for study purpose

1. COPD
Chronic obstructive pulmonary
disease
ROSHNA.P

2. • Chronic Obstructive Pulmonary Disease
• A progressive disease that affects the lungs,
making it difficult to breathe

3. Other names for COPD
• Chronic Obstructive Lung Disease (COLD)
• Chronic Lower Respiratory Disease (CLRD)

4. COPD
• Chronic obstructive pulmonary disease
(COPD) is a lung ailment that is characterized
by a persistent blockage of airflow from the
lungs.
• It is an under-diagnosed, life-threatening lung
disease that interferes with normal breathing
and is not fully reversible.

5. COPD: an umbrella term
• Umbrella term used to describe
progressive lung diseases which
include:
• Emphysema
• Chronic bronchitis
• Asthma
• Severe bronchiectasis
• Small airway disease

6. EMPHYSEMA
Abnormal permanent enlargement of the air
spaces distal to the terminal
bronchioles,accompanied by destruction of
their walls without significant fibrosis

7. • Cigarette smoking (20- 40% smokers)
• Air pollution
• Alpha-1-antitrypsin deficiency
• Inherited diseases (rare)
Cutis laxa
Marfan’s syndrome
Menke’s syndrome
ETIOLOGY

8. Cutis Laxa

9. Marfan’s syndrome Ether Danlos syndrome Menke’s syndrome

10. CLASSIFICATION
1. Centriacinar (centrilobular)emphysema
2. Panacinar (panlobular)emphysema
3. Paraseptal (distal acinar) emphysema
4. Irregular (para-cicatricial)
5. Mixed (unclassified)emphysema

12. CENTRILOBULAR
PANLOBULAR
PARASEPTAL
IRREGULAR

13. CENTRIACINAR
• Most common ; >20%
• Central or proximal
parts of the acini ,
respiratory bronchioles
are affected while distal
alveoli are spared
• Severe type affects the
distal alveoli as well
• Seen in cigrette smokers

14. CENTRIACINAR

15. PANACINAR
• Lower lung zone
• Acini are uniformly
enlarged , from the level
of the respiratory
bronchiole to the
terminal blind alveoli
• Usually seen in α1-
antitrypsin deficiency

17. DISTAL ACINAR
• The proximal portion of the acinus is normal but
the distal part is primarily involved
• Unknown cause spontaneous pneumothorax
in young adults
• Charecteristic finding : multiple , contigious ,
enlarged air spaces ranging in diameter from
<0.5mm to >2.0cm
• Sometimes forming cystic structures that , with
progressive enlargement , are referred to as
bullae

18. IRREGULAR EMPHYSEMA
• Acinus is irregularly involved , is almost
invariably associated with scarring
• Clinically asymtomatic

20. MACROSCOPIC FEATURES
• Voluminous ,pale with
little blood
• Edges of lungs are
rounded &show
dilatation of air spaces
• Subpleural bullae and
blebs bulging outwards

21. Sub pleural bullae

22. Irregular Emphysema with Bullae

23. MICROSCOPIC FEATURES
• Destruction of alveolar wall with out fibrosis , leading to
enlarged air spaces
• The number of alveolar capillaries is diminished
• Terminal and respiratory bronchioles may be deformed
because of the loss of septa that help tether these structures
in the parenchyma

26. CLINICAL FEATURES
• Long history of slowly increasing severe
exertional dyspnoea
• Obvius use of accessory muscles of
respiration
• Chest is barrel-shaped &
hyperresonant.
• Cough occours late after dyspnoea
starts & is associated with scanty
mucoid sputum.
• Recurrent respiratory infections are
not frequent

27. Complication of emphysema
• Pulmonary failure with respiratory acidosis
• Hypoxia
• Coma
• Right-sided heart failure (cor pulmonale)

28. CHRONIC BRONCHITIS
• It is defined clinically as a persistant cough
with expectoration most days for at least
three months of the year for two or more
consecutive years.
• The cough is caused by over secretion of
mucus

29. • SMOKING
• Atmospheric pollution
• Occupation
• Infection
• Familial and genetic factors
ETIOLOGY

30. PATHOGENESIS
• Irritants
• Hypertrophy of mucous glands in trachea &main
bronchi
• Hyper secretion of mucus (begin in large airways)
• Marked increase in mucin-secreting globlet cells
• Small airway disease & coexist
• Secondary microbial infection

31. MORPHOLOGIC FEATURES
• Grossly bronchial wall
Thickened
Hyperemic
Oedematous
• Lumina of the bronchi &
bronchioles
Mucus plug
Purulent exudate

33. MICROSCOPY
• Increased Reid index
ie hypertrophy &hyperplasia
• Assed using micrometer lens
or by morphometry
• Bronchial epithelium
squamous metaplasia &dysplasia
• Chronic infiltrate
• Non cartilage containing small
airways
Goblet cell hyperplasia
Intra luminal fibrosis
&Peribronchial fibrosis

35. CLINICAL FEATURES
• Persistent cough
• Sputum may persist indefinitely without
ventilatory dysfunction
• Hypercapnia ,hypoxemia ,& (in severe cases)
cyanosis
• ‟Blue bloaters”
• Recurrent respiratory infections
• Dyspnoea

36. Complications of chronic bronchitis
• Pulmonary hypertension
• Cardiac failure
• Recurrent infections
• Respiratory failure

39. BRONCHIAL ASTHMA
• Asthma is a chronic inflammatory disorder of
the airways that causes recurrent episodes of
wheezing ,breathlessness ,chest tightness ,&
cough particularly at night and /or early in the
morning.

40. • Intermittent & reversible airway obstruction
• Chronic bronchial inflammation with
eosinophils
• Bronchial smooth muscle cell hypertrophy &
hyperreactivity
• Increased mucus secretion

41. • Atopic
Evidence of allergen sensitization ,often in a patient
with a history of allergic rhinitis,eczema
• Nonatopic
• Bronchospasm can be triggered by
1.Respiratory infections
2.Environmental exposure to irritants
3.Cold air
4.Stress
5.Exercise

43. Atopic Asthma
• Most common
• Usually begin in childhood , classic example of type 1
IgE-mediated HS
• A positive family history ;Dusts ,pollen ,animal
dander , and foods
• Infections can also be a trigger
• A skin test ; immediate wheal- and flare reaction
• Diagnosis based on serum radioallergenosorbent
tests (RASTs) that identify the presence of IgE
specific for a panel of allergens.

44. Non-Atopic Asthma
• No evidence of allergen sensitization
• Skin test ;usually negative
• A positive family history of asthma is less common
• Respiratory infections due to viruses and inhaled air
pollutants are common triggers
• It is thought that virus- inducedinflammation of the
respiratory mucosa lowers the threshold of the subepithelial
vagal receptors to irritants
• Humoral and cellular mediators of airway obstruction are
common to atopic and nonatopic variants of asthma

45. Drug induced asthma
• Aspirin
• Patients with aspirin sensitivity present with
recurrent rhinitis & nasal polyps ,urticaria ,and
bronchospasm
• Mechanism remains unknown
• It is presumed that aspirin inhibit the cyclooxygnase-
1 pathway of arachidonic acid metabolism without
affecting the lipoxygenase route
• Thereby shifting the balance of production towards
leukotrienes that cause bronchial spasm

46. Occupational Asthma
• Stimulated by fumes (epoxy resins plastics)
,organic and chemical dusts (wood , cotton ,
platinum) ,gases (toluene) ,and other
chemicals
• Asthma attacks usually develop after repeated
exposure to the inciting antigen

47. MORPHOLOGY
Gross
• lungs are overdistended because of
overinflation
• Small areas of atelectasis
• Occlusion of bronchi and bronchioles by thick ,
tenacious mucous plugs

48. MICROSCOPY
• Mucous plugs contain whorls of shed epithelium (curschmann
spirals)
• Numerous eosinophils and Charcot-leyden crystals (collection
of crystalloids made up of eosinophil proteins)
• Airway remodelling include
• Thickening of airway wall
• Sub-basement membrane fibrosis
• Increased vascularity in sub mucosa
• An increase in size of the sub mucosal glands and globlet cell
metaplasia of the airway epithelium
• Hypertrophy and/or hyperplasia of the bronchial muscle

51. CLINICAL FEATURES

52. BRONCHIECTASIS
• Bronchiectasis is the permanent dilation of
bronchi and bronchioles caused by
destruction of the muscle and the supporting
elastic tissue , resulting from or associated
with chronic necrotizing infections

53. • Secondary to persisting infection or
obstruction caused by a variety of conditions
• Charecteristic symptom:cough
&expectoration of copious amounts of foul
purulent sputum
• Diagnosis: patient history +radiographic
bronchial dilatation

54. Etiology
• Bronchial obstruction
• Congenital or heriditary conditions :-
o In cystic fibrosis
o In immunodeficiency state
o Kartagener syndrome
• Necrotizing or suppurative pneumonia

55. pathogenesis
• Two processes are crucial
Obstruction
Chronic persistant infection
• Either of these may come first
• Usually affects the lower lobes bilaterally

56. Morphology
GROSS
• Most severe involvement is more distal
bronchi and bronchioles
• Airways are dilated
• Bronchioles can be seen on the pleural
surfaces

58. Microscopy
• Vary with the activity and chronicity of the
disease
• In the usual case, a mixed flora can be
cultured from the involved bronchi
• Hyperplasia of epithilium metaplasia of
epithelium in to squamous cell

59. • Full blown active case:-
• An intense acute and chronic inflammatory
exudate with in the walls of the bronchi and
bronchioles
• Desqumation of lining epithelium cause
extensive areas of ulceration

60. • Healing-lining epithelium may regenerate
completely
• Healing in chronic case- fibrosis of the
bronchial and bronchiolar wall and
peribronchiolar fibrosis
• In some instances , necrosis destroys the
bronchial or bronchiolar walls
formation of an abcess cavity within which a
fungus ball may develop

61. Clinical features
• Severe , persistant cough with expectoration
of mucopurilent , sometimes fetid sputum
• Sputum: flecks of blood , frank hemoptysis
• Symptoms are episodic , precipitated by upper
respiratory tract infections or new pathogenic
agents
• Clubbing
• Hypoxemia , hypercapnia , pulmonary
hypertension and cor pulmonale (rare)

62. Complications
• Metastatic brain abscesses
• Reactive amyloidosis

63. thankyou