RHS10 - Pulmonary Pathology 5 Flashcards
(30 cards)
What is pneumoconiosis? What are the most common types of this diseaes?
Pneumoconiosis is a restrictive lung disease caused by inhalation of particulates or vapors. The most common kinds of pneumoconiosis are:
- Asbestosis
- Silicosis
- Coal Worker Pneumoconiosis (CWP)
What determines the severity of symptoms of pneumoconiosis?
The fibrogenicity (potential to cause fibrosis) of the inhaled particle?
List the particulates we need to know that cause pneumoconiosis and say how fibrogenic they are.
Fibrogenic - asbestos and silica
Inert or Weakly Fibrogenic - carbon and iron oxides
Describe the general pathogenesis of pneumoconiosis diseases.
- Alveolar macrophages engulf the inhaled particle and release various lysosomal enzymes and free radicals, causing tissue injury which leads to inflammation and fibroblast proliferation.
- Alveolar macrophages also secrete growth factor IL-1, causing more fibroblast proliferation.
- The increased fibroblast proliferation leads to lung fibrosis
What is the primary cause of asbestosis? What occupations are at greatest risk for this disease?
Asbestos (fibrous silicates)
Mining, milling, insulation, construction, and demolition
Describe the specfific pathogenesis of asbestosis.
- Alveolar macrophages engulf asbestos fibers
- The macrophages cannot digest the fibers so they die, leaving behind an asbestos body which is an asbestos fiber surrounded by a protein and iron complex. The iron comes from the macrophage’s ferritin
- The body responds to the asbestos body by generating free radicals and secreting cytokines and other inflammatory mediators. This leads to cell injury and proliferation
- The increased cell injury and proliferation increases the rate of DNA damage and eventually leads to carcinogenesis
Describe the histological appearance of asbestosis
Presence of asbestos bodies with appear as elongated, translucent particles with a beaded end
List the various lesions associated with asbestosis.
- Lung
- Asbestos bodies
- Peribronchiolar fibrosis which can progress to diffuse interstitial fibrosis
- Bronchogenic carcinoma
- Pleura
- Plaques (collagen deposits)
- Mesothelioma (malignancy of mesothelial cells in the pleura)
Describe the gross features of asbestosis
Whitish, large, discrete, collagen plaques on the lung pleura (left)
Thick, firm, whitish pleural tumor (right)
Important note about asbestos exposure, smoking, and lung cancer.
Asbestos and smoking are lung cancer risks independently but they drastically increase the risk for lung cancer if an individual is exposed to both.
What is the cause of silicosis? What occupations are at the greatest risk for developing silicosis?
Inhilation of silicon dioxide (silica)
Mining, stonecutting, sandblasting, grinding, foundry work, and ceramic work
Describe the gross appearance of silicosis.
A fibrotic and shrunken upper lobe
Describe the histological appearance of silicosis.
Presence of central collagenous silicotic nodules with dust laden nodules on the periphery.
What other diseases does silicosis increase the risk of? Why?
Pulmonary Tuberculosis
The silical inhibits the ability of the macrophages to kill phacgocytosed mycobacteria
What is the cause of coal workers pneumoconiosis?
The inhalation of coal dust. But the carbon itself is actually harmless. The real problem is the organic and inorganic compounds also in the coal dust
List and describe the categories of coal workers’ pneumoconiosis (CWP).
- Anthracosis
- Accumulation of carbon pigment in the macrophages in the lymph nodes and perilymphatic regions. Asymptomatic
- Simple CWP
- Carbon-laden (dust-laden) macrophages begin to aggregate into macules (smaller) and nodules (larger). Little to no fibrosis or pulmonary dysfunction
- Complicated CWP (progressive massive fibrosis)
- Nodules coalesce and fibrous scars begin to appear (depending upon the amount of non-carbon material). There will be impaired pulmonary function
Describe the gross appearance of CWP
The presence of antracotic pigment and fibrosis
Fibrosis can be spotted by looking at the pleural border. Fibrosis causes shrinking and if it present the border will be sunken in
Give the definition of pulmonary edema and list the non-acrdiogenic causes we need to know.
The accumulation of fluid in the alveolar space
- ARDS (increased capillary permeability)
- High Altitude (exaggerated pulmonary capillary vasoconstriction in response to the hypoxic envrionment)
- Neurogenic (mechanism not completely understood)
- Pulmonary embolism (increased pressure)
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What are the three things needed for thrombus formation?
- Hypercoagulability
- Stasis
- Endothelial Injury
List the major risk factors for pulmonary thromboembolism
- Immobility (blood stasis)
- Surgery (both for immobility afterwards and because many surgeries (orthopedic) utilize prothrombotic measures)
- Severe Trauma
- CHF (stasis)
- Oral Contraceptive Pills (OCPs) (elevated estrogen increased coagulability)
- Disseminated Malignancy
- Hypercoagulability Disorders (Factor V Leiden, protein C, protein S, Anitthrombin III deficiency)
What determines the Sx severity of a pulmonary thromboembolism
The percentage of pulmonary vasculature blocked (so one large or several smaller emboli) and cardiopulmonary status of the patient
What are the consequences of a pulmonarythromboembolism?
- Upstream increase of PA pressure +/- vasospasm
- Ischemia (but usually not infarct) of downstream pulmonary parenchyma
- Acute increase in pressure on the right heart
- Secondary Hypoxia from
- Atelectasis - reduced surfactant production in ischemic areas
- Blood flow redirected to normally hypoventilated areas of the lung
- R to L shunt through patent foramen ovale (30% of population)
When can a pulmonary embolism lead to sudden death?
Sudden death from a pulmonary thromboembolism is usually the result of acute cor pulmonale (RH failure), shock, or hypoxia.
This usually only occurs if the embolus or emboli obstruct _>_60% of the pulmonary vasculature.
What is a saddle embolus?
A large embolus lodged in the bifurcation of the pulmonary trunk
