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Pneumoconiosis
Pneumoconiosis-
• Pneumoconioses encompass a group of chronic fibrosing diseases of
the lung resulting from exposure to organic and inorganic
particulates, most commonly mineral dust
• Pathogenesis-
(1) amount of dust
(2) size, shape, and buoyancy of the particles
o small particles,1 to 5 μm –acute lung injury
o Large particle-evoke fibrosing collagenous pneumoconioses
(3) particle solubility and physiochemical reactivity-small particles composed of
injurious substances of high solubility
(4) additional effects of other irritants
• particles stimulate resident innate immune cells in the lung
• invokes systemic response
• a genetic predisposition
Particles size
2.5–10 μm-
• bronchi and bronchioles
• removed by mucociliary action
 <2.5 μm- acini
<100 nm-penetrate alveolar walls
Silicosis
• Silicosis is the most common pneumoconiosis in the world, and
crystalline silica (e.g., quartz) is the usual culprit
• caused by inhalation of proinflammatory crystalline silicon dioxide
Pathogenesis-
crystalline and amorphous forms
• crystalline forms (including quartz, cristobalite, and tridymite)- much more
fibrogenic
• Phagocytosed silica crystals activate the inflammasome, leading to the release of
inflammatory mediators, particularly IL-1 and IL-18
• disease may continue to worsen even if the patient is no longer
exposed
• It is associated with an increased susceptibility to tuberculosis
• Patients with silicosis have double the risk for developing lung cancer
SIMPLE NODULAR SILICOSIS: most common form of silicosis
PROGRESSIVE MASSIVE FIBROSIS: nodular masses greater than 2 cm
in diameter, in a background of simple silicosis
• bilateral
• 5–10 cm
• Central cavitation
ACUTE SILICOSIS:
• heavy exposure to finely particulate silica during sandblasting or boiler scaling
• it is associated with diffuse fibrosis of the lung
• Silicotic nodules are not found
• Microscopically,Dense eosinophilic material accumulates in alveolar spaces
Gross
Progressive massive fibrosis
Several coalescent collagenous silicotic nodules
Coal Workers’ Pneumoconiosis
• caused by inhalation of coal particles and other admixed forms of
dust
• Contaminating silica in the coal dust favour progressive disease
• develop emphysema and chronic bronchitis independent of smoking
MORPHOLOGY
• Anthracosis is the most innocuous coal-induced pulmonary lesion in coal miners
coal macules (1 to 2 mm in diameter) and somewhat larger coal nodules
• Coal macules consist of carbon-laden macrophages
• Complication- centrilobular emphysema
Complicated coal workers’ pneumoconiosis (progressive massive fibrosis)
• intensely blackened multiple scars 1 cm or larger
• Microscopy- dense collagen, pigment ,+/- necrosis
• Caplan syndrome- combination of rheumatoid arthritis (RA) and pneumoconiosis
that manifests as intrapulmonary nodules, which appear homogenous and well-
defined on chest X-ray.
• Nodular lesions are large (1–10 cm), multiple, bilateral
• Caplan nodule- combination of silicotic and rheumatoid nodule
Asbestos-Related Diseases
• Asbestos (Greek, “unquenchable”) includes a group of fibrous silicate minerals
that occur as thin fibers
 Chrysotile accounts for the bulk of commercially used asbestos
 The amphiboles include amosite, crocidolite, tremolite, actinolite and
anthophyllite.
• ASBESTOSIS: Asbestosis is diffuse interstitial fibrosis resulting from
inhalation of asbestos fibers
• historically seen in asbestos miners, millers and insulators
ETIOLOGIC FACTORS:
• Asbestos fibers may be long (up to 100 μm) but thin (0.5–1 μm), so
their aerodynamic particle diameter is small
• They deposit in distal airways and alveoli, particularly at bifurcations
of alveolar ducts
• first lesion is an alveolitis
PATHOLOGY:
• bilateral, diffuse interstitial fibrosis
• asbestos bodies in the lung In early stages, fibrosis
• end-stage or “honeycomb” lung
Asbestosis
Asbestos bodies
Pleural plaque
• BENIGN PLEURAL EFFUSION
• PLEURAL PLAQUES-
most common manifestation of asbestos
well-circumscribed plaques of dense collagen often calcified
• DIFFUSE PLEURAL FIBROSIS
• ROUNDED ATELECTASIS
• MESOTHELIOMA
• CARCINOMA OF THE LUNG
Berylliosis
• pulmonary disease that follows the inhalation of beryllium
• materials in aerospace, industrial ceramics and nuclear industries
Pathology
• Acute chemical pneumonitis or a chronic pneumoconiosis
• 10% progress to chronic disease, Chronic berylliosis
• Exposure may be minimal and brief
• Microscopically, Multiple noncaseating granulomas are distributed
along the pleura, septa and bronchovascular bundles
• may progress to end-stage fibrosis and honeycomb lung
• associated with an increased risk of lung cancer
Berylliosis
Talcosis
• Prolonged and Heavy Exposure to Talc Dust
• magnesium silicates
• lubricants, and in cosmetics and pharmaceuticals
• Associated minerals such as silica may contribute to the fibrotic
changes
• Tiny nodules to severe fibrosis
• Foreign body granulomas associated with birefringent plate-like talc
particles
Thank you

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981_ppt_pneumoconiosis_pathology.pptx

  • 2. Pneumoconiosis- • Pneumoconioses encompass a group of chronic fibrosing diseases of the lung resulting from exposure to organic and inorganic particulates, most commonly mineral dust
  • 3.
  • 4. • Pathogenesis- (1) amount of dust (2) size, shape, and buoyancy of the particles o small particles,1 to 5 μm –acute lung injury o Large particle-evoke fibrosing collagenous pneumoconioses (3) particle solubility and physiochemical reactivity-small particles composed of injurious substances of high solubility (4) additional effects of other irritants
  • 5. • particles stimulate resident innate immune cells in the lung • invokes systemic response • a genetic predisposition
  • 6. Particles size 2.5–10 μm- • bronchi and bronchioles • removed by mucociliary action  <2.5 μm- acini <100 nm-penetrate alveolar walls
  • 7.
  • 8. Silicosis • Silicosis is the most common pneumoconiosis in the world, and crystalline silica (e.g., quartz) is the usual culprit • caused by inhalation of proinflammatory crystalline silicon dioxide
  • 9. Pathogenesis- crystalline and amorphous forms • crystalline forms (including quartz, cristobalite, and tridymite)- much more fibrogenic • Phagocytosed silica crystals activate the inflammasome, leading to the release of inflammatory mediators, particularly IL-1 and IL-18
  • 10. • disease may continue to worsen even if the patient is no longer exposed • It is associated with an increased susceptibility to tuberculosis • Patients with silicosis have double the risk for developing lung cancer
  • 11. SIMPLE NODULAR SILICOSIS: most common form of silicosis PROGRESSIVE MASSIVE FIBROSIS: nodular masses greater than 2 cm in diameter, in a background of simple silicosis • bilateral • 5–10 cm • Central cavitation
  • 12. ACUTE SILICOSIS: • heavy exposure to finely particulate silica during sandblasting or boiler scaling • it is associated with diffuse fibrosis of the lung • Silicotic nodules are not found • Microscopically,Dense eosinophilic material accumulates in alveolar spaces
  • 13. Gross
  • 15. Several coalescent collagenous silicotic nodules
  • 16. Coal Workers’ Pneumoconiosis • caused by inhalation of coal particles and other admixed forms of dust • Contaminating silica in the coal dust favour progressive disease • develop emphysema and chronic bronchitis independent of smoking
  • 17. MORPHOLOGY • Anthracosis is the most innocuous coal-induced pulmonary lesion in coal miners coal macules (1 to 2 mm in diameter) and somewhat larger coal nodules • Coal macules consist of carbon-laden macrophages • Complication- centrilobular emphysema Complicated coal workers’ pneumoconiosis (progressive massive fibrosis) • intensely blackened multiple scars 1 cm or larger • Microscopy- dense collagen, pigment ,+/- necrosis
  • 18. • Caplan syndrome- combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogenous and well- defined on chest X-ray. • Nodular lesions are large (1–10 cm), multiple, bilateral • Caplan nodule- combination of silicotic and rheumatoid nodule
  • 19.
  • 20. Asbestos-Related Diseases • Asbestos (Greek, “unquenchable”) includes a group of fibrous silicate minerals that occur as thin fibers  Chrysotile accounts for the bulk of commercially used asbestos  The amphiboles include amosite, crocidolite, tremolite, actinolite and anthophyllite.
  • 21. • ASBESTOSIS: Asbestosis is diffuse interstitial fibrosis resulting from inhalation of asbestos fibers • historically seen in asbestos miners, millers and insulators
  • 22. ETIOLOGIC FACTORS: • Asbestos fibers may be long (up to 100 μm) but thin (0.5–1 μm), so their aerodynamic particle diameter is small • They deposit in distal airways and alveoli, particularly at bifurcations of alveolar ducts • first lesion is an alveolitis
  • 23. PATHOLOGY: • bilateral, diffuse interstitial fibrosis • asbestos bodies in the lung In early stages, fibrosis • end-stage or “honeycomb” lung
  • 27. • BENIGN PLEURAL EFFUSION • PLEURAL PLAQUES- most common manifestation of asbestos well-circumscribed plaques of dense collagen often calcified • DIFFUSE PLEURAL FIBROSIS • ROUNDED ATELECTASIS • MESOTHELIOMA • CARCINOMA OF THE LUNG
  • 28. Berylliosis • pulmonary disease that follows the inhalation of beryllium • materials in aerospace, industrial ceramics and nuclear industries
  • 29. Pathology • Acute chemical pneumonitis or a chronic pneumoconiosis • 10% progress to chronic disease, Chronic berylliosis • Exposure may be minimal and brief • Microscopically, Multiple noncaseating granulomas are distributed along the pleura, septa and bronchovascular bundles
  • 30. • may progress to end-stage fibrosis and honeycomb lung • associated with an increased risk of lung cancer
  • 32. Talcosis • Prolonged and Heavy Exposure to Talc Dust • magnesium silicates • lubricants, and in cosmetics and pharmaceuticals • Associated minerals such as silica may contribute to the fibrotic changes • Tiny nodules to severe fibrosis • Foreign body granulomas associated with birefringent plate-like talc particles

Notas do Editor

  1. Mineral dust is mainly constituted of the oxides (SiO2, Al2O3, FeO, Fe2O3, CaO, and others) and carbonates (CaCO3, MgCO3) that constitute the Earth's crust.
  2. 1-cigarette smoking, that impairs mucociliary clearance significantly increases the accumulation of dust in the lungs.
  3. Il 1il18 prion inflammasome is a multiprotein intracellular complex that activates the highly pro-inflammatory cytokines interleukin-1b (IL-1b) and IL-18.
  4. because crystalline silica inhibits the ability of pulmonary macrophages to kill phagocytosed mycobacteria
  5. Advanced silicosis. Scarring has contracted the upper lobe into a small dark mass (arrow). Note the dense pleural thickening.
  6. large area of dense fibrosis containing entrapped carbon particles.
  7. Microscopy-central area of whorled collagen fibers with a more peripheral zone of dust-laden macrophages
  8. Progressive massive fibrosis superimposed on coal workers’ pneumoconiosis. The large, blackened scars are located principally in the upper lobe. Note the extensions of scars into surrounding parenchyma and retraction of adjacent pleura
  9. The lung shows patchy, dense, interstitial fibrosis.
  10. These ferruginous bodies are golden brown and beaded, with a central, colorless, nonbirefringent core fiber. Asbestos bodies are encrusted with protein and iron.
  11. The dome of the diaphragm is covered by a pearly white, nodular plaque.
  12. . A noncaseating granuloma consists of a nodular collection of epithelioid macrophages and multinucleated giant cells.