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Flashcards in COPD Deck (28):
1

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

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

2

How should acute exacerbations of COPD be treated?

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

3

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

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

4

What changes occur in the alveoli of lungs with emphysema?

Destruction of alveolar walls by proteases
Loss of elasticity

5

What are proteases?

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

6

Why does air trapping occur in patients with emphysema?

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.

7

Why is protease activity increased in smokers?

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

8

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

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

9

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

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

10

Which immune cells secrete proteases in emphysema?

Neutrophils and macrophages.

11

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

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

12

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

Muscarininc antagonism.

13

What does the M1 muscarinic receptor facilitate?

ACh transmission on nicotinic receptors of ganglia

14

What does the M2 muscarinic receptor facilitate?

Autoreception of ACh - thus reduces release of ACh

15

What does the M3 muscarinic receptor facilitate?

Smooth muscle contraction in response to ACh

16

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

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

17

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

Ipratropium

18

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

Tiotropium

19

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

Delivered by inhalational route
Both contain quaternary ammonium group which reduces systemic exposure

20

Why is tiotropium superior to ipratropium in treatment of COPD?

Shows selectivity for M3 receptor
Longer half life at this receptor

21

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

More useful combination than either drug alone in improving FEV1

22

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

Symptomatic patients
Patients with FEV1 < 50% of expected

23

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

LAMA i.e. tiotropium

24

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

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

25

What is the Haldane effect?

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.

26

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

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

27

Which two pathologies characteristically define COPD?

Chronic bronchitis & emphysema

28

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

Obstructive - reduced FEV1