Q1.

Sand blasting results in potentially high levels of silicon dioxide (silica), usually in crystalline form as quartz, which is inhaled into the lung. It is a requirement of all sandblasters that they wear protective gear to prevent inhalation. Although compulsory, there is some question over whether this patient had worn protective gear. Inhaling silica results in silicosis. Silicosis is one of a number of diseases of the lung due to inhaled inorganic dusts.

Q2. There is essentially no normal lung although small residual areas of red tissue are seen between the dense grey black nodules. These nodules are of varying caliber but are all less than 10mm and show areas of coalescence. The nodules are present in all the areas of the lung seen and include the upper and lower lobes. There is no spared area. Some residual vascular and bronchiole structures are evident, although appearing compressed. The pleural surface is unremarkable.

Q3. The structure circled is a bronchus that appears partly destroyed by an irregular edged, yellow grey tissue cavity with central haemorrhage. On the symptomatology given the most likely relevant feature is the sudden severe haemoptysis. A postulated diagnosis would be that he has ruptured a bronchus with resultant terminal haemoptysis occurring as a vessel involved in the rupture is also torn. The tissue looks soft and necrotic around the edge of the cavity and it does not appear to be due to a tumour, which would give the edge of the lesion a bulky solid appearance due to the expanding tumour. The soft necrotic edge is more likely due to an infective aetiology. However to reach a satisfactory diagnosis I would need to see tissue sections of the edge of the lesion to determine the cause more exactly.

Q4. The structures circled are hilar lymph nodes. The accumulation of carbon pigment in the macrophages of the node makes the node look black. The node is not normal although the size of the nodes is only slightly increased. Normal nodes (in an urban dweller or smoker) are grey to black throughout the node. These nodes have a rim of grey white tissue, which is not normally seen.

Q5. Inorganic dusts especially silica and asbestos, cause lung injury by stimulating fibrosis. The fibrosis occurs secondary to the release of inflammatory mediators that happens when the macrophages attempt to engulf the particles. With asbestosis the particles that are particularly aggravating to the lung are the long thin aerodynamic particles that extend to the distal airway and can extend into the walls of the bronchioles and through the alveolar wall. The lodging of these particles elicits the macrophage response that leads to secondary fibrosis in the interstitial spaces. Asbestos also causes pleural plaques and is clearly linked to malignant mesothelioma, a primary tumour arising from the pleura. Bronchogenic carcinoma is also increased in this population, especially in those that smoke.

In coal miners, the coal particles are also taken up by macrophages and these concentrate around the distal bronchiole and infiltrate the peri-bronchiolar connective tissues. There is an accompanying mild dilation of the respiratory bronchioles. The mechanism of silicosis is discussed in the following answers in more detail.

Q6. Type 1 pneumocytes cover 95% of the surface of the alveolar lining and type II cells, although accounting for 60% of the cells are more cuboidal and hence do not cover so much of the surface area. The alveolar wall contains a dense meshwork of capillaries. The fusion of the endothelial (capillary) and epithelial (alveolar) basement membranes, constitute the alveolar capillary membrane, across which gas exchange occurs. Therefore the barriers are Pneumocyte Pneumocyte basement membrane Endothelial basement membrane (fused with above) Endothelial cell

Q7. The lining of respiratory epithelium is a pseudostratified columnar ciliated epithelium with goblet cells. The ciliated cells and the mucous secreting cells form a mucociliary blanket over the airway epithelium that disposes of particles 2 to 20mm. The cilia beat the mucous blanker toward the trachea, and the particles that land on it are thus removed from the lung. Other cells in the epithelium are basal cells that are precursor cells that differentiate to form the neuroendocrine cells of the tracheobronchial epithelium. As the bronchi branch to become bronchioles, the epithelium becomes thinner until only one cell layer is left. The mucous cells disappear and are replaced by a non-ciliated columnar cell. This answer goes toward the prize along with the other questions you may have attempted in the case studies so far. Sorry no answer from me.

Q8. Macrophages are cells that have the capacity to engulf and breakdown particles. They are particularly effective if the particle is less than 2 microns. The process is called phagocytosis. The cells are medium to large in size and have abundant cytoplasm containing numerous lysosomes and mitochondria. Macrophages are one of the most synthetically active cells in the body, producing a variety of factors that control cell proliferation and maturation. Macrophages are also important in processing foreign antigens following presentation of their surface HLA proteins for lymphocyte activation. They also clear senescent red blood cells and salvage the iron for re-use as well as clearing the body of neoplastic and foreign cells.

Q9. Fibroblasts produce collagen that leads to fibrosis as the collagen fibres accumulate. Fibroblasts are stimulated but fibrinogenic factors (FGF) released by macrophages. Other factors stimulating fibroblastic growth include platelet derived growth factor (PDGF), TGF and plasma fibronectin. Macrophage release FGF following the engulfment of the irritant particles, in this case silica. Fibroblasts are stimulated during the process of any form of healing and lead to the development of scar tissue. The classical example is wound healing which can be taken on a broader context to be most forms of injury and chronic inflammation in any part of the body with the exception of the brain which heals using a different (brain specific) cell type due to the blood brain barrier.

Q10. The pink stuff is the collagen. It is pink because it is acidic and acidic things are pink using a standard Haematoxylin and Eosin stained section. There is a problem with gas exchange if these collagenous nodules are replacing and destroying the gas exchange potential over such a large proportion of the lung. This mans lung changes are particularly florid and relatively acute. This probably relates to the amount of exposure to silica he received. In these acute forms of silicosis, where disease progresses rapidly over a few years, the extent and the florid nature of the lung involvement leads to a defective gas exchange as illustrated by his respiratory rate is 20/min and his oxygen saturation of 93% on 2L/min of O2/minute whilst resting in bed.

Q11. This series of photographs relate to Q3 and illustrate fungal hyphae forming a mass within a necrotic lumen. Fungal hyphae, are branching and have septa. These features raise the possibility of an Aspergillus fungus. This fungus is capable of invading into and destroying vessels and tissues. It is this destructive capacity that has led to the terminal haemoptysis. The lower image illustrates blood extending into lung parenchyma as a secondary effect of the blood also extending down into lung.