Obstructive diseases : Chr.by Obstruction to airflow out of the lungs Due to partial or complete obstruction in airway. Increase in lung compliance and Decrease in lung elasticity. Restrictive diseases : Chr by reduced expansion of lung parenchyma with problems in getting air in the lungs. Lung compliance is decreased Elasticity is increased: once air is in the lungs it comes out rapidly on expiration.

1. Obstructive versus Restrictive Lung
Diseases
Spr 09 1

2. 1. Obstructive diseases : Chr.by
• Obstruction to airflow out of the lungs
Due to partial or complete obstruction in
airway.
Increase in lung compliance and
Decrease in lung elasticity.
2. Restrictive diseases : Chr by
• reduced expansion of lung parenchyma with
problems in getting air in the lungs.
• Lung compliance is decreased
• Elasticity is increased: once air is in the
lungs it comes out rapidly on expiration.
Spr 09 2

3. Problem with getting air out of the lungs.
Pulmonary function tests:
Forced expiratory volume in 1 sec (FEV 1sec) is
Decreased
Normal FEV 1sec = 4L
Usually <2 L in obstructive diseases.
Forced vital capacity (FVC) is decreased
Normal is 5 L
Usually < 4 L due to decreased elasticity
FEV 1sec / FVC ratio is decreased:
Normal is 4/5 = 80%
In obstructive diseases (1/3 = 33%)
Obstructive diseases
Spr 09 3

4. 1. Chronic obstructive pulmonary disease
(COPD)
1. Emphysema
2. Chronic bronchitis
2. Asthma
3. Bronchiectasis
The obstructive lung diseases
Spr 09 4

5. Chronic obstructive pulmonary disease
(COPD)
Includes two conditions that typically occur
together.
Chronic bronchitis
Emphysema
Both cause chronic or recurrent obstruction to
the airflow out of the lungs.
Both associated with one major symptom –
dyspnea.
Major pathogenetic mechanism:
Cigarette smoking.
Proven association between COPD and
smoking
Spr 09 5

6. Emphysema
Spr 09 6

7. Acinus= the respiratory unit
Is the basic gas
exchange unit of lungs
Also Known As = The
respiratory unit
Composed of:
Respiratory bronchiole
Alveolar ducts
Alveolar sacs
Alveolus
Spr 09 7

8. Emphysema
Characterized by:
Permanent Enlargement of all or part of the
respiratory unit.
respiratory bronchiole, alveolar ducts and
alveoli.
Due to destruction of their elastic tissue
support (walls).
Results in: Loss of elastic recoil and
enlarged air spaces.
Spr 09 8

9. Acinus
Resp. bronchiole
Alveolar ducts
Alveoli
1.Permanent enlargement
2.Destruction of elastic
tissue support
Pure emphysema
Spr 09 9

10. Normal lung gross
Normal lung gross
Lung with Emphysema
A
C
B
Spr 09 10

11. Emphysema
Causes:
1. Cigarette smoking is the MC cause
2. α1-Antitrypsin (AAT) deficiency
Pathogenesis:
1. Imbalance between elastase and anti-
elastase (α1-Antitrypsin).
2. Imbalance between oxidants (free radicals)
and antioxidants (e.g. glutathione)
3. Elastase and oxidants
Derived from neutrophils and macrophages
4. Net effect of preceding imbalances is
Destruction of elastic tissue of airways.Spr 09 11

12. Emphysema: Pathogenesis
Cigarette smoke is chemotactic to neutrophils
and macrophages
Accumulate in respiratory unit
Release free radicals and elastases.
Free radicals can inactivate AAT and
antioxidants.
Elastases destroy elastic tissue
Net effect:
Destruction of elastic tissue of airways.
Spr 09 12

13. Pathogenesis
Normal function of elastic tissue:
Apply radial traction to keep airways
open.
Destruction of elastic tissue causes:
Loss of radial traction
Small airways collapse on expiration.
Prevents egress of air out of the
respiratory unit
Trapped air distends the respiratory
unit.
Spr 09 13

14. Types of emphysema
 Four anatomical
types of
emphysema
1. Centriacinar*
2. Panacinar*
3. Distal acinar
4. Irregular
Respiratory
Bronchiole
Alveolar duct
Alveolus
Normal acinus
Spr 09 14

15. Centriacinar (centri-lobular ) emphysema
Most common type of emphysema in
smokers.
Respiratory bronchioles : primary site of
elastic tissue damage.
Usually involves the apical segments of
upper lobes.
Spr 09 15

16. Distended
respiratory
bronchiole
Centriacinar emphysema
Spr 09 16

17. Panacinar emphysema
It is characterized by:
Uniform destruction and enlargement of
respiratory unit (respiratory bronchiole,
alveolar duct and alveoli).
Mainly affects the lower lobes.
Associated with α1-Antitrypsin (AAT)
deficiency
1. Genetic
2. Acquired
Spr 09 17

18. Panacinar emphysema
Distended
respiratory unit
Spr 09 18

19. Panacinar emphysema
Genetic type of AAT deficiency
Autosomal recessive disorder
MM phenotype is normal
Normal amounts of AAT synthesized in the
liver
ZZ phenotype has decreased synthesis of AAT
Emphysema develops at an early age in the
genetic type.
Acquired AAT deficiency:
Cigarette smoke inactivates AAT
Spr 09 19

20. Distal acinar (Paraseptal) emphysema
Does not produce obstructive lung disease
Mainly involves the alveolar ducts and the alveoli
sparing the proximal part of respiratory unit.
Appear as large air filled spaces located beneath
the pleura.
Note: if the air filled spaces >1cm in
diameter , they are called bullae.
Increased incidence of pneumothorax
Spr 09 20

21. Distal acinar (Paraseptal) emphysema
Spr 09 21

22. Emphysema: Microscopy
Thinning and destruction of alveolar walls.
Adjacent alveoli fuse  large airspaces.
Loss of alveolar capillaries.
Normal lung : micro Emphysema
Spr 09 22

23. Emphysema
Loss of elastic recoil causes small airways to collapse
during expiration – trapping the air.
Clinical findings:
Dyspnea: Severe and occurs early
Hyperventilation: Well oxygenated blood  pink
puffers.
Increased TLC
Diminished breath sounds due to lung hyperinflation.
Change in the shape of chest : Barrel chest
Decreased FEV 1sec/FVC ratio
Cor pulmonale is uncommon
Blood gas values = usually normal
Spr 09 23

24. Emphysema
Chest radiograph:
Hyperluscent lung fields
Increased Anterior posterior (AP)
diameter
Vertically oriented heart
Depressed diaphragm.
Spr 09 24

25. Spr 09 25

26. A typical patient
Barrel-chested and
dyspneic with prolonged
expiration.
Sitting forward in a
hunched over position
Attempting to squeeze air
out of the lungs with
pursed lips .
= Pink puffers
Spr 09 26

27. Chronic bronchitis
Most common form of COPD
Chronic bronchitis has a clinical definition,
requiring :
1. Persistent cough and sputum production
2. Present for at least 3 months
3. Present for at least 2 consecutive years
Etiology:
Strong association with cigarette smoking and
Urban residence (air pollution).
Spr 09 27

28. Large airways (trachea,bronchi)
•Inflammation
•Mucus gland hyperplasia
•Mucus hypersecretion
Small airways (T.bronchioles)
•Inflammation
•Goblet cell metaplasia
•Mucus plugs
•SMC hypertrophy
Pure chronic bronchitis
Spr 09 28

29. Pathogenesis
Chronic irritation by inhaled substances.
1. Hyperplasia of submucosal glands
resulting in
Hypersecretion of mucus in bronchi.
2. Obstruction to airflow in the terminal
bronchioles.
Spr 09 29

30. Effects of cigarette smoke and air pollutants
Changes in Bronchi:
Inflammation
Mucous gland hypertrophy and hyperplasia
which results in an increased Reid Index.
Result: excessive mucous production.
Changes in Terminal bronchioles:
Inflammation and fibrosis
Goblet cell metaplasia and Mucous plugs
Smooth muscle hypertrophy
Result: Narrowing  airflow obstruction.
Spr 09 30

31. CD:AB = Reid index
Mucous gland
hyperplasia
Ratio of the thickness of submucosal mucous
glands to entire submucosa
Spr 09 31

32. Clinical features
Persistent cough productive of copious sputum*.
Dyspnea occurs late in the disease.
Tend to be stocky and obese
Hypercarbia (CO2 retention)
Cyanosis of mucous membrane and skin.
Patients called as blue bloaters.
Severe hypoxemia  vasoconstriction
Pulmonary HT and Cor pulmonale is common.
Frequent infections
Spr 09 32

33. Effects of COPD
In Emphysema
Airways collapse and become obstructed.
In Chronic bronchitis
mucous hypersecretion and airway edema and
inflammation leads to airway plugging.
The net effect of COPD
is to make it difficult to get air out of lungs
Spr 09 33

34. Effects of COPD
Pulmonary hypertension: results from a
combination of:
pulmonary vasoconstriction (induced
by hypoxemia
Loss of pulmonary vasculature surface
area and
increased blood viscosity (due to polycythemia
induced by chronic hypoxia)
The Heart develops right ventricular hypertrophy
Right ventricular failure and Cor Pulmonale
Spr 09 34

35. Effects of COPD
Spr 09 35

36. Blue bloaterPink Puffer
Spr 09 36