FIGURE 7.1

Model of normal respiratory acinus: each acinus is formed by branching of a terminal bronchiole into a number of respiratory bronchioles, which eventually form alveolar ducts, whose walls are lined entirely by alveoli.

FIGURE 7.2

High-power view of a section of an allergic nasal polyp. It is lined by respiratory epithelium (left ) and inflamed by masses of eosinophils and some plasma cells.

FIGURE 7.3

Bronchiectasis. A slice of left lung showing markedly dilated bronchi, scarring and loss of lung parenchyma.

FIGURE 7.4

Asthma. Microscopic view of a bronchiole with mucus in the lumen, submucosal oedema and inflammation, and prominent smooth muscle.

FIGURE 7.5

Aspergilloma. This slice of lung shows a large pale ball of fungus (Aspergillus) mixed with mucus in a markedly dilated bronchus.

FIGURE 7.6

Microscopic view of bronchial wall in chronic bronchitis. There are prominent mucous glands in the submucosa.

FIGURE 7.7

Centriacinar emphysema. This slice of lung shows expanded air spaces around respiratory bronchioles.

FIGURE 7.8

Panacinar emphysema. This slice of upper lobe shows more diffuse enlargement of air spaces than seen in Figure 7.7.

FIGURE 7.9

Lung section from autopsy on a patient who developed adult respiratory distress syndrome following peritonitis. Neutrophil polymorphs are packed in the alveolar capillaries and fibrin is present in alveoli, in places forming hyaline membranes (arrows).

FIGURE 7.10

Pathogenesis of adult respiratory distress syndrome. Initial injury is to the capillary endothelium or the alveolar epithelium. The endothelial damage is often initiated by endotoxin and is sustained by interactions between neutrophils, macrophages, cytokines, oxygen radicals, complement and arachidonate metabolites. Fluid and proteins leak from the capillary into the interstitium and alveoli.

FIGURE 7.11

Honeycomb lung. This can be the end result of a number of fibrosing lung diseases, including cryptogenic fibrosing alveolitis.

FIGURE 7.12

Sarcoidosis. Microscopic view of non-caseating granulomatous inflammation, including giant cells.

FIGURE 7.13

Asbestos body in a high-power view of a section of scarred lung tissue. It appears golden brown and beaded as it is coated with iron.

FIGURE 7.14

Pale yellowish-white fibrous plaques on the posterior parietal pleural surface at autopsy on a patient who had a history of occupational exposure to asbestos.

FIGURE 7.15

Lobar pneumonia affecting the whole of the lower lung on the left of the picture. This is solid and dull red (red hepatization) due to inflammatory exudates filling alveoli and small bronchi.

FIGURE 7.16

Bronchopneumonia. There is patchy consolidation (paler areas) of this lung. This case was due to aspiration of gastric contents (not shown).

FIGURE 7.17

Secondary pulmonary tuberculosis. There is caseation, fibrosis and developing cavitation toward the apex of the upper lobe.

FIGURE 7.18

Pulmonary infarction. The dark haemorrhagic areas towards the periphery of the lung in the lower part of the field are infarcted.

FIGURE 7.19

Slice of lung hilum showing an invasive carcinoma (white) originating in the wall of a bronchus. This is a small cell carcinoma, but one could not tell that without microscopy.

FIGURE 7.20

Small cell carcinoma of lung. Microscopic view showing sheets of small, hyperchromatic nuclei with nuclear moulding.

FIGURE 7.21

A large squamous cell carcinoma of lung. Such tumours generally metastasize later than small cell carcinomas and are thus more often amenable to surgery.

FIGURE 7.22

An adenocarcinoma with associated scarring and carbon pigmentation occupies most of the upper lobe of this lung and extends into the fissure and lower lobe.

FIGURE 7.23

Cytological preparation from a large cell carcinoma of lung showing an enormous malignant cell (compare size with adjacent red blood cells) with prominent vesicular nucleus and nucleoli. Papanicolaou.

FIGURE 7.25

Malignant mesothelioma encasing most of the lobe shown in this field.