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Diseases of the Lung and Respiratory Tract, Part I
William Bligh-Glover M.D.Department of Anatomy, CWRU
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Educational objectives:
• Distinguish the types of atelectasis and their etiologies
• Distinguish the types of obstructive lung disease,– Etiology, epidemiology, pathogenesis,
pathophysiology, and consequences • Distinguish the types of restrictive pulmonary
disease – Etiology, epidemiology, pathogenesis,
pathophysiology, and consequences
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Normal Lung
• Function– Exchange gases between inspired air and
blood– O2 in CO2 out.
• Progressively smaller air passages– Lining pseudostratified, tall columnar ciliated
epithelial cells– Alveoli type I, type II pneumocytes and
capillaries
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Normal Lung Gross
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Normal Lung Micro
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Atelectasis
• “Collapsed lung”– Collapse of previously inflated lung
• Anectasis never inflated lung.
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Atelectasis Gross
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Types of Atelectasis
• Obstruction (resorption)• Compression• Contraction
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Resorption Atelectasis
• Complete obstruction of an airway– Resorption of trapped oxygen– Unimpaired blood flow
• Excessive secretions – Mucous plugging
• Asthma, bronchitis, bronchiectasis, aspiration
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Atelectasis
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Compression Atelectasis
• Pleural cavity filled with fluid– Hemothorax (blood)– Pneumothorax (air)– Pleural effusion– Tumor
• Most often occurs in the setting of heart failure with pleural effusions or malignant pleural effusions
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Compression Atelectasis
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Contraction Atelectasis
• Fibrosis of pulmonary parenchyma prevents full expansion
• Pneumoconioses
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Contraction AtelectasisHoneycomb lung
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Mediastinal Shifts
• Resorption Atelectasis– Towards Affected Side
• Compression Atelectasis– Away from Affected Side
• Contraction Atelectasis– No Shift
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Mediastinal shift
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Obstructive vs. Restrictive
• Airway diseases• Increased resistance
to airflow• Decreased FEV1
forced expiratory volume 1 sec
• Parenchymal diseases
• Reduced expansion, decreased total lung capacity
• Normal airflow
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Obstructive vs. Restrictive
• Obstructive Lung Diseases– Asthma– Bronchiectasis– Chronic Bronchitis– Emphysema– Tumor
• Restrictive Lung Disease– Chest wall
abnormalities– ARDS– Pneumoconioses
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Asthma
• Reactive airways• Production of excessive mucus• Allergies• Eosinophils
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Asthma Inflamed mucosa with mucus
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AsthmaMucus plug with eosinophils
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Asthma Mucus
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Bronchiectasis
• Sequelae of chronic infections• Lung tissue destroyed by necrotizing
infections• Compounded by stasis of secretions
– CF
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Bronchiectasis Gross
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BronchiectasisLarge bronchi close to pleura
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Bronchiectasis Micro
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Bronchiectasis
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Chronic Bronchitis
• Productive cough• Lasting for three months• Two or more years running• Associated with smoking
– Impairment of muco-cilliary elevator
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Chronic Bronchitis Micro
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Emphysema
• Destruction of pulmonary parenchyma• Dilated air spaces• “Septae in space”• Destruction of lung by neutrophil enzymes
– Alpha-1-antitrypsinase deficiency– Smoking
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Emphysema-Physical
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Emphysema Gross
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Emphysema Micro
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Tumors
• Squamous cell carcinomas– Most common – Hilar origin– Associated with
smoking
• Adenocarcinomas– Less common– Not associated with
smoking– Peripheral location
• Neuroendocrine– Treatment amenable
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Tumors
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ARDS
• Initial damage to pulmonary capillaries• Leakage of fluid, production of hyaline
membranes• Tremendous disruption of gas exchange
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ARDS
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Occupational Lung Disease
• Coal Worker’s Pneumoconiosis• Silicosis• Farmer’s Lung• Silo Filler’s Lung
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Coal Worker’s Pneumoconiosis
• Shaft miners > pit miners• Reaction to silica in coal matrix• Gradually worsening lung disease
– Coal macules– Black lung– Progressive Massive Fibrosis
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Coal Macule
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Coal Macule
• Anthracotic pigment in interstitial macrophages
• Prominent nodules of black in grey background
• Deeply pigmented, irregular nodules. – micronodular (< 7 mm in diameter) – macronodular (> 7 mm) forms
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Progressive Massive Fibrosis
• Multiple, retracted scars of lung
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PMF