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OBSTRUCTIVE AIRWAYS DISEASE & SMOKING- ASSOCIATED INTERSTITIAL LUNG DISEASE.

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Presentation on theme: "OBSTRUCTIVE AIRWAYS DISEASE & SMOKING- ASSOCIATED INTERSTITIAL LUNG DISEASE."— Presentation transcript:

1 OBSTRUCTIVE AIRWAYS DISEASE & SMOKING- ASSOCIATED INTERSTITIAL LUNG DISEASE

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

3 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” OBSTRUCTIVE AIRWAYS DISEASE

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5 “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 OBSTRUCTIVE AIRWAYS DISEASE – Chronic Bronchitis

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7 OBSTRUCTIVE AIRWAYS DISEASE Acute on chronic bronchitis

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

9 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 OBSTRUCTIVE AIRWAYS DISEASE – Small Airway Disease

10 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 OBSTRUCTIVE AIRWAYS DISEASE – Emphysema

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

12 OBSTRUCTIVE AIRWAYS DISEASE CENTRILOBULAR EMPHYSEMASEPTAL 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

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15 OBSTRUCTIVE AIRWAYS DISEASE PANACINAR EMPHYSEMA

16 OBSTRUCTIVE AIRWAYS DISEASE PANACINAR EMPHYSEMA

17 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 OBSTRUCTIVE AIRWAYS DISEASE – Emphysema - pathogenesis

18 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 OBSTRUCTIVE AIRWAYS DISEASE – Bronchial Asthma

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

20 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 OBSTRUCTIVE AIRWAYS DISEASE – Nonatopic Asthma

21 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 OBSTRUCTIVE AIRWAYS DISEASE – Asthma

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

23 OBSTRUCTIVE AIRWAYS DISEASE Hyperinflated lungs in status asthmaticus

24 OBSTRUCTIVE AIRWAYS DISEASE Sticky mucus plugs in status asthmaticus

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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

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39 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 LANGERHAN’S CELL HISTIOCYTOSIS (LCH) EOSINOPHILIC GRANULOMA (EG) HISTIOCYTOSIS X (HX)

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