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Peptic Ulcer Disease and Related Disorders

Chapter 335 | Harrison's 22e

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[PAGE 2514] 2514 PART Disorders the Gastrointestinal System the need for diagnostic testing in most patients. When endoscopy is Shaheen NJ et al: Diagnosis and management of Barrett’s esophagus: performed, localized ulceration or inflammation is evident. Histologi- An updated ACG guideline. Am J Gastroenterol 117:559, 2022. cally, acute inflammation is typical. Chest CT imaging will sometimes Straumann A, Katzka DA: Diagnosis and treatment of eosinophilic reveal esophageal thickening consistent with transmural inflammation. esophagitis. Gastroenterology 154:346, 2018. Although the condition usually resolves within days to weeks, symp- Von Arnim U et al: Monitoring patients with eosinophilic esophagitis toms may persist for months and stricture can develop in severe cases. in routine clinical practice – international expert recommendations. No specific therapy is known to hasten the healing process, but antise- Clin Gastroenterol Hepatol 21:2526, 2023. cretory medications are frequently prescribed to remove concomitant reflux as an aggravating factor. When healing results in stricture forma- tion, dilation is indicated. FOREIGN BODIES AND FOOD IMPACTION Food or foreign bodies may lodge in the esophagus, causing complete obstruction, which in turn can cause an inability to handle secretions (foaming at the mouth) and severe chest pain. Food impaction may 335 Peptic Ulcer Disease occur due to peptic stricture, carcinoma, Schatzki ring, EoE, achala- and Related Disorders sia, or simply inattentive eating. If it does not resolve spontaneously, impacted food should be removed endoscopically. Use of meat ten- derizer enzymes to facilitate passage of a meat bolus is discouraged John Del Valle because of potential esophageal injury. Glucagon (1 mg IV) is some- times tried before endoscopic dislodgement. After emergent treatment, patients should be evaluated for potential causes of the impaction with PEPTIC ULCER DISEASE treatment rendered as indicated. A peptic ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due ESOPHAGEAL MANIFESTATIONS OF to active inflammation. Although burning epigastric pain exacerbated SYSTEMIC DISEASE by fasting and improved with meals is a symptom complex associated with peptic ulcer disease (PUD), it is now clear that >90% patients with SCLERODERMA AND CONNECTIVE this symptom complex (dyspepsia) do not have ulcers and that the TISSUE DISORDERS majority of patients with peptic ulcers may be asymptomatic. Ulcers Scleroderma esophagus (hypotensive LES and absent esophageal con- occur within the stomach and/or duodenum and are often chronic in tractility) was initially described as a manifestation of scleroderma or nature. Acid peptic disorders are very common in the United States, other collagen vascular diseases and thought to be specific for these with 4 million individuals (new cases and recurrences) affected per disorders. However, this nomenclature subsequently has been dis- year. Lifetime overall prevalence of PUD in the United States is ~8.4% carded because an estimated half of qualifying patients do not have an with a slightly higher prevalence in men. PUD significantly affects identifiable rheumatologic disease, and reflux disease is often the only quality of life by impairing overall patient well-being and contribut- identifiable association. When scleroderma esophagus occurs as a man- ing substantially to work absenteeism. Moreover, an estimated 15,000 ifestation of a connective tissue disorder, the histopathologic findings deaths per year occur as a consequence of complicated PUD. The are of infiltration and destruction of the esophageal muscularis propria financial impact of these common disorders has been substantial, with with collagen deposition and fibrosis and reduction in the number of an estimated burden on direct and indirect health care costs of ~$6 bil- interstitial cells of Cajal. The pathogenesis of absent peristalsis and LES lion per year in the United States, with $3 billion spent on hospitaliza- hypotension in the absence of a connective tissue disorder is unknown. tions, $2 billion on physician office visits, and $1 billion in decreased Regardless of the underlying cause, the manometric abnormalities pre- productivity and days lost from work. dispose patients to severe GERD due to inadequate LES barrier function combined with poor esophageal clearance of refluxed acid. Dysphagia may also be manifest but is generally mild and alleviated by eating in an I GASTRIC PHYSIOLOGY upright position and using liquids to facilitate solid transit. Gastric Anatomy The gastric epithelial lining consists of rugae DERMATOLOGIC DISEASES that contain microscopic gastric pits, each branching into four or A host of dermatologic disorders (lichen planus, pemphigus vulgaris, five gastric glands made up of highly specialized epithelial cells. The bullous pemphigoid, cicatricial pemphigoid, Behçet’s syndrome, and makeup of gastric glands varies with their anatomic location. Glands epidermolysis bullosa) can affect the oropharynx and esophagus, within the gastric cardia comprise <5% of the gastric gland area and particularly the proximal esophagus, with blisters, bullae, ulceration, contain mucous and endocrine cells. The 75% of gastric glands are webs, and strictures. Topical or systemic anti-inflammatory therapy found within the oxyntic mucosa and contain mucous neck, parietal, is effective for mucosal healing. Stevens-Johnson syndrome and graft- chief, endocrine, enterochromaffin, and enterochromaffin-like (ECL) versus-host disease can also involve the esophagus. Esophageal dilation cells (Fig. 335-1). Highly specialized tuft cells are located in the neck may be necessary to treat strictures. region of the gastric gland. These specialized cells are thought to sample luminal contents, which in turn may be important in regulating FURTHER READING gastric acid secretion. Pyloric glands contain mucous and endocrine Hirano I et al: American Gastroenterological Institute and the joint cells (including gastrin cells) and are found in the antrum. task force on allergy-immunology practice parameters clinical guide- The parietal cell, also known as the oxyntic cell, is usually found in lines for the management of eosinophilic esophagitis. Gastroenterol- the neck or isthmus or in the oxyntic gland. The resting, or unstimu- ogy 158:1776, 2020. lated, parietal cell has prominent cytoplasmic tubulovesicles and intra- Kahrilas PJ et al: Advances in the management of oesophageal motil- cellular canaliculi containing short microvilli along its apical surface ity disorders in the era of high-resolution manometry: A focus on (Fig. 335-2). H+,K+-adenosine triphosphatase (ATPase) is expressed achalasia syndromes. Nat Rev Gastroenterol Hepatol 15:323, 2018. in the tubulovesicle membrane; upon cell stimulation, this membrane, Katzka DA, Kahrilas PJ: Advances in the diagnosis and manage- along with apical membranes, transforms into a dense network of api- ment of gastroesophageal reflux disease. BMJ 23:371, 2020. cal intracellular canaliculi containing long microvilli. Acid secretion, a Katzka DA et al: Phenotypes of gastroesophageal reflux disease: process requiring high energy, occurs at the apical canalicular surface. Where Rome, Lyon, and Montreal meet. Clin Gastroenterol Hepatol Numerous mitochondria (30–40% of total cell volume) generate the 18:767, 2020. energy required for secretion. [PAGE 2515] Peptic Ulcer Disease and Related Disorders 2515 CHAPTER 335 Surface cells Corpus gland (MUC5AC) Progenitor cells Pit (foveolus) Mucous neck cells (MUC6, TFF2) Human Parietal cells Isthmus ( I / I - IIII s I ) D cells (Somatostatin) Corpus ECL cells Neck (Histidine decarboxylase) EC cells (Serotonin) Antrum X Cell (Ghrelin) Base Chief cells (MIST1, PGC) Mouse Antral gland Surface cells (MUC5AC) G cells (Gastrin) Corpus D cells Pit (Somatostatin) Antrum ECL cells (Histidi