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Emphysema
Dr. Salman Ansari
Dept. of Pathology
Kanachur Institute of Medical Sciences
Contents
● Definition
● Types of emphysema
● Pathogenesis
● Morphology
● Clinical features
● Complications
Emphysema
Definition: Irreversible dilation of air spaces distal to terminal
bronchiole, accompanied by destruction of their walls.
Types of emphysema
Classified according to anatomic distribution.
1. Centriacinar
2. Panacinar
3. Paraseptal
4. Irregular
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
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.
4. Irregular :
- Acinus is irregularly involved
- associated with scarring.
- asymptomatic and clinically insignificant.
- most common type
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
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.
● 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.
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.
Clinical features
● Dyspnea , cough, wheezing
● Prolonged expiration
● Barrel chest
● Pink puffers
Complications
(i) Cor pulmonale
(ii) congestive heart failure due to secondary pulmonary
hypertension and pneumothorax.
(iii) death
Death is due to:
● Respiratory acidosis and coma
● Rt sided heart failure
● Massive collapse secondary to pneumothorax
References:
Ramadas Nayak - Exam Prep Manual for Undergraduates
Questions:
salman.s.ansari92@gmail.com
For PPT, scan:
For notes, click here
or scan:

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Emphysema - Pathology - ATOT

  • 1. Emphysema Dr. Salman Ansari Dept. of Pathology Kanachur Institute of Medical Sciences
  • 2. Contents ● Definition ● Types of emphysema ● Pathogenesis ● Morphology ● Clinical features ● Complications
  • 3. Emphysema Definition: Irreversible dilation of air spaces distal to terminal bronchiole, accompanied by destruction of their walls.
  • 4.
  • 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.
  • 18.
  • 19.
  • 20.
  • 21. Clinical features ● Dyspnea , cough, wheezing ● Prolonged expiration ● Barrel chest ● Pink puffers
  • 22.
  • 23.
  • 24. Complications (i) Cor pulmonale (ii) congestive heart failure due to secondary pulmonary hypertension and pneumothorax. (iii) death
  • 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 Questions: salman.s.ansari92@gmail.com For PPT, scan: For notes, click here or scan: