Occupational & Traumatic Disorders Flashcards
Define acute respiratory distress syndrome
Manifestation of severe acute lung injury
Define acute lung injury
Abrupt onset of hypoxemia and bilateral pulmonary infiltrates in the absence of heart failure
Both ARDS & ALI involve inflammation-associated increases in _______.
- pulmonary vascular permeability
- edema
- epithelial cell
Define diffuse alveolar damage (DAD)
Histologic manifestation of ARDS/ALI
Describe the pathophysiology of ARDS/ALI
Injury → neutrophil recruitment & endothelial activation/injury → release of proteases, ROS → leakage of proteins into alveoli → hyaline membrane → interference w/gas exchange.
- blue arrow: collapsed alveoli
- black arrows: hyaline membranes formed due to damage (these interfere with gas exchange & decrease lung compliance)
Organizing phase of ALI/ARDS. About one week after the initial injury, fibroblasts begin to proliferate within the alveolar walls.
- Yellow arrow: scattered residual alveoli containing proteinaceous fluid
- Yellow circle: alveolar wall which is thickened by loosely arranged fibroblastic tissue (i.e. granulation tissue).
ARDS/ALI clinical presentation
- Tachypnea
- Dyspnea → hypoxemia
- Respiratory acidosis (⇡ PCO2)
(mechanical ventilators often become necessary)
Prognosis of ARDS/ALI
40% mortality
(survivors may heal with fibrosis → chronic pulmonary disease)
CXR findings of ARDS/ALI
Diffuse bilateral infiltrates
Define pneumoconiosis
Lung disease caused by the inhalation of mineral or organic dust or chronic or vapors
(typically occupational disease)
Many cases of pneumoconiosis results in _______.
pulmonary fibrosis
(regulations limiting worker exposure have decrease this)
List 4 factors that increase the likelihood of pneumoconiosis development
- Amount of dust retained in the lungs
- particle size of 1-5 micrometers in diameter
- Particle solubility
- genetics
The most common chronic occupational disease in the world
Silicosis
(type of pneumoconiosis)
Define silicosis
Fibrosing lung disease caused by inhalation of silicon dioxide (silica) particles
most commonly implicated particle in silicosis
Quartz
Silica occurs in both crystalline and amorphous forms. _____ is more fibrogenic. ______ is more pathogenic.
- Crystalline
- Amorphous
Pathogenesis of silicosis
macrophages phagocytize a silica particle → become activated → inflammatory mediators released → fibrosis
Silicosis
(Black Arrow: dense fibrosis)
silicotic nodule composed of dense collagenous fibrous connective tissue
(these coalesce)
Silicotic nodule w/birefringent silica particles
3 Occupations at risk for silicosis
- miners
- Sand blasters
- Quartz stone cutters
CXR findings for silicosis
Fine nodularity in the upper zones of the lung
silicosis is associated with an increased susceptibility to ______
tuberculosis
(“slow to kill” disease; most patients do not developed dyspnea until they have massive fibrosis)
Define asbestos
a family of hydrated silicates that form fibers
Occupational exposure to asbestos is linked to ______(6).
- pleural plaques
- Pleural effusion
- Pulmonary interstitial fibrosis (asbestosis)
- Lung carcinoma
- Mesothelioma
- Laryngeal, ovarian malignancies
The oncogenicity related to asbestos-related disease is due to the _____.
Generation of free radicals and adsorption of carcinogens on to the fibers
asbestosis
Define asbestosis
interstitial fibrosis due to asbestos exposure
Asbestos bodies (golden-brown beaded batons)
pleural plaques due to asbestos exposure
Define hypersensitivity pneumonitis
Immune-mediated lung disorders caused by exposure to inhaled organic antigens (bacterial, fungal or animal proteins)
Hypersensitivity pneumonitis is also known as
Extrinsic allergy alveolitis
(important to recognize these disorders early)
Farmer’s lung: source of antigen
Thermophilic actinomycetes spores in warm moist air
Pigeon breeder’s lung: source of antigen
Proteins from serum, excreta or feathers of birds
Humidifier lung: source of Antigen
(air conditioner)
thermophilic bacteria and heated water reservoirs
hypersensitivity pneumonitis pathogenesis: type III hypersensitivity
complement and Igs in vessel walls
Hypersensitivity pneumonitis pathogenesis: Type IV hypersensitivity
(delayed type: after 2-3 days)
noncaseating granulomas
Hypersensitivity pneumonitis clinical symptoms: acute attack (4)
- Fever
- Dyspnea
- Cough
- Leukocytosis
CXR findings: hypersensitivity pneumonitis
Interstitial infiltrates
Hypersensitivity pneumonitis: Long-term exposure symptoms
Progressive respiratory failure with a restrictive pattern
hypersensitivity pneumonitis: noncaseating interstitial granuloma containing a Langhans giant cell (yellow arrow) consistent with a type IV hypersensitivity reaction.
(If exposure to the offending antigen persists, then the patient can go on to develop interstitial fibrosis, obliterative bronchiolitis and honeycombing).
