2)Distinguish the Various Morphologic Patterns of Lung Injury from Dusts and Give Examples
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 / Lung defense mechanismsAmount 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 / 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 / Lung reaction / ExamplesMineral / Accumulation in macrophages; no appreciable fibrosis / Iron, barium
Mineral / Sarcoid like granulomas / Beryllium
Mineral / Nodular or massive fibrosis / Quartz (silica), coal
Mineral / Diffuse interstitial fibrosis (fibrosing alveolitis) / Asbestos
Organic / Allergic alveolitis / 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 / Clinical Associations / Gross / Microscopic / Disease AssociationsCoal Workers Pneumoconiosis (CWP) / Little or no functional impairment / Fibrous nodules >2 cm with black pigment in upper lobes / Dense collagen and pigment with necrotic center / Anthracosis (any black dust accumulation) Tuberculosis
Silicosis / Most prevalent chronic occupational disease. Silica produces free radicals, damaging macrophages to release cytokines (inflammation) / 1-5 mm nodules in upper lobes of lungs / Nodular lesions of concentric layers of hyalinized collagen with a dense capsule / PMF - right heart failure, tuberculosis, Caplan's
Berylliosis / Type IV cellular immune response (hypersensitivity) forms granulomas / Usually no demonstrable alteration, although coalescence of granulomas may produce small nodules / Granulomatous disease virtually identical to sarcoidosis / Increased risk of lung cancer, HLA-DPβ-Glu69 allele confers greater risk to those exposed.
Asbestos Exposure–
Two forms serpentine and amphibole (↑pathogenic) / Dyspnea and cough. Fibrogenic, asbestos fibers are phagocytized causing the release of chemical mediators resulting in fibrosis. / Pleural plaques of dense collagen develop on the anterior and posterolateral aspects of the parietal pleura and over the domes of the diaphragm. / Asbestos bodies, golden brown, fusiform or beaded rods consisting of asbestos fibers coated with iron and proteins / Lung cancers, potentiates the effects of smoking, 50-80% of all diffuse mesotheliomas.