Chapter 14

Geriatric GI Tract Physiology Colette LaSalle, PhD, RD San Jose State University Several subtle alterations in gastric physiology occur with aging. These changes can reduce overall gastrointestinal function, increase the risk of malabsorption, and affect both intake and output. Oral Cavity The oral cavity is affected by aging in several ways; for example, dental status is often impaired as teeth are ground down or lost, and mouth sores or ulcers from poorly fitting dentures are not uncommon. Dry mouth is a frequent com- plaint that results from decreased basal saliva production or as a side effect of medications commonly taken in this population such as anticholinergics (e.g., antidepressants, bronchodilators, and antihistamines) and diuretics. The resulting xerostomia can reduce oral intake in addition to contributing to periodontal disease and poor dental status. Swallow function is not affected as a direct consequence of aging, but a sense of impairment may occur given decreased saliva production. Olfactory and taste perceptions may also decline with age, decreasing the pleasure of eating and thus contributing to suboptimal intake. Esophagus Possible changes in the esophagus include decreased upper esophageal sphincter pressure, diminished sensory perception, and weaker, less coordinated peristaltic contractions. Stomach Physiological changes in the stomach include gastric atrophy, altered enzymatic function, and decreased secretion of pepsin, HCl, and mucus. Low levels of HCl temperature. Dental caries can also lead to death of the nerve and blood vessels in the tooth, resulting in severe pain. Individuals at Risk for Dental Disease As stated earlier, approximately 7% of Americans over age 65 do not have their natural teeth. Additionally, the Centers for Disease Control and Prevention reports that one-third of adults over age 65 have untreated dental caries and approximately 40% have peridontal disease.11 Dental caries, tooth loss, and ill-fitting dentures may contribute to inadequate or improper intake of nutrients. At the same time, malnutrition and weight loss may contribute to the poor fit for dentures and loss of teeth. Individuals who have difficulty chewing or who are edentulous may rely on soft foods of limited variety, resulting in an inad- equate nutrient intake.12 Other medical conditions may be associated with increased dental caries. Eating disorders are frequently linked with dental disease. In bulimia nervosa, for example, the exposure to gastric juices during repetitive vomiting contributes to the demineralization of the teeth.13 impede the ability to break protein bonds and to absorb vitamin B12 and calcium, while impaired enzymatic action can lead to intolerance of certain food components (such as lactose) and malabsorption. Additionally, though the basal level of the satiety-inducing hormone cholecystokinin (CCK) tends to be higher, the stimulated release of the hormone is also increased, resulting in early satiety. Small Intestine While some physiological changes such as altered villi shape, mucosal atrophy, and decreased blood supply due to vascular changes affect the small intestine, overall, these changes are subtle and its function is maintained with age. However, older adults are at risk of malabsorption secondary to these changes, especially in the presence of other factors such as bacterial overgrowth, celiac disease, or pancreatic insufficiency. Large Intestine Constipation is one of the most common complaints among older adults. This may be due to changes in the enteric nervous system and pelvic floor dysfunction, but is likely related more to factors such as use of medications, presence of chronic disease, lack of physical activity, and a low-fiber diet. References D'Souza AL. Ageing and the gut. Postgrad Med J. 2007; 83(975): 44-53. Poh CH, Navarro-Rodriguez T, Fass R. Review: treatment of gastroesophageal reflux disease in the elderly. Am J Med. 2010; 123(6): 496-501. Rayner CK, Horowitz M. Physiology of the ageing gut. Curr Opin Clin Nutr Metab Care. 2013; 16(1): 33-38. Timiras PS, ed. Physiological Basis of Aging and Geriatrics. 4th ed. Boca Raton, FL: CRC Press; 2007: 319-21. Infants and children are also considered to be at high risk for dental disease. "Baby bottle tooth decay" can occur when an infant falls asleep with a bottle containing a high- sugar beverage such as fruit juice or infant formula. During sleep, the beverage may pool in the mouth, contributing to widespread caries. Cavities usually form on upper front teeth and back molars. It is recommended that bottles be removed from a child's mouth during sleep and that infants be weaned from a bottle starting at 12 months of age. Other preventions include brushing a child's teeth as soon as they erupt, or wiping them with a wet cloth. A child's first dental examination should occur by the end of his or her first year.10 Prevention of Dental Disease Prevention of dental caries focuses on both nutrition and public health interventions. Fluoridation of water supplies, use of topical fluoride treatments, and use of dental sealants are primary methods of preventing dental caries. Fluoride ingested when teeth are developing is incorporated into the structure of the enamel and protects it against the action of acids. Topical fluoride

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Nutrition Interventions for Xerostomia

try tart food Sip on liquids or suck on ice chips throughout the day. • Avoid caffeine, alcohol, and tobacco products. • Try using a cool mist humidifier at bedtime. • Try drinking through a straw. • Rinse mouth frequently with mild saline solution. • Add extra sauces and gravies to foods.

and sealants also provide protection for the outer covering of the tooth. Nutritional choices can play a role in the prevention of dental disease. Some foods, such as cheese, serve as a buffer that prevents decreases in pH and resulting demineralization.14,15 Sugar alcohols such as xylitol are used to sweeten products such as chewing gum, toothpaste, and mouth- washes. These carbohydrates are not metabolized by bacteria in the mouth, and current research indicates that xylitol may have an additional antimicrobial effect against dental caries. Other foods that have been identified as containing anticaries components include red grape seeds, green tea, nutmeg, apples, cranberries, chicory, and roasted coffee, all of which have demonstrated antibacterial activity against the common bacterial strains implicated in dental caries.15 The following recommendations can assist in the prevention of dental caries: • Choose fiber-rich vegetables and whole grains often. • Choose and prepare foods and beverages with little added sugars or caloric sweeteners. • Rinse the mouth after meals and snacks. • Chew sugarless gum with xylitol after meals. • Practice good oral hygiene. • Consume sugar- and starch-containing foods and beverages less frequently. 350 Part 4 Nutrition Therapy Inflammatory Conditions of the oral Cavity It is not uncommon for patients to suffer from inflammatory conditions of the mouth. When the mouth is inflamed or infected, maintaining oral intake is very difficult. Inflammatory conditions may result from poor dental hygiene and lack of dental care, and can also develop in persons who are immunosuppressed or who have undergone chemotherapy or radiation therapy. Gingivitis is an inflammation of the gingiva (gums). In gingivitis, the gums appear red and swollen and often bleed; the tissue is very tender and painful. Other symptoms include fever, loss of appetite, foul breath, and a bad taste in the mouth. Stomatitis or mucositis (see Figure 14.5) is inflammation of the oral mucosa and is often associated with fungal infections such as Candida albicans or with herpes-like viruses. It is common in stomatitis to have open ulcerations on the oral mucosa, gingiva, and palate. Nutritional strategies for indi- viduals with stomatitis are presented in Table 14.4.16 Glossitis and cheilosis are inflammatory symptoms of the oral cavity classically associated with vitamin deficien- cies. Glossitis involves increased redness, swelling, and pain of the tongue and lips. Cheilosis is fissuring and scaling at the corners or angles of the mouth (see Figure 14.6). Both cheilosis and glossitis may be a sign/symptom of riboflavin, folate, niacin, pyridoxine. vitamin B12, or iron deficiency.4 Conditions Resulting in Altered Salivary Gland Function The importance of saliva production in ensuring normal chewing and swallowing is emphasized above (see the section "Oral Cavity Secretions"). In many clinical conditions and with the use of numerous medications, saliva production may be altered, resulting in decreased oral intake and ultimately placing the patient at nutritional risk. Xerostomia may result from either a disease process or a medical treatment (see Table 14.5). Infection or dam- age to salivary glands through surgical resection or radiation

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produce mucus to facilitate movement of the bolus during swallowing. The muscle layer consists of both longitudinal and circular muscles that coordinate movement of the food bolus by alternately contracting. This "squeezing" contrac- tion easily moves the bolus down the esophagus. The outer layer (or adventitia) of tissue for the esophagus is connective tissue and has no additional outer covering. The chief function of the esophagus is motility. Its pri- mary task—transporting the bolus of food from the oral cav- ity to the stomach—sounds simple, yet several disorders of the upper GI tract actually involve derangements in this task. An individual unconsciously swallows over 600 times each day. Each swallow is composed of four phases. The first phase, described previously, is the oral preparatory phase where food is chewed and mixed with saliva. The second phase or oral transit phase was also described previously and consists of voluntary movement of the bolus of food from the front of the oral cavity to the back. The third phase of swallowing is known as the pharyngeal phase. The most important part of this phase is to ensure the bolus is directed into the esophagus and is prevented from entering the tra- chea. This is initially accomplished when the uvula seals off the nasal passage so food does not leak into the nose. Next, laryngeal muscles contract and seal off the glottis (entrance to the larynx). The epiglottis also tilts upward to assist in pre- venting food from entering the larynx. The final phase of swallowing is the esophageal phase. The upper esophageal sphincter (UES) is located at the top of the esophagus. This sphincter, when open, allows the bolus to enter the esophagus. When the sphincter is closed, it pre- vents air from entering the GI tract during breathing. After the bolus of food moves through the UES into the esophagus, the sphincter closes and normal breathing will resume. When the esophageal phase of swallowing begins, auto- nomic control initiates the peristaltic wave that moves the bolus of food down the esophagus into the stomach (see Figure 14.3). Mucus secreted by the esophagus lubricates the food bolus and aids in its successful passage. At the end of the esophagus, another sphincter muscle—the lower esophageal sphincter (LES)—controls release of the bolus from the esophagus into the stomach. This sphincter is closed except during swallow- ing. It serves as a barrier to protect the esophageal mucosa from stomach contents. Atmospheric pressure is greater in the esophagus than in the stomach under normal conditions. This positive pressure of approximately 30 cm H2O assists in pre- venting stomach contents from refluxing back into the esopha- gus and preventing large amounts of air from entering the stomach. (Gastric pressure is approximately 10 cm H2O.) Two major neurotransmitters, nitric oxide and VIP, are responsible for allowing the LES to relax: they inhibit closure of the LES, allowing it to relax so that the bolus slides from the esopha- gus into the stomach. They oppose the stimulatory action of acetylcholine. The swallow is complete when the bolus of food moves through the LES. Pharyngeal and esophageal phases of swallowing take only 6-10 seconds under normal conditions. If for some reason all food is not cleared from the esophagus, secondary peristaltic waves are initiated. This might occur when a sticky substance that does not move as readily down the esophagus is eaten. The individual, in this case, would usually be unaware of these secondary peristaltic waves.3,5,6 346 Part 4 Nutrition Therapy Figure 14.3 Peristalsis in the Esophagus Bolus Ringlike peristaltic contraction sweeping down the esophagus Source: L. Sherwood, Human Physiology: From Cells to Systems, 5e, copyright © 2004, p. 603. Normal Anatomy and Physiology of the Stomach The final portion of the upper GI tract is the stomach (see Figure 14.4). This organ lies from left to right across the upper abdomen directly under the diaphragm. Portions of the stomach (fundus, corpus, antrum, and pylorus) differ by anatomy and function. Sphincters at both ends of the stomach regulate the flow of foodstuffs from the esophagus to the small intestine. Major functions of the stomach include all four digestive processes: motility, secretion, digestion, and absorp- tion. The anatomy of the stomach plays an important role in protecting the gastric mucosa from the constant flow of

substances that are potentially toxic to its cells. Hydrochloric acid, pepsin, and bile as well as medications and alcohol can all damage the mucosa and, as this chapter explains, this con- tributes to the pathophysiology of gastritis and peptic ulcer disease. The healthy stomach provides several lines of defense against these toxins, including an unstirred mucus-water layer providing a physical barrier to hydrogen ions and other sub- stances; epithelial cells that secrete bicarbonate and maintain intracellular pH; and a complex mechanism of cellular repair that includes specific growth factors and angiogenesis.3,5 Gastric Motility Gastric motility includes filling of the stomach, storage of foodstuffs, mixing with gastric juices, and finally emptying into the small intestine. When empty, the stomach's volume is only about 50 mL, but it can stretch to hold more than 1000 mL. Storage occurs primarily in the body (corpus) of the stomach. Mixing occurs in the antrum, where the muscle is much thicker and can accommodate the strong peristaltic waves. Each peristaltic wave moves foodstuffs toward the pyloric sphincter at the bottom of the stomach. Rate of gastric emptying through the pyloric sphincter into the upper portion of the small intestine is controlled by the anatomical structure of the stomach, nutrient content of the foodstuffs, the nervous system, and the influence of specific hormones. Gastric Secretions The stomach secretes approximately 1-3 liters of gastric juices each day. Gastric juice is composed of water, mucus, hydrochloric acid, enzymes, and electrolytes. The mucosa, which lines the fundus and the body of the stomach, contains gastric glands. Several different types of cells are located within the gastric glands. The mucous cells secrete mucus, which protects the lining of the stomach from mechanical or acid insult. (Note that mucus is a noun and refers to the secretion itself; mucous is an adjective used to describe nouns associated with mucus.) Chief cells secrete the zymogen pepsinogen and the enzyme gastric lipase. (Recall that a zymogen is an inactive enzyme.) Pepsinogen, when activated, begins protein digestion. Gastric lipase ini- tiates some preliminary digestion of lipids. Parietal cells secrete hydrochloric acid and intrinsic factor. Hydrochloric Table 14.2 Control of Gastric Secretions The Stomach Mucosa and the Gastric Glands acid serves to activate pepsinogen, kill microorganisms, and denature proteins. Intrinsic factor is a protein necessary for the absorption of vitamin B12. In the pylorus, enterochromaf- fin (ECL) cells secrete histamine, G cells secrete gastrin, and D cells secrete somatostatin. All three of these substances assist in overall control and production of gastric secretions. Control of Gastric Secretions Control of gastric secretions is accomplished through complementary actions of the nervous and endocrine systems, and involves four major chemical messengers: acetylcholine, histamine, and gastrin, which stimulate gastric secretions, and somatostatin, which inhibits gastric secretions (see Table 14.2). Acetylcholine is a neurotransmitter that stimulates parietal, chief, and ECL cells. Histamine, a paracrine, acts on parietal cells to increase hydrochloric acid (HCl) release. Gastrin, a hor- mone, stimulates chief and parietal cells as well as ECL cells to release histamine. Somatostatin works as an inhibitory paracrine by providing negative feedback to the stimulatory pathways. When gastric pH falls (becomes more acidic), somatostatin acts on each of the stimulatory mechanisms to slowly decrease gastric secretions. All stimulatory pathways for production of HCl work in similar ways. The enzyme H1, K1-ATPase drives production of hydrogen ions (H1 ). Gastrin, acetylcholine, and histamine act to increase the amount of H1 available for the formation of HCl within the parietal cells. Many medications designed to decrease gastric acidity work at this cellular level to either prevent production of stimulatory factors or block transport of H1 needed for production of HCl. This is discussed in more detail in the sections on gastroesophageal reflux disease and peptic ulcer disease. Release of Gastric Secretions Gastric secretions are produced even before food enters the stomach and serve to prepare the stomach for its eventual role in digestion. Thus, release of gastric secretions in response to a meal is divided into three phases: cephalic, gastric, and intestinal phases. The cephalic ("head") phase refers to release of HCl and pepsinogen when stimulated by tasting, smelling, or even seeing food. The gas- tric phase begins when food enters the stomach. Both the

Dysphagia severity scale

1-Minimal dysphagia—video swallow shows slight deviance from a normal swallow. Patient may report a change in sensation during swallow. No change in diet is required. 2 Mild dysphagia—oropharyngeal dysphagia present, which can be managed by specific swallow suggestions. Slight modification in consistency of diet may be indicated. 3 Mild-moderate dysphagia—potential for aspiration exists but is diminished by specific swallow techniques and a modified diet. Time for eating is significantly increased; thus, supplemental nutrition may be indicated. 4 Moderate dysphagia—significant potential for aspiration exists. Trace aspiration of one or more consistencies may be seen under videofluoroscopy. Patient may eat certain consistencies by using specific techniques to minimize potential for aspiration and/or to facilitate swallowing. Supervision at mealtimes required. May require supplemental nutrition orally or via feeding tube. 5 Moderately severe dysphagia—patient aspirates 5% to 10% on one or more consistencies, with potential for aspiration on all consistencies. Potential for aspiration minimized by specific swallow instructions. Cough reflex absent or nonprotective. Alternative mode of feeding required to maintain patient's nutritional needs. If pulmonary status is compromised, "nothing by mouth" may be indicated. 6 Severe dysphagia—more than 10% aspiration for all consistencies. "Nothing by mouth" recommended.

Nutrition Interventions to Reduce Nausea and Vomiting table on 364

1. Liquids to try after vomiting has stopped: Source: © Cengage Learning. • Water • Applejuice • Sportsdrink • Warmorcoldtea • Lemonade Instructions First suck on ice chips if over 3 years of age. If tolerated, start with 1 tsp (5 g) every 10 minutes. Increase to 1 tbsp (15 g) every 20 minutes. Double the amount of fluid every hour. Progress to the other liquids as tolerated. If diarrhea is present, use only rehydration beverage. 2. Solid Food Introduction When there has been no vomiting for at least 8 hours, start oral intake slowly by adding one solid food at a time in very small increments. Avoid food that is high in fat or fiber as well as food that has a strong odor or is gas producing. The use of ginger to treat nausea and vomiting may help. Take medications after eating. Foods Recommended for Initial Introduction of Solid Food Grains Dry toast, crackers, pretzels, rice or rice cereal, potato Milk and dairy products Yogurt, sherbet Meat, poultry, and fish Clear broths, baked chicken, eggs

Monitoring and Evaluation Depending on the origin of the patient's dysphagia, tolerance of an oral diet may improve with treatment. The registered dietitian, with the other health care team members, will reevaluate the ability of the patient to progress in use of the prescribed diet. If problems arise, Figure 14.9 Dysphagia Products Can you tell that the foods in this photo are pureed foods shaped with commercial thickeners? Source: S. Rolfes, K. Pinna and E. Whitney, Understanding Normal and Clinical Nutrition, 7e, copyright © 2006, p. 719. 362 Part 4 Nutrition Therapy the diet may also need to be further restricted or changed in texture or consistency. Patients' weight, nutritional parameters, and hydration should be monitored closely to ensure adequacy of nutritional intake. Hiatal Hernia Hiatal hernia is a condition where the upper portion of the stomach protrudes through the esophageal hiatus into the thoracic cavity. Most cases of hiatal hernia are designated as type 1 (sliding), where both the LES and some portion of the upper stomach protrude through the esophageal hiatus or diaphragm into the chest (see Figure 14.10). In type 2 (rolling hiatal hernia), the LES remains below the diaphragm. Incidence of hiatal hernia increases with age. Any factor that increases intra-abdominal pressure, such as obesity or preg- nancy, will also increase the risk of hiatal hernia. Symptoms of hiatal hernia are consistent with those of GERD. First-line interventions, both medically and nutrition- ally, are the same as those previously discussed for GERD. Some patients require surgical repair of the hernia. In this procedure, which may be performed conventionally or laparoscopically, the surgeon retracts the hernia and repairs the hole in the diaphragm. Fundoplication (previously described

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Prolonged nausea and vomiting can have significant clinical consequences. Forceful vomiting can either rupture the esophagus (Boerhaave's syndrome) or tear the lower esophageal sphincter (Mallory-Weiss tear). Bleeding or hematemesis is a serious outcome of these injuries. Continued vomiting can also result in dehydration and acid-base imbalances. Malnutrition can be a long-term consequence for the patient if he or she is not able to ingest an adequate diet for a pro- longed amount of time. If gastric contents are aspirated into the lungs, aspiration pneumonia is a likely result. Sample PES statement: Inadequate oral intake related to nausea and vomiting as evidenced by ,300 kcal ingestion for previous 48 hours reported by patient and nursing records. Nutrition Therapy for Nausea and Vomiting Nutritional Implications Nausea and vomiting can result in inadequate nutrient intake, dehydration, and acid-base imbalances, and over time can lead to learned food aversions. This is similar to anticipatory nausea and vomiting. When a negative consequence is linked to a particular food, most people choose to avoid eating that food. Nutrition Diagnosis Nutrition diagnoses secondary to nausea and vomiting may include altered GI function; involuntary weight loss; inadequate fluid intake; and inadequate oral intake. Nutrition Intervention Nutrition therapy does not necessarily treat nausea and vomiting but can minimize symptoms and discomfort. Appropriate nutrition therapy can assist in maintaining nutritional status during periods of nausea and vomiting. If patients can manage oral intake, foods that are cold and have minimal smell usually are best tolerated. Table 14.15 outlines suggestions for foods and food-related activities that may reduce nausea and vomiting. Close monitoring of hydration status and length of time that the patient is without adequate oral intake will be crucial in preventing long-term nutritional consequences. Nutrition support will be necessary for those individuals who are unable to meet their nutritional needs orally.

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Gastritis Definition Gastritis is inflammation of the gastric mucosa. This condition is not a discrete disorder, as it may result from numerous conditions. Gastritis is generally classified as acute or chronic. Etiology Acute gastritis is typically related to infection, which may be viral, bacterial, fungal, or parasitic in nature. Acute gastritis can also occur with food poisoning, alcohol ingestion, or medications such as nonsteroidal anti- inflammatory drugs (NSAIDs). Chronic gastritis is further classified as Type A or Type B but, in reality, it is often difficult to distinguish the two clinically. Type A is a condition often related to pernicious anemia. Pernicious anemia has an autoimmune component whereby antibodies are formed against parietal cells and achlorhydria results. This may lead to vitamin B12-deficiency anemia because intrinsic factor, which is produced in the parietal cells, is necessary for absorption of vitamin B12. (See Chapter 19). Type B chronic gastritis is the more common condition and is related to H. pylori infection.53,54 Pathophysiology Under normal conditions, the gastric mucosa is well protected against injury. The production of mucus provides a barrier that prevents damage to the cells, and their high turnover rate allows for efficient recovery from injury. Prostaglandins also assist in support of the mucosal defense by stimulating mucus production, inhibiting acid pro- duction and release, and regulating blood flow to the mucosal cells. When infection or trauma interrupts these protective mechanisms, an acute inflammatory condition initiates. Thus, acute gastritis is due to the localized inflammatory state of the gastric mucosa. By blocking prostaglandin release, NSAIDs assist in control of inflammation but may also inhibit their protective function for the gastric mucosa, leading to gastritis. Generally, acute gastritis is short lived and causes no long- term problems. In chronic gastritis, initially only the surface mucosa is affected but as time progresses, inflammation deep- ens to other layers of the gastric mucosa and damages the gas- tric glands, causing gastric atrophy.53,54 Symptoms of gastritis can include belching, anorexia, abdominal pain, vomiting, and, in the more severe cases, bleeding and hematemesis. Medi- cal treatment for gastritis includes identifying and treating the cause; for example, an antibiotic and medication regimen may be used to treat infections caused by H. pylori that are responsible for gastritis. Medications that reduce acid secretions may also be used. Alternative anti-inflammatory medications rather than NSAIDs are prescribed. See Tables 14.16 and 14.17 for lists of these medications. Peptic Ulcer Disease Definition Peptic ulcer disease (PUD) involves ulcerations of the gastric or duodenal mucosa that penetrate the submucosa (see Figure 14.11). They usually occur in the antrum of the stomach or in the first few centimeters of the duodenum. Erosion may proceed to other levels of tissue and can eventually perforate. Breakdown in the tissue allows for continued insult by the highly acidic environment of the stomach as well as damage from other secretions of the stomach, such as pepsin.55,56 Figure 14.11 Peptic Ulcer Disease Copyright 2016 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. Source: BSIP SA/Alamy. Epidemiology In the United States, 15.5 million people were diagnosed with PUD in 2011. PUD accounted for over 600,000 health care visits and over 350,000 hospitalizations.22 Historically, the epidemiology of PUD was redefined after H. pylori was recognized as a pivotal factor in development of gastric and duodenal ulcers. It is estimated that 92% of duodenal ulcers and 70% of gastric ulcers are caused by H. pylori. Nonetheless, there are still quite a large number of individuals who suffer from ulcer disease and are not infected with H. pylori.53 This section describes the role of H. pylori and other factors that have been correlated to the development of PUD. Etiology Helicobacter pylori is a spiral-shaped, flagellated, Gram-negative rod that lives under the mucous layer of the stomach and attaches to mucus-secreting cells lining the stomach. Many individuals (30%-60% in developed countries) are positive for H. pylori but most do not develop PUD or any other clinical signs or symptoms associated with this bacteria. The potential for complications from H. pylori depends on the individual's immune response, the strain of H. pylori, and other environmental differences.57 H. pylori organisms break down urea to produce ammonia, which helps neutralize acid in the immediate vicinity of these bacteria and enhances their survival. The H. pylori organisms subsequently produce various proteins that may damage mucosal cells, attracting lymphocytes and causing persistent inflammation. By-products released by the organism result in damage to the epithelium and impair the mucous barrier within the stomach. H. pylori has also been linked to gastric malignancies such as adenocarcinoma and lymphoma. Additional etiology of PUD also involves factors that may decrease mucosal integrity, such as a reduction of protective prostaglandins through the use of NSAIDs (e.g., ibuprofen) or alcohol, excessive glucocorticoid secretion or steroid medication, and factors that decrease the blood sup- ply, such as smoking, stress, or shock. Factors that increase acid secretions, including rapid gastric emptying or increased gastrin secretions, also contribute to the development of PUD. The genetic link to PUD has also been explored; ulcers

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are approximately three times more common in first-degree relatives than in the general population. This may be related to an increased susceptibility to infection from H. pylori.53,56,57 Clinical Manifestations The most common symptom related to PUD is epigastric pain, but this pattern is not con- sistent. In general, patients will complain of abdominal pain and a burning sensation, which may be precipitated by certain types of foods or accentuated by food intake. For others, epi- gastric pain may be relieved by food intake due to its ability to dilute any irritants. For a duodenal ulcer, pain characteristi- cally occurs from 90 minutes to 3 hours after eating, and is usually relieved within minutes either by eating or by use of antacids. Unfortunately, partial neutralization of gastric acid is followed by a rebound of gastrin release, causing additional stimulation of HCl and probably more pain.53 The presence of blood in stool or vomit may be indicative of active bleed- ing from the ulcer. Changes in hematological indices such as hemoglobin or hematocrit will also be indicative of active bleeding. If there is an active infection, changes in white blood cell counts will be consistent with the inflammatory process. Diagnosis The same diagnostic procedures that have been discussed earlier in this chapter will allow for a definitive diag- nosis of PUD. Endoscopy coupled with a tissue biopsy permits visualization of the ulcer and confirmation of H. pylori infec- tion. Less invasive testing for H. pylori includes the C-urea breath test, stool antigen test, and serum testing for antibod- ies. At present, the most accurate and reliable test for both diagnosis and follow-up is the urea breath test.57 Treatment Treatment of peptic ulcer disease associated with H. pylori infections includes regimens of three to four medica- tions (triple/quadruple therapy). The recommended therapy involves a 7- to 14-day course of two antibiotics and one of the proton pump inhibitors. Eradication rates associated with tri- ple/quadruple therapy range from 86% to 98% if patients com- ply with the treatment regimens (see Table 14.16). However, the frequency of adverse effects such as nausea, vomiting, and abdominal pain associated with these regimens significantly hinders patient compliance and often the 7-day treatment is recommended.53,57 Other treatment for PUD focuses on use of medications to suppress acid secretion, which will ultimately promote healing of the ulceration (see Table 14.17). These medica- tions, as discussed in the section on treatment for GERD, include antacids, proton pump inhibitors, histamine blocking agents, prokinetic agents, and mucosal protectants. Table 14.16 Examples for FDA-Approved Treatment Options for Eradication of H. pylori Infection 1. Omeprazole 1 clarithromycin 1 metronidazole (14 days) Source: Atherton JC. Helicobacter pylori infections. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. 366 Part 4 Nutrition Therapy Table 14.17 Drugs Used in Treatment of Peptic Ulcer Disease Antibiotics Metronidazole, tetracycline, clarithromycin, amoxicillin Antacids Mylanta, Maalox, Tums, Gaviscon H2 blockers Cimetidine, ranitidine, famotidine, nizatidine Proton pump inhibitors Omeprazole, esomeprazole, lansoprazole, rabeprazole, pantoprazole, dexlansoprazole Cytoprotective agents Sucralfate, prostaglandin analogue (Misoprostol), bismuth subsalicylate Source: © Cengage Learning. For those patients who are refractory to treatment or who suffer from complications such as hemorrhage, perfora- tion, or gastric outlet obstruction, surgical resection may be necessary (discussed later in this chapter). Nutrition Therapy for Peptic Ulcer Disease Nutritional Implications and Assessment Among patients with PUD, symptomatic abdominal pain can impair oral intake and result in weight loss and/or nutrient imbal- ances. Therefore, it is important to obtain as much informa- tion as possible regarding weight and dietary intake changes and to evaluate this data in the context of the medical history of abdominal pain and symptoms. Nutrition Diagnosis Nutrition diagnoses associated with peptic ulcer disease include inadequate beverage intake; altered GI function; involuntary weight loss; and food- and nutrition-related knowledge deficit. Nutrition Intervention For several decades, dietary fac- tors have gained and lost favor as a significant component in both the cause and treatment of peptic ulcers. Currently, goals for nutrition therapy include supporting medical treatment, maintaining or improving nutritional status, and providing a diet that minimizes symptoms of PUD. There are no data indi- cating that diet is a causative factor for PUD.53,55 Current nutrition therapy for PUD (see Table 14.18) includes recommending a trial of restriction of foods that may increase acid secretion or cause direct irritation to gastric mucosa. These foods include black and red pepper, caffeine, coffee (including decaffeinated), and alcohol. Additionally, it is recommended that patients avoid any foods they do not individually tolerate. Historically, milk and cream were used to treat PUD, but it is now known that their consumption increases both gastrin and pepsin secretion. Furthermore, the pH of a food prior to its consumption has little effect after it is consumed. Restricting acidic juices or other foods is not consistently warranted unless the patient identifies intoler- ance to them. Other components of MNT will include timing and size of meals. Patients should not lie down after eating and avoid eating large meals close to bedtime. Smaller, more frequent meals may be better tolerated. Micronutrients of concern may include iron, calcium, and B12, as previously discussed in this chapter. The need for additional supplementation should be evaluated for each client individually.

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Monitoring and Evaluation Follow-up for the patient with PUD will focus on adequacy of the patient's nutritional intake and tolerance to the oral diet. Normal nutrition assessment indices will be monitored to ensure maintenance of nutritional status. Gastric Surgery When peptic ulcer disease does not respond adequately to medical treatment, or when the patient experiences a complication of PUD, surgery is often the next step. Complications from PUD may include hemorrhage, perforation, or obstruction of the pyloric sphincter. The decision to perform surgery is based on the patient's current medical status and prior surgical history. The same procedures are used for surgical resections required for other diagnoses such as gastric malignancy. Vagotomy The purpose of the vagotomy is to eliminate the cholinergic stimulation of the stomach. Selective vagotomy eliminates innervations from the vagus nerve to parietal cells, resulting in decreased acid production and a decreased response to gastrin. Other functions of the vagus nerve remain intact, and the normal pathway for gastric emptying and peristalsis continues. In many patients, total vagotomy with pyloroplasty is chosen. In this procedure, innervations to the parietal cells are severed, and the portion of the vagus nerve controlling gastric emptying is also eliminated. Pyloroplasty enlarges the pyloric sphincter. Gastric resection is also an option depending on the location of the ulcer and extent of the stomach that requires removal. Reconstruction after pyloroplasty or gastric resection will generally use one of three procedures: a gastroduodenostomy (Billroth I), gastrojejunostomy (Billroth II), or Roux-en-Y procedure (see Figure 14.12).

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Gastroduodenostomy (Billroth I), Gastrojejunostomy (Billroth II), and Roux-en-y Procedure Figure 14.12 and Figure 12.7 (in Chapter 12) illustrate these types of surgery. In the procedure gastroduodenostomy, or Billroth I, a partial gastrectomy or pyloroplasty is performed with a reconstruc- tion that consists of an anastomosis of the proximal end of the duodenum to the distal end of the stomach. A gastrojejunostomy, or Billroth II, is a partial gastrectomy with a recon- struction that consists of an anastomosis of the proximal end of the jejunum to the distal end of the stomach. In this surgical procedure, a blind loop of the duodenum is created. The Roux-en-Y procedure accomplishes the same thing as the Billroth II but creates a very small pouch after the gastric resection and connects the jejunum to the upper portion of the stomach. Although the Roux-en-Y procedure (or gastric bypass) has most recently featured prominently as a treatment for morbid obesity, it originated as a treatment for PUD and other gastric diseases.53 Nutrition Therapy for Gastric Surgery Nutritional Implications Nutritional risk is due to reduced capacity of the stomach and potential changes in gastric emptying and transit time when the normal pathway for digestion and absorption is interrupted. Additionally, when portions of the stomach are resected, valuable components of digestion may be altered or lost. These issues combine to place the patient at significant nutritional risk due to decreased oral intake, maldigestion, and/or malabsorption. Additional nutrition concerns include the potential for vitamin and mineral deficiencies. Deficiencies of thiamin, vitamin B12, vitamin D, iron, and copper have been documented.58-60 With changes in gastric anatomy, intrinsic factor secretion may be reduced or absent. This prevents normal B12 absorption and leads to a subsequent deficiency. Research has confirmed that patients who have had gastric surgery have a high prevalence of vitamin B12 deficiency. Treatment of the defi- ciency can prevent cardiovascular, hematologic, and neurologic abnormalities seen with B12 deficiency or pernicious anemia. Levels of methylmalonic acid and homocysteine are measured in addition to serum B12 to determine deficient levels, but it is also standard practice to prescribe prophylactic B12 injections for these patients. Iron deficiency is also common. The cause is multifactorial, including a decrease in HCl, decreased dietary intake, and possible malabsorption. Risk of osteoporosis is also increased due to decreased absorption of calcium. It is recommended that both calcium and vitamin D supplements be prescribed for these patients.60 Dumping Syndrome One of the most common complications after gastric surgery is dumping syndrome. Dumping syndrome occurs when an increased osmolar load enters the small intestine too quickly from the stomach. Severity of the symptoms varies depending on the extent of gastric surgery and the overall change in gastric emptying. When the stomach is removed or partially resected, important steps in digestion are missed. As discussed earlier, in a healthy person food may remain in the stomach anywhere from 1 to 3 hours as it becomes liquefied and partially digested. It then enters the duodenum via the pyloric sphincter slowly, so the acidic chyme is neutralized by pancreatic bicarbonate. When the pyloric portion of the stomach is removed, bypassed, or destroyed, the rate of gastric emptying is increased. Additionally, when the duodenum is bypassed, feedback inhibition is lost. Furthermore, surgery will affect the release of hormones, enzymes, and other secretions. If stomach function is altered (as it is in gastric resections), food "dumps" into the small intestine (see Figure 14.13). Because the chyme is hyperosmolar, fluid is drawn into the small intestine from the vascular compartment in an attempt to dilute intestinal contents. These processes result in cramping, abdominal pain, hypermotility, and diarrhea. Furthermore, fluid changes in the vascular compartment result in dizziness, weakness, and tachycardia. These symptoms constitute what is generally referred to as "early" dumping syndrome, which actually occurs within 10-20 minutes after eating. "Intermediate" dumping syndrome occurs approximately 20-30 minutes after eating. As foodstuffs enter the colon, fermentation and action of microflora cause the production of gas, abdominal pain, cramping, and diarrhea. "Late" dumping syndrome can occur anywhere from 1 to 3 hours after eating, and is especially common after consuming simple carbohydrates. In this situation, rapid absorption in the small intestine stimulates

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insulin release. After quick movement and absorption of food through the small intestine, blood glucose levels drop rapidly as insulin promotes glucose uptake into the cells. This results in hypoglycemia and its symptoms of shakiness, sweating, confusion, and weakness. The Sigstad diagnostic scoring system (see Table 14.19) assesses these symptoms.61,62 Sample PES statement: Inappropriate intake of carbohydrates (simple vs. complex) related to food and nutrition knowledge deficit as evidenced by frequent ingestion of simple carbohydrates such as regular sweetened sodas with meals. Medications that have been used for the prevention of dumping symptoms include acarbose and octreotide.61 Nutrition Intervention Nutrition therapy can prevent and treat many complications of gastric surgery (see Table 14.20 for an overview). The post-gastrectomy or "antidumping" diet encourages a well-balanced diet slightly higher in protein and fat than what is recommended by the U.S. Dietary Guidelines. Simple sugars (including clear liquids) are avoided in order to prevent hyperosmolality and hypoglycemia associated with dumping syndrome. Lactose is often not tolerated. If the patient is lactose intolerant, commercial products that provide lactase or are lactose-free can be recommended. This is an additional reason to recommend calcium and vitamin D supplements. Liquids should be consumed between meals to prevent their contribution to dumping syndrome because they facilitate quick movement through the small intestine. The patient is encouraged to consume five to six small meals throughout the day and, if necessary, lie down after meals. See Table 14.21 for an outline of nutrition recommendations for gastric surgery patients. Nutrition support is recommended if advancement to solid food does not progress Table 14.19 Dumping Symptoms According to Sigstad's Scoring System Shock 15 Source: Sigstad H. A clinical diagnostic index in the diagnosis of the dumping syndrome; changes in plasma volume and blood sugar after a test meal. Acta Med Scand. 1970; 188: 479-86. successfully or if there is preexisting malnutrition. Enteral immunonutrition has demonstrated positive results in these surgical patients.63,64 See Chapter 5 for guidance on nutrition therapy with enteral nutrition. Monitoring and Evaluation Patients who have had gas- tric surgery should be monitored closely to assess for weight loss and for symptoms of malabsorption and steatorrhea. Biochemical indices monitoring hemoglobin, hematocrit, ferritin, serum iron, and serum B12 will assist in detecting deficient iron, B12, or folate levels. Other biochemical indices that should be monitored include other vitamin and mineral levels that are at risk for deficiency. Bariatric Surgery As discussed earlier in this section, the treatment of morbid obesity may include gastric surgery. Restricted access procedures include vertical banded gas- troplasty, adjustable banded gastroplasty, and gastric sleeve. The most common bariatric surgical procedures include Roux-en-Y gastric bypass and biliopancreatic diversion (BPD). These are discussed fully in Chapter 12. Gastroparesis Definition The American College of Gastroenterology defines gastroparesis as a "syndrome of objectively delayed gastric emptying in the absence of mechanical obstruction

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Medication treatment for Gerd Page 356

Antacids Use different combinations of three basic salts— magnesium, calcium, and aluminum—with hydroxide or bicarbonate ions to neutralize HCl. Examples include Alka-Seltzer, Maalox, Mylanta, Pepto-Bismol, Rolaids, and Riopan. May have side effects. Magnesium salt can lead to diarrhea, and aluminum salts can cause constipation. Aluminum and magnesium salts are often combined in a single product to balance these effects. Calcium carbonate antacids, such as Tums, Titralac, and Alka-2, can also be a supplemental source of calcium. They can cause constipation as well. Foaming agents Combinations of aluminum, magnesium, and sodium bicarbonate. Reduce the symptoms associated with reflux. Examples include Gaviscon, Foamicon. H2 antagonists Block histamine receptors that are a component of one of the stimulatory paths for acid secretion. Medications available include cimetidine (Tagamet HB), famotidine (Pepcid AC), nizatidine (Axid AR), and ranitidine (Zantac 75). They are available in prescription strength and over-the-counter. Provide short-term relief, but over-the-counter (OTC) H2 antagonists should not be used for more than a few weeks at a time. They are effective for about half of those who have GERD symptoms. Proton pump inhibitors Block the H1, K1-ATPase enzyme, a component in HCl production. They include omeprazole (Prilosec, Zegerid), lansoprazole (Prevacid), pantoprazole (Protonix), rabeprazole (Aciphex), and esomeprazole (Nexium), which are all available by prescription. OTC-strength Prilosec is also available. Prokinetics Help strengthen the pyloric sphincter and increase speed of gastric emptying. This group includes bethanechol (Urecholine), metoclopramide (Reglan), and erythromycin. May have frequent side effects that can limit their usefulness in treatment of GERD.

Diseases and Conditions Associated with Dysphagia

Chronic neurological diseases Amyotrophic lateral sclerosis, Parkinson's, multiple sclerosis, myasthenia gravis, Alzheimer's, Huntington's, neuropathy associated with type 1 diabetes mellitus Muscle disorders Myositis, myopathies; scleroderma Gastrointestinal disease GERD, hiatal hernia, achalasia, gastroparesis Malignancy Head and neck cancers; stomatitis, mucositis, esophagitis associated with chemotherapy and radiation therapy Other Inflammatory secondary to infection; post intubation; injury secondary to thermal or caustic exposure; aspiration; esophageal varices; drug side effects; aging

from their most complex form of polysaccharides to the monosaccharides: glucose, fructose, and galactose. Proteins are converted from polypeptides to single amino acids, di-, and tripeptides. Lipids are digested to their simplest forms: free fatty acids, monoglycerides, glycerol, phospholipids, and cholesterol. After digestion, these basic molecules are absorbed along with water, electrolytes, vitamins, and miner- als to provide essential nutrients to every cell. Contraction and motility are regulated through a complex network of communication paths involving autocrine, para- crine, and neuronal control systems. In particular, the GI tract's own specialized pacemaker cells called interstitial cells of Cajal control smooth muscle activity. The autonomic nervous system relays input for the smooth muscle of the GI tract through a specialized enteric nervous system. Two types of neurons regu- late contraction of smooth muscle, motility, and secretory func- tions of the GI tract. One of these neurons communicates using a variety of substances including neuropeptides, hormones, and neurotransmitters. A neuropeptide is a protein substance orig- inating from the nerve that can alter functional activity of an organ. As you may remember, a hormone is defined as a chemi- cal substance formed in one organ and carried via the circula- tory system to another target organ or cell. Hormones involved with control of the GI tract include gastrin, cholecystokinin, and secretin. These are discussed in more detail later in this section. 344 Part 4 Nutrition Therapy Primary neuropeptides involved in transmission of impulses include acetylcholine, somatostatin, vasoactive intestinal polypeptide (VIP), substance P, histamine, neuro- tensin, serotonin, and nitric oxide. Other neurotransmitters and modulators involved in neuroregulation for the GI tract include norepinephrine, neuropeptide Y, and g-aminobutyric acid (GABA). (See Table 14.1.) Major innervation for the enteric nervous system is supplied by parasympathetic and sympathetic fibers of the autonomic nervous system. Most sympathetic impulses are carried along the splanchnic nerves. Parasympathetic impulses are carried by the vagus nerve. Anatomy and Physiology of the oral Cavity The oral cavity or mouth serves as the point of entry into the digestive tract. The mouth consists of the lips, teeth, tongue, and palate. The lips assist in directing food into the oral cavity. By separating the mouth and nasal cavity, the palate (roof of the mouth) allows for chewing, swallowing, and breathing to occur all at the same time. The tongue's primary role is mov- ing food from the front of the mouth to the pharynx in prepa- ration for swallowing. Major taste buds are also located on the tongue. The tongue and lips also play a primary role in speech. oral Cavity Motility After food is voluntarily placed in the oral cavity, teeth begin their work of mastication (chewing). The purposes of mastication are (1) to break food down into smaller pieces, (2) to mix food with saliva, and (3) to stimu- late taste buds. The tongue assists by moving food in place for chewing. When the jaw is closed, upper and lower teeth fit together to mash, grind, and tear food. oral Cavity Secretions The primary secretion of the oral cavity is saliva. Saliva is produced in the mouth by three pairs of salivary glands: the parotid, submandibular, and sublin- gual. Saliva is made of water (99.5%), electrolytes, and protein.

Electrolytes include sodium chloride, bicarbonate, and potas- sium. Proteins include enzymes, mucus, and lysozyme. Lysozyme functions as part of the first level of defense for the immune system and is capable of destroying bacteria in the mouth. One to two liters of saliva are produced each day. Both autonomic and acquired reflexes can stimulate salivation. An example of an autonomic reflex is production of saliva in response to the pressure exerted by the presence of food in the mouth. An acquired reflex is learned; for example, the "mouth waters" at the sight or smell of food (saliva is pro- duced without oral stimulation). Functions of saliva include (1) moistening and lubricating food to facilitate swallowing; (2) initiating digestion of carbo- hydrate; (3) providing antibacterial protection with lysozyme and by rinsing away food from the oral cavity; (4) enhancing taste by providing a solution that can interact with taste buds; (5) serving as a buffer—the pH of saliva is approximately 6.8, which neutralizes acids and protects the teeth from dental caries; (6) promoting oral hygiene by dissolving food, dead cells, and foreign substances; and (7) assisting speech by allowing free movement of the lips and tongue.3 After food is chewed and mixed with saliva, it is shaped into a sticky ball called a bolus. The bolus is moved from the front of the oral cavity to the back, where swallowing is then initiated. Pressure of the bolus on the pharynx stimulates nerve impulses to the swallowing center. The swallowing cen- ter, located in the medulla, then stimulates the sequence of Figure 14.2 Layers of the Digestive Tract Wall Body wall Peritoneum Mesentery Serosa muscle actions that coordinate the swallow. Thus, the initia- tion of swallowing is voluntary, but thereafter swallowing is under autonomic control. Physical Assessment of the oral Cavity: An Impor- tant Component of Nutrition Assessment Nutrition- focused physical assessment is a critical element of the overall nutrition assessment. (See Chapter 3 for resources related to nutrition assessment.) The oral cavity in particular is an excel- lent site to assess for micronutrient deficiencies. Cheilosis, xerostomia, presence of candidiasis, pale tissues, bleeding gums, tooth loss, and dental caries may all be identified within the oral cavity. Assessment of the tongue for color and inflam- mation can also identify physical changes associated with several vitamin and mineral deficiencies. Correlating results of this physical examination with laboratory data, dietary his- tory, and medical history can allow for determination of any deficiencies.4 Normal Anatomy and Physiology of the Esophagus The esophagus is a straight, hollow tube approximately 25 cm long and 2 cm in diameter. The esophagus has sphincter mus- cles at either end. Walls of the esophagus consist of four lay- ers of tissue (see Figure 14.2). The inner layer is the mucosa, which is made of stratified squamous epithelial cells. The next layer is the submucosa, which contains secretory cells that

Table 14.18 Nutrition Therapy for Peptic Ulcer

Food Groups Foods Recommended Foods Not Recommended if Symptomatic Cola, coffee, tea, cocoa, alcohol 2% or whole milk, cream, high-fat yogurt, chocolate milk Fried or scrambled using high-fat cooking methods None Fried meats, bacon, sausage, pepperoni, salami, bologna, frankfurters/hot dogs None except fried Those that provoke individual intolerance Those that provoke individual intolerance Those that provoke individual intolerance High-fat or fried desserts such as pastries, doughnuts Pepper Beverages: Milk and milk products Eggs Cereals Meats and protein sources Potatoes/rice/pasta Vegetables Fruits Fat Dessert Miscellaneous Source: © Cengage Learning. Non-cola carbonated beverages, Postum®, herbal teas Skim, 1%, buttermilk, low-fat yogurt Poached, hard-cooked, or scrambled using low-fat cooking methods All ready-to-eat or cooked Baked, roasted, broiled, grilled, stewed; trimmed of visible fat; beef, veal, Iamb, pork, poultry, fish, low-fat cottage cheese, low-fat cheese, peanut butter All except fried All All As tolerated consistent with current dietary guidelines All except high-fat or fried desserts such as pastries, doughnuts All except pepper

Foods to avoid for GERD Page 357

I. Foods that may relax the lower esophageal sphincter Peppermint or spearmint Chocolate Fried foods or those with high amounts of added fat Alcohol Coffee (decaffeinated and caffeinated) II. Foods that may increase gastric acid secretion Coffee (decaffeinated and caffeinated) Alcohol Pepper Food Group Foods to Avoid (if they cause symptoms) Beverages Caffeinated and decaffeinated coffee and tea, cocoa, alcohol Milk and milk products 2% milk, whole milk, cream, high-fat yogurts, chocolate milk Eggs Fried or scrambled using high-fat cooking methods Cereals/grains High-fat choices such as pastries Meat and protein sources Fried meats, bacon, sausage, pepperoni, salami, bologna, frankfurters/hot dogs Vegetables Only those that aggravate symptoms in the individual Fruits Only those that aggravate symptoms in the individual Fat As tolerated within current recommendations of U.S. Dietary Guidelines—less than 8 tsp daily Desserts High-fa

Type of Secretory Cell Product Secreted Stimuli for Secretion Function(s) of Secretory Product Exocrine Cells Mucous cells Alkaline mucus Mechanical stimulation by contents Protects mucosa against mechanical, pepsin, and acid injury Chief cells Pepsinogen Acetyl choline (ACh), gastrin When activated, begins protein digestion Parietal cells Hydrochloric acid Intrinsic factor ACh, gastrin, histamine Activates pepsinogen, breaks down connective tissue, denatures proteins, kills microorganisms Facilitates absorption of vitamin B12 Endocrine/Paracrine Cells Enterochromaffi-like (ECL) cells Histamine ACh, gastrin Stimulates parietal cells G cells Gastrin Protein products, ACh Stimulates parietal, chief, and ECL cells D cells Somatostatin Acid Inhibits parietal, G, and ECL cells

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cephalic and gastric phases are stimulatory phases, meaning they result in production of gastric secretions. Several factors contribute to stimulation of gastric juices, including the pres- ence of protein, distention of the stomach, intake of caffeine, and intake of alcohol. Stimulation of HCl by alcohol and caf- feine may be damaging if food is not present in the stomach. Thus, alcohol and caffeine may be restricted for persons with peptic ulcer disease (PUD) or gastroesophageal reflux disease (GERD). (See "Nutrition Therapy—Gastroesophageal Reflux Disease" for further discussion.) In contrast to cephalic and gastric phases, which stimu- late gastric juices, the intestinal phase is inhibitory in that it slows gastric secretions and prepares the small intestine for receipt of the acidic chyme. Distention of the stomach, accumulation of acid, the presence of fat, and increasing osmolality of partially digested food result in release of two major hormones: cholecystokinin and secretin. These hormones act on the smooth muscle of the antrum to slow gastric motil- ity. Additionally, somatostatin is released from the antrum of the stomach. Together these chemical messengers inhibit the action of the parietal and chief cells, which reduces the amount of gastric juices. Gastric Digestion Digestion in the stomach is both mechanical and chemical in nature. Mechanical digestion occurs as contractions of the stomach shear the foodstuffs and mix the bolus of food with gastric juices. HCl causes proteins to unravel or denature, allowing for more efficient digestion. Additionally, HCl converts pepsinogen to the active enzyme, pepsin. Pepsin works to cleave amino acids, di-, and tripeptides from inner portions of the protein, and results in shorter chains of amino acids called peptones. Of the three macronutrients, proteins are subjected to the most active chemical digestion in the stomach; carbohydrate and lipid digestion are fairly limited. Gastric lipase preferentially hydrolyzes fatty acids at the third carbon position, releasing fatty acids and diglycerides. Short- and medium-chain fatty acids are more easily hydrolyzed than long-chain fatty acids in the stomach. Carbohydrate digestion that began in the oral cavity is reduced because salivary amylase is inactivated by HCl. A small amount of carbohydrate digestion may continue in the inner portions of the food bolus, which are not exposed to the acid. Gastric Absorption Absorption in the stomach is limited; no nutrients and only a small amount of water are absorbed. Exceptions include alcohol and some medications. Alcohol can be absorbed in the gastric mucosa and enters the blood- stream through capillaries of the stomach. Because the presence of food in the stomach slows this process considerably, consuming food prior to or with alcohol will slow systemic effects of alcohol ingestion. Most medications are absorbed in the small intestine, but acetylsalicylic acid (aspirin) is readily moved across the epithelial cells of the gastric mucosa. The gastric mucosa is well protected against injury. Anatomical design provides one of the strongest sources of protection. Cell membranes of the gastric mucosal cells are impermeable to hydrogen ions, so the increasing acidity can- not harm them. Secretion of mucus by the cells also provides a layer of protection. Furthermore, gastric mucosal cells have 348 Part 4 Nutrition Therapy a high turnover rate and are sloughed off approximately every 72 hours—too short a life span for these cells to experience any significant damage from acidic conditions of the stomach. Still, if for some reason injury does occur, the high acid- ity will cause tissue to erode. This tissue erosion occurs in peptic ulcer disease and is described later in this chapter. Pathophysiology of the oral Cavity In this section, general problems associated with mouth, teeth, and gums are discussed. These are of nutritional concern because most of these conditions involve problems that interfere with adequate oral intake and can lead to nutritional deficits. Conditions affecting oral health include the most common dental diseases: dental caries, gingivitis, and periodontal disease. Over the past several decades, the U.S. population has seen significant improvement in prevalence of most dental diseases. Even with these improvements, dental disease remains one of the most common health problems in our country. Approximately 15% of children age 6-19 years have untreated dental caries.7 The prevalence of untreated dental caries varies with race/ethnicity and poverty level. For all age groups, non-Hispanic blacks and Mexican Americans have higher numbers of untreated decayed teeth than non-Hispanic Caucasian individuals.7 According to the 2011 National Health Interview Survey, approximately 7% of all Americans over the age of 65 have lost all of their natural teeth.8 (See Box 14.1 for an overview of GI tract changes related to aging.) Dental Caries Dental caries or tooth decay is destruction of tooth structure through the development of small pits or cavities. The cause of dental caries is multifactorial. Individual factors may include structure of the tooth, immunologic response to bacteria, and composition of saliva in the mouth. It is currently understood that several different types of bacteria commonly found in the mouth, including Streptococcus mutans, colonize the surface of the tooth to form a substance called plaque. Plaque adheres to the tooth and, if it is not removed, will mineralize into tartar or calculus. This leads to invasion into the layers of the tooth structure and, when not treated effectively, will lead to tooth loss. Factors that contribute to the development of caries and plaque include frequency of eating, stickiness of the food, composition of saliva, presence of buffers, and overall oral hygiene.9,10 Foods that are sticky adhere to the surface of the tooth and are more likely to cause caries. Frequent snacking increases the time acids are in contact with the tooth and additionally increases risk of caries. The use of liquids with eating helps clear the mouth of food debris and can reduce the potential for caries. Crunchy, high-fiber foods also help clear the mouth of food debris and assist with cleaning the teeth. Dietary and eating patterns associated with increased and decreased risk are outlined in Table 14.3. Caries are usu- ally painless until they invade to the level of the tooth pulp. Usually, the patient first experiences increased sensitivity to

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Possible Causes of Xerostomia

Side effects of More than 400 medicines can cause the salivary some medicines glands to make less saliva. Medicines for high blood pressure and depression often cause dry mouth. Disease Some diseases affect the salivary glands, for example, Sjögren's syndrome, HIV/AIDS, diabetes, and Parkinson's disease. Radiation therapy The salivary glands can be damaged if they are exposed to radiation during cancer treatment. Consistency of saliva may also change. Chemotherapy Drugs used to treat cancer can make saliva thicker, causing the mouth to feel dry. Nerve damage Injury to the head or neck can damage the nerves to the salivary gland.

Table 14.14 Antiemetic Agents Used in the Treatment of Nausea and/or Vomiting Classification of Medication Generic and/or Trade Name Uses/Mechanism H1 antihistamines dimenhydrinate (Dramamine®) diphenhydramine (Benadryl®) hydroxyzine (Atarax®) Work by blocking histamine—may treat mild nausea such as motion sickness; also provide benefit of mild relaxation. Not effective for severe nausea and vomiting. Benzamides metoclopramide (Reglan®) Block dopamine and therefore affect the vomiting center in the brain. Side benefit of increasing gastric emptying. Benzodiazepines diazepam (Valium®) lorazepam (Ativan®) Primarily used as tranquilizers, but can also increase the effectiveness of other antiemetics. Butyrophenones droperidol (Inapsine®) Block dopamine and therefore affect the vomiting center in the brain. Phenothiazines prochlorperazine (Compazine®) Block dopamine and therefore affect the vomiting center in the brain. Corticosteroids dexamethasone methylprednisolone Reduce the effect of prostaglandins and can also improve the effectiveness of other antiemetics. Cannabinoids dronabinol (Marinol®) Mechanism unclear but produces feelings of euphoria and antiemetic effect. NK1-receptor antagonists aprepitant (Emend®) Block substance P in the brain, which appears to have a direct effect on the vomiting center. 5-HT3 receptor antagonists/ serotonin antagonists ondansetron (Zofran®) tropisetron (Navoban®) granisetron (Kytril®) dolasetron (Anzemet®) Block serotonin—usually given in combination with dexamethasone.

Table 364

Diagnostic Procedures: Upper GI Pathology A variety of standard procedures are available to assist in the diagnosis of pathology involving the upper GI system, and most specifically for the esophagus and stomach. These procedures can be divided into those tests that involve visu- alization of the GI tract and those that involve the measurement of secretions by these organs. Endoscopy During esophagogastroduodenoscopy (EGD), a fiberoptic endoscope (see Figure 14.8A) is introduced through the oral pharynx and is moved through the esophagus and stomach and into the duodenum. This is also used for the fiber- optic endoscopic evaluation of swallow- ing (FEES). The endoscope is an optical instrument that includes a lens viewer, a long flexible tube, and a light source. The lens viewer allows the physician to visually inspect the mucosa of the organs and determine any abnormalities. The patient may have clear liquids from mid- night the night before and then should be NPO for the last 6 hours prior to the procedure. The patient will also receive a variety of preparatory medications to assist in the procedure. These may include Versed (midazolam), a medication 360 Part 4 Nutrition Therapy that is given as an agent to induce seda- tion and/or amnesia prior to and during the procedure. Other medications include pain medications and antibiotic prophy- laxis. A needle biopsy can be passed through the endoscope to determine the presence of either abnormalities in the tissue or infection. Barium Radiology Studies In these procedures, the patient is given a contrast medium to drink. The most com- mon medium is barium sulfate, which is a chalky, white radiopaque substance that the patient drinks like a milkshake. The barium can be visualized by fluoroscopy or by X-ray. This is the procedure used for a videofluorographic swallowing study (VFSS). This study allows the physician to monitor swallowing and the movement through the stomach into the duode- num. It also can distinguish many other abnormalities such as ulcers, tumors, or inflammation. Esophageal Manometry Motor function of the esophagus and the lower esophageal sphincter is evaluated in this procedure. A tube is passed through the oral pharynx into the stomach. An instrument called a transducer, attached to the outer end of the tube, records the barometric pressure as the tube is pulled back from the stom- ach through the LES. The patient should be NPO for 8 hours prior to the proce- dure, and is premedicated with both antianxiety and sedative drugs. A normal manometry will indicate that the LES pressure is normal and that it relaxes during a swallow. It will also indicate that the pattern of muscle contractions is systematic and coordinated during a swallow. 24-Hour pH Monitoring This test previously involved placing a pH probe into the distal esophagus for a 12- to 24-hour period in order to gen- erate a graph depicting continuous pH readings. New technology allows for the placement of a capsule that contains an acid-sensing probe, a battery, and a trans- mitter. The probe monitors the acid in the esophagus and transmits the information to a recorder that is worn by the patient on a belt. The capsule transmits for 2 days, and then the battery dies. Within a week, the capsule is passed in the stool. Information is obtained regarding quantity and pattern of gastroesophageal reflux events, the correlation with symptoms,and the efficiency of esophageal acid clearance. Bernstein Test (Acid Perfusion Test) The Bernstein test may be used to differ- entiate between chest pain that is cardiac in origin and pain caused by acid reflux. A nasogastric tube is inserted through the nasopharynx into the esophagus. The physician attempts to replicate the symp- toms of acid reflux by alternately injecting either a mild hydrochloric acid solution or a saline solution through the tube. The patient reports the differences in symp- toms with each solution. Urea Breath Test This test is both specific and sensitive for diagnosis of Helicobacter pylori. The client ingests urea that is labeled with radioactive carbon-14 or nonradioactive carbon-13. The Helicobacter pylori, if present, will digest the urea. The by-product after digestion will be expired along with carbon dioxide and will indicate the presence of H. pylori. Electrogastrography (EGG) This procedure is used to diagnose and study stomach rhythm. Disturbances in the stomach's pacemaker can produce nausea and vomiting. This procedure can assist in determining the etiology of nausea and vomiting. Antroduodenal Manometry The purpose of 24-hour antroduodenal manometry is to measure the pressure in the small intestine before and after a meal and during sleep and waking hours. The measurements provide documentation of gastric emptying and peristalsis of the small intestine. Gastric Analysis (Basal Acid Output) This procedure measures the amount of hydrochloric acid produced by the stom- ach under baseline conditions. This test is often used to diagnose pernicious anemia, achlorhydria, and Zollinger-Ellison syn- drome or to evaluate the effectiveness of surgical or pharmacological interventions. Gastric Emptying Scintigraphy This test is used to measure gastric emptying time and can be used to diag- nose dumping syndrome or gastroparesis. After the patient consumes a standard meal with radioisotope, images are taken to document the passage of the food from the stomach.

Table page 360-361

No other system of the human body is so intimately involved in preservation of an optimal nutritional status than the gastrointestinal (GI) tract. Any pathology involving the GI tract can have a significant effect on nutritional status. A wide array of diagnoses affect normal digestion and absorption. Nausea, vomiting, diarrhea, constipation, and malabsorption, all common symptoms in GI disease, can potentially jeopardize the individual's nutritional status. For some diseases, such as celiac disease, nutrition therapy is the only treatment. GI disease is estimated to affect more than 70 million people in the United States each year. Annually, more than 48 million physician office visits are related to GI disease.1 Direct medical costs for these individuals are staggering, at over $97 billion per year.2 Prilosec, a proton pump inhibitor (PPI), was the number one prescribed medication in the United States in 2010.1 Normal Anatomy and Physiology of the Upper Gastrointestinal Tract A good working knowledge of normal anatomy and physiology of the GI tract is essential to understanding the pathophysiology and subsequent medical and nutritional care of GI disease. The GI tract is often described as a long tube approximately 15 feet in length. This description, though technically accurate, minimizes the complexity of this body system. Cell and organ function and intricacy of control factors throughout the GI tract are highly differentiated. The upper GI tract is composed of the mouth, pharynx, esophagus, and stomach, while the lower GI tract includes the small and large intestine (see Figure 14.1). These continuous organs differ from one another in both anatomical structure and specialized function. Accessory or ancillary organs that contribute to the function of the GI tract include the liver, biliary system, and pancreas. This section discusses the normal function of each upper GI tract organ in the context of the four basic functions of the GI tract as a whole: motility, secretion, digestion, and absorption. GI disease can affect any one or all of these functions. Motility, Secretion, Digestion, and Absorption Motility is the movement of the food consumed along the GI tract. Both propulsive contractions and mixing movements serve not only to move foodstuffs toward sites of digestion and absorption, but to mix foods with digestive secretions and maximize potential absorption. Secretions of the GI tract include water, electrolytes, enzymes, bile salts, and mucus. Through the process of digestion, complex molecules are converted to their simplest form. Carbohydrates are digested

acarbose—also known as PrecoseTM; a medication—an alpha glucoside inhibitor— that slows the digestion of starch; used in diabetes treatment and to prevent dumping syndrome acetylcholine—excitatory neurotransmitter involved in stimulation of parietal cells achalasia—motility disorder characterized by an absence of or weakened peristalsis within the esophagus achlorhydria—lack of gastric hydrochloric acid secretions ageusia—inability to taste anastomosis—the surgical connection of body parts, especially hollow tubular parts like those of the GI tract aspiration—the accidental inhalation of food particles or fluids into the lungs autocrine—describes a type of communica- tion via hormones and other chemical messen- gers that when released from that cell results in an action or change within that same cell bariatric—referring to medical treatment of morbid obesity Barrett's esophagus—a complication of severe chronic GERD involving changes in the cells of the tissue that line the bottom of the esophagus bezoar—accumulation of undigested food- stuffs in the stomach borborygmus—rumbling noise caused by movement of fluid or gas through the GI tract calculus—calcified deposits that have formed around the teeth cheilosis—fissures that develop at the edges of the mouth cholinergic—resembling acetylcholine; stimu- lated by or releasing acetylcholine or a related compound chyme—partially digested food in a semi-fluid state dental caries—decay of the teeth that begins when acid dissolves the enamel that covers the tooth dumping syndrome—a group of symp- toms that occurs with rapid passage of large amounts of food into the small intestine; symptoms include dizziness, sweating, decreased blood pressure, and diarrhea dysgeusia—abnormalities in or reduced ability to taste dyspepsia—vague upper abdominal symp- toms that may include upper abdominal pain, bloating, early satiety, nausea, or belching dysphagia—difficulty swallowing edentulous—without any teeth enamel—hard outer layer of teeth consisting of hydroxyapatite; this mineral is composed of calcium, phosphorous, fluoride, chloride, sodium, and magnesium endoscopy—examination of the interior of a canal by means of an endoscope eosinophilic esophagitis (EoE)—an aller- gic inflammatory response affecting the esophagus epigastric—referring to the upper abdominal region eructation—belching or burping esophageal phase of swallowing—phase in which esophageal peristalsis carries the bolus through the esophagus and LES and into the stomach gastrectomy—surgery to resect a portion of or the entire stomach gastrin—primary hormone released to stimu- late digestion and production of hydrochloric acid in the stomach gastritis—inflammation of the gastric mucosa gastroesophageal reflux disease (GERD)—chronic or recurrent gastric pain due to reflux of gastric secretions into the lower esophagus gingiva—the gums glossitis—inflammation of the tongue hematemesis—the vomiting of blood hemorrhage—bleeding hiatal hernia—protrusion of part of the stomach through the diaphragm into the space normally occupied by the esophagus, heart, and lungs histamine—paracrine compound released from parietal cells involved in production of hydrochloric acid; also released from mast cells and basophils as a component of inflamma- tory and immune responses hyperosmolar—having a higher osmolality than body fluids (.300 mOsm/kg) hypoglycemia—a low serum glucose; generally considered to be ,70 mg/dL laparoscopically—describes a method of performing surgical procedures within the abdomen and pelvis in which an instrument (endoscope) used to view the structures and other instruments are inserted through small incisions, avoiding the need for a large surgical incision learned food aversion—avoidance of certain foods due to association with unpleasant GI symptoms lower esophageal sphincter (LES)—the junction between the esophagus and the stomach Nissen fundoplication—a surgical technique used to suture the fundus of the stomach around the esophagus to prevent reflux obstruction—blockage octreotide—medication that mimics the action of somatostatin oral preparatory phase of swallowing— phase involving the chewing of food and preparation of a bolus by the tongue, teeth, and mandible; food is mixed with saliva, pressed against the hard palate, and formed into a bolus oral transit phase of swallowing—phase in which the tongue moves the bolus to the back of the throat osmolality—number of water-attracting particles per kilogram of water (expressed as mOsm/kg) paracrine—describes a neurotransmitter that is released from a cell that is close to the tar- get cell parietal cell—one of the gastric gland cells that lies on the basement membrane covered by chief cells and secretes hydrochloric acid peptic ulcer disease (PUD)—ulceration or perforation in the lining of the stomach, duo- denum, or esophagus perforation—a break in the integrity of the tissue periodontal disease—a bacterial infection that destroys the attachment fibers and sup- porting bone that hold the teeth in the mouth pharyngeal phase of swallowing—phase in which the involuntary swallowing reflux begins and the bolus is carried through the pharynx to the top of the esophagus; the entrance to the trachea (larynx) closes; and the soft palate lifts and closes off the entrance to the nose plaque—the noncalcified accumulation of oral microorganisms and their by-products that adhere to the teeth proton pump inhibitors (PPIs)—class of medications that block the H1, K1-ATPase enzyme, a component in HCl production pyloroplasty—surgical enlargement of the pyloric sphincter reduction and fixation of fracture—a method to surgically repair a bone fracture Sjögren's syndrome—a chronic systematic inflammatory disorder, etiology unknown, characterized by dryness of mucous mem- branes and destruction of the moisture- producing glands somatostatin—a hormone and neurotrans- mitter that inhibits release of peptide hor- mones in several tissues sphincter—a circular muscle that prevents movement or passage through the circle when contracted; sphincter muscles are located throughout the GI tract and are crucial control factors for peristalsis steatorrhea—excessive fat in the feces stomatitis—inflammation of the membrane in the mouth syncope—temporary loss of consciousness; fainting vagotomy—severing of the vagus nerve; often a component of gastric surgery vagus nerve—tenth cranial nerve; one of its major functions is to coordinate the autonomic nervous system communication between organs of digestion xerostomia—decreased saliva production and dry mouth

Nutrition interventions for Stomatosis

and mouth every 4 hours and at bedtime. Use frequent mouth rinses and avoid alcohol-based products. • Treat oral lesions pharmacologically as appropriate (antifungal medications if needed). • Consider using oral topical agents and anesthetics, such as viscous lidocaine and institution-specific mouth rinses, which are combinations of nystatin, Maalox® (Novartis, Parsippany, NJ), diphenhydramine, hydrocortisone, and viscous lidocaine. • Adjust texture and temperature as tolerated. Extremes of very hot or cold are often not tolerated. • Avoid carbonated beverages. • Avoid caffeine, alcohol, and tobacco products. • Avoid other irritants (e.g., acidic, spicy foods). • Try oral glutamine supplementation—optimal dose is 10 g three times daily. • Consider enteral nutrition support if unable to maintain nutritional status orally.

therapy can interrupt normal saliva production. The salivary ducts may also become blocked as a result of a tumor or other medical condition. Systemic changes such as those seen in Sjögren's syndrome or with dehydration can also change saliva production. Many medications cause a reduction of saliva by affecting the parasympathetic nervous system. For instance, medications called anticholinergics, which act to block the effect of acetylcholine, reduce the amount of saliva as a major side effect. Groups of medications that have anticholinergic effects include antihistamines and anti- depressants. Table 14.6 outlines interventions to assist with xerostomia. Excessive saliva production may also be a concern, but in general does not pose the nutritional problems that xerostomia can. Nervous system diseases such as Parkinson's disease Figure 14.6 Cheilosis Source: Wellcome Image Library/Custom Medical Stock Photo—All rights reserved. Table 14.5 Possible Causes of Xerostomia © Cengage Learning. may interfere with autonomic control of saliva production. Other situations that increase saliva production, such as seeing, tasting, or smelling food or the consumption of sour- tasting food, involve the autonomic reflex. Surgical Procedures for the oral Cavity Surgical resections of the tongue, palate, or pharynx occur with head/neck malignancies. Fractures of the mandible (lower jaw) are a common consequence of accidents, trauma, and certain disease states. Repair of these fractures requires surgery and immobilization to ensure adequate healing. Jaw fractures are described as follows: open (exposed to open area of mouth or skin); closed (within tissue); complete (in two separate pieces); incomplete (splintered); and comminuted (multiple pieces). The type of fracture, as well as other medical and psychosocial factors, will determine the type of surgery that the patient will have and, ultimately, the type of nutrition therapy that is required. Surgical repair includes reduction and fixation of the fracture. Fixation will include either an external or internal use of the upper jaw to hold the lower jaw in place while healing occurs. This is what is commonly referred to as "wiring the jaw," or maxillomandibular fixation.17 These procedures require significant nutrition interventions to ensure maintenance of nutritional status. Nutritional intake is limited to those liquids and blenderized foods that can be put through a straw or syringe (see Table 14.7 later in this section).

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Nutrition Assessment and Diagnosis Since this procedure severely limits the type of foods the patient can consume, a past diet history may not be that useful other than as a means to obtain a sense of food likes and dislikes. Depending on the age of the patient, interviewing a parent or care- giver helps the clinician to evaluate behaviors associated with food and meal preparation and the patient's social network and support. Common nutritional diagnoses associated with a jaw fracture may include inadequate oral food/beverage intake; inadequate fluid intake; increased nutrient needs; biting/chewing difficulty; involuntary weight loss; and food and nutrition knowledge-related deficit. Nutrition Intervention Nutrition interventions will center around modification of texture and consistency, increasing the nutrient density of nutritional intake, and nutrition education to ensure adequacy and safety of food preparation. All foods must be prepared so that each easily moves through a straw or syringe. Table 14.7 summarizes the blenderized diet recommended for a jaw fracture, and Box 14.2 presents a case example. If the patient is unable to maintain his or her nutritional intake through these interventions or if the nutritional status of the patient warrants, enteral feeding may be recommended. Impaired Taste: Dysgeusia/Ageusia Dysgeusia is the condition of altered or impaired sense of taste. Ageusia is the inability to taste or "mouth blindness." Many clinical conditions affect the ability to taste. For example, patients undergoing treatment for cancer relate changes in both taste and smell.19 Epithelial cells of the oral mucosa have a high turnover rate and can be affected by either chemotherapy or radiation therapy (see Chapter 23). Diseases of the tongue and palate can interfere with normal function of taste buds. Nervous system diseases can also affect transmission of sensory information. Many patients relate changes in taste that are associated with certain medications.20 For example, the use of methotrexate (a common medication used in treatment of cancer and autoimmune diseases) can cause a strong metallic taste.

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Nutrition Therapy for Pathophysiology of the oral Cavity Nutritional Implications The primary nutrition problem for diseases involving the oral cavity is the inability to maintain adequate oral intake (see Box 14.3). Foods may be difficult to swallow due to lack of saliva, thickened saliva, or the pain of an inflammatory condition or dental disease. When saliva production or quality is impaired, there is an additional risk of infection and dental caries. Dysgeusia can reduce overall oral intake due to changes in appetite. If appropriate medical and nutrition interventions do not improve dietary intake, the patient is at risk for malnutrition. Nutrition Diagnosis Common nutrition diagnoses associated with pathology of the oral cavity include inadequate oral intake; inadequate fluid intake; inadequate protein-energy intake; biting/chewing difficulty; swallowing difficulty; and unintended weight loss. Nutrition Intervention Nutrition intervention strategies will primarily be focused on modification of the distribution, type, or amount of foods provided. Texture modification of

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the current diet will be necessary for most of these clinical conditions. Changing the diet to include soft, moist foods, liquids, or blenderized foods will allow for increased intake. Use of gravies, sauces, and soft casseroles should be encouraged, while foods that are dry, crunchy, or have sharp edges should be avoided. Liquids should be consumed with meals. Medical food supplements may also be appropriate. Kilocalorie and protein density can be increased by using modular com®ponents (such as dry skim milk powder or Beneprotein ) and high-kcalorie, high-protein liquid sup- plements (such as Ensure®, Boost®, or milkshakes), and by increasing fat intake (serving cream soups or adding margarine to mashed potatoes). Increasing frequency of meals may also allow for overall improved intake. Many patients may need to be prescribed a general multivitamin supplement. If specific deficiencies are confirmed, then appropriate supplementation should begin. Extreme temperatures and spices in foods may increase pain and intolerance to oral intake. Foods at room temperature and foods that are bland in flavor such as custards, yogurt, or pudding are generally well tolerated. Feeding assistance in terms of mouth care may also be beneficial. Liberally using fluids will increase moisture in the mouth and assist with increasing solid food intake. Ensure adequate hydration at all times. Spraying the mouth with 354 Part 4 Nutrition Therapy water or sucking on ice chips may be helpful. Sugar-free beverages containing citric acid (lemonade, etc.) may stimulate saliva production. Though usually a temporary intervention, using sugar-free gum or mints can also help. Cold and frozen foods are sometimes preferred. In extreme conditions, artificial saliva can be used. Oral hygiene is an important part of nutritional care. Frequently rinsing the mouth to remove food particles can help prevent a bad taste in the mouth and an increase in dental caries. Alcohol-containing mouthwashes tend to dry the mouth, so other choices such as lemon-glycerine solutions or warm water with baking soda can be used. Using 1⁄4 tsp of baking soda in 1 cup of water is recommended. If pain is severe, coordinating pain medication with oral intake is important. Oral agents that provide localized numbing can be used, but in severe inflammatory conditions, systemic pain medications are frequently prescribed. Monitoring and Evaluation Oral intake can be monitored by observation, a kcalorie count, or a food diary. Adequacy of intake is compared to estimated kcalorie and protein requirements. Every effort should be made to meet the patient's food preferences and tolerances. Success of nutrition interventions will be measured by weight gain or weight maintenance and the evaluation of biochemical parameters.

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Nutrition Assessment of the Upper GI Tract Client History Personal history: Socioeconomic status/ food security; support systems; education level—primary language Medical and health history for client and family: Diagnoses; medications; previous medical conditions or surgeries Anthropometric Measurements Height; current weight; weight history: highest adult weight, usual body weight, reference weight (BMI) If other areas of the nutrition assessment indicate that the patient may be at nutritional risk, other anthropomet- ric measures would be assessed to sub- stantiate the presence of malnutrition. Biochemical Data Laboratory measures of protein status are evaluated to establish any chronic visceral protein deficit. Other laboratory indices would be assessed depending on the underlying medical condition; for instance, in dehydration and/or anemia, electrolytes, BUN, creatinine, hemoglobin, and hematocrit would be evaluated. Nutrition-Focused Physical Findings Examination of the head, neck, and oral cavity is a standard component of physi- cal assessment and a crucial component of nutrition assessment for conditions of the oral cavity. Review results of swallowing evaluations. Assess for clinical symptoms of malnutrition; identify signs and symptoms that may be associated with dehydration. These may include increased pulse and orthostatic hypoten- sion. Physical exam may reveal: weight loss, lethargy, sunken eyes, absence of tears, dry mucous membranes, dry skin, decreased capillary refill, and decreased skin turgor. Patient interview can confirm actual fluid intake. (See Chapters 3 and 7.) Food-/Nutrition-Related History Dietary assessment will focus on deter- mining the changes in oral intake that have occurred due to the disease condi- tion. Methods to obtain this information include a 24-hour recall, a diet history, or direct observation of the patient's intake. Evaluate tolerance to different textures and consistencies. Evaluate for supplement intake. Note: • Ability to chew; use and fit of dentures; problems swallowing • Nausea, vomiting; constipation, diarrhea; heartburn • Any other symptoms interfering with ability to ingest normal diet • Ability to feed self; ability to cook and prepare meals • Food allergies, preferences, or intoler- ances: spicy foods, high-fat foods, pepper, caffeine, coffee, tea, alcohol, spearmint, peppermint, chocolate • Previous food restrictions • Ethnic, cultural, and religious influences • Use of alcohol; use of vitamin, mineral, herbal, or other type of supplements • Previous nutrition education or nutrition therapy • Eating pattern: 24-hour recall, food history, food frequency

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Pathophysiology of the Esophagus This section discusses the most common diseases or conditions involving the esophagus, including gastroesophageal reflux disease, Barrett's esophagus, eosinophilic esophagitis, hiatal hernia, and dysphagia. Gastroesophageal Reflux Disease Definition The most recent medical guidelines for the management of gastroesophageal reflux disease (GERD) define this condition as "symptoms or complications resulting from the reflux of gastric contents into the esophagus or beyond, into the oral cavity (including larynx) or lung."21 Epidemiology Each year, more than 20 million Americans suffer daily symptoms of gastroesophageal reflux, while more than 100 million suffer occasional symptoms.22 The frequency of GERD symptoms does not appear to rise with increased age, but the rate of complications does.23 GERD is also a common condition during pregnancy but generally resolves after delivery. Pathophysiology As discussed earlier in this chapter, the lower esophageal sphincter (LES) normally serves as a barrier between the esophagus and stomach. Under normal conditions, atmospheric pressure is greater in the esophagus than in the stomach, and this pressure differential typically prevents reflux of gastric contents. Transient relaxation of the LES is normal but becomes a problem when ongoing LES incompetence develops. LES incompetence may result from these normal transient relaxations, a change in LES pressure, or some type of anatomical change such as that seen with hiatal hernia.24 The signs and symptoms experienced with GERD are attributed to a reflux of both gastric acid and pepsin. The etiology of the reflux is multifactorial and can include both physical and lifestyle factors. Factors that can lower LES pressure and thus contribute to LES incompetence include (1) increased secretion of the hormones gastrin, estrogen, and progesterone; (2) presence of other medical conditions, such as hiatal hernia, scleroderma, or obesity; (3) cigarette smoking; (4) use of medications, including dopamine, morphine, and theophylline; and (5) specific foods. Foods high in fat, chocolate, spearmint, peppermint, alcohol, and caffeine all may decrease LES pressure.24,25 As is discussed later in this section, research that supports the effectiveness of restriction of these foods in successful elimination of GERD symptoms is lacking, despite the continued use of food restrictions based on anecdotal evidence.21,26 Clinical Manifestations Symptoms of GERD may include dysphagia (difficulty swallowing), heartburn, increased salivation, and belching. In some situations, pain is severe and may radiate to the back, neck, or jaw. In fact, pain from GERD can be confused with pain that is cardiac in origin because of the diffuse spread of pain into these other areas. For many patients, pain is worse at night when they are lying down. Complications of untreated or unresponsive GERD may include impaired swallowing, aspiration of gastric contents into the lungs, ulceration, and perforation or stricture of the esophagus. Barrett's esophagus is also considered to be a complication of GERD (see the section "Barrett's Esophagus— A Complication of GERD"). Medical Diagnosis Medical diagnosis of GERD can be made clinically based on the presence of associated symptoms and their relief after prescription and use of a proton pump inhibitor (PPI). Further diagnosis is made by endoscopy. Other tests such as biopsy of damaged mucosa, esophageal manometry, and barium X-rays are not necessarily used for diagnosis of GERD but will be used in evaluation of complications or other upper GI conditions. (See Box 14.5 later in this chapter for a summary of diagnostic procedures.) Treatment Treatment for GERD includes three major goals: (1) increasing LES competence; (2) decreasing gastric acidity, and thus decreasing the severity of symptoms; and (3) improving clearance of contents from the esophagus. Surgical intervention may be warranted if the disease is unresponsive to medical management or if the patient experiences complications. Decreasing gastric acidity involves the use of several groups of medications and, for some patients, nutrition therapy. Medications fall into five major categories: (1) antacids or buffering agents, (2) histamine blocking agents, (3) prokinetic agents, (4) proton pump inhibitors, and (5) mucosal protectants. Gastric secretions are controlled in several different ways (see the section "Control of Gastric Secretions") and medications used to treat GERD interfere with control of gastric secretions by blocking several of those regulatory pathways.21,24 See Table 14.8 for a summary of these medications. Lifestyle factors that compromise LES competence such as cigarette smoking, use of medications, obesity, and nutritional history should be addressed. Patient education can focus on ways to improve clearance in the esophagus; for example, patients may be instructed to remain upright after eating, to lose weight, to wear loose-fitting clothing, and to raise the head of their bed for sleeping.21 The most common surgical procedure used for refractory GERD is the Nissen fundoplication (see Figure 14.7). This procedure takes the fundus of the stomach and wraps it around the lower esophagus. This provides additional strength to the LES and assists in preventing the reflux. This procedure can be done laparoscopically, which avoids an abdominal incision and considerably reduces the recovery time.27 Other treatment options include partial fundoplications and Roux- en-Y gastric bypass for the patient who is morbidly obese. Another surgica®l procedure places an expandable device called the LINX management system around the LES; this device helps tighten the sphincter, preventing the reflux.28 Nutrition Therapy for GERD The goals of nutrition therapy are consistent with the goals of medical care discussed earlier. These goals include reducing gastric acidity and a trial of food restriction excluding those foods that may lower LES pressure. Most patients identify foods they feel make their symptoms worse and decrease intake of those foods. In these situations, restriction of food groups may result in weight loss or nutritional deficiency. Nutritional therapy may assist not only by addressing these nutritional problems but also by decreasing the symptoms that the patient is experiencing. Long-term use of medications for GERD may impair calcium absorption and iron and

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B12 status, but long-term prospective studies to confirm this have not been completed at this time.29-35 Nutrition Diagnosis Common nutrition diagnoses asso- ciated with GERD include overweight or obesity, impaired nutrient utilization, inadequate vitamin or mineral intake, swallowing difficulty, or altered GI function. Nutrition Assessment See Box 14.3 for general guidelines for nutrition assessment of disorders involving the upper GI system. Nutrition Intervention Unfortunately, most nutrition therapy interventions that have been used historically have not been tested through rigorous scientific study.21

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Nevertheless, recommendations to reduce gastric acidity typically include a trial of elimination of black and red pepper, coffee (both caffeinated and decaffeinated), and alcohol. These have been identified as stimulants for gastric acid production. Likewise, meals of larger quantity tend to stimulate more acid production, delay gastric emptying, and increase the risk of reflux. Thus, smaller, more frequent meals may be indicated. Foods that have been identified as potentially lowering LES pressure may also be restricted. An initial trial to avoid chocolate, mint, and foods with a high fat content is recommended. Furthermore, any food the client identifies as irritating should be avoided. Nutrition interventions for GERD are outlined in Table 14.9 (see Box 14.4 for a discussion of GER in infants). There is a strong association between obesity and GERD. For patients who are overweight or obese, weight loss is recommended and has been associated with an overall improvement of GERD symptoms and esophageal pH.21 Monitoring and Evaluation Ongoing monitoring is recommended to assess the effectiveness of any food restrictions in controlling symptoms. If there has been no improvement, then there is no need for the patient to continue these dietary restrictions. Continued monitoring and support for weight loss improves success and will assist with the maintenance of Table 14.9 Nutrition Interventions for GERD Foods to Avoid Source: Nahikian-Nelms M. Gastrointestinal disease. In: Nutrition Care Manual. Chicago, IL: American Dietetic Association; 2013. Copyright 2013 by the American Dietetic Association. Adapted with permission. weight loss. Laboratory values should be monitored for indications of nutrient deficiencies with long-term use of GERD medications. Barrett's Esophagus—A Complication of GERD Barrett's esophagus, or Barrett's metaplasia, involves a change in the epithelial cells of the esophageal mucosa and is usually considered a complication of GERD. Barrett's esophagus is detected in approximately 10% of patients undergoing endoscopy for GERD. Furthermore, it has been established that patients with refractory GERD (unresponsive to treatment) are much more likely to develop Barrett's esophagus. For example, patients with Barrett's esophagus have been shown to have persistent abnormal pH monitoring results even on maximum pharmacological treatment.36 In this condition, the normal squamous cell epithelium of the esophagus changes to metaplastic columnar cell epithelium. This dysplastic cellular change is considered to be a precursor to a malignancy. Those patients with Barrett's esophagus are at higher risk for adenocarcinoma of the esophagus.24,36,37 Current research is focusing on determining better ways to identify high-risk patients; for example, establishing biomarkers would allow for early detection and treatment. Patients do not experience any specific symptoms with this condition outside of those experienced with GERD. It is generally undetected unless the patient has a biopsy done as part of an upper GI diagnostic work-up, usually for the treat- ment of GERD. There are no specific nutritional concerns unless the patient is diagnosed with esophageal cancer. In the case of a malignancy, nutritional issues are addressed as the patient begins treatment for that diagnosis. Eosinophilic Esophagitis Definition Eosinophilic esophagitis (EoE) is defined both clinically and pathologically using the following criteria: symptoms consistent with esophageal dysfunction; biopsy revealing $15 eosinophils per high power field (hpf); mucosal eosinophilia limited to the esophagus that persists after a trial of PPI; and exclusion of secondary causes of esophageal eosinophilia.38 A response to treatment supports the diagnosis but is not required. Epidemiology EoE is a fairly new diagnosis, as it only began to be recognized within the past 20 years among young men, and is associated with a specific genetic profile.39 A recent review of the literature demonstrated the incidence of EoE in children to vary from 0.7 to 10/100,000 per person-year and the prevalence to range from 0.2 to 43/100,000.40 Prevalence and incidence of EoE appear to be increasing. Etiology EoE is an inflammatory condition characterized by infiltration of eosinophils within the esophageal mucosa. Other immune cells involved in this condition include mast cells and T lymphocytes. There is a definite link to food as a disease trigger. Standard allergy testing does not successfully identify the food trigger, and thus it is common for individuals with EoE to eliminate all common food allergens (see the "Treatment" section). The diagnosis of an allergic response to

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food is confirmed by the successful resolution of symptoms after elimination of common food allergens.38 Diagnosis The American Gastroenterology Association guidelines state that diagnosis requires endoscopy with biopsy revealing $15 eosinophils per high-powered field (hpf ). A trial of PPI is recommended, as in many situations EoE is difficult to distinguish from GERD. If eosinophilia remains, EoE is diagnosed.38,39 Clinical Manifestations Symptoms of EoE in adults include heartburn, non-cardiac chest pain, dysphagia, and food impaction. Infants and children may also present with a history of feeding dysfunction, nausea, vomiting, and abdominal pain. Individuals may have a history of food allergy, asthma, eczema, or allergic rhinitis. Treatment Pharmacological treatment includes swallowed topical steroids and systemic steroids. Three different nutrition interventions are currently attempted for EoE. The first is an elimination of all food allergens by substituting a chemically defined formula as the only source of nutrients. This has been documented to successfully resolve symptoms but often requires long-term enteral feeding. Tolerance of and successful adherence to this strict protocol are difficult. The next nutrition therapy options include either a directed or an empiric elimination diet. The directed elimination diet restricts specific foods identified by allergy testing such as skin prick or atopy patch testing. These tests have limitations (see Chapter 9) and may eliminate foods that are not necessarily food triggers for the allergic reaction. The empiric elimination diet removes the most common food allergens: soy, milk, egg, wheat, peanuts, tree nuts, and seafood. After elimination for 8 weeks, foods are reintroduced one at a time. Repeat biopsies for presence of eosinophils will document a successful remission and response to the dietary elimination. These nutrition therapies require extensive education and follow-up by the registered dietitian to ensure successful adherence and maintenance of nutritional status for each patient.40,41 Chapter 9 provides additional information regarding the elimination diet for food allergies. Dysphagia Definition Dysphagia, or difficulty swallowing, is not gener- ally considered a diagnosis but a symptom caused by a variety of disorders. Since many conditions of the esophagus involve dysphagia, it is important to understand this "symptom" and the importance of nutrition therapy in its treatment. There are numerous medical conditions and treatments that can ultimately affect one or more of the four phases of swallowing: oral preparatory, oral, pharyngeal, and esophageal. Medical conditions that are often associated with dysphagia include neurological, immunological, gastroesophageal, congenital, and oncological disorders.42 See Table 14.10 for an outline of potential diagnoses associated with dysphagia. Clinical Manifestations The symptoms of dysphagia experienced by a patient depend on the phase of swallowing that is impaired. For example, if the problem originates in the oral preparation phase, food may be pocketed in the buccal mucosa (cheek area) because the patient cannot propel the bolus of food effectively from the front of the oral cavity to the Table 14.10 Diseases and Conditions Associated with Dysphagia Acute neurological Stroke, closed head injury Sources: Roden DF, Altman KW. Causes of dysphagia among different age groups: a systematic review of the literature. Otolaryngol Clin N Am. 2013; 46: 965-87. Logemann JA. Swallowing disorders. Best Pract Res Clin Gastroenterol. 2007; 21(4): 563-73. pharyngeal area. Other general symptoms may include drooling, coughing, and choking. Many patients will experience weight loss and generalized malnutrition due to inadequate nutritional intake.43-46 Aspiration or inhalation of oropharyngeal contents is a primary complication. This can lead to aspiration pneumonia with the accompanying infections and is the most common reason enteral nutrition support is recommended.45 Diagnosis Diagnosis and treatment of dysphagia involve many different members of the health care team. Many institutions have a dysphagia team consisting of physicians, nurses, speech-language pathologist, dietitian, physical therapist, and occupational therapist. Diagnosis of dysphagia begins with a clinical bedside evaluation and bedside swallowing assessment usually performed by the speech-language pathologist. Conclusive evaluation uses a videofluoroscopy swallow- ing study or fiberoptic endoscopic evaluation of swallowing (FEES) (see Figure 14.8 and Box 14.5). In these diagnostic procedures, barium is added to foods and liquids with a variety of textures. The patient is then monitored to determine his or her ability to swallow each of these foods. From these evaluations, a specific site of the dysphagia can be determined and a care plan can be developed. The severity of dysphagia may be evaluated using a variety of descriptions and scales. In one such scale, described in Table 14.11, the swallow is ranked from normal to a profound disruption, where oral intake is prohibited. Nutrition Therapy for Dysphagia Nutritional Implications and Assessment The primary nutritional implications are weight loss and subsequent development of nutrient deficiencies that can result from an inadequate dietary intake. Therefore, it is very important to accurately evaluate anthropometric measures and obtain as

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much information as possible regarding dietary intake and food patterns. After reviewing results of swallowing diagnos- tic tests, the health care team will be able to determine how the patient handles various textures of foods and liquids. Nutrition Diagnosis Common nutrition diagnoses asso- ciated with dysphagia include inadequate oral intake; inad- equate fluid intake; malnutrition; inadequate protein-energy intake; altered GI function; and swallowing difficulty. Nutrition Intervention Once the patient's swallowing ability has been evaluated, the registered dietitian can then use foods of acceptable textures to develop an adequate menu. The standard definitions for foods, liquids, and levels of nutri- tion intervention for dysphagia diets were developed by a United States task force in 2002. These levels of diet interven- tion are the National Dysphagia Diets 1, 2, and 3. Table 14.12 outlines the foods allowed on each level of the National Dysphagia Diet.47 There are many specialty products appropriate for dys- phagia diets available. These include a variety of thicken- ing agents and texture-modified products (see Figure 14.9) pre-prepared to meet a specific consistency for the diets; see Table 14.13 for examples. Thickening agents are primarily made from carbohydrates, and many foods included in the dysphagia diets are also high in simple sugars. Successfully managing blood glucose for individuals with diabetes is chal- lenging in this context. For those individuals who are unable to safely swallow or to consume adequate nutrition orally, enteral feeding should be considered (see Chapter 5). Enteral feeding may be tran- sitional until the patient successfully rehabilitates or may be a long-term support. Long-term nutritional support often poses ethical challenges for those individuals with chronic, terminal illnesses. (See Chapter 5.)

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in the section on GERD) can also be done at this time, if needed. The combination of surgical repair with fundoplication provides additional support of the LES, which prevents the stomach from sliding back through the diaphragm.27 Pathophysiology of the Stomach Diseases and clinical disorders that affect the stomach can certainly influence nutritional status. Some disorders, such as indigestion, are mild and temporary conditions that resolve easily. Others, such as peptic ulcer disease, are chronic and require aggressive medical intervention. Indigestion Indigestion, or dyspepsia, is not considered to be a specific condition. Most people use the term "indigestion" to refer to a wide range of symptoms that may include abdominal pain, abdominal fullness, gas, bloating, belching, nausea, or even gastroesophageal reflux. Nausea and Vomiting Nausea is the unpleasant sensation that there is a need to vomit; vomiting is the expulsion of gastric contents. Even though nausea does not always lead to vomiting, they are often considered together because they are controlled through the same neural pathways. Neural signals are sent to the vomiting center located in the medulla. As a result of these stimuli, the steps of vomiting or emesis occur. In this sequence of events, gastric contents are pushed upward by the constriction of the respiratory muscles, the esophageal sphincter opens, the glottis closes (to prevent aspiration), and gastric contents are expelled through the mouth. Additionally, chemoreceptor zones in the medullary nucleus can also trigger the vomiting center. Drugs, toxins, metabolic conditions (such as renal failure or acid-base imbalances), and motion affect chemoreceptor zones, which can lead to nausea and emesis. Vomiting may also occur as a result of stress or extreme emotions. Nausea and vomiting occur with many different medi- cal conditions. These may include infection, pain, pregnancy, syncope, headache, metabolic disorders, motion sickness, kidney failure, myocardial infarction, and a host of other possibilities. Therefore, treatment of the underlying cause is the most important step in treating nausea and vomiting. The patient's history and physical examination will assist in deter- mining the cause of nausea and vomiting. The etiology may be further clarified through assessment of the symptoms the patient experiences prior to and after vomiting. For example, if vomiting occurs within a very short time after eating, it may be indicative of an obstruction. Abdominal pain is symptomatic of an inflammatory process. Simple regurgitation of food occurs when gastric contents move easily from stomach to the mouth and is not a forceful expulsion like that seen in vomiting. After determining the etiology of nausea and vomiting, the next step for treatment is use of medications or antiemetics. Table 14.14 provides a summary of antiemetics used to treat nausea and vomiting. Medication action may decrease the sensitivity of the chemoreceptor trigger zones. In many situations, such as in the use of chemotherapy, antiemetics are prescribed at the onset of treatment to prevent nausea. Controlling nausea from the very beginning of treatment prevents anticipatory nausea and/or vomiting, which can develop when the patient comes to associate nausea and vomiting with a specific event, food, or smell. For instance, an individual who has gotten sick after eating a specific food may experience similar symptoms when faced with that food again because it evokes memories of prior illness. Complementary and alternative medicine (CAM) may provide some additional avenues for controlling and treating symptoms experienced with nausea as well as other symptoms experienced with diagnoses involving the upper gastrointestinal tract. These may include the use of ginger and peppermint oil in treatment of nausea. Acupuncture, aromatherapy, meditation, and guided imagery have also been used to treat nausea and vomiting, but with mixed results.4

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Nutrition therapy for jaw fracture

• Cut foods into small pieces and place in a strong blender or food processor. • Commercially prepared baby food is available to use (do not use "junior" foods), but you will need to experiment with herbs and spices to add flavor. Adding extra protein: • Dry milk powder—this can be added to thin cooked cereal, cocoa, eggnog, blenderized soups and casseroles, milkshakes, pudding, and gravy. • Double-strength milk—add 1 cup dry milk powder to 1 cup whole milk. Use this as a beverage or in place of milk in recipes. • Liquid egg substitutes—add EggBeaters® or other pasteurized egg substitutes. • Blenderized meats. • Cottage cheese. • Yogurt, smooth blended. • Commercial liquid nutritional supplements such as Ensure®, Boost®, or Carnation® Breakfast Essentials. To add extra kcalories: • Use whole milk, half and half, or evaporated milk in place of water as the fluid when blenderizing. • Add extra butter or margarine to blenderized vegetables, soups, or thin cereals. Add gravy to blenderized meats. • Add sugar or honey to blenderized fruits, squash, pumpkin, or carrots. Food Group Recommended Foods Food Group Recommended Foods Milk and milk products All Fruits Any cooked or canned fruits without seeds and skins Fresh, peeled soft fruits (like peaches and bananas) that can be blended until smooth Meat and other protein foods Tender, well-cooked meat, poultry, or fish prepared without bones, skin, or added fat Well-cooked eggs prepared without added fat Soft soy foods (like tofu) Smooth nut butters Fats and oils Any oils Melted butter or margarine Grains Rice Pasta Couscous without seeds and nuts Cooked cereals, such as oatmeal and cream of wheat Beverages Any Look for liquid supplements that provide both calories and protein, such as Carnation Breakfast Essentials, Boost, or Ensure Vegetables Any cooked or canned vegetables without seeds and skins Other Ground spices, seeds, and nuts Smooth condiments, such as mustard

Dental health risk increased with

• Sugar-sweetened liquids, such as carbonated beverages, fruit drinks, energy drinks, and sweetened teas and coffees • Sticky foods, such as raisins • Slowly dissolving candies • Sugary, starchy snacks, such as cookies, cakes, etc. • Simple sugars, such as sucrose, honey, and molasses Dietary Factors Associated with Decreased Risk • Sugar-free chewing gum, mints, and candies • Fresh fruits and vegetables • High-quality protein foods, such as meats, eggs, cheese, fish, beans, and legumes • Whole-grain, low-sugar breads and cereals Eating Patterns Associated with Increased Risk • Frequent and prolonged intake of foods rich in simple sugar • Eating sticky, retentive foods alone • Sipping sugar-sweetened beverages for prolonged periods Eating Patterns Associated with Decreased Risk • Space frequency of food and beverage intake at least 2 hours apart • Select fresh, whole, unprocessed food to stimulate salivary output • Chew sugarless