By Dan Longo, Anthony Fauci
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Additional info for Harrison's Gastroenterology and Hepatology
Oropharyngeal motor dysphagia results from impairment of the voluntary effort required in bolus preparation or neuromuscular disorders affecting bolus preparation, initiation of the swallowing reﬂex, timely passage of food through the pharynx, and prevention of entry of food into the nasal and the laryngeal opening. Paralysis of the suprahyoid muscles leads to loss of opening of the UES and severe dysphagia. Because each side of the pharynx is innervated by ipsilateral nerves, a unilateral lesion of motor neurons leads to unilateral pharyngeal paralysis.
FIGURE 3-14 Geographic tongue. FIGURE 3-17 Heavy calculus and gingival inﬂammation. FIGURE 3-15 Moderate gingivitis. FIGURE 3-18 Severe gingival inﬂammation and heavy calculus. 25 CHAPTER 3 FIGURE 3-22 Severe periodontal disease, missing tooth, very mobile teeth. FIGURE 3-20 Ulcer on lateral border of tongue—potential carcinoma. FIGURE 3-23 Salivary stone. FIGURE 3-21 Osteonecrosis. FIGURE 3-24 A. Calculus. B. Teeth cleaned. Atlas of Oral Manifestations of Disease FIGURE 3-19 Heavy plaque and gingival inﬂammation.
Diseases of the smooth-muscle segment involve the thoracic part of the esophagus and the LES. Dysphagia occurs when the peristaltic contractions are weak or absent or when the contractions are nonperistaltic. Loss of peristalsis may be associated with failure of LES relaxation. Weakness of contractile power occurs due to muscle weakness, as in scleroderma or impaired cholinergic effect. Nonperistaltic contractions and failure of LES relaxation occur due to impaired inhibitory innervation. In diffuse esophageal spasm (DES), inhibitory innervation only to the esophageal body is impaired, whereas in achalasia inhibitory innervation to both the esophageal body and LES is impaired.