Pneumoconiosis

pathology

1. PNEUMOCONIOSIS Dr.Sundaresan Pathology Loyola college

2. PNEUMOCONIOSIS Pneumoconiosis is a disease of lung caused by inhalation of organic & inorganic particles,fumes & vapours . Important types of pneumoconiosis Asbestosis ASBESTOS Berylliosis BERYLLIUM Siderosis IRON Stannosis TIN Byssinosis COTTON Silicosis SILICA

3. Coal Workers Pneumoconiosis Coal dust exposure occurs in coal miners. PATHOGENESIS Coal dust contains amorphous carbon and variable amount of Silica. It induces fibrosis OR Failure of normal clearance mechanism to remove excess coal leads to fibrosis by accumulated coal.

4. Accumulated coal dust induces fibrosis by ( i )Lung injury by reactive oxygen (ii)Stimulation of macrophages to produce cytokines (iii)Increase protease activity MORPHOLOGY -Types 1 .Asymptomatic -Carbon pigment accumulates in the macrophages and connective tissues 2.Simple Coal Pneumoconiosis -Collection of Carbon laden macrophages- macules Macules coalesce to form nodule surrounded by fibro collagenous tissue.The fibro collagenous tissue can obliterate alveoli-EMPHYSEMA UPPER LOBE

5. 3. Progressive massive fibrosis Over years simple coal workers pneumoconiosis progresses to progressive massive fibrosis. There are large areas of scarring and carbon pigmented areas. There is lung dysfunction.

6. COMPLICATIONS 1.Simple Coal workers pneumoconiosis cause chronic bronchiotis and Bronchiolitis . 2.Progressive Coal Workers pneumoconiosis cause (a) Cor Pulmonale (b) Caplan Syndrome-Coal worker pneumoconiosis along with rheumatoid nodule.It can also be seen in association with silicosis or asbestosis.The Lesions are nodular with central necrosis surrounded by fibroblasts and macrophages.

7. CLINICAL PICTURE Coal workers pneumoconiosis is a Benign asymptomatic disease. Rarely progressive massive fibrosis occurs patient develops dyspnoea cough and respiratory dysfunction.

8. Silicosis It is the most common occupational disease caused by inhalation of Silica.It is seen in sand Blasting ,foundry work and stone cutting.

9. PATHOGENESIS Inhalation of Silica Engulfment by Release mediators alveolar macrophages Binds with membrane protein and phospholipids Damages cell membrane Kills Macrophages Free Silica particle FIBROSIS

10. Following inhalation of Silica it is engulfed by alveolar macrophages Silicon Hydroxide groups on the surface of particles form hydrogen bond with membrane protein.

11. Denaturation of membrane protein and damage of microphage cell membrane. Macrophage is killed and silica particle is released. The free silica is re-ingested by other macrophages and cycle goes on. The silica ingested alveolar macrophages gets activated and release mediators-IL1, TNF,O2 derived radicles , fibrogenic cytokines. These cause fibrosis.

12. MORPHOLOGY: Early silicosis- Macroscopic features. Upper zone- small nodules Large areas of focal to confluent consolidation. Microscopic features Chronic inflammation of alveoli and septa. Alveolar spaces filled with amorphous material. Long needle like space contain bifringent silica particles Fibrinous pleuritis

13. CHRONIC NODULAR SILICOSIS Macroscopic Tiny nodules like sand grains, initially in the upper lobe, later spread to other areas. Tiny nodules coalesce to form hard visible scars. Lung parenchyma between the scars is compressed or emphysematous.

14. MICROSCOPIC FEATURES: Nodules are made up of concentric layers of hyalinised collagen surrounded by a dense collagenous capsule. Pleura shows dense plaques with adhesion obliterating the pleural cavity. Hilar nodes - show thin calcification- these appears like egg shell in xray chest

15. CLINICAL PICTURE : Dysnoea on exertion, later during rest. Respiratory dysfunction . DIAGNOSIS X ray chest shows nodularity . Complications Caplan syndrome Chronic bronchitis Emphysema Cor pulmonale Pulmonary tuberculosis

16. ASBESTOSIS: Inlation of asbestos fibres is called asbestosis . Asbestosis is seen in the following occupation, Manufacturing of car components Flooring and roofing Mining Sewage

17. TYPE OF ASBESTOS FIBRES : Amphibole- straight and stiff fibres . Less soluble and mere pathogenic. Chrysotile- curled, flexible and more soluble than amphibole

18. Amphibole fibres are straight and stiff. They move along airflow and penetrate deep into lung. Chrysotile fibres are curled and flexible. They get stuck in the upper respiratory passages and are removed by mucociliary action of air passages. They are more soluble than amphibole fibres and are easily removed . They are less pathogenic.

19. Disease occurs after 10 years of exposure. The asbestos fibres are indicators as well as promotors of carcinogenesis. Fibres contain trace metals such as nickel and chromium which are carcinogenic. Tobacco and asbestos act together and produce malignancy. Asbestos fibres are ingested by macrophages they get activated and release cytokines Cytokines induce fibrosis .

20. Straight and stiff asbestos fibres Align along air flow Penetrate deep into lung Ingested by alveolar and intestinal macrophage Activation of macrophages Release cytokines

21. -FIBRONECTIN -PLATELET DERIVED GROWTH FACTOR -IGF-1 FIBROSIS

22. Straight and stiff asbestos fibres Align along air flow Penetrate deep into lung contains adsorped Tobacco carcinogen MALIGNANCY Failure to destroy or recognize Malignant cells Fibres contains Nickel chromium Supress NK cells Benzopyrene

23. Morphology Diffuse pulmonary interstitial Fibrosis with presence of asbestos bodies. Fibrosis starts around respiratory bronchioles and alveolar ducts. Fibrosis spreads to alveolar sacs and alveoli. Due to fibrosis the adjacent alveoli become dilated- compensatory dilatation giving a honey comb appearance to the lung. In the areas of fibrosis asbestos bodies are seen .

24. Asbestos bodies or Ferrugenous bodies They are club shaped or dumble shaped Golden brown in colour . The case of the body contains asbestos fibre . The fibre is coated by glycoprotein with haemosiderins . The haemosiderin give its golden brown colour and beaded appearance

25. PLEURAL PLAQUES -Pleural plaques are well demarcated. Pearly white smooth or nodular areas in pleura. -These are dense hyaline tissue with calcification. -Diffuse pleural fibrosis may lead to adhesion to chest wall.

26. COMPLICATIONS - Emphysema - Bronchiectasis - Cor pulmonale - Caplan syndrome - Mesothelioma - Bronchogenic carcinoma -Gastrointestinal carcinoma -Renal carcinoma -Lymphoma