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Year 1 SBA revision > 103 - COPD > Flashcards

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
What causes emphysema?
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.
26
Signs/symptoms of emphysema
``` Airflow obstruction Gas trapping Hyperinflation of chest Loss of capillary bed Reduced blood flow through lungs Pulmonary hypertension/cor pulmonale ```
27
Signs/symptoms of bronchitis
Production of purulent sputum.
28
Treatment of COPD
Stop smoking Pulmonary rehabilitation Surgery - lung transplant, lung volume reduction surgery B2 agonists and muscarinic antagonists (short/long acting)
29
Why are bronchodilators used?
Reduce acute breathlessness (Short acting) and reduce freq of exacerbations (long acting)
30
B agonists - what do they do?
Agonists at B2-adrenergic receptors. | Side effects - tachycardia
31
Muscarinic antagonists - what do they do?
Inhibit parasympathetic receptors in smooth muscle. | Side effects - dry mouth
32
What is Symbicort and why is it used?
Combination bronchodilator & corticosteroid. Used to reduce freq of exacerbations. Combination of formoterol and budesonide
33
What do Xanthines do?
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
34
Toxicity symptoms of Xanthines
``` Nausea and vomiting Tachycardia Tremor Agitation Diuresis Seizures ```
35
Role of mucolytics
Decrease number/severity of exacerbations. Thin the mucous, decrease chance of infection, decrease cough.
36
Role of pulmonary rehab
Increase quality of life. Increase mobility etc. Limits speed of downwards spiral
37
Role of long term O2 therapy
If given for >18hrs/day - only treatment that increases life expectancy.
38
Role of smoking cessation
Reduces speed of disease progression - increases life expectancy.
39
Role of surgery
Resection of bullae (focal regions of emphysema) - increases O2 sats gradually.
40
Why no long term oxygen for smokers?
Boom | Fire + O2 = BAD
41
Long term management for all patients
Smoking cessation advice | Pneumococcal & annual flu vaccination.
42
Inhaled COPD therapies
1 - SABA or SAMA 2 - FEV1 >50% expected - switch to LABA/LAMA 3. Persistant breathlessness/exacerbations or FEV1
43
Why is oxygen needed
To release energy by oxidative phosphorylation of glucose to form ATP
44
Upper respiratory tract - what is it, what does it do
Nasal and oral cavities, pharynx, larynx and trachea.
45
What does upper respiratory tract do
Warms, moistens and filters air before it reaches lungs
46
How is the upper respiratory tract specialised?
Large surface area with rich blood supply and epithelium coated in mucous secretions.
47
What is the lower respiratory tract?
Main bronchi and lungs
48
What is the acinus
Part of airway involved in gaseous exchange - respiratory bronchioles onwards.
49
Conducting airway
Part of airway that transports gases but doesn't directly participate in gaseous exchange
50
3 steps involved in gas exchange
Ventilation - Va Perfusion Diffusion
51
What is hypocapnia
Decreased CO2 in arterial blood
52
What is hypercapnia
Increased CO2 in arterial blood
53
Hypoxaemia
Deficient oxygenation of arterial blood
54
Hypoxia
Deficient oxygenation of tissues
55
Boyles law
Pressure of gas decreases as volume of gas increases
56
Inspiratory reserve volume
Maximum volume of air that can be further inhaled after normal inhalation.
57
Tidal volume
Volume of air moved into/out of lungs during quiet breathing.
58
Functional residual capacity
Volume of air remaining in lungs after normal exhalation.
59
Residual volume
volume of air still in lungs after maximum exhalation.
60
Expiratory reserve volume
Maximum volume of air that can be forced out after normal exhalation.
61
Inspiratory capacity
Maximum volume of air that can be inhaled (normal and forced) from point of normal exhalation.
62
Vital capacity
Maximum volume of air that can be exhaled after deepest inhalation
63
Total lung capacity
Volume of air in lungs at maximum inflation
64
2 main types of disorder that impair ventilation
Obstructive disorders | Restrictive disorders
65
Obstructive disorder
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
Restrictive disorder
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
Control of respiration
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
Ventilation:Perfusion
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
Most common cause of hypoxaemia
Ventilation:Perfusion mismatch
70
Effect of gravity on ventilation:perfusion mismatch
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
What is COPD
Non-reversible airflow obstruction. Usually progressive and not associated with abnormal inflammatory response
72
Consider asthma if:
``` Never smoker Family history Dinural variation Exacerbating factors (animals) Childhood atopy Nasal symptoms ```
73
Likely Chronic bronchitis if:
(Ex)smoker | Purulent sputumn
74
Emphysema likely if:
Smoking history | Weight loss
75
COPD - Pink & puffing
Classic tripod shape to support muscles in breathing Hyperexpanded chest with prominent accessory muscles Decreased chest expansion Intercostal recesion
76
COPD - Blue and bloated patients
``` 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
Asthma and diffusing capacity
Capacity unaffected. Takes longer to breathe in due to obstructed narrow airways.
78
Emphysema and diffusing capacity
Diffusing capacity reduced to to alveolar and capillary bed destruction
79
COPD patients with Cor Pulmonale - how to treat?
Loop diuretic - Furosemide Consider long term O2 therapy AVOID - ACE inhibitors/Alpha blockers/Calcium channel blockers
80
How do molecules move by diffusion
From area of [high] to [low] by random movement (brownian motion) - movement in all directions but average direction.
81
Ficks Law of diffusion
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
Normal lung - Ventilation perfusion mismatch at apex when sitting
Both VA & Q reduced due to gravity • But gravity has largest effect on blood • Th. = >1 – Apex poorly perfused
83
Normal lung - Ventilation perfusion mismatch at base when sitting
Both VA & Q increased due to gravity • But gravity has greatest effect on blood • Th. =
84
What is shunt
No ventilation of blood.
85
What is dead space
No perfusion of ventilated areas
86
Control centres for respiration
Pons - initiates inspiratory/expiratory impulses | Medulla - modifies rate of breathing
87
Most important drive for breathing
PCO2 - overstimulated and desensitised in blue bloaters who use PO2 instead.

Year 1 SBA revision (37 decks)

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