COPD

Question 1

What are the most common causal bacteria in acute infective exacerbation of COPD?

Answer 1

Haemophilus influenzae
Streptococcus pneumoniae
Moraxella catarrhalis
All three are present in upper respiratory tract flora.

Question 2

How should acute exacerbations of COPD be treated?

Answer 2

Give antibiotics if increased sputum purulence or signs of consolidation on CXR.
1st line - amoxicillin 500mg 3x daily
2nd line - doxycycline 200mg on day 1, 100mg for next 4 days

Question 3

Why do acute exacerbations of COPD become progressively more difficult to treat?

Answer 3

Patients acquire more resistant microorganisms and more atypical organisms.
Remember - COPD is a progressive, irreversible disease.

Question 4

What changes occur in the alveoli of lungs with emphysema?

Answer 4

Destruction of alveolar walls by proteases

Loss of elasticity

Question 5

What are proteases?

Answer 5

Chemicals secreted by immune cells which cause destruction of alveolar walls and elastic

Question 6

Why does air trapping occur in patients with emphysema?

Answer 6

Loss of elastic fibres in alveolar walls and bronchioles mean the recoil effect during expiration is lost. The alveoli and bronchioles struggle to deflate in order to breathe out air.

Question 7

Why is protease activity increased in smokers?

Answer 7

Inhalation of toxins - e.g. free radical oxygen species - initiates an inflammatory immune response within the lungs.

Question 8

Which inflammatory mediators are released in emphysema from the resident alveolar macrophages?

Answer 8

IL-6
IL-8
IL-1
TNF-alpha

Question 9

What does the release of inflammatory mediators from resident alveolar macrophages do?

Answer 9

These exacerbate inflammatory response:
IL-1 and TNF-alpha recruit neutrophils by chemotaxis. These release elastase.
Other inflammatory mediators secrete other proteases.

Question 10

Which immune cells secrete proteases in emphysema?

Answer 10

Neutrophils and macrophages.

Question 11

Why is the recruitment of T-lymphocytes into alveoli in emphysema bad?

Answer 11

They cause more damage to alveolar walls - potentially by T cell mediated apoptosis

Question 12

Which method of treatment is the cornerstone of dealing with COPD - muscarinic antagonism or beta agonism?

Answer 12

Muscarininc antagonism.

Question 13

What does the M1 muscarinic receptor facilitate?

Answer 13

ACh transmission on nicotinic receptors of ganglia

Question 14

What does the M2 muscarinic receptor facilitate?

Answer 14

Autoreception of ACh - thus reduces release of ACh

Question 15

What does the M3 muscarinic receptor facilitate?

Answer 15

Smooth muscle contraction in response to ACh

Question 16

How does antagonism of the M3 muscarinic receptor assist in the treatment of COPD?

Answer 16

Inhibits release of Ca2+ from sarcoplasmic reticulum which normally occurs through coupling with Gq/11 receptor. This reduces contraction of smooth muscle.

Question 17

Give an example of a short acting muscarinic antagonist (SAMA).

Answer 17

Ipratropium

Question 18

Give an example of a long acting muscarinic antagonist (LAMA).

Answer 18

Tiotropium

Question 19

How is systemic absorption minimised in administration of ipratropium and tiotropium?

Answer 19

Delivered by inhalational route

Both contain quaternary ammonium group which reduces systemic exposure

Question 20

Why is tiotropium superior to ipratropium in treatment of COPD?

Answer 20

Shows selectivity for M3 receptor

Longer half life at this receptor

Question 21

Why is a combination of LABA/LAMA indicated in moderate COPD?

Answer 21

More useful combination than either drug alone in improving FEV1

Question 22

In which patients is a combination inhaler of LABA and corticosteroid useful?

Answer 22

Symptomatic patients

Patients with FEV1 < 50% of expected

Question 23

What treatment should be added to a patient when COPD remains uncontrolled with treatment of LABA/corticosteroid inhaler combination?

Answer 23

LAMA i.e. tiotropium

Question 24

In patients with chronic CO2 retention, which receptors in the brain do they depend on to detect desaturation?

Answer 24

O2 receptors - this is the ‘hypoxic drive’
If O2 sats in these patients reach 100% or there abouts, they will stop breathing
In normal patients, CO2 receptors used to detect desaturation

Question 25

What is the Haldane effect?

Answer 25

In chronic CO2 retention, haemoglobin becomes saturated with CO2. High-flow oxygen can push this CO2 from the haemoglobin and cause CO2 levels in blood to become increased, rendering the patient acidotic.

Question 26

Why is it dangerous to give patients with chronic CO2 retention high flow oxygen?

Answer 26

Loss of hypoxic drive
V/Q mismatching means high flow oxygen will cause shunting in these patients
Haldane effect

Question 27

Which two pathologies characteristically define COPD?

Answer 27

Chronic bronchitis & emphysema

Question 28

Does COPD produce an obstructive or a restrictive pattern on spirometry?

Answer 28

Obstructive - reduced FEV1