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Medicine Year 1 > Week 102 COPD > Flashcards

Week 102 COPD Flashcards

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1
Q

What is the composition of air?

A

N2- 78%
O2- 21%
Ar- 1%
CO2- 0.04%

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2
Q

What’s the equation for diffusion?

A

Time (t) taken for a molecule to diffuse a specified distance (x) in one direction (from “start” to “end”

x^2 alpha t

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3
Q

What is in-between the parietal and visceral pleura of the thorax?

A

Interpleural space containing fluid with a negative pressure

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4
Q

Give 3 facts of parietal and visceral pleura of the thorax

A

• Superior and anterior borders of lungs and
pleura → identical

• Cupula of pleura – 1-2 cm above the clavicle; 2-3 cm above the 1st rib ́s border

• Sup. interpleural space at the level of the 2nd
rib ́s cartilage (thymus, Hassal’s corpuscles, connective and fatty tissue)

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5
Q

Name pleural recesses of the thorax

A

Right costodiaphragmatic recess of pleural cavity

Left costodiaphragmatic recess of pleural cavity

• Superior and anterior borders of lungs and
pleura → identical

• Cupula of pleura – 1-2 cm above the clavicle; 2-3 cm above the 1st rib ́s border

• Sup. interpleural space at the level of the 2nd
rib ́s cartilage (thymus, Hassal’s corpuscles, connective and fatty tissue)

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6
Q

Why is the right main bronchus more vulnerable to inhalation injury?

A

Shorter
Straighter
Wider
More vertical

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7
Q

What plain film projection is best for an accurate heart size?

A

PA projection (AP projection is not reliable)

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8
Q

Name pathological changes that occur in COPD:

A

Chronic bronchitis
Emphysema
Small airways disease

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9
Q

What are the clinical implications for the patient dependent on?

A
  • History
  • Physical signs on examination
  • Radiology
  • Lung function tests
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10
Q

What 2 disease in COPD go together?

A

Chronic bronchitis

Emphysema

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11
Q

Describe the anatomy of the normal human airway

A
  • Cartilage is present to level of proximal bronchioles
  • Gas exchange occurs beyond terminal bronchiole
  • Distal airspaces kept open by elastic tension in alveolar walls
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12
Q

Name the cells found in the normal bronchial epithelium

A
  • Ciliated columnar cells
  • Goblet cells
  • Bronchial gland
  • Basement membrane
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13
Q

Describe a major indicative symptom of chronic bronchitis, but what must you beware of?

A

Symptom: cough productive of purulent sputum for at least 3 months of the year for at least 2 successive years

Beware: other chronic conditions with wheeze may fit this definition e.g. asthma, bronchiectasis

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14
Q

What is the WHO definition of chronic bronchitis?

A

Chronic bronchitis refers to an inflammatory
process in the wall of the bronchioles with
excessive production of mucus and sputum
from hypertrophic glands. The small airways
are narrow, and there is morning cough more
than 3 months per year

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15
Q

What can contribute to the pathology of chronic bronchitis?

A

-Cigarette smoke and other irritants

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16
Q

Describe the pathophysiology of chronic bronchitis

A

Irritated epithelial cells increase numbers of goblet cells, mucous glands and mucous in the airway lumen.

Increased CD8 +ve lymphocytes and neutrophils occur- inflammatory cell infiltration.

Increased inflammatory cells in submucosa.

Excess abnormal mucous “glues” and flattens cilia.

Bacterial adherence to bronchial secretions.

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17
Q

What do the submucosal macrophages release in chronic bronchitis?

A

Proteases

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18
Q

Name other pathological changes in bronchial epithelium

A
  • Loss of ciliated cells

- Squamous metaplasia

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19
Q

How are distal airspaces of the airways kept open?

A

By elastic tension in alveolar walls

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20
Q

What is emphysema?

A 
Destruction
of lung tissue distal to the
terminal bronchioles. There
is degenerative loss of radial
traction of the bronchial walls
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21
Q

What is the protease/anti-protease theory of emphysema?

A

Observation

Patients with alpha-1-antitrypsin deficiency (an anti-protease) develop
emphysema

Theory

Smoke causes inflammatory cell infiltration
Cells release proteases (elastase, matrix metalloproteases)
These overwhelm body’s natural anti-proteases (like α-1AT )
Causing destruction of structural proteins in alveolar walls

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22
Q

Describe connective tissue in the normal alveolar wall

A 
Elastin - E
• 30% lung extracellular matrix
• Hydrophobic, highly X-linked
complex, 3D molecule
• Elastic properties
• Sheets surround alveoli
• Stretch & elastic recoil

Collagen - C 
• 60% lung extracellular matrix
• Triple helical structure
• Molecules overlap + X-link to
form fibrils of high tensile
strength
• Meshwork for lung structure
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23
Q

Name structural abnormalities in emphysema

A

Loss of elastin/connective tissue in alveolar walls

Dilated airspaces

Loss of elastic tissue to support small airways

Causes floppy airways which narrow or collapse on expiration (higher intrathoracic pressure)

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24
Q

Describe small airway disease in COPD

A 
Increasingly appreciated
Small airway thickening & fibrosis
(unlike emphysema)
Progression of COPD correlates
with:
  • Wall volume
  • Inflammatory cells
  • Mucous in lumen
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25
What are pointers towards asthma?
``` Never-smokers Nasal symptoms Diurnal variation Family history Exacerbating factors Childhood atopy ```
26
What are pointers towards chronic bronchitis?
Smoking history | Purulent sputum > 3 months for > 2years
27
What are pointers towards emphysema?
Smoking history, weight loss
28
What are physiological consequences of emphysema?
* Airflow obstruction * Gas trapping (can’t get air out) * Hyperinflation of the chest
29
Name physical signs of COPD:
``` Pursed lip breathing Hyperexpanded chest ↑ accessory muscles 1 ↓ cricoid /sternal notch 2 ↓ chest expansion Intercostal recession 3 Paradoxical costal margin ↓ hepatic /cardiac dullness to percussion ```
30
What is audible with a stethoscope in COPD?
* Heart sounds in epigastrium * ↓ breath sounds * Polyphonic wheezes * Scanty insp. Crackles
31
Name physiological consequences of emphysema
``` Loss of capillary bed • Reduced blood flow through the lungs • Hypoxia & hypercarbia • Pulmonary hypertension / cor pulmonale ```
32
Name physical signs of COPD
``` Bounding pulse (CO2 retention) • Flapping tremor (CO2 retention) • Cyanosis (from hypoxia) • ↑ JVP • Ankle swelling • Tricuspid regurgitation • Large (pulsatile) liver ```
33
What receptor controls broncodilation?
Beta 2
34
What receptor controls | bronchoconstriction?
M
35
What type of drugs can facilitate bronchodilatation?
B2 receptor agonists
36
Explain the physiology when an agonist binds to a B2 receptor in the airwyas
- binds to 7 TMD - Activates coupled Gs protein (alpha subunits detethers from beta/gamma and = conformational change) - GDP--> GTP - ATP--> cAMP by adenylate cyclase = GI/vascular/bronchial/ciliary/smooth muscle relaxation
37
Name short acting B2 agonists (SABAs)
Salbutamol | Terbutaline
38
Name long acting beta2 agonists (LABAs)
Salmeterol Formoterol Indacaterol Vilanterol
39
How can beta 2 agonists be administered?
By inhalation
40
How long do SABAs work for?
Acts within minutes and lasts for 4-6 hours
41
How long do LABAs work for?
12-24 hours after acting in minutes
42
What are side effects of B2 agonists?
Tremor Hypokalaemia Tachycardia
43
What type of antagonist can be used to ease airways?
Muscarinic anatagonists because they antagonise Ach to reduce bronchoconstriction Block M1 and M3 --> bronchodilation
44
What pathway do M1/M3 receptors work by?
PLC--> IP3/DAG --> Ca+
45
Name short acting muscarinic antagnoists (SAMAs)
Ipratrpoium
46
Name long acting muscarinic antagonists (LAMA)
Tiotropium Umeclidinium Aclidinium Glycopyrronium
47
How are muscarinic antagonists administered?
Inhalation
48
How long does ipratropium last for?
Can be used as and when required Lasts 4-6 hours
49
How long do LAMAs last for?
Should be used regularly\ 12-24 hr duration of action
50
What are side effects of LAMAs?
Dry mouth Blurred vision GI disturbances Can ppt glaucoma in susceptible individuals
51
What typed of administrations of bronchodilators exist?
Inhaler: aerosol, dry powder Nebuliser
52
Describe the step by step treatment algorithm for COPD
Step 1: SABA Step 2: SABA LAMA Step 3: SABA LAMA LABA Step 4: SABA LAMA LABA ICS At each stage give smoking cessation advice
53
What is most important in advising patients at all stages of COPD?
SMOKING CESSATION ``` • Cannot replace lost lung function but reduces rate of decline • Active programmes + nicotine replacement chance of quitting ```
54
What vaccinations can you give to help manage COPD?
Influenza (annual) | Pneumococcus (every 10 years)
55
How can you manage COPD pharmacologically?
Rational use of bronchodilators Inhaled corticosteroids Mucolytics - carbocisteine
56
What drugs are controversial in managing stable COPD?
Inhaled corticosteroids There is limited evidence for the benefit of inhaled corticosteroids: • No survival benefit independent of effects of long acting bronchodilators • No effect in decline in FEV1 • Possible effect of reducing rate of acute exacerbations is unclear • Substantial adverse effects notably increased risk of pneumonia
57
What hospital investigations take place when managing acute exacerbations of COPD?
``` Arterial blood gas ideally breathing air - or note inspired pO2) • CXR (?pneumonia. ? pneumothorax) • ECG • FBC & renal profile • CRP (crude measure of ‘infection’) • Theophylline blood level (if taking) • Sputum for bacteriology – but don’t wait to treat • Blood culture (if febrile) ```
58
How can acute exacerbations of COPD be managed?
* Nebulised bronchodilators * Controlled oxygen therapy (? risk of CO2 retention) * Antibiotics if sputum purulent * IV fluids * IV or oral corticosteroids * Consider iv aminophylline (monitor blood levels beware interactions) * Chest physiotherapy * Consider Non-Invasive Ventilation (NIV) if CO2 rising * Consider ITU if appropriate (? ceiling of treatment)
59
What are advantages of acute Non-Invasive Ventilation (NIV) | for exacerbations of COPD?
``` • reduces mortality, rate of intubation & LOS • more cost effective than intubation / ventilation on ITU ```
60
When do you administer long-term o2 therapy (LTOT)?
* Patients with COPD and cor pulmonale * Arterial pO2 < 7.3 kPa – when stable * Flow rate to bring pO2 < 10 kPa * Without significant ↑ pCO2
61
Name common causes of obstructive lung diseases
Asthma Emphysema Chronic bronchitis
62
Name less common causes of obstructive lung disease
``` Bronchiectasis Cystic fibrosis (inherited form of bronchiectasis) ```
63
Name rare causes of obstructive lung disease
Obliterative bronchiolitis
64
What are common COPD symptoms
Cough Sputum Wheeze Breathlessness
65
What does diagnosis of asthma require?
demonstration of variability or reversibility in lung function e.g. spirometry before and after bronchodilator
66
How can you identify asthma in particular from histology of the bronchial epithelium?
Eosinophil infiltration
67
What is stridor?
• High-pitched inspiratory wheeze • Audible at a distance • Caused by laryngeal oedema, vocal cord spasm or tracheal obstruction e.g.
68
Describe wheeze
Continuous musical sound with a definite pitch • Generated at site of stenosis when walls of lightly touching bronchi are set in oscillation by jet of air • Wheeze frequency is independent of airway size • Varies with velocity of airflow at point of stenosis • Most prominent in EXPIRATION
69
What are the types of wheeze?
Monophonic | Polyphonic
70
Describe polyphonic wheeze
• Common in COPD and asthma • ‘Polyphonic’ = cluster of harmonically unrelated sounds • Regional variations in airway narrowing and ‘floppiness’ result in sequential, dynamic compression • May be absent on tidal breathing (if present = severe disease • Number increase with forced expiratory effort§
71
Describe monophonic wheeze
• Low pitched • Occurs when bronchus narrowed by critical stenosis or intrabronchial mass (tumour) • Tend to be ‘focal’ or at least louder in one lung than the other • Relatively uncommon • Can get transient & random monophonic wheeze with COPD / Asthma
72
Name some causes of monophonic wheeze
Bronchial tumour | Inhaled foreign body e.g. peanut
73
Describe crackles
``` • Non-musical explosive sounds • Most common in inspiration • Airways that have closed during expiration ‘snap’ open on inspiration • Can be early, middle or late ```
74
What types of crackles can you get?
early mid late
75
Describe features of early inspiratory crackles
* Typical of COPD (though rarely appreciated!) * Scanty - only present in severe disease * Also audible at the mouth (i.e. larger airways)
76
Describe features of mid inspiratory crackles
* Typical of bronchiectasis * Also audible at the mouth (i.e. larger airways) * May also represent bubbling secretions
77
Describe features of late inspiratory crackles
``` Generated by small, sub-pleural, fibrotic airways Sound like ‘velcro’ and usually profuse Predominantly basal Not audible at the mouth ```

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