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RS Pathology
Respiratory System Pathology - Silicosis, Asbestosis & Diffuse Alveolar Hemmo...
| Question | Answer |
|---|---|
| What is silicosis? | Most prevalent chronic occupational disease in the world and caused by inhalation of crystalline silica |
| Which workers are at particular risk for silicosis? | Workers in sandblasting |
| What are the different forms of silica? | 1) Crystalline (such as quartz) 2) Amorphous forms |
| Characteristics of the crystalline form of silica? | The most toxic and fibrogenic Quartz is most commonly implicated in silicosis and when mixed with other minerals, it has been observed to have a reduced fibrogenic effect and quartz in the workplace is rarely pure |
| Morphology of silicosis: | Pale-to-blackened (if coal dust is present) nodules in the upper zones of the lungs As disease progresses, individual nodules may become hard, collagenous scars, with progression to PMF Fibrotic lesions may occur in the hilar lymph nodes & pleura |
| Microscopic appearance of silicosis: | Concentrically arranged hyalinized collagen fibers surrounding amorphous center and this whirled appearance of the collagen fibers Polarized microscopy reveals weakly birefringent silica particles in the center of the nodules |
| Radiographic appearance of silicosis: | Eggshell calcification |
| Clinical features of silicosis: | Usually detected on routine chest radiographs in asymptomatic workers Pulmonary function either normal or only moderately affected Patients do not develop dyspnea until late, after PMF is present Develop pulmonary hypertension and cor pulmonale |
| How does silicosis affect the effected? | The disease is slow to kill, but impaired pulmonary function may severely limit activity Associated with an increased susceptibility to tuberculosis |
| Crystaline silica may inhibit | The ability of pulmonary macrophages to kill phagocytosed mycobacteria |
| Nodules of silicotuberculosis often contain: | A central zone of caseation |
| Occupational exposure to asbestos is linked to: | 1) Parenchymal interstitial fibrosis (asbestosis) 2) Localized fibrous plaques and rarely, diffuse fibrosis in the pleura 3) Pleural effusions 4) Lung carcinomas; 5) Malignant pleural and peritoneal mesothelioma 6) Laryngeal carcinoma |
| What are the forms of asbestosis? | 1) Serpentine 2) Amphibole 3) |
| Appearance of asbestos in serpentine: | The fiber is curly and flexible and chrysotile accounts for most of the asbestos used in industry |
| How does the structure of serpentine asbestos affect the lungs? | Likely to become impacted in the upper respiratory passages and removed by the mucociliary elevator Those that are trapped in the lungs are gradually leached from the tissues, because they are more soluble than amphiboles |
| Appearance of fibers in amphibole asbestos: | Fiber is straight, stiff |
| Difference between amphibole and serptentine asbestos: | Amphiboles, are less prevalent but more pathogenic than the serpentine Serpentine are more soluble than amphiboles |
| How do amphiboles affect the lungs? | Align themselves in the airstream and are delivered deeper into the lungs They may penetrate epithelial cells to reach the interstitium |
| Why is asbestos considered carcinogenic? | Functions as both a tumor initiator and a promoter Some of the oncogenic effects of asbestos on the mesothelium are mediated by reactive free radicals generated by asbestos fibers |
| Morphology of asbestosis: | Diffuse pulmonary interstitial fibrosis Asbestos bodies Distortion of normal architecture Adhesion between the lungs and the chest wall Scarring may narrow pulmonary arteries Pleural plaques |
| What are asbestos bodies? | Golden brown, beaded rods with a translucent center and consists of asbestos fibers coated with an iron |
| How are asbestos bodies formed? | When macrophages attempt to phagocytose fibers The iron is derived from phagocyte ferritin |
| Asbestosis begins in which zone of the lung: | The lower lobes and subpleurally |
| What is the most common manifestation of asbestos exposure? | Pleural plaques |
| What are pleural plaques? | Well-circumscribed plaques of dense collagen , often containing calcium |
| Where do pleural plaques develop? | Most frequently on the anterior and posterolateral aspects of the parietal pleura |
| Uncommonly, asbestos exposure induces | Pleural effusion Diffuse pleural fibrosis |
| Clinical manifestations of asbestosis: | Progressive worsening dyspnea-10 to 20 years after exposure Cough associated with production of sputum. Disease may remain static or progress to CHF and death. Pleural plaques are usually asymptomatic- detected on radiographs as circumscribed densities |
| What cancers can appear in workers exposed to asbestos? | Lung carcinoma Malignant mesothelioma |
| The risk of lung carcinoma and malignant mesolthelioma is increased by how much after asbestos exposure: | Lung carcinoma - 5x Malignant mesothelima - 1000x |
| Concomitant cigarette smoking increases the risk of lung carcinoma and malignant mesothelioma by how much: | Mesothelioma, not at all Lung carcinoma - greatly increased |
| Examples of diffuse alveolar hemorrhagic syndromes: | 1) Goodpasture syndrome 2) Idiopathic pulmonary hemosiderosis |
| Goodpasture syndrome is characterized by: | Proliferative, rapidly progressive, glomerulonephritis and hemorrhagic interstitial pneumonitis |
| The renal and pulmonary lesions in Goodpasture syndrome are caused by: | Antibodies targeted against the noncollagenous domain of the α3 chain of collagen IV |
| The antibodies are found in the serum of how many patients of Goodpasture syndrome? | 90% |
| What is the hallmark diagnostic finding in renal biopsy specimens for Goodpasture syndrome? | Linear pattern of immunoglobulin deposition,usually IgG Seen along the alveolar septa by immunoflurescence studies |
| How can the prognosis of Goodpasture syndrome be improved? | By Plasmapheresis which removes the offending agent Immunosuppressive therapy which inhibits antibody formation |
| What is the treatment for severe renal disease? | Renal transplantation |
| What is the difference between Idiopathic pulmonary hemosiderosis and Goodpasture syndrome? | 1) No associated renal disease in IPH 2) No circulating anti-basement membrane antibody in IPH |
| Who has a better prognosis for IPH? Children or adults? | Adults |
| How can the prognosis for IPH be improved? | With steroid and immunosuppressive therapy Which is why we assume the disease is immunologic in origin |
Created by:
Ulaisl
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