Session 24 Lung Pathology

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Lecture Notes

Session 24: Lung Pathology

Alex Simon (MD)

Learning tasks

At the end of this session, students are expected to be able to:

Describe pulmonary infections.

Explain industrial lung diseases.

Explain atelectasis.

Explain diseases of pleura.

Pulmonary (Lung) infections

Common at all ages and are a frequent cause of death.

Caused by a wide variety of microorganisms.

Examples

Acute pulmonary infections

Pneumonia.

Lung abscess.

Chronic lung infections

Pulmonary tuberculosis.

Pulmonary (Lung) infections cont…

Pulmonary infections in the form of pneumonia are common because of

The epithelial surfaces of the lung are constantly exposed to many liters of air containing various levels of microbial contaminants.

Nasopharyngeal flora are regularly aspirated during sleep, even by healthy persons.

Other common lung diseases render the lung parenchyma vulnerable to virulent organisms.

Pneumonia

Pneumonia is defined as acute inflammation of the lung parenchyma distal to the terminal bronchioles.

The terms ‘pneumonia’ and ‘pneumonitis’ are often used synonymously for inflammation of the lungs.

The term ‘consolidation’ (meaning solidification) is the term used for gross and radiologic appearance of the lungs in pneumonia.

Pathogenesis of Pneumonia

Before a respiratory disease can be established, the following conditions need to be met

There must be a sufficient number or sufficient ‘dose’ of infectious agent inhaled.

The infectious particles must be airborne.

The infectious organism must remain alive and viable while in the air.

The organism must be deposited on susceptible tissue in the host.

Pathogenesis of Pneumonia cont…

The microorganisms gain entry into the lungs by one of the following four (4) routes:

Inhalation of the microbes present in the air.

Aspiration of organisms from the nasopharynx or oropharynx.

Haematogenous spread from a distant focus of infection.

Direct spread from an adjoining site of infection.

Pathogenesis of Pneumonia cont…

Once a pathogen is in the respiratory tract, it is essential that it colonizes these surfaces before it can cause obvious disease.

Most microorganisms cause disease by the following pathogenic mechanisms

Bacterial adherence factors.

Extracellular toxins.

Growth in host tissue.

Evasion of host defence mechanism by inhibiting phagocytosis.

Predisposing factors for Pneumonia

Broadly divided into factors which

Impair defense mechanisms.

Decrease host resistance to infections.

Failure of these result in pneumonias.

Refer to Handout 24.1 for additional information on predisposing factors for pneumonia.

Classification of Pneumonia

Duration

Acute.

Chronic.

Etiology

Bacterial.

Viral.

Other etiologies (fungal, parasitic, lipid)

Anatomic part of the lung parenchyma involved

Lobar pneumonia.

Bronchopneumonia (or Lobular pneumonia).

Interstitial pneumonia.

Clinical setting

Community acquired.

Hospital acquired.

Disease of immunosuppression.

Aspiration pneumonia.

Distinct clinical settings Pneumonias

Community-acquired acute pneumonia.

Community-acquired atypical pneumonia.

Nosocomial pneumonia.

Aspiration pneumonia.

Chronic pneumonia.

Necrotizing pneumonia and lung abscess.

Pneumonia in the immunocompromised host.

Refer to Handout 24.2 for additional information on pathogens implicated in above mentioned pneumonias.

Pneumonia cont…

Histologic spectrum of pneumonia

A fibrinopurulent alveolar exudate seen in acute bacterial pneumonias.

Mononuclear interstitial infiltrates in viral and other atypical pneumonias.

Granulomas and cavitation seen in many of the chronic pneumonias.

Acute bacterial pneumonias can manifest as one of two (2) anatomic and radiographic patterns:

Bronchopneumonia (Lobular pneumonia).

Lobar pneumonia.

Bronchopneumonia (Lobular pneumonia)

Patchy distribution of inflammation that involves more than one lobe.

Resulted from an initial infection of the bronchi and bronchioles with extension into the adjacent alveoli.

Thus infection of the terminal bronchioles that extends inflammatory exudate into the surrounding alveoli resulting in patchy consolidation of the lung(lobular distribution).

Lobar pneumonia

Homogenous consolidation of part of a lobe or of the whole lobe or even two lobes of one or both the lungs caused by acute bacterial infection.

Contiguous air spaces of part or all of a lobe are homogeneously filled with an exudate that can be visualized on radiographs as a lobar or segmental consolidation.

Streptococcus pneumoniae is responsible for more than 90% of lobar pneumonias.

Acute bacterial pneumonia: Anatomic and radiographic patterns

Lobar pneumonia

Bronchopneumonia

Morphology of Lobar pneumonia

In the era before antibiotics, pneumococcal pneumonia involved entire or almost entire lobes and evolved through four (4) stages described by Laennec:

Congestion.

Red hepatization.

Gray hepatization.

Resolution.

Early antibiotic therapy alters or halts this typical progression.

Congestion stage

The affected lobe(s) is (are) heavy, red, and boggy.

Histologically

Vascular congestion.

Proteinaceous fluid.

Scattered neutrophils.

Many bacteria in the alveoli.

Red hepatization stage

Lung lobe has a liver-like consistency.

The alveolar spaces are packed with

Neutrophils.

Red cells.

Fibrin.

Gray hepatization stage

The lung is dry, gray, and firm, because the red cells are lysed.

Fibrinosuppurative exudate persists within the alveoli.

Resolution stage

Resolution follows in uncomplicated cases.

Exudates within the alveoli are enzymatically digested to produce granular, semifluid debris that is:

Resorbed.

Ingested by macrophages.

Coughed up.

Organized by fibroblasts growing into it.

The pleural reaction (fibrinous or fibrinopurulent pleuritis) may similarly resolve or undergo organization, leaving fibrous thickening or permanent adhesions.

Morphology of Bronchopneumonia

Foci of inflammatory consolidation are distributed in patches throughout one or several lobes.

Most frequently bilateral and basal.

The lung substance immediately surrounding areas of consolidation is usually hyperemic and edematous, but the large intervening areas are generally normal.

Pleural involvement is less common than in lobar pneumonia.

Histologically, the reaction consists of focal suppurative exudate that fills the bronchi, bronchioles, and adjacent alveolar spaces.

Complications of Pneumococcal Pneumonia

Tissue destruction and necrosis may lead to lung abscess formation

Suppurative material may accumulate in the pleural cavity, producing an empyema thoracis.

Organization of the intraalveolar exudate may convert areas of the lung into solid fibrous tissue (Lung fibrosis).

Pleural effusion can occur.

Bacteremic dissemination may lead to meningitis, arthritis, or infective endocarditis (Bacteremia/Septicemia)

Lung abscess

Localized area of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities.

Refer to Handout 24.3 for additional information on Lung abscess morphology.

Complications of Lung abscess

Pneumothorax.

Empyema thoracis.

Meningitis.

Brain abscess.

Chronic Pneumonia:Pulmonary Tuberculosis

Communicable chronic granulomatous disease caused by Mycobacterium tuberculosis.

It usually involves the lungs but may affect any organ or tissue in the body.

Presence of granulomas with central caseous necrosis.

Initial exposure to Mycobacteria results in development of an immune response that confers resistance but also leads to hypersensitivity

Determined by a positive result on the tuberculin skin test.

Pathogenesis of Tuberculosis

Develops in a previously unexposed and therefore unsensitized patient.

Elderly persons and immunosuppressed patients may lose their sensitivity to the tubercle bacillus.

They may develop primary tuberculosis more than once.

About 5% of those newly infected acquire significant disease.

Refer to Handout 24.4 for additional information on pathogenesis of Pulmonary Tuberculosis and types of TB.

Histopathological features of Pulmonary Tuberculosis

Caseous necrosis

Formation of Granuloma

Industrial lung diseases(Pneumoconiosis)

Lung diseases caused by inhalation of dust.

Group of chronic fibrosing diseases of the lung.

Factors which determine extent of damage are

Size and shape of the particles.

Their solubility and physicochemical composition.

The amount of dust retained in the lungs.

Additional effect of other irritants e.g. tobacco smoke.

Host factors e.g. efficiency of clearance mechanism and immune status of the host.

Pathogenesis of Industrial lung diseases (Pneumoconiosis)

Pulmonary alveolar macrophages play key role in initiation and perpetuation of lung injury and fibrosis.

This triggers macrophages to release a number of products that mediate inflammatory response, initiate fibroblast proliferation and collagen deposition.

The tissue response to inhaled dust may be one of the following three (3) types:

Fibrous nodules e.g. in Coal-workers’ pneumoconiosis and Silicosis.

Interstitial fibrosis e.g. in Asbestosis.

Hypersensitivity reaction e.g. in Berylliosis.

Coal workers pneumoconiosis

Coal dust–induced disease varies from

Asymptomatic anthracosis.

Simple coal worker’s pneumoconiosis (coal macules or nodules, and centrilobular emphysema).

Progressive massive lung fibrosis.

Progressive massive lung fibrosis is manifested by increasing pulmonary dysfunction, pulmonary hypertension, and cor pulmonale.

Silicosis

Silicosis is the most common pneumoconiosis.

Crystalline silica (e.g., quartz) is the usual culprit.

Manifestations of silicosis can range from asymptomatic silicotic nodules to progressive massive lung fibrosis .

Persons with silicosis also have an increased susceptibility to tuberculosis.

The relationship between silica exposure and subsequent lung cancer is controversial.

Asbestosis

Asbestos fibers come in two forms

Stiff amphiboles (more fibrogenic and carcinogenic)

Serpentine chrysotiles.

Asbestos exposure is linked with six (6) disease processes

Parenchymal interstitial fibrosis (asbestosis).

Localized fibrous plaques or, rarely, diffuse pleural fibrosis.

Pleural effusions.

Lung cancer.

Malignant pleural and peritoneal mesotheliomas.

Laryngeal cancer.

Berylliosis

Berylliosis is caused by heavy exposure to dust or fumes of metallic beryllium or its salts.

Two (2) forms of pulmonary berylliosis are recognised

Acute berylliosis: Causes exudative chemical pneumonitis.

Chronic berylliosis: Development of non-caseating epithelioid granulomas.

Atelectasis (lung collapse)

Atelectasis (lung collapse) is loss of lung volume caused by inadequate expansion of air spaces.

It is classified into three (3) forms.

Resorption atelectasis.

Compression atelectasis.

Contraction atelectasis.

Refer to Handout 24.5 for additional information on types of Atelectasis.

Diseases of Pleura

Diseases affecting the pleura are nearly always secondary to some other underlying disease.

Broadly, they fall into

Inflammations.

Non-inflammatory pleural effusions.

Pneumothorax.

Tumours.

Inflammatory pleural effusions

Inflammatory involvement of the pleura is termed as pleuritis or pleurisy.

Depending the character of exudate, pleuritis can be

Serous.

Fibrinous.

Serofibrinous.

Suppurative (empyema thoracis).

Haemorrhagic.

Refer to Handout 24.6 for additional information on types of pleuritis.

Non-inflammatory pleural effusions

Hydrothorax.

Accumulation of serous fluid within the pleural cavities.

Haemothorax.

Accumulation of pure blood in the pleural cavity.

Chylothorax.

Accumulation of milky fluid of lymphatic origin into the pleural cavity.

Pneumothorax.

Accumulation of air in the pleural cavity.

Tumors of Pleura

Pleural tumours may be primary or secondary.

Secondary tumours in the pleura are more common.

The only important primary tumour of pleura is mesothelioma.

Malignant mesothelioma is recognised to be associated with occupational exposure to asbestos (particularly crocidolite) for a number of years, usually 20 to 40 years.

Key points

pneumoniae (Pneumococcus) is the most common cause of community-acquired acute pneumonia.

Morphologically, lobar pneumonias evolve through four stages: congestion, red hepatization, gray hepatization, and resolution.

Tuberculosis is associated with caseous necrosis and granuloma formation (tuberculoma)

Tobacco smoking worsens the effects of all inhaled mineral dusts.

Malignant mesothelioma is associated with occupational exposure to asbestos.

Review questions

How can pneumonia be classified?

Explain pathogenesis of lobar pneumonia.

List four (4) industrial lung diseases.

Explain pathogenesis of pulmonary tuberculosis.

Mention five (5) causes of pleural effusion.

References

Goljan E.;(2007): Rapid Review Pathology (2th Ed.) Elsevier Saunders, USA. Pg. 290-303, 325-326.

Kumar V. ; Abbas A. K. ; Aster J. C.;(2013): Robbins and Contran Pathologic Basis of Disease (9th Ed.) Elsevier Saunders, USA. Pg. 460, 486-511.

Mohan H.;(2010): Text book of Pathology (6th Ed.) Jaypee Brothers Medical Publishers, India. Pg. 165, 465-477.

Xiu P.;(2012): Crash Course Pathology (4th Ed.) Elsevier Saunders, USA. Pg. 87-89.

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Session 24 Lung Pathology

Contents

Lecture Notes