1. OBSTRUCTIVE AIRWAYS DISEASE &
SMOKING-ASSOCIATED INTERSTITIAL LUNG DISEASE

2. OBSTRUCTIVE AIRWAYS DISEASE
Chronic bronchitis
Chronic bronchiolitis (Small Airways Disease)
Emphysema
Bronchiectasis
Bronchial asthma

3. OBSTRUCTIVE AIRWAYS DISEASE
All characterized by airflow limitation, but involve
different mechanisms and parts of the respiratory
tree
Chronic bronchitis hypersecretory
Chronic bronchiolitis obstructive
Emphysema destructive
NB Cigarette smoking
Frequently co-exist – but 2 clinical syndromes
“Blue bloater vs. Pink puffer”

5. OBSTRUCTIVE AIRWAYS DISEASE – Chronic Bronchitis
“Persistent or recurrent excess of secretion in the bronchial tree on most days for at least 3 months in the year, over 2 years”
Middle-aged & elderly, M > F
Mucoid sputum – H. Inf, Strep pneum., Bran. Cat
Cigarette smoke, air pollution, dust exposure – cadmium, smog
At PM - bronchi filled with mucous / pus
Enlargement of submucosal glands (Reid Index)
shift to pure mucous from mixed sero-mucinous type
Inceased nos of goblet cells in epithelium, at expense of ciliated cells and Clara cells

7. OBSTRUCTIVE AIRWAYS DISEASE
Acute on chronic bronchitis

8. OBSTRUCTIVE AIRWAYS DISEASE
Loss of airway ‘tapering’ in chronic bronchitis

9. OBSTRUCTIVE AIRWAYS DISEASE – Small Airway Disease
Airways < 2mm = small bronchi, proximal bronchioles
Bronchiolar goblet cell metaplasia – loss of clara cells – loss of protease inhibitor
Chronic inflammation & fibrosis – focal stenoses
Hypoxic pulmonary vasoconstriction – hypertension – cor pulmonale
Compensatory polycythaemia

10. OBSTRUCTIVE AIRWAYS DISEASE – Emphysema
Emphysema is a condition of the lung characterized by abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
Airflow limitation is due to premature closure of airways because of diminished elastic recoil

11. OBSTRUCTIVE AIRWAYS DISEASE – Emphysema
Morphologic types according to part of acinus affected
Centriacinar – cigs, UL
Panacinar 1-AT defficiency, LL
Paraseptal septal / subpleural

12. OBSTRUCTIVE AIRWAYS DISEASE
CENTRILOBULAR EMPHYSEMA
SEPTAL EMPHYSEMA

13. OBSTRUCTIVE AIRWAYS DISEASE
PARASEPTAL EMPHYSEMA
Large solitary bullae
These may grow large
enough to cause
respiratory failure by
compressing adjacent
‘normal’ lung.
Corrective bullectomy or
‘lung reduction’ may return
pulmonary function to
normal

15. OBSTRUCTIVE AIRWAYS DISEASE
PANACINAR EMPHYSEMA

16. OBSTRUCTIVE AIRWAYS DISEASE
PANACINAR EMPHYSEMA

17. OBSTRUCTIVE AIRWAYS DISEASE – Emphysema - pathogenesis
Proteases (elastase) vs. Antiproteases
Neutrophils & macrophages - sources of elastase – increased in smokers / infection / inflamm
Smoking stimulates release and enhances activity of elastase
Oxidants in cig smoke inhibit native 1-AT activity
1-AT defficiency - unopposed elastase activity
1-AT specified by proteinase inhibitor (Pi) locus – chrom 14, polymorphism – 70 different variants
PiMM – normal, Z and S mutants NB medical relevance

18. OBSTRUCTIVE AIRWAYS DISEASE – Bronchial Asthma
Asthma - characterized by hyperreactive airways leading to episodic, reversible bronchconstriction, owing to increased responsiveness of the tracheobronchial tree to various stimuli
Extrinsic / Atopic / Allergic = allergy to exogenous substances
Intrinsic / idiosyncratic / Non-atopic = no exogenous factors identified

19. OBSTRUCTIVE AIRWAYS DISEASE – Atopic Asthma
Commoner
Childhood, M>F
Less severe as age – but 30% symptoms as adults
Assoc eczema, rhinitis
Environmental triggers
Type I (IgE-mediated) hypersensitivity reaction

20. OBSTRUCTIVE AIRWAYS DISEASE – Nonatopic Asthma
Adult onset
Chronic, tending to worsen with age
Triggered by respiratory tract infxn – viral
Family hx – uncommon
Serum IgE – normal
Virus-induced inflammation may lower threshold of receptors to irritants

21. OBSTRUCTIVE AIRWAYS DISEASE – Asthma
Sputum – yellow – MPO
Eosinophils, Charcot-Leyden crystals, Curschmann’s spirals and Creola bodies
Lungs at PM – Status Asthmaticus – overdistension, mucous plugging
Micro – luminal mucous & eo, goblet cell hyperplasia, infiltration by eosinophils, BM thickening, bronchial smooth muscle hyperplasia, hypertrophy

22. OBSTRUCTIVE AIRWAYS DISEASE
(a) Curschmann
spiral
OBSTRUCTIVE AIRWAYS DISEASE
(b) Creola body b a

23. OBSTRUCTIVE AIRWAYS DISEASE
Hyperinflated
lungs in status
asthmaticus

24. OBSTRUCTIVE AIRWAYS DISEASE
Sticky mucus
plugs in status
asthmaticus

31. “SMOKING-ASSOCIATED” INTERSTITIAL LUNG DISEASE
Respiratory-bronchiolitis (RB)
Desquamative interstitial pneumonia (DIP)
Langerhan’s cell histiocytosis (LCH) Eosinophilic granuloma (EG) Histiocytosis X (HX)

32. RESPIRATORY (SMOKERS) BRONCHIOLITIS (RB) and DIP
Cough & dyspnoea
LL interstitial infiltrates, restrictive PFTs
Patchy disease
Accumulation of macrophages containing yellow-brown pigment in lumens of distal bronchioles, alveolar ducts & spaces
Mild interstitial thickening
DIP – diffuse filling of alveolar spaces
?different ends of the spectrum of one disease

39. LANGERHAN’S CELL HISTIOCYTOSIS (LCH) EOSINOPHILIC GRANULOMA
LANGERHAN’S CELL HISTIOCYTOSIS (LCH) EOSINOPHILIC GRANULOMA (EG) HISTIOCYTOSIS X (HX)
Pulmonary LCH – smokers
Cough, dyspnoea, fever, malaise, spontaneous pneumothorax
Imaging – UL, cysts and nodules
Micro: discrete stellate nodules, bronchocentric
Langerhan’s cells, histiocytes, eosinophils,
Langerhan’s cells – large histiocytes – “groovy” nuclei
Cysts, stellate or starfish-shaped scars
H&E diagnosis, IHC has replaced EM as a diagnostic tool