obstructive diseases 2 Flashcards

1
Q

emphysema pathogenesis

A

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

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2
Q

smoking as a cause of emphysema

A

exposure causes accumulation of neutrophils and macrophages in respiratory bronchioles
inhibits a1-antitrypsin and other anti-proteases
results in inflammation and protease activity

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3
Q

genetics as a cause of emphysema

A

most common is a1-antitrypsin deficiency

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4
Q

homozygous genetic a1 antitrypsin deficiency

A

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

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5
Q

heterozygous genetic a1-antitrypsin deficiency

A

60% of normal level

may be asymptomatic but develop emphysema much earlier if exposed to environmental pollutants

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6
Q

symptoms of emphysema occur once

A

1/3 tissue of the lung is infected

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7
Q

emphysema clinical presentations

A
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
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8
Q

2 types of emphysema

A

centriacinar

panacinar

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9
Q

canrtiaciner emphysema

A

upper lobes
loss of respiratory bronchioles in the proximal portion of the acinus
usually seen in smokers
more common than panacinar

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10
Q

panacinar emphysema

A

typical of a1-antitrypsin deficiency

all lung fields

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11
Q

2 minor types of emphysema

A

distal acinar

irregular

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12
Q

distal acinar

A

least common form
sub pleural and paraseptal
often forms bullae (bubbles)

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13
Q

irregular emphysema

A

acinus is irregularly involved

associated with scarring, usually clinically insignificant

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14
Q

bullae

A

blisters - where many damaged acini merge and trap air

can rupture and cause spontaneous pneumothorax

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15
Q

anthracosis

A

carbon pigment from smoking, air pollution

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16
Q

microscopic pathology of emphysema

A

damage to alveolar spaces

larger alveolar spaces

17
Q

chronic bronchitis as a clinical diagnosis

A

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

18
Q

symptoms and signs of CB

A

dyspnoea, eventually respiratory failure with hypoxaemia, hypercapnia and cyanosis

19
Q

CB caused by

A

chronic irritation - smoking/pollution

20
Q

chronic bronchitis vs bronchiolitis

A

inflammation of bronchi vs bronchioles

21
Q

complications of chronic bronchitis

A

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

22
Q

CB pathology

A

inflammation
increased mucus without eosinophils
plugging of bronchi in acute exacerbations
squamous metaplasia

23
Q

bronchiectasis

A

parmanent and abnormal dilatation of the bronchi and bronchioles as a result of bronchial obstruction or infection or both

24
Q

dilated bronchi

A

leads to mucus pooling
persistent cough with foul smelling sputum
if localised, surgery may be curative

25
Q

causes of bronchiectasis

A

tumour or foreign body obstructing bronchi
infection
congenital disorders
- cystic fibrosis, mucoviscidossis, kartgegener’s syndrome, defect in development of bronchi