Flashcards in Lung Deck (452)
Goodpasture's syndrome: Relevance of epidemiology to presentation (2).
Young white males: Pulmonary symptoms often precede renal symptoms.
Elderly women: Glomerulonephritis and renal failure precede pulmonary disease.
Goodpasture's syndrome: Pulmonary manifestation.
Hemoptysis, which may be mild or life-threatening.
Goodpasture's syndrome: Histology of pulmonary disease (3).
Intraalveolar hemorrhage with many hemosiderin-laden macrophages.
Fibrous thickening of alveolar septa.
Hyperplasia of pneumocytes.
Goodpasture's syndrome: Ancillary tests (2).
Immunofluorescence: Linear IgG, IgM, or IgA and complement along the alveolar basement membrane.
Serology: Circulating autoantibodies.
Goodpasture's syndrome: Electron microscopy.
Fragmented capillary basement membranes.
Widened gaps between endothelial cells.
Goodpasture's syndrome: Antibodies (2).
Anti-GBM against the non-collagenous domain of the α₃ chain of type IV collagen.
Concurrent c-ANCA or p-ANCA in one third of patients.
Goodpasture's syndrome: Associated HLA type.
Pulmonary silicosis: Classification according to timing.
Acute: Symptoms within 3 years after exposure.
Accelerated: Within 3-10 years.
Chronic: At least 20 years.
Pulmonary silicosis: Classification according to gross pathology.
Simple: Nodules up to 1 cm.
Progressive massive: Nodules >1 cm.
Pulmonary silicosis, acute: Histology (3).
PAS-positive granular substance fills alveoli.
Pulmonary silicosis, chronic: Histology.
Discrete fibrous nodules of variable size, mainly in the upper lobes and subpleural regions.
Pulmonary silicosis, chronic: Structure of nodules.
Middle zone: Layers of dense collagen with focal calcification and necrosis.
Periphery: Particle-laden macrophages, lymphocytes, fibroblasts.
Microbiological association of pulmonary silicosis:
A. Mycobacterium tuberculosis (silicotuberculosis).
B. Silicotic nodules with central necrosis and epithelioid granulomas.
Pulmonary silicosis vs. pulmonary alveolar proteinosis.
Pulmonary alveolar proteinosis:
− Little inflammation or fibrosis.
− Protein is reactive for antibodies to surfactant apoptotein.
Pulmonary alveolar proteinosis: Associations (3).
Pulmonary alveolar proteinosis: Complication.
Secondary infection by
− Pneumocystis jiroveci.
Pneumoconiosis: Particles that induce fibrosis (5).
Pneumoconiosis: Particles that induce little or no fibrosis (3).
B. Clinical presentation (3).
A. Symptoms appear 15-20 years after exposure.
B. Dyspnea, clubbing, restrictive lung disease.
Asbestosis: Location of lesions.
Mostly in the lower lobes.
Asbestosis: How the inhaled fibers get to the pleura.
Through the lymphatic channels (carried in macrophages) or by direct penetration.
Asbestos: Chemical composition.
Hydrated magnesium silicates.
Asbestosis: Appearance of fibers in tissue (2).
Asbestos body: Brown (due to hemosiderin), beaded, two bulbous ends, clear core.
Ferruginous body: No clear core.
Asbestosis: Histology of tissue reaction (3).
Diffuse interstitial fibrosis with chronic inflammation.
Hyperplasia of type 2 pneumocytes.
Alveolar epithelial cells may contain a substance that resembles Mallory's hyaline.
Asbestosis: Preferred sample for recovery of asbestos bodies.
Asbestosis: Related cancers.
Radiation pneumonitis, acute:
B. Clinical presentation.
A. Symptoms begin between 6 weeks and 6 months after exposure.
B. Cough, dyspnea on exertion.
Radiation pneumonitis: Exacerbating factors (3).
Radiation pneumonitis, acute: Histology.
Hyaline membranes as in diffuse alveolar damage.
Interstitial proliferation of atypical fibroblasts within young fibrosis.