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CR - Interstitial Lung Disease (Pul Fibrosis) (ii) (Silicosis (acute (from…
CR - Interstitial Lung Disease (Pul Fibrosis) (ii)
CWP
pathogenesis
particle in alveolus
proinflamm, toxic + fibrinogenic factors
lung injury, then fibrosis
carbon, trace metals, inorganic materials + silica in coal
most cases are mild = pul anthracosis
lesions in lymphatics + nodes
common in urban dwellers + smokers
accumulation of inhaled carbon taken up by alveolar macrophages
simple CWP
focal dust accumulation around resp bronchioles
macules (dust-laden macrophages) + larger nodules (collections of collagen fibres)
upper zone predominant
can eventually cause alveolar dilation -> centrilobar emphysema -> COPD
usually not functionally disabling
PMF
progression/complication of simple CWP due to increased exposure (increased total dust burden)
after 10-20 yrs
nodules coalesce
intense black multiplying scars/lesion of collagen + pigment
upper zone predominant
rarely leads to pul dysfunction, pul hypertension, cor pulmonale
Caplan syndrome
unsure why coexistence exists
distinctive nodular pul lesions that develop rapidly
central necrosis
surrounding fibroblasts, plasma cells + macrophages all contain coal dust + collagen
also occurs in asbestosis + silicosis
Silicosis
silica can be crystalline (more toxic + fibrinogenic) or amorphous
rock/stone cutting, mining, drilling, tunnelling, sandblasting, glass + pottery making
acute
from exposure to high levels
rapid onset
tachypnoea, cough, cyanosis, resp failure
interstitial inflamm + accumulation of proteinaceous fluid in alv spaces
chronic/nodular
silicotic nodules = collagen deposition + surrounding inflamm
inhalation over prolonged period
upper zone + sub pleural predominant
complicated/conglomerale
progression of chronic
expansion + coalescence of nodules
destruction of parenchyma -> PMF
Caplan syndrome
increases risk of TB + lung carcinoma (esp adenocarcinoma)
clinical course: progressive resp failure, pul hypertension, cor pulmonale
Asbestosis
asbestos = family of crystalline hydrated silicates
sources = construction materials, insulation, cement, roofing materials, electric motor components, textiles
2 different forms
serpentine (curly, flexible, used more in industry, e.g. chrysotile)
amphibole (straight, still, brittle, more pathogenic)
related disorders...
pleural plaques
most common
well-circumscribed
consist of dense collagen
most frequently on parietal pleura
pleural effusions
asbestosis
diffuse interstitial fibrosis
lower zone + sub pleural predominant but spreads up to middle + upper lobes as fibrosis progresses
asbestos bodies
mesothelioma
pleural
rarely peritoneal
bronchogenic carcinoma (esp with smoking)
fibres inhaled, surrounded by macrophages, coated in fe to form dumbbell-shaped ferruginous bodies
latency period = 10-30 yrs
fibrosis begins around resp bronchioles + alv ducts before moving into sacs
advanced - honeycombing (enlarged air spaces + thick fibrous walls)
Berylliosis
similar process to silicosis, just different source