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Pneumoconioses

Pneumoconioses: Pathogenesis and Clinical Findings Authors: Austin Laing Reviewers: Yan Yu* Tara Lohmann* * MD at time of publication Bronchogenic carcinoma and mesothelioma Inhalation of asbestos (Asbestosis) Inhalation of carbonaceous dust (Carboconiosis) Inhalation of metal dust (Metaloconiosis) Inhalation of silica dust (Silicosis) “-Coniosis”: disease which comes from inhaling dust particles Internalized asbestos fibers disrupt cellular processes through a complex series of theorized mechanisms Inhaled dust particles (1-5μm in size) are trapped and deposited in the alveolar airspaces Alveolar macrophages ingest dust particles, which activates the macrophages and sometimes causes apoptosis Activated macrophages create an inflammatory microenvironment by releasing pro-inflammatory cytokines, chemokines and reactive oxygen species Inflammatory products (e.g. reactive oxygen species) damage alveolar epithelial cells, causing activation and release of inflammatory cytokines into the alveolar space Inhaled dust particles, inflammatory products & other pro- tussive mediators activate airway vagal afferent receptors Activated receptors stimulate the cough center located in the medulla oblongata Cough Alveolar capillaries vasoconstrict in response to hypoxia à↑ Pulmonary vascular resistance Pulmonary Hypertension Right heart must pump blood into lungs against higher pressure àcardiomyocyte growth (via sarcomeres formed in parallel within myofibrils)àconcentric hypertrophy of right heart Cor Pulmonale (right heart failure due to pulmonary hypertension) Asbestos fibers accumulate in the airspace and translocate to the pleural surface Macrophage apoptosis: ↓ alveolar macrophages Fibroblasts are recruited to the alveolar wall and are activated Activated fibroblasts produce and deposit collagen in the extracellular space between alveoli Thickening of tissue between alveoli and capillaries ↑ the diffusion distance of atmospheric and blood gasses ↓ Diffusion of CO2 from blood to alveoli and ↓ diffusion of O2 from alveoli to blood ↑ Respiratory rate to maintain minute ventilation due to ↓ lung volumes and diffusion limitations Dyspnea and Exertional Hypoxemia ↓ Innate immune response in the lungs Chest X-Ray: Nodular and reticulonodular opacities are seen in varying lung regions depending on the underlying inhaled dust Excessive collagen deposition ↓ lung compliance and ↓ lung expansion ↓ Diffusing capacity for carbon monoxide (DLCO) on pulmonary function test ↓ Arterial oxygen contentà ↑ deoxyhemoglobin and ↓ oxyhemoglobin ↑ Deoxyhemoglobin within the vasculature causes the skin and mucous membranes to appear blue Cyanosis ↑ Risk of respiratory infections. Mycobacterial infections (e.g. tuberculosis) associated primarily with silicosis ↓ Inhalation volume ↓ Expiratory volume Hypoxemia ↓Total lung capacity (TLC) and ↓ residual volume (RV) on pulmonary function test ↓Forced vital capacity (FVC) and ↓ forced expiratory volume in 1 second (FEV1) on pulmonary function test Note: Forced Vital Capacity: the volume of air that can forcibly be blown out after full inspiration Forced Expiratory Volume in 1 second: the volume of air that can forcibly be blown out in first 1 second, after full inspiration Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published September 12, 2021 on www.thecalgaryguide.com

rheumatoid-pneumoconiosis-caplans-syndrome-pathogenesis-and-clinical-findings

Rheumatoid Pneumoconiosis (Caplan’s Syndrome): Pathogenesis and clinical findings Authors: Christopher Li Keerthana Pasumarthi Reviewers: Daniela Urrego, Ben Campbell, Liam Martin* * MD at time of publication Dust-exposed occupation (e.g. coal, asbestos, silica) ↑ Accumulation of dust particles in lungs Dust (e.g. silica) mobilizes from the lungs to other organs such as the kidneys, lymph nodes, and spleen Accumulation of silica in other organs which activate the immune system to secrete cytokines, chemokines, and lysosomal enzymes Activation of antigen- presenting and antibody- producing cells Increased risk to produce autoantibodies Increased risk for autoimmune conditions such as rheumatoid arthritis See slide: Rheumatoid Arthritis (RA): Extra- articular manifestations for mechanism of systemic inflammation See slide Pneumoconioses: Pathogenesis and clinical findings for mechanism Note: Rheumatoid arthritis may precede lung nodules or develop later in the course Rheumatoid arthritis Systemic autoimmune inflammatory disease that mainly involves synovial joints (+) Alveolar macrophages and neutrophils ingest dust particles ↑ Inflammation and cytokine production in pulmonary parenchyma (e.g. interleukin-1, tumor necrosis factor-α) Rheumatoid pneumoconiosis Interstitial lung disease, with characteristic nodules, resulting from the interaction between dust inhalation and rheumatoid arthritis inflammation Cytokines recruit histiocytes, neutrophils, lymphocytes, and fibroblasts to the area to produce a zone of inflammation around the dust-containing cell Necrosis and apoptosis of dust-containing cells, macrophages, and surrounding collagen Necrotic cells are digested by new macrophages to restart the process Production of nodules that contain a central necrotic area surrounded by alternate layers of dust and necrotic tissue (Caplan nodules) Hyperactive immune response to foreign materials in lungs Multiple concentric rings of dust seen histologically on light microscopy 0.5-5 cm rounded opacities on chest X-ray in periphery of lungs See slide on Pneumoconioses for symptoms and pulmonary function test results Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 17, 2022 on www.thecalgaryguide.com