Circulatory disturbances are usually a part of similar troubles of neighboring tissues.

Inflammation

The acute catarrhal pharyngitis or angina may result from exposure to cold, to the irritating action of various substances, as tobacco smoke and dust, or may occur as a part of an intestinal derangement. The mucous membranes become red and swollen with decreased secretion at first. As the process goes on there is frequently an abundance of a thick, tenacious secretion composed of mucus and desquamated columnar epithelial cells. In severe cases true ulcers may form along the posterior wall.

In chronic pharyngitis, such as occurs in excessive smokers and in those who use their voice a great deal, the posterior wall and the faucial pillars are particularly involved. There is chronic congestion and the lymphoid collections become hyperplastic, causing slight granular elevations. The secretions become less, as a rule, but may be increased and mucopurulent. The pharyngeal tonsils are usually hyperplastic.

Phlegmonous Pharyngitis

Phlegmonous Pharyngitis and retropharyngeal abscess follow the entrance of bacteria, usually pyogenic, into the deeper tissues or may result from caries of the spinal column, from diphtheria or scarlet fever. If there is rapid abscess formation there is bulging into the pharynx and rupture may take place. If the process has been slower the pus will extend along the deep fascia till perforation into the posterior mediastinum, bronchi, or esophagus occurs. General septicemia not infrequently occurs.

Syphilitic Pharyngitis

Syphilitic Pharyngitis is common as a secondary symptom, but it has no characteristic appearance that renders it easily recognizable.

Tuberculous Pharyngitis

Tuberculous Pharyngitis is unusual. Is generally secondary to tuberculosis of the lungs. The tubercles ultimately soften, break down and form ulcers of varying extent.

Pseudo-Membranous Pharyngitis

Pseudo-Membranous Pharyngitis may be diphtheritic or non-diphtheritic.

Vincent's Angina

Vincent's Angina is an infection of the pharyngeal mucous membrane due to the presence of fusiform bacilli and spirochete. They cause the formation of a dense exudate which when removed causes bleeding and discloses more or less extensive ulcerations which are very persistent. At times the uvula and even portions of the hard palate are involved.

The non-diphtheritic pharyngitis is generally caused by the streptococcus pyogenes or may result from the action of very irritating substances, as steam or ammonia. The appearance of the pseudo-membrane is, to the naked eye, similar to that of the diphtheritic variety. It is not, however, accompanied by the same constitutional depression, nor is it followed by paralyses.

Diphtheritic Pharyngitis

Diphtheritic Pharyngitis is caused by the Klebs-Loeffler bacillus and characterized by a pseudo-membrane that is yellowish or dirty gray in color. The involvement may be limited to a small portion of the pharynx, being most common on the arches of the fauces, or the tonsils and nares as well may be concerned. It may extend even into the esophagus and stomach. This pseudo-membrane is laminated, being composed of fibrin in the meshes of which are desquamated epithelial cells, leukocytes and erythrocytes, and the diphtheria bacilli in great numbers. It is formed by the coagulation of the exudate and by coagulation necrosis of the superficial tissues.

This membrane can be removed, exposing a raw ulcerated surface upon which a new membrane quickly forms. The lymph-nodes near-by may enlarge and undergo suppuration.

The extent of the pseudo-membrane does not denote the gravity of the infection. The severity depends upon the virulence of the particular bacillus that has caused the infection; it is the expression of the intensity of the toxin present. In severe forms it spreads rapidly, and if there is a mixed infection with streptococci, hemorrhage and gangrene may result, as well as secondary abscess formation elsewhere in the body.

Fig. 148. - -Diphtheric Membrane from the Uvula. X 50 (Ziegler).

a, b, c, Layers of fibrin containing epithelial cells, leukocytes, and bacteria; d, e, cellular infiltration of the connective tissue; f, collections of red corpuscles; g, dilated blood-vessels.

Besides the local manifestations there are marked general symptoms due to the presence of a dangerous toxin. The action of this body is seen in the form of small foci of necrosis in various tissues of the body. Death may result from cardiac paralysis resulting from the presence of the toxin.

Of the internal organs the liver especially shows focal necrosis, in which the cells are degenerated and the nuclei show hyperchromatosis. There is hyperemia of the kidney with cloudy swelling of the epithelium, edema, and hemorrhage. Myocarditis and degeneration of the cardiac muscle also occur. The spleen is also hyperemia.

During convalescence paralysis, particularly of the throat, may occur, also of the muscles of the eyes, the larynx, and the diaphragm. The muscles will show a round-cell infiltration between the fibers and a granular and fatty change of the cells.

There may be degeneration of the ganglion cells of the cord.

Tumors of the pharynx are rare. Squamous epithelioma as a result of extension is the most common, but fibromata and sarcomata have been encountered.