COPD

Question 1

What is COPD?

Answer 1

Common progressive disorder where abnormal inflammatory response to noxious particles/gases causes mainly irreversible airway obstruction. Includes chronic bronchitis and emphysema.
[OHCM, pts]

Question 2

What is chronic bronchitis?

Answer 2

Clinically defined as a productive cough, most days for 3 months for 2 successive years. Symptoms improve when smoking ceases, and there is no excess mortality if lung function is normal. [ohcm]

Question 3

What is the pathophysiology of bronchitis?

Answer 3

Inflammation causes hyperplasia and hypertrophy of the mucous glands. Excess mucus and wall thickening lead to airflow obstruction.

Question 4

Give 3 risk factors for COPD.

Answer 4

Smoking (>90%)
Age >35
Pollution
Alpha-1 antitrypsin defficiency
Men > women, although gap decreasing
Low socioeconomic status

Question 5

How does alpha-1 antitrypsin deficiency cause COPD?

Answer 5

A1ATD is an autosomal recessive disease where homozygotes develop severe panacinar emphysema which progresses to respiratory failure in their 40s/50s. Smoking exacerbates it by activating protease.

Question 6

Describe the clinical features of bronchitis.

Answer 6

(Blue bloaters [medcomic]):
Rhonchi (sounds like snoring), wheezing
Cough with sputum
Cyanosed, not breathless
Peripheral oedema
Cor pulmonale may occur

Question 7

Why should you be careful when giving supplemental oxygen to someone with bronchitis?

Answer 7

Their respiratory centres and relatively insensitive to CO2, their respiratory drive relies on hypoxia. Giving them oxygen can therefore deplete their respiratory drive so they stop breathing.
[ohcm, pts]

Question 8

How is the diagnosis of chronic bronchitis made?

Answer 8

Clinically: Cough with sputum most days for 3 months of 2 successive years.

Question 9

What causes rhonchi?

Answer 9

Rhonchi are low-pitched, rattling lung sounds caused by secretions (eg mucus) and obstruction (eg inflammation) in the bronchi. They usually clear after coughing.

Question 10

What investigations would you do for chronic bronchitis and what would they show?

Answer 10

Alveolar ventilation - decreased because thicker diffusion barrier
PaO2 low, PaCO2 high - decreased alveolar ventilation

Question 11

Give 3 differential diagnoses for COPD.

Answer 11

Asthma - breathlessness, younger age of onset.
Pulmonary embolism
Emphysema - pink puffers
Bronchitis - blue bloaters

Question 12

Give 3 symptoms of COPD.

Answer 12

Cough, sputum, dyspnoea, wheeze, fatigue, low mood.

Question 13

Give 3 signs of COPD.

Answer 13

Tachypnoea
Use of accessory muscles of respiration
Ankle swelling due to resulting RHF

Question 14

How is emphysema diagnosed?

Answer 14

Histologically:
Enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls.
Often visualised on CT.

Question 15

Describe the presentation of emphysema.

Answer 15

‘Pink puffers’ [medcomic]:
severe dyspnoea, not cyanosed,
quiet chest (no rhonchi)
Barrel chest

Question 16

What would alveolar ventilation, PaO2 and PaCO2 show in emphysema?

Answer 16

Alveolar ventilation increased because there is increased lung volume (fewer acini).
PaO2 is normal and PaCO2 is normal/low.

Question 17

What investigations are done to diagnose COPD?

Answer 17

Chest X ray
Spirometry
ABG
ECG

Question 18

What would you see on CXR for COPD?

Answer 18

Large central pulmonary arteries
Flattened diaphragm
Emphysema: hypodense bullae, hyperinflation. [ohcm, pts]

Question 19

What would you see on spirometry for COPD?

Answer 19

Obstructive air air trapping:
FEV1 <80% predicted; FVC normal/low; overall effect is:
FEV1:FVC <70%
Increased TLC and RV
Decreased DLCO in emphysema.
[ohcm]
reduced PEFR [pts]

Question 20

What would ABGs show for COPD?

Answer 20

Decreased PaO2.[ohcm]
Raised HCO3 shows compensation due to a chronic CO2 retention.
Hypoxia with low PaCO2 =high resp. drive, pink puffer
Hypoxia with high PaCO2 = low resp. drive, blue bloater
[pts]

Question 21

What may be seen on ECG in COPD?

Answer 21

Cor pulmonale: right atrial and ventricular hypertrophy.

Question 22

What may be seen on CT for COPD?

Answer 22

Bronchial wall thickening (bronchitis), scarring, airspace enlargement (emphysema).

Question 23

Describe the pathophysiology of emphysema.

Answer 23

Many types, most common in centrolobular, affecting the proximal acinus, asso with smoking. May also see panacinar pattern in lower lobes. Loss of elasticity in alveolar walls causes them to burst, reducing surface area for gas exchange.

Question 24

What are the aims of treatment for COPD?

Answer 24

Reduce symptoms - improve exercise tolerance, relieve symptoms
Reduce risk - prevent exacerbations, mortality and progression

Question 25

Describe the non-pharmacological management of COPD.

Answer 25

Smoking cessation
Avoid infections and increase tolerance with exercise
Diet advice, supplements

Question 26

What is first-line treatment for advanced COPD?

Answer 26

SABA (salbutamol) / SAMA (ipratropium)

Question 27

What is the treatment for advanced COPD if SAMA/SABAs fail?

Answer 27

LAMA (tiotropium)
If FEV1 >50%, LABA (salmeterol)
If FEV1 <50%, LABA plus ICS (beclomethasone) in combined inhaler.

Question 28

Salmeterol - class, mechanism?

Answer 28

Long-acting beta(-adrenoreceptor) agonist. Cause calcium channels to close and stimulates beta-2 receptors in bronchial smooth muscle, causing relaxation of muscle and therefore dilation of the airways.

Question 29

Give a major side-effect and CI of salmeterol.

Answer 29

Muscle relaxation causes tachycardia and hypertension.

Do not use with beta-blockers as this will diminish the effect.

Question 30

Ipratropium - class, mechanism?

Answer 30

Long-acting muscarinic antagonist. Blocks activity of muscarinic acetylcholine receptors (the ones which respond to muscarine), causing bronchial smooth muscle relaxation.

Question 31

Give a SE and interaction of ipratropium.

Answer 31

Dry mouth, sedation

Interaction with other anticholinergics eg tricyclic antidepressants.

Question 32

Give 3 pathogens which exacerbate COPD.

Answer 32

Viral upper RTIs, tracheobronchial tree infections [lecture 12.12.17]
Strep pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
[pts, 2011 SAQ]

Question 33

Describe the first-line management of a COPD exacerbation.

Answer 33

SABA (salbutamol) +/- SAMA (ipratropium).

Systemic corticosteroids and antibiotics can also help.

Question 34

Give 3 investigations for a COPD exacerbation and why you would do them.

Answer 34

ABG - respiratory failure? PaO2<8kPa.
CXR - exclude alternative diagnoses
ECG - aid in diagnosis of co-existing cardiac problems.
FBC - identify polycythaemia, anaemia or bleeding.
Sputum - if purulent, begin empirical antibiotics.
U&E - detect electrolyte imbalance, diabetes, poor nutrition.

Question 35

What is the target saturation of oxygen therapy in COPD?

Answer 35

88-92%.

Question 36

What are the effects of systemic corticosteroids in COPD exacerbations? Give an example of a CS used.

Answer 36

Prednisolone

• Shortens recovery time + hospital stay
• Improves lung function (FEV1) and hypoxemia (PaO2)
• reduces risk of early relapse

Question 37

What indicates need for antibiotics in COPD patients?

Answer 37

1. Increased dyspnoea+ sputum volume+sputum purulence OR

2. Requiring mechanical ventilation.

Question 38

What indicates need for hospital admission in COPD patients?

Answer 38

Marked increase in severity of symptoms
Severe underlying COPD
Onset of new physical signs
Frequent exacerbations
Older age

Question 39

What would high PaCO2 and pH <7.36 indicate in someone with COPD?

Answer 39

Acute respiratory acidosis. Exacerbation of COPD