the pathology of lung diseases
DESCRIPTION
The Pathology of Lung Diseases. I. RESTRICTIVE LUNG DISEAS ES II. OBSTRUCTIVE LUNG DISEASES. I. RESTRICTIVE LUNG DISEAS ES - Diffuse Interstitial Lung Disease - Infiltrative Lung Disease - F ibrosing alveolitis -H oneycomb lung. - PowerPoint PPT PresentationTRANSCRIPT
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The Pathology of Lung Diseases
I. RESTRICTIVE I. RESTRICTIVE LUNG DISEASLUNG DISEASESES
II. OBSTRUCTIVE LUNG DISEASES
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I.RESTRICTIVE LUNG DISEASES
-Diffuse Interstitial Lung Disease-Infiltrative Lung Disease-Fibrosing alveolitis-Honeycomb lung
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Restrictive lung diseases are characterized by reduced lung volume, an alteration in lung parenchyma a disease of the pleura or chest wall a disease of neuromuscular apparatus
In physiological terms, restrictive lung diseases are characterized by reduced lung capacity;
reduced total lung capacity (TLC) reduced vital capacity reduced resting lung volume
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The many disorders that cause reduction or restriction of lung volumes may be divided into 2 groups based on anatomical structures: 1. 1. Intrinsic lung diseasesIntrinsic lung diseases (or
diseases of the lung parenchyma), 2.2. Extrinsic disordersExtrinsic disorders (or
extraparenchymal diseases).
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1.
Intrinsic lung diseases or diseases of the lung parenchyma:
The diseases cause inflammation or scarring of the lung tissue (interstitial lung disease) or result in filling of the air spaces with exudate and debris (pneumonitis).
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2.
Extrinsic disorders or extraparenchymal diseases:
Nonmuscular diseases of the chest wall, and neuromuscular disorders
The chest wall, pleura, and respiratory muscles are the components of the respiratory pump, and they need to function normally for effective ventilation.
If not; impaired ventilatory function, respiratory failure.
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Intrinsic lung diseases or Diseases of the lung parenchyma
RESTRICTIVE LUNG DISEASES
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These diseases can be characterized according to etiological factors:
Acute restrictive pulmonary diseases (acute lung injury)
Acute Respiratory Distress Syndrome (ARDS) Acute Hypersensitivity Pneumonitis
Chronic restrictive pulmonary diseases Idiopathic fibrotic diseases Connective tissue diseases Drug-induced lung disease Primary diseases of the lungs (including sarcoidosis)
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Acute restrictive pulmonary diseases
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Acute Lung Injury
1. Diffuse Alveolar Damage (Acute Respiratory Distress Syndrome - ARDS)
2. Acute Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)
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1. Diffuse Alveolar Damage (Acute Respiratory Distress Syndrome - ARDS)
Diffuse alveolar damage (DAD) refers to a pattern of reaction to injury of alveolar epithelial and endothelial cells from a variety of acute insults.
The clinical counterpart of severe DAD is the acute respiratory distress syndrome (ARDS).
In this disorder, a patient with apparently normal lungs sustains pulmonary damage and then develops rapidly progressive respiratory failure.
The condition reflects decreased lung compliance (usually requiring mechanical ventilation) and hypoxemia and features extensive radiologic opacities in both lungs (white-out).
The overall mortality of ARDS is more than 50%, and in patients older than 60 years, it is as high as 90%.
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ETIOLOGY: Important Causes of the Acute Respiratory Distress Syndrome
Nonthoracic Trauma
Shock due to any cause
Fat embolism
Infection
Gram-negative septicemia
Other bacterial infections
Viral infections
Aspiration
Near-drowning
Aspiration of gastric contents
Drugs and Therapeutic Agents
Heroin
Oxygen
Radiation
Paraquat
Cytotoxic drugs
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Acute Respiratory Distress Syndrome: Pathogenesis
Endothelial/capillary injury alveolar capillary membrane damage
increased vascular permeability edema (interstitial/alveolar) increased synthesis of neutrophil
chemotacatic & activating agents (IL) activated neutrophils oxidants, proteases, PAF, leukotriens tissue damage other mediators stimulating collagen
production Fibrosis
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Pathology
Exudative phase (0-7 days): congestion, necrosis of alveolar epithelial cells, edema, hemorrhage, neutrophils in capillaries, Destruction of type I pneumocytes
permits exudation of fluid into alveolar spaces, where deposition of plasma proteins results in formation of fibrin-containing precipitates (hyaline membranes) on the injured alveolar walls
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congestion
necrosis of alveolar epithelial cells
edema
hemorrhage
neutrophils in capillaries
hyaline membranes
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If the patient survives the acute phase of ARDS
Proliferative phase (1-3 weeks): Proliferation of type II pneumocytes Cleaning of remnant hyaline membranes
by pulmonary macrophages Expansion of alveolar septa Proliferation of fibroblasts Collagen tissue production Healing or Fibrosing
Fibrosing phase: Diffuse interstitial fibrosis Honeycomb lung
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Proliferation of type II pneumocytes
Cleaning of remnant hyaline membranes by pulmonary macrophages
Expansion of alveolar septa
Proliferation of fibroblasts
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Diffuse interstitial fibrosis
Honeycomb lung.
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2. Acute Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)
A response to inhaled antigens Farmer's lung occurs in farmers exposed to Micropolyspora
faeni from moldy hay Bagassosis results from exposure to Thermoactinomyces
sacchari in moldy sugar cane Maple bark-stripper's disease is seen in persons exposed to
the fungus Cryptostroma corticale from moldy maple bark Bird fancier's lung affects bird keepers with long-term
exposure to proteins from bird feathers, blood and excrement
Hypersensitivity pneumonitis may also be caused by fungi growing in stagnant water in air conditioners, swimming pools, hot tubs, and central heating units.
Skin tests and serum precipitating antibodies are often used to confirm the diagnosis.
In many cases, especially in the chronic form of hypersensitivity pneumonitis, the inciting antigen is never identified.
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Chronic restrictive Chronic restrictive pulmonary diseasespulmonary diseases
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CHRONIC INTERSTITIAL LUNG DISEASES
Characterized by - decreased lung volume - decreased oxygen-diffusing capacity on pulmonary function studies
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A large number of pulmonary disorders are grouped as interstitial, infiltrative, or restrictive diseases
They are characterized by inflammatory infiltrates in the interstitial space and have similar clinical and radiologic presentations
These diverse maladies (1) are of known or unknown etiology, and (2) vary from minimally symptomatic conditions to
severely incapacitating and lethal interstitial fibrosis
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Etiology
Occupational/environmental diseases (24%)
Sarcoidosis (20%) Idiopathic pulmonary fibrosis (15%) Collagen-vascular diseases (8%)
The remainder have more than 100 different causes and associations.
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The most striking findings are; Longstanding inflammatory damage Fibrosis of the alveolar walls Fibrosis finally wipes out groups of alveoli Scar contraction of respiratory bronchioles The radiographic and autopsy diagnosis of
"honeycomb lung"
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ORGANIC DUST EXPOSURE
Chronic Hypersensitivity Pneumonitis Chronic form of Acute Hypersensitivity
Pneumonitis The prototype of hypersensitivity pneumonitis
is farmer's lung Cause: Inhalation of thermophilic
actinomycetes that grow in moldy hay Patients with the chronic form of
hypersensitivity pneumonitis have a more nonspecific presentation, with indolent onset of dyspnea and cor pulmonale.
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Pathology: The main microscopic features of chronic
hypersensitivity pneumonitis include bronchiolocentric cellular interstitial pneumonia noncaseating granulomas (in two thirds of cases) organizing pneumonia
The bronchiolocentric cellular interstitial infiltrate
lymphocytes plasma cells macrophages
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Patchy mononuclear cell infiltrates,
Lymphocytes
Plasma cells
Epitheloid histiocytes
Interstitial noncaseating granulomas,
Interstitial fibrosis.
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INORGANIC DUST EXPOSURE
Pneumoconioses Dust inhalation
Silicosis Asbestosis Talcosis
Historically, knife grinder's lung (silicosis).
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Mineral dust-induced lung diseases Coal dust (upper
lobe) Silica (upper lobe)
Asbestos (lower lobe)
Beryllium
: Coal workers: Stone, Ceramics,
Sandblasting: Mining, Milling,
Insulation: Nuclear energy,
Aircraft industry
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Particles over 10 µm in diameter deposit on bronchi and bronchioles and are removed by the mucociliary escalator.
Smaller particles reach the acinus, and the smallest ones behave as a gas and are exhaled.
Alveolar macrophages ingest the inhaled particles and are the primary defenders of the alveolar space.
Most phagocytosed particles ascend to the mucociliary carpet and are expectorated or swallowed.
Others migrate into the interstitium of the lung, then into the lymphatics.
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Air particulate exposure Pneumoconioses Pulmonary fibrosis Asthma Chronic bronchitis Lung cancer
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INORGANIC DUST EXPOSURE: Silicosis Inhalation of silicon dioxide (silica) History: Dyspnea in metal diggers was
reported by Hippocrates Early Dutch pathologists wrote that the lungs
of stone cutters sectioned like a mass of sand. The major cause of death in workers exposed
to silica dust for the first half of the 20th century
Sandblasters Stone cutting Polishing and sharpening of metals Ceramic manufacturing Foundry work
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After their inhalation, silica particles are ingested by alveolar macrophages
Silicon hydroxide groups on the surface of the particles form hydrogen bonds with phospholipids and proteins, an interaction that is presumed to damage cellular membranes and thereby kill the macrophages
The dead cells release free silica particles and fibrogenic factors progressive massive fibrosis
The released silica is then reingested by macrophages and the process is amplified
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The nodular lesions consist of concentric layers of hyalinized collagen
Surrounded by a dense capsule of more condensed collagen
Examination of the nodules by polarized microscopy reveals the birefringent silica particles.
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INORGANIC DUST EXPOSURE: Coal Workers' Pneumoconiosis (CWP)
Coal dust is composed of amorphous carbon and other constituents of the earth's surface, including variable amounts of silica.
Anthracite (hard) coal contains significantly more quartz
Amorphous carbon by itself is not fibrogenic Silica is highly fibrogenic, and inhaled
anthracotic particles may thus lead to anthracosilicosis.
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Asymptomatic anthracosis Simple CWP:
Coal macules Coal nodules
Complicated CWP Caplan syndrome
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Asymptomatic anthracosis
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CWP Simple CWP Complicated CWP (progressive massive fibrosis)
Coal-dust macules and coal-dust nodules: Both are typically multiple and scattered throughout
the lung as 1- to 4-mm black foci Microscopy
Coal-dust macule: numerous carbon-laden macrophages
Coal-dust nodule: round or irregular; dust-laden macrophages associated + fibrotic stroma
Focal dust emphysema
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Coal workers’ pneumoconiosis (CWP)
Coal-dust nodule +Focal dust emphysema
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Caplan syndrome Rheumatoid nodules (Caplan nodules) in
the lungs of coal miners with rheumatoid arthritis.
Nodular lesions (1-10 cm in diameter) Multiple, bilateral, and usually peripheral
Microscopy Rheumatoid nodule + dust deposits
Rheumatoid nodules consist of large, central, necrotic areas surrounded by a border of chronic inflammation and palisading macrophages.
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INORGANIC DUST EXPOSURE: Asbestosis Asbestos - a group of fibrous silicate
minerals Insulation Construction materials Automative brake linings
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Asbestos is a naturally occurring fibrous silicate that was widely used in the past for commercial applications because of its heat-resistance properties.
Geometric forms of asbestos: 1. Amphibole (straight, stiff, and brittle
fibers). 2. Serpentine (curly and flexible fibers;
90% used in wide-world).
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Asbestos exposure has been industrial or occupational and primarily affects workers involved in: mining or processing asbestos shipbuilding construction textile insulation-manufacturing industries
However, because the latency period between an initial exposure and the development of most asbestos-related disease is 20 years or longer,
Asbestos-related disease remains an important public health issue.
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Exposure to asbestos can cause a number of thoracic complications Asbestosis Benign pleural effusion Pleural plaques Diffuse pleural fibrosis Rounded atelectasis Mesothelioma Lung carcinoma
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Asbestos-Related Lung Disease
Pleural lesions Benign pleural effusion Parietal pleural plaques Diffuse pleural fibrosis Rounded atelectasisInterstitial lung disease AsbestosisMalignant mesothelioma*Carcinoma of the lung (in smokers)
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ASBESTOSIS Asbestosis is diffuse interstitial fibrosis resulting
from inhalation of asbestos fibers The development of asbestosis requires heavy
exposure to asbestos Asbestos may produce obstructive as well as
restrictive defects As the disease progresses, fibrosis spreads beyond
the peribronchiolar location and eventually results in an end-stage or (honeycomb) lung
Asbestosis is usually more severe in the lower zones of the lung
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Pathology Lower lobes and subpleural Diffuse pulmonary interstitial fibrosis Asbestos bodies (golden brown, fusiform or beaded
rods with a translucent center and knobbod ends) Asbestos fibers coated with an iron-containing
proteinaceous material (ferruginous body)
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Lower lobes and subpleural
Diffuse pulmonary interstitial fibrosis
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Asbestos fibers coated with an iron-containing proteinaceous material (ferruginous body)
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Asbestos-Related Lung Disease & Complications
Pleural lesions Benign pleural effusion Parietal pleural plaques Diffuse pleural fibrosis Rounded atelectasis
Interstitial lung diseaseAsbestosis Progressive fibrosis Pulmonary hypertension and cor pulmonale
Malignant mesothelioma (80% pleural; 20% peritoneal in origin)
Bronchogenic carcinoma (20-25% of heavily exposed asbestos worker)
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Berryliosis
Aerospace industry Dusts/fumes of berrylium Acute pneumonitis (high doses) Pulmonary/systemic
granulomatous lesions Progressively fibrotic lung
pathology
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Primary or Unclassified diseases
SARCOIDOSIS A granulomatous disease of unknown etiology Sarcoidosis can involve many systems and organs
bilateral hilar lymphadenopathy (75-90 %) lung involvement (90%) eye and skin lesions
Most sarcoid patients are young adults Exact pathogenesis of sarcoidosis remains obscure
T lymphocyte response to exogenous or autologous antigens These cells accumulate in the affected organs, where they
secrete lymphokines and recruit macrophages, which participate in the formation of noncaseating granulomas.
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Pathology Multiple sarcoid granulomas are scattered in
the interstitium of the lung. Frequent bronchial or bronchiolar submucosal
infiltration by sarcoid granulomas accounts for the high diagnostic yield (<90%) on bronchoscopic biopsy.
The cellular granulomatous phase of sarcoidosis can progress to a fibrotic phase.
Significant necrosis is usually absent, small foci of necrosis are seen in one third of open lung biopsies.
Asteroid bodies (star-shaped crystals) Schaumann bodies (small calcifications with
a lamellar structure)
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Kveim test
Kveim test, which involves taking ground-up spleen from someone with sarcoidosis and injecting it into the dermis,
If a granuloma forms, the living patient supposedly has sarcoidosis,
80% sensitive, 95% specific.
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noncaseating granulomas
Schaumann’s bodies
asteroid bodies
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IDIOPATHIC PULMONARY FIBROSIS
Usual Interstitial Pneumonia (UIP) Syn: Chronic interstitial pneumonitis, Interstitial
pneumonitis, Idiopathic pulmonary fibrosis, Cryptogenic fibrosing alveolitis
One of the most common types of interstitial pneumonia Middle-aged men Unknown etiology (?)
Viral (flu-like illness) Genetic (familial UIP; UIP-like diseases in neurofibromatosis and
Hermansky-Pudlak syndrome) Immunologic factors (collagen vascular diseases; autoimmune
disorders)
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Circulating autoantibodies (e.g., antinuclear antibodies and rheumatoid factor).
Immune complexes (antigen?) circulation, inflamed alveolar walls, bronchoalveolar-lavage specimens.
Immune complexes activated alveolar macrophages phagocytosis of immune complexes release of cytokines neutrophil migratrion damage of alveolar walls progression interstitial fibrosis
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Pathology
The histologic hallmark: patchy chronic inflammation and interstitial fibrosis with areas of dense scarring and honeycomb cystic change
The lungs are small Fibrosis tends to be worse in the
lower lobes, subpleural regions, and along interlobular septa
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The honeycomb cystic spaces lined by bronchiolar or cuboidal
epithelium contain mucus, macrophages, or
neutrophils interstitial chronic inflammation lymphoid aggregates, sometimes
containing germinal centers, in UIP associated with rheumatoid arthritis
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Vascular changes intimal fibrosis thickening of the media
Progressive fibrosis of lungs respiratory insufficiency pulmonary hypertension cor pulmonale cardiac failure
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Desquamative Interstitial Pneumonia (DIP) Pathologically described entity A diffuse lung disease characterized by marked
accumulation of intraalveolar macrophages intra-alveolar cells were desquamated epithelial cells,
whereas they are now recognized as macrophages The macrophages contain a fine golden-brown
pigment. Alveolar walls show mild thickening by chronic
inflammation and interstitial fibrosis. Scattered lymphoid aggregates also may be
present. Hyperplasia of type II pneumocytes is often
prominent.
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In cigarette smokers The radiographic picture of DIP is not
specific but is most frequently described as bilateral ground glass infiltrates with a lower lobe predominance
DIP has a much better prognosis than UIP Most patients respond well to steroid
therapy and smoking cessation
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Collagen-Vascular Diseases & Drugs and other Treatments
Nonspecific Interstitial Pneumonia (NSIP) Etiology
infection collagen vascular disease hypersensitivity pneumonitis drug reaction, and others) or it may be idiopathic.
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Pathology
Diffuse uniform changes in the lung NSIP
Cellular type: alveolar septa are diffusely involved by a mild to moderate lymphcytic infiltrate.
Fibrosing type: septa are diffusely involved by fibrosis, with or without significant associated inflammation.