L34 Environmental Lung Disease

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jknell
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202803
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L34 Environmental Lung Disease
Updated:
2013-02-23 13:37:44
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Pulmonary II
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Pulmonary II
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  1. Pneumoconiosis Definition
    • -Retention of and pathologic effects from inhalation of dust particles
    • -typically due to inorganic dusts
    • -most don't develop disease
  2. Hypersensitivity Pneumonitis Definition
    • -Complex syndromes with various antigens
    • -Organic antigens (proteins from bacteria, mold, fungi, myocbacterium)
  3. General Pathogenesis
    • Development depends on:
    • 1. Amount of dust retained in the lung -concentration
    • -duration of exposure
    • -effectiveness of clearance mechanisms

    • 2. Size, shape and buoyancy of particles
    • -1-5um
    • -asbestos is larger by narrower width
    • -curly fibers not dangerous

    • 3. Particle solubility and physiochemical properties
    • -smaller/soluble: dissolve in blood
    • -larger/non-soluble: inflammation and fibrosis
    • -quartz: interact with free radicals
  4. Protection Mechanisms
    • 1. Tortuous passages of upper airways
    • 2. Bronchoconstriction
    • 3. Entrapment in mucus blanket
    • 4. Mucocilliary clearance
    • 5. Phagocytosis by macrophages
    • 6. Transport to lymphatics
    • 7. Metabolic modifications
  5. Pathophysiology of Environmental Lung Disease
    • -typical reaction to chronic injury is fibrosis
    • -mechanism depends on agent
    • -some directly injure lung parenchyma
    • -some trigger macrophages --> inflammatory response
    • -fibrosis may lead to pulmonary HTN and death from respiratory failure or RHF
  6. Coal Workers Pneumoconiosis
    -"black lung"

    • Range of Disease:
    • 1. Asymptomatic anthracosis
    • 2. Simple coal workers pneumoconiosis
    • 3. Complicated coal workers pneumoconiosis/Progressive Massive Fibrosis
  7. Anthracosis
    • -asymptomatic
    • -coal workers lung, urban dwellers, tobacco smokers
    • -carbon pigment taken up in MPs which accumulate in lymphatics in CT and LNs
  8. Simple Coal Workers Pneumoconiosis
    • -usually asymptomatic
    • -may have chronic productive cough with blank-tinged sputum

    • Coal macules
    • -1-2mm
    • -carbon laden macrophages

    • Coal nodules
    • -<1cm
    • -collagen fibers and carbon laden macrophages
  9. Complicated Coal Workers Pneumoconiosis/Progressive Massive Fibrosis
    -develops in the background of simple CWP

    • Symptoms:
    • -dyspnea
    • -cough
    • -sputum
    • -may develop R sided congestive HF

    *may progress even after exposure is stopped

    • Diagnosis:
    • -coal nodules > 1cm
    • -nodules contain dense collagen and pigment and may have central necrosis
  10. Silicosis
    • -most prevalent pneumoconiosis in the world
    • -sandblasters, mine workers
    • -inhalation of silicon dioxide

    • Two forms of silica:
    • 1. Crystalline (more fibrogenic)
    • 2. Amorphous (can cause fibrosis with heavy burden)

    • Pathogenesis:
    • -silica is toxic to macrophages
    • -fibrosis
    • -lesions in upper portion of lungs

    • Gross:
    • -hard collagenous scars

    • Histology:
    • -concentric layers of hyalinized collagen
    • -particles visible under polarized light

    *Increased susceptibility to TB (maybe due to depressed cell mediated immunity)
  11. Asbestosis
    • Different types of fibers
    • 1. Serpentines
    • -curly and flexible
    • -get stuck in upper respiratory tract and cleared
    • 2. Amphobiles
    • -straight stiff and brittle
    • -less prevalent
    • -more pathogenic (mesothelioma)

    • Pathophysiology:
    • -crystals activate macrophages
    • -stimulate production of ROS and cytokines
    • -promote fibroblast and mesothelial cell proliferation

    • Histology:
    • -Ferruginous bodies: iron from phagocyte ferritin coats fibers
    • -more commonly in lung parenchyma

    • Pathology of chronic exposure:
    • 1. Benign pleural effusions (asbestos pleurisy)
    • 2. Focal or diffuse pulmonary interstitial fibrosis (lower lobes)
    • 3. Parietal pleural plaques
    • 4. Mesothelioma
  12. Focal or Diffuse Pulmonary Interstitial Fibrosis
    • -affects lower lobes and subpleural lung first
    • -begins as fibrosis around respiratory bronchioles
    • -extends to involve adjacent alveolar sacs and alveoli
    • -fibrosis creates enlarged airspaces enclosed within thick fibrous walls

  13. Pleural Plaques
    • -most common manifestation of asbestos
    • -typically parietal
    • -typically do NOT contain ferruginous obides
    • -eventually calcify
    • -dense periauricular collagen with slit like retraction spaces parallel to pleural surface
  14. Malignant Mesothelioma
    • Epidemiology:
    • -rare neoplasm
    • -2-10% of pts with heavy asbestos exposure
    • -long latency: 25-45yrs
    • -other risk factors: radiation, chronic inflammation

    *No increase in risk in asbestos workers who smoke

    • Clinical Presentation:
    • -pleural effusion
    • -chest pain
    • -dyspnea

    • Pathogenesis:
    • -asbestos causes chronic irritation of mesothelial cells
    • -generate ROS --> DNA damage
    • -can eventually encase the lung

    • Gross:
    • -multiple gray-white ill defined noduels
    • -diffusely thickened pleura

    • Three Main Histological Types:
    • 1. Epithelial (resembles adenocarcinoma)
    • 2. Sarcomatoid (spindle cells)
    • 3. Mixed or biphasic
    • *has no prognostic value
  15. Epithelial Mesothelioma
    • -sheets of rounded cells infiltrating down into fat

    • -can mimic adenocarcinoma
  16. Sarcomatoid Mesothelioma
    • -spindle fibers
    • -not in sheets

  17. Asbestos and Lung Carcinoma
    • -most frequent malignancy in asbestos exposure
    • -risk for developing lung carcinoma is exacerbated by cigarette smoking (50-90X)
    • -carcinogens from smoke may absorb into asbestos fibers
    • -1/5 exposed die of lung carcinoma
    • -1/10 die of mesothelioma
    • -1/10 die of GI carcinomas
  18. Hypersensitivity Pneumonitis
    All the funny names

    • -Immunologic reaction to inhaled organic antigens
    • -both type III and type IV hypersensitivity responses

    • Type III
    • -immune complex mediated
    • -abs present in blood
    • -C' and Ig in vessel walls

    • Type IV:
    • -cell mediated
    • -"attempt" to form a granulomatous response
    • -increased chemokines and T cells in BAL
    • -non-caseating granulomas are present

    • Diagnosis:
    • -known exposure
    • -BAL with T lymphocytosis (CD8>CD4)
    • -positive inhalation test

    • Histopathology:
    • -diffuse mononuclear cell infiltrates (lymphocytes)

    • -poorly formed non-caseating granulomas (peribronchiolar localization)

    -interstitial fibrosis and obliterative bronchiolitis in advanced cases
  19. Treatment of HP
    • -remove source of antigen
    • -corticosteroids
    • -prognosis good unless fibrosis has already developed
  20. Iatrogenic/Drug-Induced Lung Disease
    • Drugs:
    • Bleomycin
    • Methotrexate
    • AMiodarone
    • Nitrofurantoin
    • Aspirin
    • β-blockers

    Radiation

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