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21 Cards in this Set
- Front
- Back
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Dust Macules
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Materials in this category are inhaled and retained in the lungs.
1. There is little host reaction to the foreign material. 2. Generally there are no clinical symptoms 3. There are no pulmonary function abnormalities. 4. There is no progressive lung disease. Iron (red macules) Tin (gray macules) Titanium (white) Urban pollution, cigarette smoking (black) The chest radiograph may show small scattered densities. |
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Acute silicosis
Silicoproteinosis |
1. Rare today
2. Progressive & fatal to massive exposure Symptoms: 1. Hypoxia 2. Respiratory failure 3. Lung edema “Ground glass” CXR esp upper lobes Finely divided birefringent material |
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Chronic (simple) silicosis
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Rarely have significant symptoms
Min to no change in PFTs - Silicotic nodules (blue/green) present (<1-1.5cm) (DIAGNOSITIC) Sharply demarcated round borders, whorled collagenous center - upper lobes - “egg shell” calcifications of hilar lymph nodes - more changes w/ greater exposure |
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Complicated Silicosis
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- Progressive lung disease even in absence of continued exposure
- restrictive (reduced VC, TLC, compliance) but also obstructive secondary to distortion of airways (bulla) - Anti-nuclear antibody & rheumatoid factor Symptoms: Cough Progressive dysnea Hypoxia, cor pulmonale Caplan’s Syndrome: lung disease (silica exposure) + rheumatoid arthritis (nodules bigger but disease itself more benign) Simple nodules coalesce, creating large densities -> involve entire hemithorax (DIAGNOSITIC) |
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Progressive Massive Fibrosis
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- Traction on lower lung by the fibrosing upper lobes leads to retraction bullae at the lung bases (look like emphysema)
- As fibrosis progresses, the great vessels can be involved. The superior vena cava can be compromised, leading to lack of adequate blood return to the heart - This process is most often fatal due to extensive lung disease as well as cv compromise - Alveolar macs -> fibroblast growth factors & IL1. T cells proliferate -> cytokines (gamma interferon, IL2, MMIF) -> fibrosis CXR: Massive coalescence of upper lobe nodules |
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Silicotuberculosis
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- Silica poisons macrophages
- Macrophages are first line of defense for TB - Persons infected w/ TB (+PPD skin test) have 4-6x increased risk of developing active TB - Annual PPD – evidence or exposure to silicosis Upper lobes |
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Non-fibrous silicates
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Can produce similar disease to fibrous silica: simple pneumoconiosis or complicated, with PMF
- Agents: talc, kaolin, bentonite |
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Coal Worker’s Pneumoconiosis (CWP)
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accumulation of coal dust in lungs + tissues’ reaction
- 10 yrs of exposure - nodules on CXR - no need to demonstrate disability or physiologic impairment |
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Simple CWP
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- accumulation of coal dust in the lungs - Cough w/ blackish sputum common
- PFTs normal - many coal miners smoked, COPD is common finding - Black Macules- airspaces around macules enlarge in pattern like centrilobular emphysema “focal emphysema” - Fine nodules (smaller than in silicosis) (if have exposure to silica -> silicotic nodules (hilar lymph nodes) - Massive fibrosis - Caplan’s lesions -Interstitial fibrosis |
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Complicated CWP
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Similar in all respects to complicated silicosis
Theories (mostly untrue) why some individuals react with fibrosis (PMF): • Silica + coal dust exposure (during rock blasting to get at coal) • Massive coal dust exposure with host reaction in susceptible individuals • Infection (TB) + coal dust exposure • Immunological (macs -> fibroblast growth factor, IL1 & collagen formation) Tend to progress, even after contact ended Symptoms: - shortness of breath - DOE (dysnea on exertion) - Hypercapnia PFTs for PMF Restrictive & obstructive (worse) DLco reduced Increase A-a gradient Bilateral lesions upper zone Consist of 1cm nodules which may coalesce Or Single large lesion Usually darkly pigmented & may have necrotic centers |
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Asbestos Pleural Disease
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Pleural plaques
Pleural fibrosis Pleural effusions Pleural pseudotumors (rounded atelectasis) – infolding of lung causes by scarring, mistaken for tumor, no functional impairment There is no apparent direct association btw asbestos-induced benign pleural disease & development of malignant mesothelioma Exudative, bloody pleural effusions 1. Pleural Plaques a. thickened pleural in patches along lateral chest walls &/or diaphragm &/or mediastinal pleural b. often calcified & appear as hard white areas on CXR 2. Diffuse pleural thickening- less common & less characteristic of asbestos exposure |
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Asbestosis
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- Progressive (over decades, despite cessation of exposure)
- diffuse interstitial fibrosis - Fibers too large to be digested by macrophages - Cycle of inflamm (macs & T cells) & fibrosis - Asbestos direct stimulate fibroblast Symptoms: 1. dry cough 2. crackles on exam 3. exertional dsypnea DOE PFTs: Restrictive with low lung volumes ↓VC, TLC compliance, DLco, ↑A-a gradient Hyperventilation, hypoxemia, clubbing, cor pulmonale, respiratory failure - Lung bases - “shaggy heart” - pleural plaques (indicative of exposure) - effusions - similar to idiopathic interstitial fibrosis (revised air spaces + honeycombing) Light microscope: Ferruginous bodies (mineral particle with iron-protein coats)-> indicative of exposure |
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Bronchogenic (lung) cancer
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1. Asbestos alone: 5x increase in risk for lung cancer
2. smoking alone: 10x increase in risk 3. Smoking + asbestos = synergistic = 90x increase risk |
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Malignant Mesothelioma
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- Malignant tumor of pleural mesothelial cells
- Prognosis worse than lung cancer- not as responsive to radiation or chemotherapy; very difficult to resect surgically - long latency period 30-40 years min 15 years Gross: - visceral (lung or bowel) - soft grey-white mass - most marked over lower lobes - lines pleural cavity & fissures - rarely invades - cavitation - metastases are present in half cases but usually small & clinically insignificant Microscopic: Adenocarcinoma pattern |
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Other cancers associated with asbestos
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Swallowed asbestos: laryngeal & GI cancers
Bladder cancer incidence increased |
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Hypersensitivity Pneumonitis
Extrinsic Allergic Alveolitis Farmer’s Lung Pigeon Breeder’s Lung Sauna Taker’s Lung Mushroom Worker’s Lung Bagassosis |
- Type III Hypersensitivity to organic dusts
- “Farmers lung” – thermophyllic actinomyces & micropolyspora in moldy hay - Key to making diagnosis is clinical & temporal association of symptoms to exposure - Symptoms occur 4-8 hours after exposure or long latency - Most common in spring, when hay has been molding & forked out - resolved spontaneously w/in 18-24 hrs - repeated exposure -> progressively more severe attacks - continued exposure -> restrictive lung disease - Type IV hypersensitivity can occur as well Symptoms: - fever - chills - malaise - sweating - unproductive cough - dyspnea (sounds a lot like pneumonia) Mixed restrictive/obstructive CXR: Bilateral reticulonodular infiltrates Pathology: Interstitial lymphocytes Mild interstitial fibrosis Interstitial granulomas Often peribronchiolar inflammation Produce small airway obstruction Bronchiolitis obliterans Rare progression to honeycomb end stage lung Schaumann bodies (old calcified concretions representing the site of previous granulomas) |
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Occupational Asthma
Obstructive lung disease |
- Temporal relationship to work exposure
Worsen during each day on the job Improve away from work - Perform spirometry before & after work shift - Respond to bronchodilators but avoiding exposure is true treatment - chronic exposure -> COPD Symptoms: Wheezing Cough Shortness of breath worsening in work place |
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Eosinophilic Granuloma
Langerhans Cell Histiocytosis Pulmonary Histiocytosis X |
Proliferation & tissue infiltration by langerhans cells
Birbeck Granules (racket shaped inclusions) CD1a antigen + - Only involves the lung - strong association with smoking Symptoms often improve w/ smoking cessation - Focal lesions around smaller bronchioles that produce stellate lesions Contain eosinophils, PMNs, & lymphocytes Important to note that eosinophils are now always present (misnomer) - Granulomatous infiltrations - Favors upper lobes - Crease in nuclei |
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Silo Filler’s Disease
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- Oxides of nitrogen from fresh cut hay.
- Yellow brown gas seen overlying the hay - Note: more common in the autumn when hay is harvested and stored in the silo. - Effects can be nearly immediate with high exposure or evolve over 18 to 24+ hours with lower level exposures. - ARDS type picture/diffuse alveolar damage &/or bronchiolitis obliterans - Treatment: oxygen & respiratory support; corticosteroids Symptoms: Severe shortness of breath Hypoxemia Bilateral diffuse lung infiltrates Ground Glass |
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Diffuse Alveolar Damage (pathology)
Acute Respiratory Distress Syndrome Acute interstitial pneumonia (Hamman-Rich syndrome) |
- Diffuse distribution
- Uniform temporal appearance - alveolar septal thickening due to organizing fibrosis, usually diffuse - airspace organization (may be patchy or diffuse) - Hyaline membranes (may be focal or diffuse) - Pertinent negatives Granulomas, necrosis, pneumonia, abscesses, infectious agents, prominent eosinophils, neutrophils, cultures - Any irritant gas in [high] can produce Cadmium, fire smoke, nitrogen oxides, chlorine, ozone, ammonia, phosgene Symptoms: Severe shortness of breath Severly hypoxemic CXR: Bilateral alveolar infiltrates Gross: diffuse consolidation with loss of normal markings Microscopically: hyaline membranes in alveolar ducts & collapse of alveolar parenchyma |
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Bronchiolitis Obliterans
Bronchiolitis Obliterans Organizing Pneumonia (BOOP) Cryptogenic Organizing Pneumonia (COP) |
- Granulation tissue (myofibroblast) plugs in alveoli and or bronchi
- Non specific pattern of organizing pneumonia - Heterogenous etiological factors - Fume, gas inhalation, viral infections Symptoms: Shortness of breath developing several weeks after exposure CXR: Tufts of granulation tissue in respiratory bronchioles |
