Lecture 16, 18: Occupational Lung Disease and Pathology Flashcards
Pneumoconiosis
Lung disease secondary to dust inhalation
Mechanisms of aerosol deposition: 3, by particle size (large –> small)
Impaction (filtered by nose, >5 um), sedimentation (small airways 1-5 um), diffusion (alveoli
Silicosis: who? how long?
Sandblasters, rock miners, quarry workers, stonecutters; ~20 years unless very heavy dose
Silicosis: pathogenesis
Silica particles phagocystosed by alveolar macrophages –> apoptosis –> alveolitis and fibrosis –> SILICOTIC NODULE
Two stages of silicosis
- Simple (small nodules) –> 2. Complicated (nodules coalescent)
What lung zone more affected in silicosis?
Upper lung zone
How does silicosis usually present (predominant symptom)
Dyspnea
Someone with silicosis is particularly susceptible to…
Infections with mycobacteria (perhaps due to impaired macrophage function)
Pneumoconiosis (CWP): who?
Coal miners
CWP: pathogenesis
Dust engulfed by macrophages –> aggregate around respiratory bronchioles –> broncholes dilate –> focal dust emphysema
Simple CWP
Coal macules (aggregation of dust and macrophages around respiratory bronchioles with little tissue reaction) and coal nodules (above + collagen)
Complicated CWP (progrssive massive fibrosis)
Coalesced nodules: bulky, irregular, well-defined, heavily pigmented black tissue masses
CWP: symptoms according to type
Simple –> few symptoms w/ preserved pulmonary function; Complicated –> pronounced symptoms
Abestos: who? how long?
People who work with insulation, shipyard and construction workers, and brake linings; 10-20 years
Asbestos-related lung disease (3)
- Asbestosis; 2. Pleural disease (mesothelioma); 3. Lung cancer
Asbestosis: pathogenesis
Clearence of fibers differs based on size; short –> phagocytosed and drained into pleural space; longer –> incompletely phagocytosed and become core of asbestos body, fibrosis throughout alveolar walls
Characteristic finding of asbestosis. What does it look like?
Asbestos body; rod-shaped body with clubbed ends that appears yellow-brown in stained tissue due to iron
Where in the lung does asbestosis have its largest affect?
Lung bases and subpleural regions
Asbestosis: radiology (include advanced cases findings)
Pattern of linear streaking that is generally most prominent at the lung bases; advanced cases can have cyst formation and honeycombing; often associated pleural disease
Asbestosis: pleural findings (2)
Diffuse pleural thickening and plaques
T/F: Pleural plaques related to asbestos exposure are malignant
False: non-malignant, assymptomatic
Berylliosis: who?
Workers in aerospace, nuclear weapons and electronics industries
Berrylliosis: pathogenosis
Hypersensitivity to beryllium –> granulomas
What does berrylliosis mimic?
Sarcoidosis
First line treatment for pneumoconiosis
Removing occupasional exposure
Hypersensitivity pneumonitis (HP): definition
Result of immunologic phenomena directed against an antigen
Steps of hypersensitivity pneumonitis (3)
- Repeated antigen exposure –> 2. Immunologic sensitiziation of host to antigen –> 3. Immune-mediated damage to lung
How is HP typically categorized?
Acute, subacute, and chronic
HP: pathogenesis
Exposed to antigen –> Th1 (acute) and Th2 (subacute/chronic) response –> inflammation, tissue damage, fibrosis
HP involves what types of immune responses?
Type 1, Type 3, Type 4
Type 1
Allergic response/asthma due to IgE binding of sensitized mast cells –> degranulation
Type 2
Antibody-initiated –> direct binding of antibody to surface molecules (autoimmunity)
Type 3
Antibody-initiated –> formation of immune complexes which are deposited (autoimmunity)
Type 4
T-cell dependent starting with primed T cells –> inflammation and T cell-mediated (CD8+) cytotoxicity
With HP, can you simply test for IgG antibodies?
Nope: not sensitive or specific
HP: pathology (triad)
Triad: cellular bronchiolitis (airway-centered inflammation), organizing pneumonia, scattered, small, non-necrotizing granulomas
Acute HP: clinical features
4-12 hours after exposure with viral-like respiratory symptoms (cough, dyspnea, chest tightness, fevers, chills, malaise) with tachypnea, rales
PFTs reveal what kind of defect with Acute HP?
Restrictive ventilatory defect
Acute HP: treatment
Remove exposure to inciting antigen
Chronic HP: clinical features
Insidious development of dyspnea, cough, and systemic features (fatigue, loss of appetite, weight loss) with tachypnea, rales, clubbing
PFTs reveal what kind of defect with Chronic HP?
Restrictive (fibrotic), obstructive, (reduced airway diameter) or combined
Chronic HP: treatment (besides removing antigen)
Corticosteroids
Definition of a restrictive lung disease
Reduced TLC
Definition of an obstructive lung disease
Less than 0.7 FEV1 / FVC ratio
What is a Ferruginous body
General term referring to any inorganic substance with a coating of iron and protein (graphite, ceramic, iron, etc)
What is an Asbestos body
Ferruginous body formed on an asbestos fiber—characterized by a clear internal core and beaded ferruginous coating
Asbestos causes what pulmonary parenchymal fibrosis (the term) which leads to what end-stage fibrosis (the term)
Asbestosis –> honeycomb lung
Describe the fibrosis progression of asbestosis
Begins around respiratory bronchioles and alveolar ducts and extends distally until it causes honeycomb lung; begins lower lube and subpleurally –> moves to middle and upper
Silicosis is marked by what major finding? What do these cause?
Silicotic nodule; enlarge and eventually obstruct airways and blood vessels
What does the silicotic nodule look like grossly? Where are they found at first?
Stellate shape at the edges; found in upper lung and hilar lymph nodes
What does the silicotic nodule look like microscopically?
Small nodules of fibroblasts and histiocytes with silica (under polarization, this can be visualized), that become less cellular and more hyalinized with time
What can silicosis lead to?
Progressive massive fibrosis
Coal workers’ pneumoconiosis begins as what and then progresses to what…(%)
Simple CWP: coal macules/nodules –> 10% develop progressive massive fibrosis
What is Caplan syndrome
Rheumatoid arthritis AND pneumoconiosis cause rapidly developing nodular pulmonary lesions histologically identical to rheumatoid nodules more commonly seen in soft tissue
