Pathology of Obstructive Lung Disease Flashcards
Obstructive airway diseases
Chronic bronchitis
Emphysema
Asthma
Chronic bronchitis and emphysema are better known as
Chronic obstructive pulmonary disease (COPD)
Normal FEV1
3.5-4 litres
Normal FVC
5 litres
Investigations for obstructive lung disease
Spirometry
Peak expiratory flow rate (PEFR)
Normal range of peak flow
80-100%
Moderate fall range of peak flow
50-80%
Marked fall range of peak flow
<50%
PEFR in obstructive lung disease
Reduced
FEV1 in obstructive ling disease
Reduced
FEV in obstructive lung disease
May be reduced
FEV1/FVC ratio in obstructive lung disease
<70%
Bronchial asthma is a reflection of
Type 1 hypersensitivity
Bronchial asthma
Bronchial smooth muscle contraction and inflammation
Bronchial asthma is generally considered to be
Reversible airway obstruction
Causes of chronic bronchitis and emphysema
Smoking Atmospheric pollution Occupation - dust Age Susceptibility
Prevalence of chronic bronchitis and emphysema
Men>women
Increasing in developing countries
Why are chronic bronchitis and emphysema more common in men than women
Men tend to smoke more and are occupied in jobs that are more likely to have them around atmospheric pollution
Clinical presentation of chronic bronchitis
Cough with sputum most days in at least 3 consecutive months for 2 or more consecutive years
Complicated chronic bronchitis when
Mucopurulent
Mucopurulent
Excess production of mucous in the respiratory tract - result in coughing it out
Morphological changes in large airways in chronic bronchitis
Mucous gland hyperplasia
Goblet cell hyperplasia
Inflammation and fibrosis - minor
Morphological changes in small airways in chronic bronchitis
Goblet cells appear
Inflammation and fibrosis in long standing disease
Emphysema
Increase in the size or airspace’s distal to the terminal bronchiole arising either from dilation or from destruction of their walls and without obvious fibrosis
Acinus
Area of lung where gas exchange takes place
Forms of emphysema
Centriacinar Panacinar Periacinar Scar 'irregular' Bullous emphysema
Centriacinar emphysema
Emphysema in the centre of the acinus, begins with bronchiolar dilation then alveolar tissue is lost
Panacinar emphysema
Emphysema in entire acinus, from bronchiole to alveoli expanded, more common in lower lobes
Periacinar emphysema
Emphysema adjacent to pleura and septal lines, distributed within secondary pulmonary lobule, subpleaural
Bulla
Emphysematous space greater than 1cm
Bleb
Bulla just underneath the pleura
Pathogenesis of emphysema
Smoking
Protease-antiprotease imbalance
Ageing
Alpha-1-antitrypsin deficiency
Apha-1-antitrypsin deficiency caused emphysema
Prevents production of anti-elastase (anti-protease) so too much elastase (protease) present leading to tissue destruction
Smoking caused emphysema
Increases the production of inflammatory cells (macrophages and neutrophils) which produce elastase (protease) production and lead to more tissue destruction. Repair mechanisms and anti-elastase proaction are inhibited.
Most of airflow limitation in COPD is
Irreversible
Mechanisms of airway obstruction in COPD in small airways
Smooth muscle tone, inflammation. fibrosis, partial collapse on expiration
Mechanisms of airway obstruction in COPD in large airways
Little contribution by glands and mucous
Mechanisms of airway obstruction that respond to pharmacological intervention
Smooth muscle tone and inflammation (like asthma)
Function of alveolar attachments
Stop alveoli from collapsing at expiration and so keep airways open
Effect of emphysema on alveolar attachments
Attachments are cut resulting in loss of pull and so flopping airways and airflow limitation
Why COPD results in hypoxaemia
Airway obstruction
Reduced respiratory drive
Loss of al velour surface are
Only during acute infective exacerbation
Chronic (hypoxic) cor pulmonale
Hypertrophy of the right ventricle resulting from disease affecting the function and/or structure of the lung
Why does chronic (hypoxic) cor pulmonate result sin pulmonary hypertension
Pulmonary vasoconsriction
Loss of capillary bed
Muscle hypertrophy and intimal fibrosis of pulmonary arterioles
Secondary polychthemia