Copd 2 5-2016 madhu

1. COPD- CHRONIC
OBSTRUCTIVE PULMONARY
DISEASE
DR. T.Matumithra MDDNB(Pathology)
Assistant Professor

3. OBSTRUCTIVE AND
RESTRICTIVE LUNG
DISAEASES
 OBSTRUCTIVE DISEASE:
restriction to airflow entry(eg: mucous plugs,
bronchoconstriction)
 RESTRICTIVE LUNG DISEASE:
Restriction to expansion of alveoli( interstial lung
disease, pneumoconioses)

4. OBSTRUCTIVE LUNG
DISEASE
 1. Emphysema
 2. Chronic bronchitis
 3. Bronchiectasis
 4. Asthma
COPD

5. 1. EMPHYSEMA
abnormal permanent enlargement of the airspaces
distal to the terminal bronchiole, accompanied by
destruction of their walls without obvious fibrosis.

6. Types of emphysema
According to its anatomic distribution within the
lobule,
a. Centriacinar (centilobular)
b. Panacinar (panlobular)
c. Paraseptal (distal acinar)
d. Irregular
 First two cause clinically significant airflow
obstruction
 Centriacinar type constitute >95% of cases

7. a. Centriacinar Emphysema
 The central or proximal part of the acini -affected.
 both emphysematous & normal airspaces exist in a
acinus
 More frequent in heavy smokers

8. Centriacinar Emphysema

9. b. Panacinar Emphysema
 The acini are
uniformly
enlarged
 Lower lung
lobes
 associated with
α1-antitrypsin
(α1-AT)
deficiency

10. Panacinar Emphysema

11. c. Distal Acinar Emphysema
(Paraseptal Emphysema)
 The proximal portion of the acinus is normal, but
the distal part is predominantly involved
 More severe in the upper half of lungs
 Characteristic findings are multiple, continuous,
enlarged airspaces from 0.5 cm to >2cm in dia

12. Irregular Emphysema
 The acinus is irregularly involved, and is
almost invariably associated with scarring
(airspace enlargement with fibrosis)
 In most instances foci of irregular emphysema
are asymptomatic & clinically insignificant

13. Bullous Emphysema
 Defined as subpleural emphysematous
spaces >1-2 cm in diameter
 Rupture of bullae may result in pneumothorax

14. Bullous Emphysema

15. Pathogenesis of emphysema:
Protease – antiprotease theory
↓Alpha 1 antitrypsin
↑Elastase
(PMN, macrophage)
Elastic
damage
Emphysema
Smoking

17. Smoking & emphysema
 Smokers have greater numbers of neutrophils
& macrophages in their alveoli
 Smoking stimulate release of
elastase(protease) from neutrophils
 Oxidants in smoke & free radicals released by
neutrophils inhibit alpha 1 antitrypsin
(functional alpha 1 antitrypsin deficiency)

18. Alpha 1 antitrypsin deficiency
Geno Type
% of
Population
Normal Pi MM 95% - 97%
Heterozygote Pi MZ 3% - 5%
Homozygote Pi ZZ 0.07% - 0.2%
More than 80% of PiZZ phenotype develop
symptomatic emphysema

19. Clinical course
 Do not manifest until at least 1/3rd
of
functioning lung parenchyma is damaged
 Dyspnea- insiious , slow progressive
 Cough and expectoration(ass with chronic
bronchitis)
 Weight loss
 barrel chested , sits forward in hunched up
position, breaths through pursed lips
Expiratory airflow limitation, measured through
spirometry, is the key to diagnosis

20. Mysterious
boiling river

21. 2.Chronic Bronchitis
 Is defined clinically as persistent cough with
sputum production for at least 3 months in at
least 2 consecutive years
 Tends to affect middle-aged men who are
smokers.

22. Types of chronic bronchitis
 A. Simple chronic bronchitis
 Have productive cough but no evidence of airway
obstruction
 B. Chronic asthmatic bronchitis
 Hyperreactive airways with intermittent
bronchospasm & wheezing
 C. Obstructive chronic bronchitis
 Chronic airflow obstruction with emphysema (in
chronic smokers)

23. Chronic Bronchitis-
Pathogenesis
 Chronic irritation by inhaled substances (cigarette
smoking is the single most important factor)also
grains, cotton & silica dust.
 4 – 10 times more common in smokers..

24. Pathogenesis (cont)
 To bacco irritants e licit inflam m ato ry m e diato rs
 hypertrophy of the submucosal glands in the
trachea and bronchi
 hype rse cre tio n o f m ucus in the large airways
 smoking impairs ciliary apparatus- predisposes to
infection

25. Morphologic Correlates Of Chronic
Bronchitis
1. Edematous mucous membrane with Mucous
hypersecretion and plugging
2. Goblet cell metaplasia
3. Hypertrophy and hyperplasia of mucosal
glands (Reid Index – normal .4)- increased
reid index
4. Lymphocytic infiltration

26. Clinical features
 1.Persistent cough with sputum production.
 2.Dyspnea on exertion.
 3.hypercapnia, hypoxemia, and mild cyanosis.
 Death may also result from further impairment of
respiratory function incident to acute intercurrent
bacterial infections.

27. Clinical course in Emphysema & Chronic Bronchitis
Predominate
Bronchitis
Predominant
Emphysema
Age (Yr) 40-45 50-75
Dyspnea Mild; late Severe; early
Cough Early; copious
sputum
Late; scanty
sputum
Infections Common Occasional
Cor pulmonale Common Rare; terminal

29. THANK U

32. THANK U

33. Bronchiectasis
 Bronchiectasis is characterized by permanent
dilation of bronchi and bronchioles caused by
destruction of the muscle and elastic tissue,
resulting from or associated with chronic
necrotizing infections.

34. Bronchiectasis
 Obstructive
 Tumor
 Foreign body
 Concretions/secretions
 Non-obstructive
 Post-infective
 Inherited disorders – cystic fibrosis,
immunodeficiency, and immotile cilia syndrome

35. Kartagener Syndrome
Defect in ciliary motility due to structural
abnormality in the cilia (absence of dynein
arms)
 Situs invertus
 Bronchiectasis
 Sinusitis

36. Bronchiectasis
Lung shows
markedly dilated
bronchi and
bronchioles, that
can be traced
up to pleural
surfaces.

37. Bronchiectasis - clinical
Features
 Chronic productive cough
 Hemoptysis
 Dyspnea and wheezing
 Pneumonia, abscess
 Systemic: fever, weight loss, weakness
Less frequent complications:
 Cor pulmonale
 Metastatic brain abscesses &
 Amyloidosis

38. Conditio
n
(OPD)
Site
Pathologic
Changes
Cause Signs
Chronic
bronchitis
Bronchus
Mucous gland
hyperplasia,
hypersecretion
Smoking,
pollution
Cough &
sputum
Bronchi-
ectasis
Bronchus
Airway dilation
& scarring
Persistent or
severe infection
Cough,
fever,
sputum
Asthma Bronchus
Smooth muscle
hyperplasia,
excess mucus,
inflammation
Immunologic or
unknown
Wheezing
cough
dyspnea
Emphy-
sema
Acinus
Airspace
enlargement;
wall destruction
Tobacco
smoke
Dyspnea
Small
airway
Bronch- Inflammatory
scarring/oblite-
Smoking, Cough,