The epithelium lining the trachea is typical respiratory epithelium (ciliated pseudostratified columnar) [example] , which, like the nasal epithelium, contains numerous goblet cells. This epithelium has an unusually thick basementmembrane, which you can see as a narrow pink-staining region immediately basal to the epithelium. This epithelium plus its underlying layer of loose connective tissue (the lamina propria) make up the tracheal mucosa. The layer under the mucosa is the submucosa wherein you’ll find numerous seromucous glands [example] . The mucosa is separated from the submucosa by a layer of longitudinal elastic fibers. This elastic layer is often not obvious in your sections, so we do not require you to decide where the division occurs. However, as you may recall from the connective tissue lab session, slide #40 happens to show these fibers quite well (cut in cross section, so they appear as eosinophilic, glass-like dots) [example] .
Outside the connective tissue layers, observe the C-shaped rings of hyaline cartilage [example] which help to keep the lumen of the trachea from collapsing. It is unlikely that your histological section will follow the same C-shaped ring all the way around the trachea; instead, it will probably pass in and out of two or more rings. The ends of the rings are bridged by horizontally oriented smooth muscle (the trachealis muscle) [example] , which can act to adjust the diameter of the trachea. This muscle is seen especially well in those examples of slide #127 that are stained with Masson’s trichrome [example] . Outermost is a layer of connective tissue, the adventitia.
A. Bronchi: The trachea bifurcates into two primary bronchi, which enter the lung and then branch several times to give rise to smaller secondary and tertiary bronchi [example] . Bronchi differ from the trachea in having plates rather than rings of cartilage, and in having a layer of smooth muscle between the lamina propria and submucosa. In smaller branches, the amount of cartilage decreases, whereas the amount of smooth muscle increases. Also, the number of glands and goblet cells decreases. Don’t worry about trying to distinguish among primary, secondary, and tertiary bronchi, but you should be able to distiguish bronchi in general from the trachea and bronchioles (discussed below).
B. Bronchioles: Bronchioles [example] are smaller branches of the bronchi, and are distinguished from them by the absence of cartilage and glands. In larger bronchioles, the epithelium is still ciliated, but is now usually simple columnar, whereas in the smallest bronchioles, the epithelium will be simple cuboidal (mostly Clara cells) and lack cilia altogether. The smooth muscle layer is generally quite prominent in these structures as demonstrated in slide 132-2 [example] where the bronchiole was cut in a grazing longitudinal section allowing you to see the circularly arranged bundles of smooth muscle in the bronchiolar wall. As mentioned above, the smallest conducting bronchioles consist of a simple cuboidal (or perhaps “low columnar”) epithelium of mostly Clara cells, a few ciliated cells, and NO goblet cells, and are called terminal bronchioles [example].
A. Respiratory Bronchioles: You might see short, transitional regions of bronchioles which have alveoli in their walls. These bronchioles with alveoli in their walls are called respiratory bronchioles [example] . They characteristically exhibit a progressive reduction in height of the epithelium and in the amount of smooth muscle between the openings of adjacent alveoli.
B. Alveolar ducts: The walls of alveolar ducts [example] are so interrupted by alveoli and alveolar sacs (clusters of alveoli) that all that can be seen of the wall proper is small knobs of smooth muscle, collagen and elastic fibers. You can spot the knobs, but shouldn’t try to distinguish the constituents, which are covered by a squamous epithelium too thin to see with the light microscope.
C. Alveoli: The walls of these structures are covered on both sides by squamous epithelium (too thin to see) of Type I cells lining adjacent alveolar lumens. Within the walls is an extensive capillary network. You may see the space within these capillaries, or they may be filled with RBCs. The Type II pneumocytes [example] , which secrete surfactant, have large, rounded nuclei and vacuolated cytoplasm and are often difficult to identify in the light microscope (the “vacuoles” are actually granules of phospolipids that, unfortunately, are often extracted during tissue processing). In the lumen of some alveoli, you will see macrophages, called alveolar phagocytes or dust cells [example].
While components of the alveolus may be difficult to see in normal lung tissue, pathological changes that occur in the lung as the result of congestive heart failure shown here in slide 42 from your histopathology collection ImageScope WebScope exaggerate many of these features making them a bit easier to see:
Poor venous return causes dilation of the alveolar capillaries.
Type II pneumocytes with large round nuclei and clear cytoplasm are much more numerous and can be easily seen in the alveolar walls because they proliferate in an attempt to repair damaged alveoli.
Alveolar macrophages characteristic of this condition (also known as “heart failure” cells) become laden with brownish-black hemosiderin pigment resulting from the breakdown of erythrocytes leaking from the engorged capillaries.
Although it is almost impossible to appreciate in these adult tissue sections, the lung is divided into lobules with a bronchiole at the center of each lobule. The blood supply is organized according to the lobule:
A. Large, thin-walled pulmonary arteries [example] run alongside the bronchi and bronchioles. These arteries are the main blood supply to the lungs. They carry large volumes of deoxygenated blood at low pressure from the right side of the heart to pulmonary capillaries in the alveoli.
B. Smaller bronchial arteries also accompany the bronchi and bronchioles. These vessels arise from the thoracic descending aorta and carry oxygenated blood at systemicpressure. They supply blood to the tissue comprising the bronchi and bronchioles and thus may be seen as part of a neurovascular bundle (artery, vein, and nerve) either in cross section [example] or longitudinal section [example] in close association with the bronchial walls. These arteries are quite a bit smaller than pulmonary arteries and for their size, have relatively thick walls.
C. Large thin-walled pulmonary veins [example] are found at the periphery of the lobules, at some distance from bronchi or bronchioles. These veins drain the intrapulmonary circulation and carry oxygenated blood (also at rather low pressure).
A 24-year-old man presented to the emergency room with dyspnea, cough, and wheezing. He had had numerous similar episodes, usually triggered or exacerbated by exposure to cold air, physical activity, and exposure to cats and birds. Physical examination revealed wheezing prominent in both phases of respiration which was relieved upon administration of inhaled albuterol. The sample shown is from another individual who had similar a similar bout of wheezing and lost consciousness while driving, resulting in a fatal motor vehicle crash.
What disorder is strongly suggested by the gross and microscopic findings?
Predict the gross autopsy appearance of the lung.
What histologic abnormalities are manifested by the bronchioles?
A middle-aged man sought medical attention because of increasing breathlessness. He had had a long history of mild exertional dyspnea and a minimal cough productive of small amounts of mucoid sputum. He had lost some weight and he appeared distressed. His lower intercostal spaces retracted with each inspiration. The patient had a long history of cigarette smoking. He underwent lung volume reduction surgery to ameliorate his condition.
Based on the pathologic features and the clinical history, what is your diagnosis?
What other clinical signs and symptoms were likely present in this case?
Predict the results of these pulmonary function tests (normal, increased, or decreased): total lung capacity (TLC), funtional residual capacity (FRC), forced vital capacity (FVC), forced expiratory volume (FEV).
The slide contains fragments of alveolar walls. What is the most likely explanation for this?
What roles do neutrophil elastase and matrix metalloproteinases purportedly play in the development of this disorder?
If the patient were to come to autopsy, what would the patient’s lungs look like grossly?
This histologic section was prepared from the lung of an elderly man who died of a myocardial infarct. At autopsy, the pleural surfaces of both lungs were fibrotic. The cut surfaces of the lungs manifested diffuse fibrosis with extensive “honeycombing.” The hilar lymph nodes were not enlarged. When examining this slide, notice that many of the alveolar walls contain more nuclei than usual and that there are detached fragments of alveolar septa. Small deposits of anthracotic pigment are also evident. Many of the alveolar septa are thickened by fibrosis. Within these areas of fibrosis are golden brown beaded or “knobby” structures [example].
The fibrotic alveolar walls represent a nonspecific reaction to injury that is a common pathologic feature in many of the restrictive lung diseases. In this case, the golden brown bodies represent the etiologic agent. What are these bodies?
How did the fibrosis come about?
Predict the results of these pulmonary function tests (normal, increased, or decreased): total lung capacity (TLC), funtional residual capacity (FRC), forced vital capacity (FVC), forced expiratory volume (FEV).
A 30-year-old man had a severe shaking chill that lasted for an hour. Shortly afterwards, he developed a fever of 40.0 degrees centigrade, marked tachycardia and tachypnea, a dry cough, and right-sided severe pleuritic chest pain. His cough became productive of thick, tenacious, rust-colored sputum. He had been previously well. The patient sought medical attention.
He appeared toxic and was in moderate respiratory distress. His respirations were shallow and there was increased tactile fremitus and dullness to percussion over the right hemithorax. Fever and tachypnea were present as were bronchial breath sounds and crackles. Laboratory values included a leukocytosis with a left shift and an elevated sedimentation rate. Arterial blood gases determination revealed hypoxemia. A chest radiograph demonstrated opacification and air bronchograms of the right middle and lower lobes. Despite aggressive medical treatment, the patient died.
How might the right lung have appeared at the autopsy table?
Describe the pathologic features manifested in your histologic section.
What is your pathologic diagnosis?
Had the patient lived, what other changes would have been manifested by the lung as the patient recovered?
A 60-year-old man sought medical attention because of weight loss. During his evaluation, the patient also complained of a decreased appetite, weakness, and night sweats. A non-productive cough had recently developed. Physical examination revealed hepatomegaly and splenomegaly. A chest radiograph manifested a diffuse reticulonodular infiltrate. A lung biopsy sample was obtained and a diagnosis was established. The patient responded promptly to treatment. Slide 26 was obtained from a similar patient at autopsy.
Based on the clinical presentation and the findings contained in the autopsy slide [hint], what diagnoses are most likely?
How could you confirm your diagnosis?
How does your diagnosis explain the clinical, radiographic, and laboratory findings?
What types of social settings increase the risk of infection by the agent responsible for the pathologic features manifested by this patient?
