional residual capacity

A

Helium dilution

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10
Q

What should be encouraged at all stages of COPD? Why?

A

Stop smoking - doesn’t stop degeneration but slows rate

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11
Q

What improves quality of life and reduces mortality in COPD?

A

Pulmonary rehabilitation

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12
Q

How to treat COPD

A
Short acting bronchodilators
THEN
Long acting bronchodilators
THEN
Inhaled corticosteroids
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13
Q

What does SABA stand for? Name an example.

A

Short acting B2 adrenoreceptor agonist.

Salbutamol.

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14
Q

What does SAMA stand for? Name an example?

A

Short acting muscarinic antagonist.

Ipratropium

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15
Q

What does LABA stand for?

Name an example

A

Long acting B2 adrenoreceptor agonist.

Salmertarol

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16
Q

What does LAMA stand for?

Name an example.

A

Long acting muscarinic antagonist.

Tiotripium

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17
Q

What inhaled corticosteriod should be prescribed in COPD? When/Why

A

Beclomethasone

Anti-inflammatory immunosupressant. Used in exacerbations.

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18
Q

What is COPD?

A

Umbrella term covering chronic bronchitis, emphysema and small airways disease.

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19
Q

What is chronic bronchitis?

A

Symptom. Cough productive of purulent sputum for at least 3 months of the year for at least 2 successive years.

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20
Q

What is emphysema?

A

Structural abnormality - destruction of lung tissue distal to terminal bronchioles. Degenerative loss of radial traction to bronchiole walls

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21
Q

What is small airways disease?

A

Thickening of airway walls as part of repaid process and fibrosis.

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22
Q

COPD incidence

A

One of biggest killers in UK. Increases with age, severity and poverty. Mostly in smokers or those exposed to coal dust

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23
Q

Genetic predisposers to COPD

A

Alpha-1-antitrypsin-deficency. Patients develop empysema.

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24
Q

What causes chronic bronchitis?

A

Tobacco smoke/irritants cause inflammatory response in bronchus.
Stimuate goblet cells - increased mucus secretion in airway.
Destruction of cilia and flattening of epithelial cells.
Reduced mucosal clearance.

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25
Q

What causes emphysema?

A

Inflammatory response - cells release proteases which overwhelm natural anti-proteases to cause destruction of alveolar walls.
Loss of small airway support by elastic tissues cause floppy airways - narrow/collapse on expiration causing a wheeze.

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26
Q

Signs/symptoms of emphysema

A
Airflow obstruction
Gas trapping
Hyperinflation of chest
Loss of capillary bed
Reduced blood flow through lungs
Pulmonary hypertension/cor pulmonale
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27
Q

Signs/symptoms of bronchitis

A

Production of purulent sputum.

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28
Q

Treatment of COPD

A

Stop smoking
Pulmonary rehabilitation
Surgery - lung transplant, lung volume reduction surgery
B2 agonists and muscarinic antagonists (short/long acting)

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29
Q

Why are bronchodilators used?

A

Reduce acute breathlessness (Short acting) and reduce freq of exacerbations (long acting)

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30
Q

B agonists - what do they do?

A

Agonists at B2-adrenergic receptors.

Side effects - tachycardia

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31
Q

Muscarinic antagonists - what do they do?

A

Inhibit parasympathetic receptors in smooth muscle.

Side effects - dry mouth

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32
Q

What is Symbicort and why is it used?

A

Combination bronchodilator & corticosteroid. Used to reduce freq of exacerbations.
Combination of formoterol and budesonide

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33
Q

What do Xanthines do?

A

Bronchiodilators by inhibition of phosphodiesterase.
Need to monitor blood levels as have narrow therapeutic window as eliminate P450 liver enzymes.
Only use in severe disease

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34
Q

Toxicity symptoms of Xanthines

A
Nausea and vomiting
Tachycardia
Tremor
Agitation
Diuresis
Seizures
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35
Q

Role of mucolytics

A

Decrease number/severity of exacerbations. Thin the mucous, decrease chance of infection, decrease cough.

36
Q

Role of pulmonary rehab

A

Increase quality of life.
Increase mobility etc.
Limits speed of downwards spiral

37
Q

Role of long term O2 therapy

A

If given for >18hrs/day - only treatment that increases life expectancy.

38
Q

Role of smoking cessation

A

Reduces speed of disease progression - increases life expectancy.

39
Q

Role of surgery

A

Resection of bullae (focal regions of emphysema) - increases O2 sats gradually.

40
Q

Why no long term oxygen for smokers?

A

Boom

Fire + O2 = BAD

41
Q

Long term management for all patients

A

Smoking cessation advice

Pneumococcal & annual flu vaccination.

42
Q

Inhaled COPD therapies

A

1 - SABA or SAMA
2 - FEV1 >50% expected - switch to LABA/LAMA
3. Persistant breathlessness/exacerbations or FEV1

43
Q

Why is oxygen needed

A

To release energy by oxidative phosphorylation of glucose to form ATP

44
Q

Upper respiratory tract - what is it, what does it do

A

Nasal and oral cavities, pharynx, larynx and trachea.

45
Q

What does upper respiratory tract do

A

Warms, moistens and filters air before it reaches lungs

46
Q

How is the upper respiratory tract specialised?

A

Large surface area with rich blood supply and epithelium coated in mucous secretions.

47
Q

What is the lower respiratory tract?

A

Main bronchi and lungs

48
Q

What is the acinus

A

Part of airway involved in gaseous exchange - respiratory bronchioles onwards.

49
Q

Conducting airway

A

Part of airway that transports gases but doesn’t directly participate in gaseous exchange

50
Q

3 steps involved in gas exchange

A

Ventilation - Va
Perfusion
Diffusion

51
Q

What is hypocapnia

A

Decreased CO2 in arterial blood

52
Q

What is hypercapnia

A

Increased CO2 in arterial blood

53
Q

Hypoxaemia

A

Deficient oxygenation of arterial blood

54
Q

Hypoxia

A

Deficient oxygenation of tissues

55
Q

Boyles law

A

Pressure of gas decreases as volume of gas increases

56
Q

Inspiratory reserve volume

A

Maximum volume of air that can be further inhaled after normal inhalation.

57
Q

Tidal volume

A

Volume of air moved into/out of lungs during quiet breathing.

58
Q

Functional residual capacity

A

Volume of air remaining in lungs after normal exhalation.

59
Q

Residual volume

A

volume of air still in lungs after maximum exhalation.

60
Q

Expiratory reserve volume

A

Maximum volume of air that can be forced out after normal exhalation.

61
Q

Inspiratory capacity

A

Maximum volume of air that can be inhaled (normal and forced) from point of normal exhalation.

62
Q

Vital capacity

A

Maximum volume of air that can be exhaled after deepest inhalation

63
Q

Total lung capacity

A

Volume of air in lungs at maximum inflation

64
Q

2 main types of disorder that impair ventilation

A

Obstructive disorders

Restrictive disorders

65
Q

Obstructive disorder

A

Airways narrowed - resistance to airflow increases.
Can be due to inflammation and thickened bronchial walls (athsma), airways filled with mucus (chronic bronchitis) and airway collapse (emphysema).

66
Q

Restrictive disorder

A

o Lungs less able to expand – reduced volume of gas exchange.
o May be due to stiffening of lung tissue (Pulmonary fibrosis) or inadequate respiratory muscles (DMD).

67
Q

Control of respiration

A

Needed to ensure respiration responds to metabolic demands of body.
Changes ventilation to ensure this occurs by changing how respiratory muscles act. Appears to be located at the base of the brain in the medulla.

68
Q

Ventilation:Perfusion

A

The flow of gas (Ventilation – VA) and the flow of blood (Perfusion – Q) need to be closely matched for efficient gaseous exchange. VA/Q ratio of healthy lungs approaches 1

69
Q

Most common cause of hypoxaemia

A

Ventilation:Perfusion mismatch

70
Q

Effect of gravity on ventilation:perfusion mismatch

A

When a person is sitting upright and breathing normally, there will be more O2 at the top of the lungs and more CO2 at the bottom which results in ventilation:perfusion inequality. This is normal and is compensated for during exercise.

71
Q

What is COPD

A

Non-reversible airflow obstruction. Usually progressive and not associated with abnormal inflammatory response

72
Q

Consider asthma if:

A
Never smoker
Family history
Dinural variation
Exacerbating factors (animals)
Childhood atopy
Nasal symptoms
73
Q

Likely Chronic bronchitis if:

A

(Ex)smoker

Purulent sputumn

74
Q

Emphysema likely if:

A

Smoking history

Weight loss

75
Q

COPD - Pink & puffing

A

Classic tripod shape to support muscles in breathing
Hyperexpanded chest with prominent accessory muscles
Decreased chest expansion
Intercostal recesion

76
Q

COPD - Blue and bloated patients

A
Bounding pulse
Flapping tremor
Cyanosis
Large pulsatile liver
Cor pulmonale (right sided heart failure) - causes oedema and high JVP due to pulmonary hypertension.
Worse prognosis
77
Q

Asthma and diffusing capacity

A

Capacity unaffected. Takes longer to breathe in due to obstructed narrow airways.

78
Q

Emphysema and diffusing capacity

A

Diffusing capacity reduced to to alveolar and capillary bed destruction

79
Q

COPD patients with Cor Pulmonale - how to treat?

A

Loop diuretic - Furosemide
Consider long term O2 therapy
AVOID - ACE inhibitors/Alpha blockers/Calcium channel blockers

80
Q

How do molecules move by diffusion

A

From area of [high] to [low] by random movement (brownian motion) - movement in all directions but average direction.

81
Q

Ficks Law of diffusion

A

The net diffusion rate of a gas across a fluid membrane is proportional to the difference in partial pressure, proportional to the area of the membrane and inversely proportional to the thickness of the membrane.

82
Q

Normal lung - Ventilation perfusion mismatch at apex when sitting

A

Both VA & Q reduced due to gravity
• But gravity has largest effect on blood
• Th. = >1 – Apex poorly perfused

83
Q

Normal lung - Ventilation perfusion mismatch at base when sitting

A

Both VA & Q increased due to gravity
• But gravity has greatest effect on blood
• Th. =

84
Q

What is shunt

A

No ventilation of blood.

85
Q

What is dead space

A

No perfusion of ventilated areas

86
Q

Control centres for respiration

A

Pons - initiates inspiratory/expiratory impulses

Medulla - modifies rate of breathing

87
Q

Most important drive for breathing

A

PCO2 - overstimulated and desensitised in blue bloaters who use PO2 instead.