Emphysema is a condition characterized by irreversible enlargement of the airspaces in the lungs. There are four main types: centriacinar, panacinar, paraseptal, and irregular. Emphysema develops due to an imbalance between proteases like elastase and antiproteases like alpha-1 antitrypsin, as well as an imbalance between oxidants from cigarette smoke and antioxidants in the lungs. This protease-antiprotease and oxidant-antioxidant imbalance leads to lung tissue damage and the development of emphysema. Symptoms include progressive dyspnea, cough, and weight loss.

1. EMPHYSEMA
Dr. Sujan Vaidya

2. OBJECTIVES
1. Emphysema:
a. definition
a. types
a. pathogenesis

3. EMPHYSEMA
• condition of the lung
characterized by
irreversible
enlargement of the
airspaces distal to the
terminal bronchioles
• is accompanied by
destruction of their
walls without obvious
fibrosis.

4. TYPES OF EMPHYSEMA
1. centriacinar
1. panacinar
1. paraseptal
1. irregular

5. TERMINAL PORTION OF RESPIRATORY
TREE

6. TYPES OF EMPHYSEMA
1. centriacinar:
• central or proximal part
of acini, formed by
respiratory bronchioles,
are affected
⮚ distal alveoli are spared
• seen in heavy smokers

7. TYPES OF EMPHYSEMA
2. panacinar:
• acini uniformly
enlarged from level of
respiratory bronchiole
to terminal blind
alveoli.
• associated with
deficiency of α1-
antitrypsin

8. TYPES OF EMPHYSEMA
3. paraseptal (distal
acinar):
• distal part is
predominantly
involved.
• proximal portion of
the acinus is normal

9. TYPES OF EMPHYSEMA
4. irregular:
• acinus irregularly
involved
• almost always
associated with
scarring
• most common
form

10. PATHOGENESIS
• emphysema arises as a consequence of 2 critical
imbalances:
1. protease (elastase)- antiprotease imbalance
1. oxidant-antioxidant imbalance
⮚ effects of imbalances lead to tissue damage.

11. PROTEASE-ANTIPROTEASE IMBALANCE
• imbalance due to deficiency of α1-antitrypsin
• α1-antitrypsin:
1. normally present in serum, tissue fluids &
macrophages
1. major inhibitor of proteases (elastase), secreted by
neutrophils during inflammation.

12. • patients with genetic deficiency of α1-antitrypsin
have ↑↑ tendency to develop emphysema.
⮚ this tendency is ↑ with smoking
• about 1% of all patients with emphysema have this
defect

13. PROTEASE-ANTIPROTEASE IMBALANCE
• neutrophils (principal source of proteases) are
normally present in peripheral capillaries (including
lungs)
⮚ few gain access to the alveolar spaces
❖neutrophilic elastase capable of digesting human
lung, but inhibited by α1-antitrypsin

14. PROTEASE-ANTIPROTEASE IMBALANCE
• sequence of events:
1. in smokers, neutrophils and macrophages gain
access to alveolar spaces
1. any stimulus that ↑ no. of neutrophils and
macrophages in the lung or the release of
proteases→ ↑ proteolytic activity
1. if serum α1-antitrypsin is ↓, elastic tissue
destruction is unchecked → emphysema

15. PATHOGENESIS OF EMPHYSEMA

16. OXIDANT-ANTIOXIDANT IMBALANCE
• normally, antioxidants (Eg: glutathione) are present
in the lungs
• tobacco smoke contains abundant free radicals
⮚ smoking releases reactive oxygen species (free
radicals ) which deplete anti-oxidants present
→ inactivate anti-proteases → tissue damage

17. CLINICAL FEATURES
1. dyspnoea: begins insidiously and is progressive
⮚ expiration prolonged
2. cough
3. weight loss

18. THANK YOU