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Pathology Lecture 34 Pneumoconioses 1) Summarize the major factors in pneumoconiosis development and lung defense mechanisms in terms of particle size and site of deposition of inhaled dust. Factors in Pneumoconiosis Development Amount of dust retained in the lung size and shape of the dust particles solubility and chemical reactivity of dust particles presence of other irritants (cigarettes) or diseases Lung defense mechanisms Filtration and impaction in the upper respiratory tract Cough Mucociliary transport Phagocytosis and transport by macrophages 2) Distinguish the various morphologic patterns of lung injury from dusts and give examples. Type of dust Mineral Mineral Mineral Mineral Organic Lung reaction Accumulation in macrophages; no appreciable fibrosis Sarcoid like granulomas Nodular or massive fibrosis Diffuse interstitial fibrosis (fibrosing alveolitis) Allergic alveolitis Examples Iron, barium Beryllium Quartz (silica), coal Asbestos Fungal spores, avian proteins 3) Compare and contrast the mild and severe lesions of coal, silica, and asbestos exposure. Mild coal: Simple CWP small aggregates of dust laden macrophages. Severe coal: Complicated Coal Workers Pneumoconiosis also called Progressive Massive Fibrosis (PMF) <10% simple CWP become PMF. Mild silica: Nodular (Chronic) Silicosis presents with few symptoms, 1-5 mm parenchymal nodules consisting of layers of relatively a cellular fibrous tissue. Severe silica: Acute Silicosis is an uncommon disease characterized by large numbers of silica particles in alveoli associated with large amounts of proteinaceous debris. PNF may result from coalescence of smaller silica nodules into large fibrous masses. Mild asbestos: localized fibrous plaques, diffuse pleural fibrosis, pleural effusions, and parenchymal interstitial fibrosis. Severe asbestos: lung carcinoma, mesotheliomas, and laryngeal (also extrapulmonary) neoplasms 4) Discuss coal workers pneumoconiosis, silicosis, berylliosis, and asbestos exposure in terms of major clinical associations, gross and microscopic pathology and associations with other diseases. Disease Coal Workers Pneumoconiosis (CWP) Silicosis Berylliosis Asbestos Exposure – Two forms serpentine and amphibole (↑pathogenic) Clinical Associations Little or no functional impairment Most prevalent chronic occupational disease. Silica produces free radicals, damaging macrophages to release cytokines (inflammation) Type IV cellular immune response (hypersensitivity) forms granulomas Dyspnea and cough. Fibrogenic, asbestos fibers are phagocytized causing the release of chemical mediators resulting in fibrosis. Gross Fibrous nodules >2 cm with black pigment in upper lobes 1-5 mm nodules in upper lobes of lungs Microscopic Dense collagen and pigment with necrotic center Nodular lesions of concentric layers of hyalinized collagen with a dense capsule Disease Associations Anthracosis (any black dust accumulation) Tuberculosis PMF - right heart failure, tuberculosis, Caplan's Usually no demonstrable alteration, although coalescence of granulomas may produce small nodules Pleural plaques of dense collagen develop on the anterior and posterolateral aspects of the parietal pleura and over the domes of the diaphragm. Granulomatous disease virtually identical to sarcoidosis Asbestos bodies, golden brown, fusiform or beaded rods consisting of asbestos fibers coated with iron and proteins Increased risk of lung cancer, HLA-DPβ-Glu69 allele confers greater risk to those exposed. Lung cancers, potentiates the effects of smoking, 50-80% of all diffuse mesotheliomas.