Topic: Emphysema
Subject: Pathology
Course: ATOT 2nd year
Emphysema: Definition, Types, Pathogenesis, Morphology, Clinical features and Complications of Emphysema
Meant for BSc ATOT students and other allied health sciences
Reference: Ramadas Nayak - Exam Preparatory Manual for Undergraduates - Pathology
5. Types of emphysema
Classified according to anatomic distribution.
1. Centriacinar
2. Panacinar
3. Paraseptal
4. Irregular
6.
7.
8.
9. Centriacinar:
- upper lobes
- involve the central or proximal parts of the acini (formed by
respiratory bronchioles), whereas distal alveoli are spared.
- occurs predominantly in smokers, in association with chronic
bronchitis.
Panacinar :
- acini uniformly enlarged
- lower lobes of lung
- α1 antitrypsin deficiency
10.
11. 3. Distal/paraseptal acinar:
- Dilatation affects the distal airspace at the periphery of the lobule
and the proximal portion is normal.
- Site: Adjacent to pleura, along the lobular connective tissue septa
- Areas of fibrosis, scarring and atelectasis
- Multiple,continuous,enlarged airspaces, less than 0.5cm to more
than 2.0 cm
Cyst like structures.
Spontaneous pneumothorax.
12. 4. Irregular :
- Acinus is irregularly involved
- associated with scarring.
- asymptomatic and clinically insignificant.
- most common type
13. Pathogenesis
Factors involved in pathogenesis of emphysema are:
● Inflammatory mediators released in lung
● Protease-antiprotease mechanism
● Imbalance of oxidants and antioxidants
● Oxidative stress
● Airway infection
14. Protease- antiprotease imbalance hypothesis:
- Injury due to heavy smoking and pollution causes
activation of inflammatory cells like neutrophils
- This causes damage to epithelial cells
- genetic deficiency of the antiprotease a1-
antitrypsin: enhanced tendency to develop
emphysema which is increased by smoking.
15. ● α1-Antitrypsin: present in serum, tissue fluids, and
macrophages
● Major inhibitor of proteases (particularly elastase)
secreted by neutrophils.
● Emphysema results from destructive effect of high
protease activity in people with low antiprotease activity.
16.
17. Morphology
Gross:
● Voluminous lungs
● Upper two thirds of lung
● Large apical blebs or bullae
Microscopically :
● Large alveoli separated by thin septa
● Destruction of septal wall
● fibrosis and chronic inflammation of the walls.
25. Death is due to:
● Respiratory acidosis and coma
● Rt sided heart failure
● Massive collapse secondary to pneumothorax
26. References:
Ramadas Nayak - Exam Prep Manual for Undergraduates
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