obstructive diseases 2 Flashcards
emphysema pathogenesis
alveolar wall destruction
occurs due to
- repeated damage to alveolar acini
- chronic inflammation - triggered by inhaled particles and cell damage
- imbalance of protease/anti-protease activity
- protease in neutrophils and Mac prophages in lung
- anti-proteases found in bronchial mucus
smoking as a cause of emphysema
exposure causes accumulation of neutrophils and macrophages in respiratory bronchioles
inhibits a1-antitrypsin and other anti-proteases
results in inflammation and protease activity
genetics as a cause of emphysema
most common is a1-antitrypsin deficiency
homozygous genetic a1 antitrypsin deficiency
10% of normal level
cirrhosis of liver in infancy
because a1-antitrypsin is produced here and can’t be transported out
severe emphysema in early adult life
heterozygous genetic a1-antitrypsin deficiency
60% of normal level
may be asymptomatic but develop emphysema much earlier if exposed to environmental pollutants
symptoms of emphysema occur once
1/3 tissue of the lung is infected
emphysema clinical presentations
barrel chest - expiratory difficulty decreased exercise tolerance wheezing cough If associated chronic bronchitis chest hyper resonant to percussion decreased density of lungs on x ray
2 types of emphysema
centriacinar
panacinar
canrtiaciner emphysema
upper lobes
loss of respiratory bronchioles in the proximal portion of the acinus
usually seen in smokers
more common than panacinar
panacinar emphysema
typical of a1-antitrypsin deficiency
all lung fields
2 minor types of emphysema
distal acinar
irregular
distal acinar
least common form
sub pleural and paraseptal
often forms bullae (bubbles)
irregular emphysema
acinus is irregularly involved
associated with scarring, usually clinically insignificant
bullae
blisters - where many damaged acini merge and trap air
can rupture and cause spontaneous pneumothorax
anthracosis
carbon pigment from smoking, air pollution
microscopic pathology of emphysema
damage to alveolar spaces
larger alveolar spaces
chronic bronchitis as a clinical diagnosis
cough productive of sputum on most days for three months of the year for at least 2 consecutive years
approx 75 ml of sputum/day
symptoms and signs of CB
dyspnoea, eventually respiratory failure with hypoxaemia, hypercapnia and cyanosis
CB caused by
chronic irritation - smoking/pollution
chronic bronchitis vs bronchiolitis
inflammation of bronchi vs bronchioles
complications of chronic bronchitis
acute infective episodes with pneumonia or exacerbation or respiratory failure
cor pulmonale and right heart failure
squamous metaplasia - possibly lead to dysplasia/ malignant change in bronchial epithelium
secondary fibrosis of bronchial lumen
CB pathology
inflammation
increased mucus without eosinophils
plugging of bronchi in acute exacerbations
squamous metaplasia
bronchiectasis
parmanent and abnormal dilatation of the bronchi and bronchioles as a result of bronchial obstruction or infection or both
dilated bronchi
leads to mucus pooling
persistent cough with foul smelling sputum
if localised, surgery may be curative
causes of bronchiectasis
tumour or foreign body obstructing bronchi
infection
congenital disorders
- cystic fibrosis, mucoviscidossis, kartgegener’s syndrome, defect in development of bronchi
