Week 103 - COPD Flashcards

1
Q

What is a definition of COPD?

A

Disease causing airflow obstruction that is not fully reversible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is FEV1?

A

The volume of air that can be expired in one second and a full inspiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What affect does COPD have on FEV1?

A

Reduced, obstructive lung disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three main pathphysiologies of COPD?

A

1) Chronic Bronchitis
2) Emphysema
3) Respiratory Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Chronic Bronchitis?

A

Cough, production of purulent sputum for >3 months of at least 2 consecutive years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the pathogenesis of bronchitis?

A
  • Inflammation and narrowing of bronchi.
  • Increased mucous secretion (Due to hypertrophy of goblet cells)
  • Squamous metaplasia, resulting in loss of cilia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is emphysema?

A

Destruction of lung tissues distal to terminal bronchioles and loss of elasticity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the pathogenesis of emphysema?

A
  • Inflammation occurs, inflammatory cells infiltrate epithelium.
  • Proteases are released by the cells.
  • Collagen/ elastin is broken down.
  • This results in small bronchioles snapping shut, trapping air and resulting in hyperinflation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What deficiency can cause people to be more prone to developing emphysema?

A
  • Alpha-1 Anti Trypsin.

* Alpha-1 Anti Trypsin is an anti-protease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is respiratory failure?

A

Sufficiently impaired gas exchange that leads to hypoxaemia (<8.0 kPa O2 in arterial blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the two types of respiratory failure?

A

1) Pink puffers

2) Blue bloaters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are pink puffers?

A

These are people with a low PaO2 and a normal PaCO2, they therefore need a high respiratory effort in order to maintain normal PaCO2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the symptoms/signs of a pink puffer?

A
  • Dyspnoea
  • Barrel Chest
  • Accessory muscle use
  • Paradoxical costal margin.
  • Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are blue bloaters?

A

these are people with a low PaO2 and a high PaCO2, they can’t maintain enough respiratory effort to keep the PaCO2 down.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the signs/symptoms of blue bloaters?

A
  • Less breathless than pink puffers.
  • Cyanosis and flapping tremor.
  • Oedema and high JVP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why do blue bloaters have a high JVP and oedema?

A

Due to Cor Pulmonale (Right sided heart failure) as a result of pulmonary hypertension.

17
Q

Week 103 - COPD: To which level is cartilage present in the airways?

A

From trachea to proximal bronchioles.

18
Q

Week 103 - COPD: What three cells make up the bronchial epithelium?

A
  • Goblet cells
  • Ciliated columnar cells
  • Bronchial gland
19
Q

Week 103 - COPD: What is the WHO definition of Chronic bronchitis?

A
  • An inflammatory process in the wall of the bronchioles with excessive production of mucus and sputum from hypertrophic glands.
  • The small airways are narrow.
  • Morning cough for more than 3 months per year.
20
Q

Week 103 - COPD: What is the pathology behind chronic bronchitis?

A

• Cigarette smoke and other irritants lead to,

  • Increased goblet cells, mucous glands and mucus in the lumen.
  • Inflammatory cell infiltration.
21
Q

Week 103 - COPD: alpha-1-antitrypsin deficiency can lead to which lung pathology? What is the process behind it?

A

• Emphysema

  • Smoke causes inflammatory cell infiltration.
  • Cells release proteases.
  • These over-whelm the bodies natural anti-proteases.
  • Causing destruction of alveolar walls.
22
Q

Week 103 - COPD: What is emphysema?

A

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

23
Q

Week 103 - COPD: What distinguishes small airway disease from emphysema?

A

small airway disease has fibrosis.

24
Q

Week 103 - COPD: What is type 1 respiratory failure? How is is it typically caused?

A
  • Hypoxemia without hypercapnia.

* It is typically caused by a V/Q mismatch.

25
Week 103 - COPD: What is type 2 respiratory failure?
* Hypoxemia and hypercapnia. | * Due to inadequate alveolar ventilation.
26
Week 103 - COPD: What occurs to spirometry results in obstructive lung disease?
* FEV1 reduced * FVC normal/reduced * FEV1/FVC = reduced (normal is around 80%)
27
Week 103 - COPD: How does the FEV1 % predicted lead to staging of COPD? (NICE 2010)
• ≥80% - mild • 50-79% - moderate • 30 - 49% - severe •
28
Week 103 - COPD: What is the four stepped algorithm for inhaled drug management of COPD?
1) As required SABA. 2) As required SABA and tiotropium (long acting anticholinergic bronchodilator). 3) As required SABA, tiotropium and LABA. 4) Add ICS/LABA combined inhaler.
29
Week 103 - COPD: Give an example of a mucolytic and explain why it is good for the management of COPD.
* Carbocisteine (Mucodyne) | * Reduces acute exacerbations, the need for antibiotics, fewer days of illness.
30
Week 103 - COPD: What are the management steps for treating an acute exacerbation of COPD?
* Nebulised bronchodilators. * Controlled oxygen therapy. * Antibiotics if sputum purulent. * IV fluids * Corticosteroids * Consider IV aminophylline * Chest physio * Non-invasive ventilation * ITU if appropriate (Ceiling of treatment)
31
Week 103 - COPD: What are the two receptors responsible for smooth muscle contraction/dilatation of the bronchioles?
* M receptor - Broncho-constriction | * B2 receptor - Broncho-Dilatation
32
Week 103 - COPD: Give some examples of B2-agonists.
* SABA - Salbutamol, Terbutaline | * LABA - Salmeterol, Formoterol
33
Week 103 - COPD: What are the side effects of B2-agonists?
Tremor, Hypokalaemia, tachycardia.
34
Week 103 - COPD: How do muscarinic antagonists work? Give examples.
* Antagonises the effect of acetylcholine on the muscarinic receptors to reduce bronchoconstriction. * Ipratropium and Tiotropium