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الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 8:18:48 AM
Esophagus:
Introduction: The normal esophagus is a hollow muscular tube that extends from the pharynx to the gastroesophageal junction at the level of the T11 or T12 vertebra. Measuring between 10 and 11 cm in the newborn, it grows to a length of about 23 to 25 cm in the adult. The wall of the esophagus consists of a mucosa, submucosa, muscularis propria, and adventitia, reflecting the general structural organization of the gastrointestinal tract. The mucosa is composed of a nonkeratinizing stratified squamous epithelial layer that overlies a lamina propria. The lamina propria is the nonepithelial portion of the mucosa, above the muscularis mucosae. It consists of areolar connective tissue and contains vascular structures and scattered leukocytes. The submucosa consists of loose connective tissue containing blood vessels, a rich network of lymphatics, nerve fibers, and submucosal glands.
The muscularis propria of the proximal 6 to 8 cm of the esophagus also contains striated muscle fibers from the cricopharyngeus; this feature explains why skeletal muscle disorders can cause esophageal dysfunction. The functions of the esophagus are to conduct food and fluids from the pharynx to the stomach and to prevent reflux of gastric contents into the esophagus.
These functions require motor activity coordinated with swallowing--a wave of peristaltic contraction, relaxation of the LES in anticipation of the peristaltic wave, and closure of the LES after the swallowing reflex.
PATHOLOGY Lesions of the esophagus varies from highly lethal cancers to the merely annoying heartburn.
Clinical Symptoms
1- Dysphagia (subjective difficulty in swallowing) is seen in both esophageal abnormal motor function and with diseases that narrow or obstruct the lumen.
2- Heartburn (retrosternal burning pain) usually reflects regurgitation of gastric contents into the lower esophagus.
3- Pain and hematemesis are sometimes evoked by esophageal disease, particularly by lesions associated with inflammation or ulceration of the esophageal mucosa. The clinical diagnosis of esophageal disorders often requires specialized procedures, such as esophagoscopy, radiographic barium studies, and manometry.
ATRESIA AND FISTULAS developmental defects in the esophagus , they must be corrected early, since they are incompatible with life, because they cause immediate regurgitation when feeding is attempted, they are usually discovered soon after birth. Absence (agenesis) of the esophagus is extremely rare; much more common are atresia and fistula formation. In atresia, a segment of the esophagus is represented by only a thin, non-canalized cord, with a proximal blind pouch connected to the pharynx and a lower pouch leading to the stomach. Atresia is most commonly located at or near the tracheal bifurcation. Atresia rarely occurs alone but is usually associated with a fistula connecting the lower or upper pouch with a bronchus or the trachea. Aspiration and paroxysmal suffocation from food are obvious hazards; pneumonia and severe fluid and electrolyte imbalances may also occur.
STENOSIS, WEBS, AND RINGS Non-neoplastic constrictions of the esophagus are most often acquired conditions. Stenosis consists of fibrous thickening of the esophageal wall, particularly the submucosa, with atrophy of the muscularis propria. The lining epithelium is usually thin and sometimes ulcerated. Those in the upper esophagus are often designated as webs; those in the lower esophagus are designated rings, located at or just above the esophagogastric junction. Web is accompanied by iron deficiency anemia, glossitis, and cheilosis, the condition is referred to as the Paterson-Brown-Kelly Stenosis is the result of severe esophageal injury with inflammatory scarring, as from gastroesophageal reflux, radiation, tumors... Stenosis usually develops in adulthood and becomes manifest by progressive dysphagia, at first to solid foods only but eventually to all foods. Dysphagia constitutes the major symptom. In severe stenosis, virtually total obstruction may result. ACHALASIA Achalasia is characterized by three major abnormalities:
(1) aperistalsis,
(2) partial or incomplete relaxation of the LES with swallowing.
(3) increased resting tone of the LES.
The pathogenesis of primary achalasia is poorly understood but is thought to involve degenerative changes in neural innervation, either intrinsic to the esophagus or in the vagus nerves. Secondary achalasia may arise in Chagas disease, in which Trypanosoma cruzi causes destruction of the myenteric plexus of the esophagus, duodenum, colon, and ureter, with resultant dilation of these viscera.
MORPHOLOGY. In primary achalasia, there is progressive dilation of the esophagus above the level of the LES. 1-The wall of the esophagus may be of normal thickness, thicker than normal owing to hypertrophy of the muscularis, or markedly thinned out by dilation. 2-The myenteric ganglia are usually absent from the body of the esophagus. 3-The mucosal lining sometimes reveals inflammation, ulceration, or fibrotic thickening.
Clinical Features. Achalasia usually becomes manifest in young adulthood but may appear in infancy or childhood. The classic clinical symptom of achalasia is progressive dysphagia. Nocturnal regurgitation and aspiration of undigested food may occur.
Complications:
1-The hazard of developing esophageal squamous cell carcinoma, said to occur in about 5% of patients, typically at an earlier age than those without this disease.
2-Candida esophagitis.
3-Aspiration with pneumonia or airway obstruction.
REFLUX ESOPHAGITIS Reflux of gastric contents into the lower esophagus is the first cause of esophagitis.
Causative factors:
1- Decreased efficacy of esophageal anti-reflux mechanisms, particularly LES tone.
2-Central nervous system depressants.
3-Hypothyroidism.
4-Pregnancy.
5-Alcohol or tobacco exposure. 6 -Presence of a sliding hiatal hernia.
The acid-peptic action of gastric juices is critical to the development of esophageal mucosal injury; in severe cases, refluxed bile from the duodenum also may contribute to the mucosal disruption.
MORPHOLOGY. The anatomic changes depend on the causative agent and on the duration and severity of the exposure. Simple hyperemia (redness) may be the only alteration.
Three characteristic histological features are:
1-The presence of inflammatory cells in the epithelial layer.
2-Basal zone hyperplasia exceeding 20% of the epithelial thickness.
3-Elongation of lamina propria papillae with congestion.
Clinical Features. Mainly seen in adults over age of 40 years, clinical manifestations consist principally of dysphagia; heartburn; and sometimes regurgitation of a sour brash, hematemesis, or melena. Rarely, chronic symptoms are punctuated by attacks of severe chest pain that may be mistaken for a heart attack. Complications of severe reflux esophagitis are Bleeding, development of stricture, and a tendency to develop Barrett esophagus.
BARRETT ESOPHAGUS Barrett esophagus is a complication of long-standing gastroesophageal reflux, occurring over time in up to 11% of patients with symptomatic reflux disease.
In Barrett esophagus, the distal squamous mucosa is replaced by metaplastic columnar epithelium, as a response to prolonged injury.
Barrett esophagus patients tend to have a long history of heartburn and other reflux symptoms and appear to have more massive reflux with more and longer reflux episodes than most reflux patients.
MORPHOLOGY. Gross appearance: Barrett esophagus seen grossly as a red, tongues or patches (islands) extending up from the gastroesophageal junction or as a broad circumferential band displacing the squamocolumnar junction. Microscopically the esophageal squamous epithelium is replaced by metaplastic columnar epithelium. The metaplastic mucosa may contain only gastric surface and glandular mucus-secreting cells.
Diagnosis is more readily made when the columnar mucosa contains intestinal goblet cells.
Critical to the pathologic evaluation of patients with Barrett mucosa is the search for dysplasia in columnar epithelium with intestinal metaplasia. Dysplasia is recognized by the presence of cytologic and architectural abnormalities extending to the luminal surface of the columnar epithelium.
These abnormalities consist of:
1- Enlarged, crowded, and stratified hyperchromatic nuclei.
2- Loss of intervening stroma between adjacent glandular structures.
Dysplasia is classified as low grade or high grade, with the predominant distinction being a basal epithelial orientation of all nuclei in low-grade dysplasia versus nuclei consistently reaching the apex of epithelial cells in high-grade dysplasia.
Persistent high-grade dysplasia demands clinical intervention. Clinical Features. In addition to the symptoms of reflux esophagitis, the clinical significance of Barrett esophagus relates to the secondary complications of local ulceration with bleeding and stricture. Of greatest importance is the development of adenocarcinoma that occurs at an estimated 30-fold to 40-fold increased rate over the general population.
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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