Lung Flashcards
Congenital pulmonary-airway malformation: Blood supply.
Derived from the pulmonary circulation.
Congenital pulmonary-airway malformation: Definition.
Malformation of part of the lung parenchyma, with abnormal direct connections to the normal tracheobronchial tree.
Congenital pulmonary-airway malformation, type 0: Gross pathology.
Lung parenchyma appears solid.
Congenital pulmonary-airway malformation, type 0: Histology (2).
Disorganized proximal airways; no distal airways.
Intervening tissue consists of connective tissue, thick-walled arteries, and extramedullary hematopoiesis.
Congenital pulmonary-airway malformation, type 1: Gross pathology.
Medium and large interconnecting cysts, usually limited to one lobe.
Congenital pulmonary-airway malformation, type 1: Histology.
Cysts are lined by bronchial epithelium and often contain bands of smooth muscle.
Congenital pulmonary-airway malformation, type 2: Gross pathology.
Back-to-back cysts, smaller than the cysts of type 1.
Congenital pulmonary-airway malformation, type 2: Histology.
Cysts are separated by alveolar ductlike structures, blood vessels, skeletal muscle.
Congenital pulmonary-airway malformation, type 2: Associations.
Sirenomelia.
Renal malformations.
Diaphragmatic hernia.
Cardiovascular abnormalities.
Congenital pulmonary-airway malformation, type 3: Gross pathology.
Solid mass involving the lobe or the entire lung, with hypoplasia of the other lung.
Congenital pulmonary-airway malformation, type 3: Histology.
Glandlike structures lined by low cuboidal epithelium.
Congenital pulmonary-airway malformation, type 3: Associations.
Male sex.
Polyhydramnios.
Congenital pulmonary-airway malformation, type 4: Gross pathology.
Peripherally located cysts of variable size.
Congenital pulmonary-airway malformation, type 4: Histology.
Cysts can have thick walls and are lined by a single layer of pneumocytes.
Capillary beds beneath the epithelial lining.
Congenital pulmonary-airway malformation, type 4: IHC.
Pneumocytes express TTF-1 and surfactant proteins A and B.
Congenital pulmonary-airway malformation: Limitations on diagnosis.
Diagnosis cannot be made when there is chronic inflammation and fibrosis.
Bronchopulmonary sequestration: Definition (2).
Anomalous segment of lung has no connection with the normal tracheobronchial tree.
Blood supply comes from the systemic circulation.
Bronchopulmonary sequestration: Types (2).
Intralobar.
Extralobar.
Bronchopulmonary sequestration, intralobar type: Typical location.
Lower lobe.
Bronchopulmonary sequestration, intralobar type: Gross pathology (3).
No pleural covering.
Sharply demarcated from the normal lung tissue.
May have vascular pedicle.
Bronchopulmonary sequestration, intralobar type: Histology (3).
Marked chronic inflammation.
Mucus accumulation and microcyst formation.
Dense fibrosis surrounds remnants of bronchioles.
Bronchopulmonary sequestration, extralobar type: Typical location.
Left side.
Bronchopulmonary sequestration, extralobar type: Gross pathology (2).
Covered with visceral pleura.
Separate from normal lung tissue.
Bronchopulmonary sequestration, extralobar type: Histology (3).
Enlarged bronchi, bronchioles, alveoli.
No significant inflammation or fibrosis.
Dilated subpleural lymphatics.
Bronchopulmonary sequestration, extralobar type: Association.
Congenital pulmonary-airway malformation, type 2, is present in up to half of cases.
Bronchogenic cyst: Origin.
Anomalous budding of the tracheobronchial anlage during development.
Bronchogenic cyst: Most common site.
Mediastinum.
No communication with the tracheobronchial tree.
Bronchogenic cyst: Radiography.
May have an air-fluid level.
Bronchogenic cyst: Histology (3).
Epithelial lining and wall (smooth muscle, cartilage) resemble those of a normal bronchus.
Squamous metaplasia or chronic inflammation may occur.
No alveolar tissue.
Congenital lobar emphysema: Definition.
Hyperinflation of one or more lobes of the lung.
Congenital lobar emphysema:
A. Age at presentation.
B. Most common site.
A. Within 6 months after delivery.
B. Left upper lobe.
Congenital lobar emphysema: Radiography.
Compression of contralateral lung and mediastinal shift.
Congenital lobar emphysema: Histology.
Alveolar distention without fibrosis.
Congenital lobar emphysema: Etiologies.
Idiopathic: Most cases.
Intrinsic compression of the bronchus supplying the affected lobe: Structural defect of bronchus.
Extrinsic compression: Mass.
Chronic bronchitis: Histology.
Reid index >0.5 (glands make up more than half the thickness of the bronchial wall).
Mild chronic inflammation.
Asthma: Gross pathology (3).
Hyperinflated lungs.
Mucous plugging of airways.
Saccular bronchiectasis.
Asthma: Histology (3).
Mucous plugs containing eosinophils.
Fibrosis beneath the basement membrane with patchy loss of epithelium.
Thickened walls of airways due to edema, hyperplasia of smooth muscle, increased mucous glands.
Asthma vs. chronic bronchitis.
Chronic bronchitis: Few or no eosinophils.
Bronchiectasis: Definition.
The bronchus is wider than its bronchial artery.
Bronchiectasis: Clinical presentation.
Persistent cough.
Copious, foul-smelling sputum.
Bronchiectasis: Causes (8).
Primary ciliary dyskinesia. Rheumatoid arthritis. Immunodeficiency. Cystic fibrosis. Inflammatory bowel disease. No known cause (30%). Graft-versus-host disease.
Infections.
Bronchiectasis: Histology (2).
Mucosa: Variable inflammation, reactive changes, necrosis.
Wall: Chronic inflammation, fibrosis.
Middle-lobe syndrome:
A. Definition.
B. Causes.
A. Recurrent or persistent atelectasis of the right middle lobe.
B. Lymphadenopathy, malignancy.
Type of emphysema associated with
A. Cigarette smokers (2).
B. α₁-Antitrypsin deficiency.
A. Proximal acinar or centrilobular.
B. Panacinar or panlobular.
Types of emphysema associated with bullous disease and idiopathic spontaneous pneumothorax (2).
Distal acinar, paraseptal.
Emphysema: Histology (2).
Alveolar distention without fibrosis.
Club-shaped septa may project into the alveolar spaces.
Interstitial emphysema.
Presence of air outside the airways, e.g. in the connective tissue and around bronchovascular bundles.
Constrictive bronchiolitis: Site.
Terminal conducting airways.
Constrictive bronchiolitis: Associations (8).
Collagen-vascular disease.
Hypersensitivity pneumonitis.
Inhalational injury.
Neuroendocrine hyperplasia/tumors.
Viral infection.
Organ transplantation.
Inflammatory bowel disease.
Drugs.
Constrictive bronchiolitis: Histology (4).
Fibrosis.
Chronic inflammation with epithelial metaplasia.
Smooth-muscle hyperplasia.
Luminal obliteration.
Acute bronchiolitis:
A. Age group.
B. Associations (2).
A. Infants and children.
B. Viral infection, bacterial infection.
Acute bronchiolitis: Histology (3).
Intense acute and chronic inflammation of small bronchioles.
Epithelial necrosis and sloughing.
Edema.
Diffuse bronchiolitis:
A. Epidemiology.
B. Associations (4).
A. Affects Asian adults.
B. HLA Bw54; cold agglutinin, increased ESR, leukocytosis.
Diffuse bronchiolitis: Histology (3).
Lymphocytes, plasma cells, foamy macrophages.
Many intraluminal neutrophils.
Organization of exudate to form polypoid plugs.
Respiratory bronchiolitis: Association.
Cigarette smoking.
Respiratory bronchiolitis: Histology (4).
Interstitial inflammation.
Many intraluminal pigmented macrophages.
Smooth-muscle hypertrophy.
Mild fibrosis.
Mineral-dust bronchiolitis: Type of lung disease.
Restrictive, due to fibrosis.
Mineral-dust bronchiolitis: Histology (3).
Fibrosis.
Deposits of dust mainly around respiratory bronchioles.
Luminal narrowing.
Follicular bronchiolitis: Type of lung disease.
Obstructive, due to external compression.
Follicular bronchiolitis: Histology.
Lymphoid hyperplasia with reactive germinal centers.
Follicular bronchiolitis: Associations.
Anything that causes lymphoid hyperplasia, e.g. chronic inflammation, infections.
Diffuse alveolar damage: Clinical equivalents (3).
Acute respiratory-distress syndrome.
Acute interstitial pneumonia.
Acute lung injury.
Diffuse alveolar damage: Relevance to autoimmune disease (2).
Various collagen-vascular diseases cause DAD-type inflammation.
Various vasculitides can resemble AIP clinically.
Diffuse alveolar damage: Distribution of lesions (2).
Patchy involvement of the lung, but concentrated in the lower lobes.
Diffuse involvement of the alveolus.
Diffuse alveolar damage: Radiography.
Ground-glass opacities that spare the lobules.
Diffuse alveolar damage: Phases.
Exudative: First week.
Proliferative: Second week.
Fibrotic: Late.
Diffuse alveolar damage, exudative phase: Histology.
Hyaline membranes and interstitial edema.
Diffuse alveolar damage, proliferative phase: Histology.
Interstitium and airspaces: Florid proliferation of fibroblasts, myofibroblasts, type 2 pneumocytes.
Arteries: Intimal proliferation, medial hypertrophy.
Diffuse alveolar damage, fibrotic phase: Histology.
Dense interstitial fibrosis with microcysts.
Diffuse alveolar damage vs. usual interstitial pneumonia (3).
UIP:
− No hyaline membranes.
− Temporal heterogeneity of fibrosis.
− Fibrosis has more collagen and fewer cells.
Acute respiratory-distress syndrome: Prognosis.
Most patients regain near-normal lung function.
Acute interstitial pneumonia:
A. Clinical presentation.
B. Prognosis.
A. Resembles severe community-acquired pneumonia but does not respond to antibiotics.
B. Death in 6 months in 78% of cases.
Cryptogenic organizing pneumonia:
A. Clinical presentation.
B. Duration.
A. Cough, dyspnea, and flulike symptoms.
B. Subacute.
Cryptogenic organizing pneumonia: Prognosis.
Usually responds to steroids.
Cryptogenic organizing pneumonia: Distribution of lesions.
Subpleural.
Cryptogenic organizing pneumonia: Radiography.
Peribronchial consolidation and nodularity.
Cryptogenic organizing pneumonia: Histology (2).
Masson bodies: Intraluminal plugs consisting of young fibrous tissue.
Interstitial mild chronic inflammation with foci of foamy macrophages.
Cryptogenic organizing pneumonia: Special stain.
Movat’s stain: Masson bodies appear green; dense fibrosis would appear yellow.
Cryptogenic organizing pneumonia vs. usual interstitial pneumonia.
UIP:
− Dense fibrosis (not seen in COP).
− Fibroblastic foci are interstitial, not intraluminal.
− Temporal heterogeneity of fibrosis.
Cryptogenic organizing pneumonia vs. nonspecific interstitial pneumonia.
NSIP: Interstitial chronic inflammation without Masson bodies.
Usual interstitial pneumonia:
A. Clinical presentation.
B. Duration.
A. Progressive dyspnea and cough.
B. Chronic.
Usual interstitial pneumonia:
A. Associated environmental agents (3).
B. Associated inherited diseases (2).
A. Cigarettes, asbestos, drugs.
B. Familial idiopathic pulmonary fibrosis, Hermansky-Pudlak syndrome.
Usual interstitial pneumonia: Association that imparts a better prognosis.
Collagen-vascular disease.
Usual interstitial pneumonia: Prognosis.
Median survival is 3 years.
Usual interstitial pneumonia: Distribution of lesions (2).
Subpleural.
Lower lobes.
Usual interstitial pneumonia: Radiography (3).
Honeycombing.
Ground-glass opacities.
Traction bronchiectasis.
Usual interstitial pneumonia: Histology.
Temporal heterogeneity: The same area may contain both mature fibrosis and subepithelial young fibrosis (fibroblastic foci).
Spatial heterogeneity: Some areas are affected, some not.
Usual interstitial pneumonia: Histologic findings associated with poor prognosis (4).
Diffuse alveolar damage.
Infection.
Capillaritis.
Organizing pneumonia.
Usual interstitial pneumonia vs. hypersensitivity pneumonitis with fibrosis.
Hypersensitivity pneumonitis:
− Mainly upper lobes.
− Centered on bronchioles.
− More cellular inflammation, including giant cells or poorly formed granulomas.
Usual interstitial pneumonia vs. Langerhans’ cell histiocytosis.
Langerhans’ cell histiocytosis:
− Centered on bronchioles.
− Few or no fibroblastic foci.
Usual interstitial pneumonia: How to diagnose cases that contain findings of other interstitial lung diseases.
As usual interstitial pneumonia.
Nonspecific interstitial pneumonia:
A. Clinical presentation.
B. Duration.
A. Dyspnea, cough, fever.
B. Subacute.
Nonspecific interstitial pneumonia: Associations (5).
Cigarettes.
Drugs.
Immunodeficiency.
Collagen-vascular diseases.
Hypersensitivity pneumonitis.
Nonspecific interstitial pneumonia: Distribution of lesions.
Subpleural.
Lower lobes.
Nonspecific interstitial pneumonia: Radiography.
Peribronchial ground-glass opacities.
Reticular opacities.
Nonspecific interstitial pneumonia: Long-term prognosis.
Cellular type: Excellent.
Fibrotic type: Poor.
Nonspecific interstitial pneumonia, cellular type: Histology (3).
Diffuse interstitial infiltrate of lymphocytes and plasma cells.
Preservation of the pulmonary architecture.
Hyperplasia of type 2 pneumocytes.
Nonspecific interstitial pneumonia, fibrotic type: Histology (4).
Loose to dense interstitial fibrosis that thickens the alveolar walls.
Fibrosis shows temporal homogeneity.
Preservation of the pulmonary architecture.
Mild or moderate chronic inflammation.
Nonspecific interstitial pneumonia: Histological clue to an association.
Abundance of lymphoid aggregates suggests collagen-vascular disease.
Nonspecific interstitial pneumonia: What should not be seen histologically (3).
Significant honeycombing.
Many fibroblastic foci.
Granulomas.
Nonspecific interstitial pneumonia vs. lymphoid interstitial pneumonia.
LIP:
− Denser inflammatory infiltrate.
− Architectural distortion.
Desquamative interstitial pneumonia: Clinical presentation.
Dyspnea, cough, chest pain.
Desquamative interstitial pneumonia: Duration.
Subacute.
Desquamative interstitial pneumonia: Distribution of lesions.
Subpleural.
Desquamative interstitial pneumonia:
A. Frequent association.
B. Infrequent associations (2).
A. Cigarette smoking, even years after cessation.
B. Sirolimus; mutations in SP-C, the gene for surfactant protein C.
Desquamative interstitial pneumonia: Radiography.
Ground-glass opacities.
Thin-walled cysts.
Reticular opacities.
Desquamative interstitial pneumonia: Histology (3).
Pigmented macrophages (originally thought to be “desquamated” pneumocytes) fill alveoli.
Intraalveolar laminated basophilic concretions (“blue bodies”) sometimes present.
No significant fibrosis.
Desquamative interstitial pneumonia: Special stain.
Prussian blue highlights the finely granular pigment within the macrophages.
Desquamative interstitial pneumonia vs. respiratory bronchiolitis-interstitial lung disease.
RB-ILD: Macrophages fill the bronchioles but not the distal airspaces.
Lymphoid interstitial pneumonia: Associations.
Children: AIDS.
Adults: Immunocompromise, including AIDS.
Lymphoid interstitial pneumonia: Clinical presentation in children.
Manifestations of AIDS: Recurrent infections, parotiditis, failure to thrive.
Respiratory failure occasionally.
Lymphoid interstitial pneumonia: Radiography (2).
Children: Miliary reticulonodular infiltrates.
Adults: The same plus alveolar consolidation.
Lymphoid interstitial pneumonia: Histology (2).
Dense mononuclear inflammation of the interstitium, sometimes with germinal centers.
Partial obliteration of architecture.
Lymphoid interstitial pneumonia: Microbiological association.
ISH detects EBV in most cases.
Lymphoid interstitial pneumonia: Clinical course.
No progression to fibrosis.
Hypersensitivity pneumonitis:
A. Associations.
B. Distribution of lesions.
A. Various organic antigens, esp. those of thermophilic actinomycetes and birds.
B. Upper lobes, peribronchiolar.
Hypersensitivity pneumonitis: Phases (3).
Acute: Exposure to high concentrations of antigen; onset in 4-8 hours; resolution in 24-48 hours.
Subacute: Continuous or intermittent exposure to low concentrations of antigen; responds to steroids or to withdrawal of antigen.
Chronic: Subacute plus fibrosis; worse prognosis.
Hypersensitivity pneumonitis, subacute phase: Histology (2).
Small, poorly formed granulomas and mononuclear inflammation next to bronchioles.
Foamy histiocytes in alveoli and interstitium.
Hypersensitivity pneumonitis, chronic phase: Histologic patterns (3).
NSIP-like pattern: Homogeneous fibrosis with architectural preservation.
UIP-like: Patchy subpleural fibrosis with architectural distortion.
Irregular peribronchiolar pattern: UIP-like plus peribronchiolar fibrosis.
Hypersensitivity pneumonitis vs. usual interstitial pneumonia.
UIP:
− No giant cells, no granulomas.
− Mainly subpleural and in lower lobes.
Hypersensitivity pneumonitis vs. nonspecific interstitial pneumonia.
NSIP: No giant cells, no granulomas.
Clinical history may be required to make the distinction.
Hypersensitivity pneumonitis vs. sarcoidosis.
Sarcoidosis:
− Well-formed granulomas with hyalinized rim and location along bronchovascular bundles.
− No UIP- or NSIP-like changes.
Eosinophilic lung diseases: Unknown etiology (3)
Simple eosinophilic pneumonia.
Acute eosinophilic pneumonia.
Chronic eosinophilic pneumonia.
Eosinophilic lung diseases: Known etiology (4).
Allergic bronchopulmonary aspergillosis.
Bronchocentric granulomatosis.
Parasitic infections.
Drugs.
Eosinophilic lung diseases: Vasculitic causes (2).
Allergic angiitis.
Churg-Strauss syndrome.
Eosinophilic lung disease: How to diagnose without tissue or cytology.
Demonstrate pulmonary opacities and peripheral eosinophilia.
Acute eosinophilic pneumonia:
A. Clinical presentation.
B. Associations (2).
A. Acute respiratory distress that mimics infectious pneumonia.
B. Cigarettes, dust.
Acute eosinophilic pneumonia: Histology (3).
Resembles acute phase of DAD but with alveolar and interstitial eosinophils.
Hypertrophied and detached type 2 pneumocytes.
Intact basal lamina.
Acute eosinophilic pneumonia: Prognosis.
Rapid and complete response to corticosteroids.
Acute eosinophilic pneumonia: Degree of eosinophilia.
BAL: More than 25%.
Peripheral blood: Often no eosinophilia at first.
Chronic eosinophilic pneumonia: Radiography.
Peripheral consolidation mainly involving middle and lower zones.
Chronic eosinophilic pneumonia: Laboratory abnormalities (2).
Peripheral eosinophilia.
Elevated IgE in 7% of patients.
Chronic eosinophilic pneumonia: Histology.
Intraalveolar and interstitial eosinophils (single or in aggregates) and eosinophilic giant cells.
Damage to basal lamina, leading to fibrosis.
Parasites that can cause eosinophilic lung disease: Allergic reaction (3).
Entamoeba.
Toxocara.
Clonorchis sinensis.
Parasites that can cause eosinophilic lung disease: Direct invasion (4).
Ascaris lumbricoides.
Ankylostoma duodenale.
Paragonimus westermani.
Schistosomes.
Parasites that can cause eosinophilic lung disease: Others (3).
Strongyloides stercoralis.
Microfilariae.
Dirofilaria immitis.
Sarcoidosis: Frequency of pulmonary disease.
90-95%.
Pulmonary sarcoidosis: Clinical course (2).
Abrupt, acute illness with a better prognosis.
Chronic, insidious illness with persistent, progressive course.
Pulmonary sarcoidosis: Distribution of lesions (3).
Around the lymphatic vessels in the pleura, the interlobular septa, and the bronchovascular bundles.
Histology of pulmonary sarcoidosis:
A. Periphery of granulomas.
B. Tissues involved by granulomas.
A. Concentric fibrosis often; usually no cuff of lymphocytes.
B. Vessels, pleura.
Histology of pulmonary sarcoidosis: Inclusions that can be confused for microorganisms (2).
Hamazaki-Wesenberg bodies: GMS (+), AFB (+); mimic fungi.
Microcalcifications: Mimic fungi or P. jiroveci.
Sarcoidosis vs. hypersensitivity pneumonitis.
Hypersensitivity pneumonitis:
− Granulomas are less well formed.
− More inflammation in the interstitium.
Types of disease associated with a sarcoidosis-like disorder (2).
Malignancies.
Collagen-vascular disorders.
Idiopathic pulmonary hemosiderosis: Age group.
Children and adolescents.
Idiopathic pulmonary hemosiderosis:
A. Clinical manifestations (4).
B. Clinical course.
A. Cough, hemoptysis, iron-deficiency anemia, weight loss.
B. Subject to spontaneous remission or exacerbation.
Idiopathic pulmonary hemosiderosis: Associations (3).
IgA nephropathy.
Dermatitis herpetiformis.
Celiac disease.
Idiopathic pulmonary hemosiderosis: Gross pathology.
Heavy, red-brown lung tissue.
Idiopathic pulmonary hemosiderosis: Histology (2).
Intraalveolar dense groups of hemosiderin-laden macrophages, or frank hemorrhage.
Loss or hyperplasia of alveolar epithelium.
Idiopathic pulmonary hemosiderosis: Pertinent negative findings (5).
Granulomas.
Vasculitis.
Infarction.
Infection.
Immune complexes or immunoglobulins.
Idiopathic pulmonary hemosiderosis: Treatment.
Immunosuppression.
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.
DR2.
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).
Pulmonary edema.
Interstitial inflammation.
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.
Center: Amorphous.
Middle zone: Layers of dense collagen with focal calcification and necrosis.
Periphery: Particle-laden macrophages, lymphocytes, fibroblasts.
Microbiological association of pulmonary silicosis:
A. Organism.
B. Histology.
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).
Inorganic dust.
Hematological malignancy.
Immunodeficiency.
Pulmonary alveolar proteinosis: Complication.
Secondary infection by
− Fungi. − Viruses. − Pneumocystis jiroveci. − Nocardia. − Mycobacteria.
Pneumoconiosis: Particles that induce fibrosis (5).
Silica.
Coal dust.
Asbestos.
Beryllium.
Talc.
Pneumoconiosis: Particles that induce little or no fibrosis (3).
Iron oxide.
Tin.
Barium.
Asbestosis:
A. Timing.
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.
Bronchioloalveolar lavage.
Asbestosis: Related cancers.
Mesothelioma.
Lung cancer.
Radiation pneumonitis, acute:
A. Timing.
B. Clinical presentation.
A. Symptoms begin between 6 weeks and 6 months after exposure.
B. Cough, dyspnea on exertion.
Radiation pneumonitis: Exacerbating factors (3).
Chemotherapy.
Prior irradiation.
Infection.
Radiation pneumonitis, acute: Histology.
Hyaline membranes as in diffuse alveolar damage.
Interstitial proliferation of atypical fibroblasts within young fibrosis.
Radiation pneumonitis, fibrotic stage: Histology.
Resembles NSIP but with hyperplasia and cytologic atypia of type 2 pneumocytes.