Flashcards in Occupational and Environmental Exposure Deck (16):
1. List agents that can cause occupational/ environmental lung disease.
smaller particles can reach the distal airspaces of the lung, host factors modulate the effects of inhaled substances and inhaled cases and particulates can have serious effects on other organ systems by gaining access to the systemic circulation via the lung
offending agents include: silica, asbestos, products form fossil fuel (exhaust, soot, coke oven emissions, coal gas and coal tar volatiles) radon progeny and metals (arsenic, aluminum, beryllium, chromium, cadmium, nickel, iron, lead and mercury)
3. Describe the epidemiology, of silicosis.
diffuse parenchymal lung disease associated with mineral dust exposure leading to an accumulation of mineral dusts inciting tissue reactions from minimal stromal reaction to interstitial fibrosis that results in permanent scarring
exposure in : mining, foundries, stone work and sandblasting
3. Describe the pathogenesis of silicosis..
acute: associated with high intensity of exposure with shorter latency (dyspnea, cough, fatigue and occasional pleuritic pain) with alveolar filling with protein and lipid rich fluid with neutrophil and eos predominance
chronic: peribronchial, well formed spherical nodules with interstitial extension, upper lung predominates, and lymph nodes that develop eggshell calcifications
progressive massive fibrosis: accelerated and progressive fibrotic disease
3. Describe the clinical spectrum of silicosis.
range from asymptomatic chest x ray to accelerated and acute forms
dyspnea, malaise and cough are most common symptoms
demonstrates restrictive pattern and correlates poorly with nodules or lymphadenopathy
associated mycobacterial infections and malignancy
3. Describe the management of silicosis
no establish therapy to reduce pulmonary toxicity, avoidance and surveillance for high risk occupations
2. Describe the epidemiology of asbestosis..
asbestos is a naturally occurring crystalline mineral whose fibers are extremely durable and resistant to heat and chemical stressors
likely exposure: boilermakers, plumbers, carpenters, electricians, shipbuilders and second-had asbestos to spouse
2. Describe the pathogenesis of asbestosis.
exposure through direct inhalation; effects are combo of direct toxic effects of the fibers along with generation of mediators by inflammatory cells and other cell types
deposition of excessive matrix by mesenchymal cells can occur and lead to parenchymal fibrosis
2. Describe the pathophysiology of asbestosis
benign asbestos pleural effusions BAPE: chronic blunting of costophrenic angle
pleural plaques: desecrate areas of fibrosis on parietal pleura (not malignancy risk)
rounded atelectasis: parenchymal/pleural thickening formed as pleural fibrosis progresses
malignant mesothelioma, (not increased with tobacco)
asbestosis: diffuse parenchymal fibrotic process
primary lung cancer: asbestos is carcinogenic, increased with tobacco use
2. Describe the clinical spectrum of asbestosis.
earliest symptom is dyspnea with exertion
reduced DLCO, diminished lung compliance and reduced lung volumes
disease can range form asymptomatic pleural disease (benign asbestos pleural effusions BAPE), pleural plaques, rounded atelectasis, malignant mesothelioma, asbestosis and primary lung cancer
5. Describe course and management of silo filer's disease.
acute toxic lung injury due to inhalation of nitrogen dioxide which manifests as bronchitis, bronchiolitis and ARDS
5. Describe the pathophysiology of organic dust toxic syndrome and silo filler's disease.
inflammatory pneumonitis after massive exposure to organic dust (may contain endotoxins, myocotoxins or spores); symptoms are flu-like and typically limited, repeated exposure at lower doses do is not likely to cause recurrence of symptoms
What is hypersensitivity pneumonitis?
wide spectrum of inhalation environmental or work related exposures leading to inflammatory lung disease form particulate matter, it is immunologically induced and driven
List the causative agent for Farmer's, Humidifier, Hot-tub, machine operator, chinese washer and bird fancier's lung
Farmer's thermophilic actinomycetes
Humidifier: klebsiella oxytoca, thermoactinomyces
Hot-tub mycobacterium avium complex
machine operater pseudomonas fluorescens
chinese washer penicillium case
bird fancier's lung: serum proteins, feathers, droppings
What is the pathogenesis of HP?
inhalation of particles induces variable sensitization, after which further exposure has the potential for increased antigenic reaction
influx of neutrophils seen in BAL after exposure to antigen, while lymphocytes predominate in BAL fluid 2-5 days after exposure
How can HP be diagnosised
restrictive pattern of PFT with reduced DLCO especially with acute reactions
precipitating antibodies can demonstrate exposure to specific antigens but do not confer clinical disease
histopathology demonstrates centrilobular distribution and advanced fibrotic changes can look like UIP