COPD Flashcards

0
Q

How does bronchitis occur?

A

Increase in mucus secreting goblets cells in the bronchi. These show infiltration of CD8+ which is then followed by formation of scar tissue and thickening of bronchi walls leading to narrowed airways. As this progresses it can lead to metaplasia and fibrosis of the bronchial walls

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1
Q

What are the different types of COPD?

A

Chronic bronchitis
Emphysema
Small airway inflammation (resp bronchiolitis)

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2
Q

Define emphysema

A

An increased air space distal to the terminal bronchioles

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3
Q

What happens in emphysema?

A

There is a loss in elastic recoil of the lung with collapse of small airways during expiration obstruction the outflow of air.

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4
Q

What causes the V/Q mismatch in COPD?

A

Not all air is expired so some deoxygenated air remains in lung. Inspiration then fills lungs to normal ventilation but perfusion is low as concentration of O2 is less

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5
Q

How is CO2 retention caused in COPD?

A

Inability to fully expire leading to CO2 not being blown off and building up in the lungs and tissues

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6
Q

Why is it bad to give COPD patients oxygen?

A

If they retain CO2 and become hypoxic they may become desensitised to CO2 and regulate their respiration due to their hypoxaemia rather than the high CO2 concentration like normal. Therefore, giving oxygen restores their O2 sats causing their respiration to become uncontrolled

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7
Q

What causes the blue bloater effect in COPD?

A

Control of respiration by hypoxaemia causes renal hypoxia which causes fluid retention leading to oedema and cyanosis in the patient

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8
Q

What causes COPD and how?

A

Smoking. It increases neutrophils granulocytes which release elastases which destroy alveolar wall connective tissue. Smoking also inhibits alpha 1 antitrypsin which usually inhibits elastase further leading to destruction of alveolar walls

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9
Q

Symptoms of COPD?

A
Wheeze
Cough > 3 months
Breathlessness
Frequency chest infection
Worsened by cold
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10
Q

Signs of COPD?

A
Expiratory Wheeze
Tachypnoeic
Use of accessory muscle
Pursing of lips on expiration
Breathless
Cyanosis
CO2 flap
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11
Q

Investigations for COPD?

A

Liver function tests
CXR
CT scan

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12
Q

Treatment of COPD?

A
Smoking cessation
SABA
LABA
LABA + LAMA
LABA + corticosteroid 
Diuretic is have oedema
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13
Q

Complications of long standing COPD?

A

Cor pulmonale:

Fluid retention due to hypoxia of the kidneys leads to pulmonary hypertension and RVH.

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14
Q

Example of SABA for COPD?

A

Salbutamol

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15
Q

Examples of LABA for COPD?

A

Salmeterol

16
Q

Example of SAMA for COPD and it’s mechanism of action?

A

Ipratropium - non-selective M antagonist

17
Q

How do muscarinic antagonists work in COPD?

A

Block M receptors preventing Ca2+ release from CICR preventing bronchoconstriction. Also decreases mucus secretion which lowers surfactant and therefore lowers pressure needed to fill alveoli.

18
Q

Why do muscarinic antagonists in COPD have few side effects?

A

They have a quaternary ammonium group which prevents systemic uptake so only effect the bronchi

19
Q

When are muscarinic antagonist most effective in COPD?

A

When used in combination with a LABA like salmeterol

20
Q

How are glucocorticoids administered in COPD and when are they useful?

A

In combination inhalers with beta agonists and have a beneficial effect in those who have frequent severe exacerbations.

21
Q

What are pink puffers?

A

When CO2 is being retained these individual’s hyperventilate (puff) to blow off CO2 and return their blood gases to normal.

22
Q

What is type one respiratory failure?

A

Hypoxia with a normal or low CO2

23
Q

What is type 2 respiratory failure?

A

Hypoxia along with hypercapnia

24
Q

What are pink puffers?

A

When CO2 is being retained these individual’s hyperventilate (puff) to blow off CO2 and return their blood gases to normal.

25
Q

What is type one respiratory failure?

A

Hypoxia with a normal or low CO2

26
Q

What is type 2 respiratory failure?

A

Hypoxia along with hypercapnia