Asbestos&Berylliosis

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Asbestos&Berylliosis

  1. 1. Asbestosis and Berylliosis Dr.CSBR.Prasad., MD.,
  2. 2. Asbestos• Asbestos is a family of crystalline hydrated silicates that form fibers• Greek word – unquenchable• Coal is a lot of dust and little fibrosis• Asbestos is little dust and lot of fibrosis CSBRP-Dec-2012
  3. 3. Asbestos• In nature – exists as thin long fibrils which are fire resistant and can be spun into yarns• Applications: Thermal insulation Electrical insulation CSBRP-Dec-2012
  4. 4. Workers at risk• Miners Fabrication of Manufacture of• Pipes • Textiles• Tiles • Insulating boards• Roofs • Sewer conduits• Textiles • Water conduits• Brake lining • Clutch casting CSBRP-Dec-2012
  5. 5. Geometric formsSerpentine Amphibole• Chrysotile • Crocidolite (blue) • Amosite (brown) • Tremolite • Anthophyllite • Actinolyte CSBRP-Dec-2012
  6. 6. Geometric formsSerpentine Amphiboles• Curly and flexible • Straight,stiff,brittle• Ex.,chrysotile (90%) • Crocidolite• Less pathogenic • More fibrogenic• Soluble • Less soluble• Get impacted in upper • Reach deeper in resp tract. lungs• Removed by • Penetrate epithelial mucocilia cells, interstitium. CSBRP-Dec-2012
  7. 7. Asbestos –general remarks• Amphiboles are more pathogenic• Amphibole fibers-longer than 8 µm and thinner than 0.5 µm are more injurious than shorter and thicker ones• High dosage – high incidence of disease• Amphibole exposure – Mesothelioma CSBRP-Dec-2012
  8. 8. Asbestosis - general remarks• Both initiators and promoters• Oncogenic: free radical injury• Adsorbed toxic chemicals• Silicosis is a nodular fibrosing disease• Asbestosis is a diffuse interstitial process• Diffuse fibrosis because: • Asbestos reaches alveoli consistently • Penetrate epithelial cells CSBRP-Dec-2012
  9. 9. Asbestosis- pathogenesis• Asbestos - MØ – interstitium – lymphatic - pleura• Chemo attraction to PMN, macrophages• Asbestos bodies - coat of glycoprotein, haemosiderin• Induce fibrosis: MDGF, IL-1• Induce ANA, Rhematoid factor CSBRP-Dec-2012
  10. 10. Asbestos induced diseases1. Asbestosis2. Pleural diseases  Pleural effusion  Visceral pleural fibrosis  Pleural plaques3. Tumors Bronchogenic carcinoma Malignant mesothelioma CSBRP-Dec-2012
  11. 11. Asbestosis• Diffuse pulmonary fibrosis• Histologically: Asbestos bodies• Gross: small, firm lungs cartilage like pleura subpleural fibrosis esp. @ bases late stages: cystic change honeycomb CSBRP-Dec-2012
  12. 12. Asbestos - microscopy1. Non specific interstitial fibrosis2. Asbestos bodies3. Emphysematous changes CSBRP-Dec-2012
  13. 13. Asbestos bodies Golden brown, fusiform / beaded rods with translucent center Consists of asbestos fibres coated with iron containing protenaceous material Iron derived from phagocyte ferritin Ferruginous bodies: inorganic particulates coated by similar iron protein complexes CSBRP-Dec-2012
  14. 14. This long, thin object is an asbestos fiber CSBRP-Dec-2012
  15. 15. CSBRP-Dec-2012Asbestos body - Typical beading and knobbed ends (arrow)
  16. 16. Ferruginous body CSBRP-Dec-2012
  17. 17. Pleural disease Pleural effusion: Serous effusion Visceral pleural fibrosis: Encases the lung Pleural plaques: Fibrocalcific Micro: oHyalinised collagenous tissue oCalcification oNo asbestos bodies CSBRP-Dec-2012
  18. 18. Figure 15-22 Asbestos exposure evidenced by severe,discrete, characteristic fibrocalcific plaques on the pleural surface of the diaphragm. CSBRP-Dec-2012
  19. 19. Diffuse visceralPleural fibrosis CSBRP-Dec-2012
  20. 20. Fibrous pleural plaque CSBRP-Dec-2012
  21. 21. Asbestos - Tumors • Brochogenic carcinoma 5x • Malignant mesothelioma 1000x • Carcinoma esophagus • Carcinoma stomach • Carcinoma colon • Carcinoma kidneys • Carcinoma larynxConcomitant cigarette smoking greatly increases the CSBRP-Dec-2012risk of lung carcinoma but not that of mesothelioma.
  22. 22. Malignant Mesothelioma• Monophasic / biphasic tumor• Spindle cells / gland formations• Markers: – Calretinin – CK 5/6 – WT1 CSBRP-Dec-2012
  23. 23. CSBRP-Dec-2012
  24. 24. CSBRP-Dec-2012
  25. 25. Asbestosis - Clinical features• Slow insidious, asymptomatic• Dyspnoea• Dry / productive cough• Advanced cases: Caplan syndrome Pul. HTN cor pulmonale various Cancers CSBRP-Dec-2012
  26. 26. Berylliosis CSBRP-Dec-2012
  27. 27. Berylliosis• Exposure to dust / fumes of metallic beryullium• Past - Fluorescent tubes / light bulbs• Presently – • Aerospace industries • Electrical / electronic equipments• Two diseases – acute / chronic CSBRP-Dec-2012
  28. 28. Acute berylliosis• Unusual sensitivity• Heavy exposure over 2 to 4 wks• Alveoli filled with protein rich fluid with formation of hyaline membrane• C/F: sudden dyspnoea, hyperpnoea substernal pain• Complete recovery CSBRP-Dec-2012
  29. 29. Chronic Berylliosis• Sensitivity for over years 20 yrs or more• CMI hypersensitivity reaction• Metal beryllium acts as a hapten1-Non caseating granulomas - sarcoid like2-Birefringent crystals3-Schaumann / conchoid bodies4-Asteroid bodies CSBRP-Dec-2012
  30. 30. Immunologic Lung Disease CSBRP-Dec-2012
  31. 31. Immunologic lung disease1. Bronchial asthma2. Hypersensitivity (allergic) pneumonitis3. Pulmonary eosinophilia4. Goodpasture’s disease5. Pulmonary alveolar proteinosis CSBRP-Dec-2012
  32. 32. Hypersensitivity pneumonitis• Immunologically mediated interstitial pneumonitis• Inhaled organic antigenic material• Acute / chronic• Type III or Type IV reaction CSBRP-Dec-2012
  33. 33. Types of hypersensitivity pneumonitis• Farmers lung Thermophilic actinomycetes• Bagassosis Thermophilic actinomycetes• Byssinosis Cotton fiber, flex, hemp Bired dropping, danders• Bird breeders disease• Mushroom workers Mushroom compost dust• Malt workers lung Mouldy barley,malt dust• Maple bark disease Mouldy maple bark (canada)• Silofillers disease Toxic fumes of nitric oxide / nitric dioxide. CSBRP-Dec-2012
  34. 34. Gross and microscopy• Early stage: alveolar wall infiltrated by plasma cells histiocytes granulomas• Chronic stage: interstitial fibrosis inflammatory infiltrates honey combing of lung. CSBRP-Dec-2012
  35. 35. Pulmonary eosinophilia• Immunologically mediated• Two features 1.Infiltration of lungs chest radiographs 2.Elevated eosinophil count in blood CSBRP-Dec-2012
  36. 36. Pulmonary eosinophilia - causes1. Loeffler’s syndrome2. Tropical pulmonary eosinophilia3. Secondary chronic pulmonary eosinophilia4. Idiopathic chronic eosinophilic pneumonia5. Hypersensitivity syndrome CSBRP-Dec-2012
  37. 37. Pathology• Gross: patchy consolidation• Micro: thickening of alveolar membrane EØ, Plasma cells, Lymphocytes small granulomas lumen may show eosinophils CSBRP-Dec-2012
  38. 38. Goodpasture’s syndromeNecrotising haemorrhagic interstitial pneumonitis +Rapidly progressive glomerulnephritis CSBRP-Dec-2012
  39. 39. Goodpasture’s syndrome Etiopathogenesis• Immunologic damage• By anti BM antibodies formed against antigens common to BM of alveoli and GBM.• Trigger: not clear, ?virus ?hydrocarbons ?smoking CSBRP-Dec-2012
  40. 40. Pathology• Red brown areas of consolidation• Acute stage: focal areas of haemorrhage, necrosis in alveolar wall• Chronic cases: organisation - fibrosis CSBRP-Dec-2012
  41. 41. Pulmonary alveolar proteinosis (PAP)• Chronic disease characterized by distal air spaces filled by granular eosinophilic PAS positive material with abundant lipid in it• Material -- Surfactant• Can occur at any age• Three distinct classes: acquired congenital & secondary PAP CSBRP-Dec-2012
  42. 42. This is a rare disease known as pulmonary alveolar proteinosis. The alveolar walls are normal histologically but the alveoli become filled with a PAS postive granular exudatecontaining abundant lipid and lamellar bodies (by electron microscopy). Patients may cough CSBRP-Dec-2012 up copious amounts of gelatinous sputum. The etiology is unknown.
  43. 43. E N D CSBRP-Dec-2012

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