September 22, 1997
Pathology #15 Transcriber: Emily Carlson Monday, September 15, 1997 10am Reviewed by: Dr. Hewan-Lowe Lecturer: Dr. Karlene Hewan-Lowe Peer reviewer: Forrest Carson
This lecture follows Dr. Hewan-Lowe's handout. We are responsible for everything on the handout, whether it was mentioned in class or not. The page numbers in the handout correspond to Robbins. If you have any questions for Dr. Hewan-Lowe, her email address is: khewanl@emory.edu
This consists of local aggregates of lymphoid tissue scattered along the bronchi. The tissue secretes immunoglobulins to neutralize toxins and noxious bacteria. It also allows macrophages to come into the bronchi and help with clearance. The macrophages are motile cells, so they can simply move freely between the air space and the adjacent lung tissue.
Inflammation and permanent dilatation of the bronchi and bronchioles. We will be able to see inflammation microscopically, and just dilated bronchi (some of which contains pus) on gross observation of the lung.
A bronchus or bronchiole could become obstructed and passively dilate distal to the point of obstruction (on the alveolar side). Secretions would pool in the dilated airway, the surrounding lung parenchyma would collapse and the obstruction would prohibit clearance mechanisms from getting rid of noxious substances. Any bacteria trapped in the pooled secretions could cause infection, leading to inflammation that could destroy the bronchial wall, leading to further dilatation.
The lung around the bronchus collapses (atelectasis) due to absorption of air. With the decrease in the usual lung elastic forces, the bronchi passively dilate. The lung must be re-expanded in order for elastic forces to maintain tone and rigidity. The chronically inflamed bronchi are distal to the obstruction.
Infection produces bronchial wall inflammation, with weakening and further dilatation. Also, extensive bronchial and bronchiolar damage causes endobronchial obstruction and worsens the bronchiectasis of bronchi in the atelectatic areas.
Atelectasis= (collapse of the lung); absence of gas from a part or the whole of the lungs, due to failure of expansion or resorption of gas from the alveoli. Atelectasis may also be due to external compression caused by pleuritis or pleural effusions. Primary atelectas
Bronchiectasis usually affects the lower lobes bilaterally, particularly those air passages that are most vertical, and is most severe in the more distal bronchi and bronchioles. The airways are dilated, sometimes up to four times the normal size. These dilatations may produce long, tube-like enlargements called cylindroid bronchiectasis, or fusiform or even saccular bronchiectasis.
Characteristically, the bronchi and bronchioles can be followed out to the pleural surfaces. In a normal lung, the bronchioles cannot be followed beyond a point 2-3 cm from the pleural surfaces.
The histology findings vary in bronchiectasis. In the full-blown case, there is acute and chronic inflammatory exudation within the walls of the bronchi/bronchioles. In cases of severe inflammation, the necrosis totally destroys the bronchial/bronchiolar walls and forms a lung abscess. There is also destruction of pseudostratified columnar epithelium. Squamous metaplasia is the replacement of the pseudostratified, columnar epithelium by squamous cells during the repair (healing after the infection subsides).
SLIDE: Gross appearance of bronchiectasis. The bronchi are wider than the accompanying pulmonary artery (that's how we know it's dilated). The bronchi will stay dilated all the way up to the pleura (not found in normal lung). In asthma, there may be mucus impaction in the bronchioles.
SLIDE: Resected lung specimen with severe bronchiectasis. Fungal (Aspergillus) COLONIZATION (grungy, brown-gray material) is present in the dilated bronchi. There are gray areas of fibrosis in the lung parenchyma.
SLIDE: Cystic fibrosis lung specimen. There are dilated bronchi filled with pus.
SLIDE: Histology of bronchiectasis. There are neutrophils and other inflammatory cells in the bronchial wall. There is squamous metaplasia as a repair mechanism. Intercellular bridges are an identifying features of squamous epithelium.
Bacterial invasion of the lung parenchyma evokes exudative solidification (consolidation) of the pulmonary tissue. In these cases, most of the inflammation is in the lung parenchyma (alveolar spaces), not in the bronchial wall.
In patients with terminal illnesses, the endpoint is often pneumonia. Viral pneumonias may cause a superimposed bacterial pneumonia because the virus impairs the immune system of the host. Patients who are hospitalized for chronic disease can develop nosocomial (hospital-acquired) pneumonias which are likely to be caused by antibiotic resistant organisms.
SLIDE: Bronchopneumonia in lung, with Staphylococcus. Several different patchy areas are involved. Here, we have focal areas of inflammation, in contrast to large, confluent areas of inflammation in lobar pneumonia. In bronchopneumonia, well-developed lesions are usually 3-4 cm in diameter, slightly elevated, dry, granular, gray-red to yellow, and poorly delimited at their margins.
Histologically, the reaction usually comprises a suppurative, neutrophil-rich exudate that fills the bronchi The gross distribution of the inflammatory cells allows us to distinguish lobar pneumonia from bronchopneumonia. Under the microscope, there are inflammatory cells in the alveolar spaces in both types of bacterial pneumonia.
Complications of pneumonia include:
This is actually a misnomer. Viruses do cause viral pneumonia. But, mycoplasma and rickettsial organisms also produce the same type of inflammatory response in the lung. The viral mycoplasma pneumonia is also known as Primary Atypical Pneumonia (PAP). This is "atypical" because of a lack of alveolar exudate. PAP's are better designated as interstitial pneumonitis (there are also intersititial pneumonitis of unknown cause).
There is no obvious consolidation as there is with lobar pneumonia. The pleura is smooth, and pleuritis or pleural effusions are infrequent. The alveolar septa are widened and edematous and usually have a mononuclear inflammatory infiltrate. There may be alveolar damage similar to that seen in Adult Respiratory Distress Syndrome.
Histology of viral pneumonia: hyaline membranes, interstitial mononuclear cell infiltrate, reactive epithelial cells. Sometimes, these reactive alveolar epithelial cells exhibit a characteristic viral cytopathic effect (e.g. measles, CMV, and adenovirus pneumonia).
SLIDE: An X-ray of a patient with viral pneumonia shows a "diffuse whiteout of both lung fields." The lungs are heavier (up to 1400 grams) than normal (400-500 grams). The cut surface of that lung feels more solid, with a red, slightly watery appearance, like raw meat.
SLIDE: Histology. The alveolar space may contain some fluid and very few cells. On the surface of the alveolar septum are hyaline membranes (pink, fibrin exudate).
SLIDE: Measles pneumonia. Widening of the septa, interstitial mononuclear cell infiltrate, reactive epithelial cell and a cell showing a viral cytopathic effect- multinucleated giant cells, called "Warthin-Finkeldy" giant cells.
SLIDE: Cytomegalovirus pneumonia. There is a widened septum, with mononuclear cells. The cells and the nuclei enlarge. There are "owl's eye" inclusions of the viral particles in the nuclei. Viral particles are also present in the cytoplasm. CMV is more common in immunocompromised hosts (e.g. AIDS patients).
When the abscesses are small and multiple, the abscesses are usually due to bacterial pneumonia. When the abscesses are large and only one or two abscesses are present, they are usually due to aspiration. The cardinal histologic change in all abscesses is suppurative destruction of the lung parenchyma. Some abscesses have a central cavity.
SLIDE: Histology of a lung abscess. There are dying cells, inflammatory cells, and necrotic tissue....no normal tissue to be found.
SLIDE: Wall of the lung abscess, with fibroblasts and inflammatory cells, forming a distinct margin between the lung abscess and the lung parenchyma.
Handout: Lung Lecture