Molecular pathophysiology of COPD Flashcards
1
Q
Chronic obstructive
pulmonary disease
A
- Airflow obstruction that is not fully reversible
- Usually progressive
- chronic bronchitis
- emphysema - Change alveoli
2
Q
Chronic Bronchitis
A
- Lung damage and inflammation in large airways (bronchi) Chronic Cough productive
- Sputum production (3 month - 2yrs)
- Haemoptysis
- Blue tinge to skin and lips
- Peripheral oedema
3
Q
Emphysema
A
- Lung damage and inflammation
- Enlargement of air spaces to distal terminal bronchioles
- Minimal cough
- Pink flush in the face
- Hyperinflation
4
Q
Functional changes caused by COPD
A
- Airway obstruction and air trapping
- Hyperinflation
- Mucus hypersecreation
- Ciliary dysfunction
- Gas exchange impairment
- Pulmonary hypertension
5
Q
Cause of COPD
A
- 90% of patients are smokers
- 10% non-smokers with COPD caused by enviromental cause passive smoking, pollutants, inhalation of other toxins
- Men and increase with age
- Inflammation dominated by neutrophil invasion of the lung tissue
6
Q
Genetic risk factor of COPD
A
- Deficiency of α1-
protease (α1-antitrypsin) inhibitor
7
Q
COPD disease progeression
A
- Inflammatory and structural changes persist even after smoking cessation
- Lung function never returns to normal rate decline to those who stop smoking
- Deteriation amplified by smoke and age
8
Q
Differentiate if it is COPD
A
- over the age of 35
- who have a risk factor of smoking
- Exertional breathlessness
chronic cough regular sputum production and ‘bronchitis’
or wheeze.
9
Q
Pathophysiological changes in COPD
A
- Loss of elastic fibres
- Deacrease in SA
- Collapsed alveoli
- Smooth muscle contraction
- Mucus hypertension
10
Q
Mechanism of COPD
A
- Chronic airways inflammation
- Prolonged cigarette smoke
- Inflammatory response - Normal/Productive
- Increase in neutorphils activated macrophages and activated T-
lymphocytes
11
Q
Alpha-1 antitrypsin deficiency
A
- Alpha 1 antitrypsin deficiency known as alpha 1 protease inhibitor
- Genetic condition whereby there is a deficiency of the protease inhibitor
- Protease breaks down the elastases enhancing distruction of lungh tissue
- Deficiency of inhibitor
12
Q
Emphysema pathophysiology
A
- SA for gas exchange decreased leading to physiological dead space and poor diffusion capacity
- Lung tissue not effected evenly therefore lung is not ventilated evenly
- Loss of elastic recoil
- Floppy airways esistance is
increased and FEV1/FVC ratio is reduced
13
Q
Chronic bronchitis pathophysiology
A
- Incease in neutrophil levels
