6/12/2020 Lect. 1, 2 Medical Nutrition Therapy for Upper Gastrointestinal Tract Disorders - PowerPoint Presentation

1. 6/12/2020Lect. 1, 2Medical Nutrition Therapy for Upper Gastrointestinal Tract Disorders Abdulaziz Abbas ph.DAssociate Professor Food & NutritionDr. Abdulaziz Abbas1

2. Digestive disorders are among the most common problems in health care. Between 60 and 70 million people are affected by all digestive diseases.More than 20 million diagnostic and surgical procedures involving the gastrointestinal (GI) tract are performed each year. Dietary habits and specific food types can play an important role in the onset, treatment, and prevention of many GI disorders. 6/12/2020Dr. Abdulaziz Abbas2

3. Nutrition therapy is integral in the prevention and treatment of malnutrition and deficiencies that can develop from a GI tract disorder. Diet and lifestyle modifications can improve a patient’s quality of life by alleviating GI symptoms and decreasing the number of health care visits and costs associated with GI disease.6/12/2020Dr. Abdulaziz Abbas3

4. ASSESSMENT PARAMETERSComponents of a comprehensive nutrition assessment of patients with GI disorders include the clinical examination and evaluation of anthropometrics, biochemical markers, and the patient’s nutrition history. A detailed nutrition history includes the typical dietary intake, changes in appetite, food allergies and intolerances, mastication and swallowing ability, and GI symptoms such as nausea, vomiting, diarrhea, constipation, and the use of dietary supplements. Assessment of body weight changes and evaluation of lean body mass (LBM) guide nutrition assessment, estimation of nutritional requirements, and the development of a nutrition care plan. 6/12/2020Dr. Abdulaziz Abbas4

5. THE ESOPHAGUSThe esophagus is a muscular tube that has an average length of 25 cm in adults.It serves a single but very important function: conveying solids and liquids from the mouth to the stomach. It is lined with nonkeratinized stratified squamous epithelium, and submucosal glands secrete mucin, bicarbonate, epidermal growth factor, and prostaglandin E2, which protect the mucosa from gastric acid. 6/12/2020Dr. Abdulaziz Abbas5

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7. It is highly muscular, with muscles arranged in a way to facilitate the passage of food. As a bolus of food is moved voluntarily from the mouth to the pharynx, the upper esophageal sphincter (UES) relaxes, the food moves into the esophagus, and peristaltic waves move the bolus down the esophagus; the lower esophageal sphincter (LES) relaxes to allow the food bolus to pass into the stomach. The esophageal transit time takes an average of 5 seconds when in an upright position, and up to 30 seconds when in a supine position. 6/12/2020Dr. Abdulaziz Abbas7

8. The normal esophagus has a multitiered defense system that prevents tissue damage from exposure to gastric contents, including LES contraction, normal gastric motility, esophageal mucus, tight cellular junctions, and cellular pH regulators. Musculoskeletal disorders and motility disorders may result in dysphagia. For example, achalasia is characterized by a failure of esophageal neurons, resulting in a loss of ability to relax the LES and have normal peristalsis.6/12/2020Dr. Abdulaziz Abbas8

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10. Gastroesophageal Reflux Disease (GERD) and EsophagitisEtiologyGastroesophageal reflux (GER) is considered a normal physiologic process that occurs several times a day in healthy infants, children and adults. GER generally is associated with transient relaxation of the LES independent of swallowing, which permits gastric contents to enter the esophagus. Gastroesophageal reflux disease (GERD) is a more serious, chronic or long-lasting form of GER and is defined as symptoms or complications resulting from the reflux of gastric contents into the esophagus or beyond, and even into the oral cavity (including larynx) or lung. 6/12/2020Dr. Abdulaziz Abbas10

11. In developed countries, the prevalence of GERD (defined by symptoms of heartburn [painful, burning sensation that radiates up behind the sternum of fairly short duration] and regurgitation, or both, at least once a week). The types of GERD can be distinguished by esophagogastroduodenoscopy(EGD), which uses a fiberoptic endoscope to directly visualize the esophagus, stomach, and duodenum. GERD can be classified as the presence of symptoms without abnormalities or erosions on endoscopic examination (nonerosive disease or NERD), or GERD with symptoms and erosions present (ERD). ERD generally is associated with more severe and prolonged symptoms compared with NERD.6/12/2020Dr. Abdulaziz Abbas11

12. Some patients experience GERD symptoms primarily in the evening (nocturnal GERD), which has a greater impact on quality of life compared with daytime symptoms. Nocturnal GERD is associated significantly with severe esophagitis (inflammation of the esophagus) and intestinal metaplasia (Barrett’s esophagus) and can lead to sleep disturbance. Patients with ERD are more likely to be men, and women are more likely to have NERD. There is a definite relationship between GERD and obesity. Several meta-analyses suggest an association between body mass index (BMI), waist circumference, weight gain, and the presence of symptoms and complications of GERD. 6/12/2020Dr. Abdulaziz Abbas12

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15. GERD is frequent during pregnancy, usually manifesting as heartburn, and may begin in any trimester. Chest pain may be a symptom of GERD, and distinguishing cardiac from noncardiac chest pain is required before considering GERD as a cause of chest pain. Patients with disruptive GERD (daily or more than weekly symptoms) have an increase in time off work and decrease in work productivity, and a decrease in physical functioning.6/12/2020Dr. Abdulaziz Abbas15

16. PathophysiologyThe pathophysiology of GERD is complex. Box 27-1 describes possible mechanisms involved in GERD. Three components make up the esophagogastric junction: the lower esophageal sphincter (LES), the crural diaphragm, and the anatomic flap valve. This esophagogastric junction functions as an antireflux barrier. The lower esophageal sphincter is a 3- to 4-cm segment of circular smooth muscle at the distal end of the esophagus. The resting tone of this muscle can vary among healthy individuals, ranging from 10 mm Hg to 35 mm Hg relative to the intragastric pressure. 6/12/2020Dr. Abdulaziz Abbas16

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18. The most common mechanism for reflux is transient LES relaxations, which are triggered by gastric distention and serve to enable gas venting from the stomach. On average, transient LES relaxations persist for about 20 seconds, which is significantly longer than the typical swallow-induced relaxation. For reflux to take place, pressure in the proximal stomach must be greater than the pressure in the esophagus. Patients with chronic respiratory disorders, such as chronic obstructive pulmonary disease (COPD), are at risk for GERD because of frequent increases in intraabdominal pressure. A chronically increased pressure also is seen during pregnancy and in overweight and obese people.6/12/2020Dr. Abdulaziz Abbas18

19. Hypersensitivity to acid can occur in people with erosive esophagitis and in those with normal mucosa. A factor contributing to increased esophageal sensitivity to acid is impaired mucosal barrier function. In a systematic review, the overall rate of gastric emptying was delayed in patients with GERD .Acid pocket is an occurrence during the postprandial period when a layer of acidic gastric juice is ready to reflux resulting from absence of peristaltic contraction in the proximal stomach. 6/12/2020Dr. Abdulaziz Abbas19

20. Prolonged acid exposure can result in esophagitis, esophageal erosions, ulceration, scarring, stricture, and in some cases dysphagia.Acute esophagitis may be caused by reflux, ingestion of a corrosive agent, viral or bacterial infection, intubation, radiation.The severity of the esophagitis resulting from the gastroesophageal reflux is influenced by the composition, frequency, and volume of the gastric reflux; the health of the mucosal barrier; length of exposure of the esophagus to the gastric reflux; and the rate of gastric emptying. Symptoms of esophagitis and GERD may impair the ability to consume an adequate diet and interfere with sleep, work, social events, and the overall quality of life.6/12/2020Dr. Abdulaziz Abbas20

21. Abnormalities in the body such as hiatal hernia also may contribute to gastroesophageal reflux and esophagitis. The esophagus passes through the diaphragm by way of the esophageal hiatus or ring. The attachment of the esophagus to the hiatal ring may become compromised, allowing a portion of the upper stomach to move above the diaphragm. Table 27-2describes the four types of hiatal hernia. The most common symptom of hiatal hernia is heartburn. When acid reflux occurs with a hiatal hernia, the gastric contents remain above the hiatus longer than normal. The prolonged acid exposure increases the risk of developing more serious esophagitis.6/12/2020Dr. Abdulaziz Abbas21

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24. Epigastric pain occurs in the upper middle region of the abdomen after large, energy-dense meals. Weight reduction and decreasing meal size reduce the negative consequences of hiatal hernia. Patients with type 3 hiatal hernia may present with severe chest pain, retching, vomiting, and hematemesis (vomiting of blood), because these hernias can twist and cause strangulation in the chest, which would be considered a surgical emergency.Some patients can present with iron deficiency anemia without acute bleeding, because the diaphragm becomes so irritated that the patient may develop chronic blood loss.Barrett’s esophagus (BE) is a precancerous condition in which the normal squamous epithelium of the esophagus is replaced by an abnormal columnar-lined epithelium known as specialized intestinal metaplasia (tissue that is similar to the intestinal lining). 6/12/2020Dr. Abdulaziz Abbas24

25. The exact cause of BE is unknown, but GERD is a risk factor for the condition. People with BE are at increased risk for a cancer called esophageal adenocarcinoma with incidence rising dramatically over the past 40 years and speculated to continue to rise during coming decades. Risk factors for BE include prolonged history of GERD-related symptoms (more than 5 years), middle age, white male, obesity, smoking, and family history of BE or adenocarcinoma of the esophagus. Estrogen may be protective and account for the lower incidence of BE in females. 6/12/2020Dr. Abdulaziz Abbas25

26. Medical and Surgical ManagementThe primary medical treatment of esophageal reflux is suppression of acid secretion. The aim in acid-suppression therapy is to raise the gastric pH above 4 during periods when reflux is most likely to occur. Proton pump inhibitors (PPIs), which decrease acid production by the gastric parietal cell, have been associated with superior healing rates and decreased relapses. Milder forms of reflux are managed by H2 receptor (a type of histamine receptor on the gastric parietal cell) antagonists, and antacids, which buffer gastric acid in the esophagus or stomach to reduce heartburn. 6/12/2020Dr. Abdulaziz Abbas26

27. Of patients with severe GERD, 5% to 10% do not respond to medical therapy. The Nissen fundoplication was first described as a treatment for severe reflux esophagitis in 1956 and is still the most commonly performed antireflux surgery (Figure 27-3).6/12/2020Dr. Abdulaziz Abbas27

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30. Lifestyle Modifications and Medical Nutrition TherapyThe first step in symptom management of GERD should consist of changes in lifestyle, including diet. The main factors that trigger reflux symptoms are caffeine, alcohol, tobacco, and stress. Initial recommendations should focus on meal size and content. Eating small rather than large meals reduces the probability that gastric contents will reflux into the esophagus. Obesity is a contributing factor to GERD and hiatal hernia because it increases intragastric pressure, and weight reduction may reduce acid contact time in the esophagus leading to decreased reflux symptoms. 6/12/2020Dr. Abdulaziz Abbas30

31. The frequent advice to elevate the head of the bed by 6 to 8 inches would be rational for patients who have reflux episodes at night. Frequent bending over should be avoided. Use of loose-fitting garments in the waist area also is thought to decrease the risk of reflux. Foods such as carminatives (such as peppermint and spearmint) have been reported to lower LES pressure, but little research has been done to establish their clinical significance in GERD when used in normal or small amounts. 6/12/2020Dr. Abdulaziz Abbas31

32. Fermented alcoholic beverages (such as beer and wine) stimulate the secretion of gastric acid and should be limited. Carbonated beverages enhance gastric distention, which increases transient LES relaxations. Highly acidic foods such as citrus juices and tomatoes should be avoided because they cause pain when the esophagus is already inflamed.The role of spices in the pathologic conditions related to upper GI disorders is not clear. In patients with GI lesions, the use of foods highly seasoned with chili powder and pepper can cause discomfort. Chewing gum has been shown to increase salivary secretions, which help raise esophageal pH, but no studies have demonstrated its efficacy compared with other lifestyle measures. 6/12/2020Dr. Abdulaziz Abbas32

33. Limiting or avoiding aggravating foods may improve symptoms in some individuals. Thus recommendations are to have a generally healthy diet and to avoid food items that, in the experience of the patient, trigger symptoms. Lifestyle changes to treat GERD in infants may involve a combination of feeding changes and positioning therapy. Modifying the maternal diet if infants are breastfed, changing formulas, and reducing the feeding volume while increasing the frequency of feedings may be effective strategies to address GERD in many infants.. Thickened feedings appear to decrease observed regurgitation rather than the actual number of reflux episodes. 6/12/2020Dr. Abdulaziz Abbas33

34. Cigarette smoking should be stopped because it is associated with decreased LES pressure and decreased salivation, thus causing prolonged acid clearance. Smoking tobacco products also compromises GI integrity and increases the risk of esophageal and other cancers. Identification and treatment of the mechanism underlying the GERD is the first line of therapy. Box 27-3 lists lifestyle and dietary modifications that are aimed at minimizing the occurrence of reflux and optimizing esophageal acid clearance.6/12/2020Dr. Abdulaziz Abbas34

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36. Head and Neck CancerPathophysiologyCancers of the upper aerodigestive tract, collectively referred to as head and neck cancers, comprise malignancies of the oral cavity (lips and inside of the mouth, including the front portion of the tongue, and the roof and floor of the mouth), the oropharynx (back portion of the tongue and the part of the throat behind the oral cavity), the larynx, and the esophagus. The patient diagnosed with head and neck cancer faces unique challenges in maintaining adequate nutrition. The disease and the treatments, especially surgery, chemo- and radiation therapy, have significant impact on upper digestive tract function, and oral intake is often insufficient during and after therapy. 6/12/2020Dr. Abdulaziz Abbas36

37. Almost all patients with head and neck cancer are malnourished at the time of diagnosis. Dysphagia is a hallmark of head and neck cancer; it occurs as a result of mechanical obstruction, sensory impairment, or odynophagia (painful swallowing). In these patients there is a high prevalence of alcohol abuse and longterm tobacco use, which are also associated with chronic malnutrition.6/12/2020Dr. Abdulaziz Abbas37

38. Medical Nutrition TherapyDepending on the tumor site, the surgical procedure may significantly alter the anatomy and lead to scarring that can negatively affect swallowing. The patient is likely to be restricted from oral intake while healing from the surgery. Placement of a gastrostomy tube is the most common approach to ensure safe delivery of adequate nutrition, but the optimal timing is not defined. Although the goal is eventual transition to oral feeding, some patients will require additional enteral nutrition (EN) because of structural and sensory deficits. 6/12/2020Dr. Abdulaziz Abbas38

39. Aggressive prophylactic swallowing therapy is a recent development in the treatment of dysphagia in patients with head and neck cancer. This approach focuses on maintaining or regaining function rather than simply accommodating dysfunction (reliance on feeding tube) and empowers patients to progress carefully with oral intake despite imperfect swallowing.6/12/2020Dr. Abdulaziz Abbas39

40. THE STOMACHThe stomach accommodates and stores meals, mixes food with gastric secretions, and controls emptying into the duodenum. Gastric volume is approximately 50 ml when empty, but can expand to approximately 4 L. Gastric parietal cells (acid producing cells) produce 1.5 to 2 L of acid daily resulting in a pH between 1 and 2. The mucosa of the stomach and duodenum is protected from proteolytic actions of gastric acid and pepsin by a coating of mucus secreted by glands in the epithelial walls from the lower esophagus to the upper duodenum. The mucosa also is protected from bacterial invaction by the digestive actions of pepsin and hydrochloric acid (HCl). Prostaglandins play an important role in protecting the gastroduodenal mucosa by stimulating the secretion of mucus and bicarbonate and maintaining blood flow during periods of potential injury.6/12/2020Dr. Abdulaziz Abbas40

41. Dyspepsia and Functional DyspepsiaPathophysiologyDyspepsia (indigestion) refers to nonspecific, persistent upper abdominal discomfort or pain. It affects an estimated 20% to 40% of the general population and significantly reduces quality of life. The underlying causes of dyspepsia may include GERD, peptic ulcer disease, gastritis, gallbladder disease or other identifiable pathologic conditions. Functional dyspepsia (FD) is defined by the Rome III criteria as the presence of symptoms thought to originate in the gastroduodenal region in the absence of any organic, systemic, or metabolic disease likely to explain the symptoms. 6/12/2020Dr. Abdulaziz Abbas41

42. Epigastric pain or discomfort is the hallmark symptom in patients with FD. The word discomfort is important to emphasize, because many patients will not complain of pain, but rather complain of burning, pressure, or fullness in the epigastric area, or that they cannot finish a normal-sized meal (early satiety). Other symptoms include postprandial nausea, belching, and abdominal bloating. 6/12/2020Dr. Abdulaziz Abbas42

43. Medical Nutrition TherapyCurrent treatments for FD have generally ignored the potential role of diet. The possible effect of specific foods and macronutrients and other dietary habits to induce or exacerbate FD symptoms has been poorly studied, and often there are conflicting results.Using a food and symptom diary during a clinical evaluation of a patient with FD and assessing symptoms associated with eating patterns is useful. Dietary modifications such as consuming smaller meals with a reduction in dietary fat may be promising in FD therapy. Helping the client identify problematic foods also can be helpful.6/12/2020Dr. Abdulaziz Abbas43

44. Gastritis and Peptic UlcersPathophysiologyGastritis is a nonspecific term literally meaning inflammation of the stomach. It can be used to describe symptoms relating to the stomach, an endoscopic appearance of the gastric mucosa, or a histologic change characterized by infiltration of the epithelium with inflammatory cells such as polymorphonuclear cells (PMNs). 6/12/2020Dr. Abdulaziz Abbas44

45. Acute gastritis refers to rapid onset of inflammation and symptoms. Chronic gastritis may occur over a period of months to decades, with reoccurring symptoms. Symptoms include nausea, vomiting, malaise, anorexia, hemorrhage, and epigastric pain. Prolonged gastritis may result in atrophy and loss of stomach parietal cells, with a loss of HCL secretion (achlorhydria) and intrinsic factor, resulting in pernicious anemia. 6/12/2020Dr. Abdulaziz Abbas45

46. Helicobacter pylori GastritisHelicobacter pylori is a gram-negative bacteria that is somewhat resistant to the acidic environment in the stomach. H. pylori infection is responsible for most cases of chronic inflammation of the gastric mucosa and peptic ulcer, gastric cancer, and atrophic gastritis (chronic inflammation with deterioration of the mucous membrane and glands), resulting in achlorhydria and loss of intrinsic factor.H. pylori infection prevalence generally correlates with geography and the socioeconomic status of the population and begins during childhood, but generally is not diagnosed until adulthood. H. pylori is believed to be spread through contaminated food and water. 6/12/2020Dr. Abdulaziz Abbas46

47. Its prevalence ranges from approximately 10% in developed countries to 80% to 90% in developing countries. Although gastritis is a characteristic observation, most people infected with H. pylori never develop ulcers. H. pylori infection does not resolve spontaneously, and risks of complications increase with the duration of the infection. Other risk factors contributing to pathology and disease severity include patient age at onset, specific strain and concentration of the organism, genetic factors related to the host, and the patient’s lifestyle and overall health.6/12/2020Dr. Abdulaziz Abbas47

48. In the first week after H. pylori infection, many PMNs and a few eosinophils infiltrate the gastric mucosa. These are replaced gradually with the mononuclear cells. H. pylori can cause duodenitis if it colonizes gastric tissue that may be present in the duodenum. Treating H. pylori with antibiotics can cause PMNs to disappear within a week or two, but a mild gastritis can persist for several years as the reduction in mononuclear cells is slow. In countries where H. pylori is common, so is gastric cancer. Because H. pylori can cause peptic ulcer and gastric cancer, antibiotic treatment is favored when it is diagnosed.6/12/2020Dr. Abdulaziz Abbas48

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50. Non-Helicobacter pylori GastritisAspirin and non-steroidal antiinflammatory drugs (NSAIDs) are corrosive; both inhibit prostaglandin synthesis, which is essential for maintaining the mucus and bicarbonate barrier in the stomach. Thus chronic use of aspirin or other NSAIDs, steroids, alcohol, erosive substances, tobacco, or any combination of these factors may compromise mucosal integrity and increase the chance for acquiring acute or chronic gastritis. Poor nutrition and general poor health may contribute to the onset and severity of the symptoms and can delay the healing process.6/12/2020Dr. Abdulaziz Abbas50

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52. Medical TreatmentTreatment for gastritis involves removing the inciting agent (e.g., pathogenic organism, NSAIDs). Noninvasive methods for diagnosing H. pylori include a blood test for H. pylori antibodies, a urea breath test, or a stool antigen test. Endoscopy is a common invasive diagnostic tool (see Focus On: Endoscopy and Capsules). Antibiotics and proton pump inhibitors (PPIs) are the primary medical treatments. Side effects of chronic acid suppression either from disease or chronic use of PPIs should be considered. These include reduction of gastric secretion of HCL, which can reduce absorption of nutrients (e.g., vitamin B12, calcium, and nonheme iron) that require intragastric proteolysis to make them bioavailable.Acid suppression may increase incidence of some bone fractures, as well as increase the risk for intestinal infection because gastric acidity is a primary defense against ingested pathogens. 6/12/2020Dr. Abdulaziz Abbas52

53. Peptic UlcersEtiologyNormal gastric and duodenal mucosa is protected from the digestive actions of acid and pepsin by the secretion of mucus, the production of bicarbonate, the removal of excess acid by normal blood flow, and the rapid renewal and repair of epithelial cell injury. Peptic ulcer refers to an ulcer that occurs as a result of the breakdown of these normal defense and repair mechanisms. Typically more than one of the mechanisms must be malfunctioning for symptomatic peptic ulcers to develop. Peptic ulcers typically show evidence of chronic inflammation and repair processes surrounding the lesion. The primary causes of peptic ulcers are H. pylori infection, gastritis, use of aspirin, other NSAIDs and corticosteroids, and severe illness.6/12/2020Dr. Abdulaziz Abbas53

54. Use of tobacco products also is linked with peptic ulcer risk, because tobacco decreases bicarbonate secretion and mucosal blood flow, exacerbates inflammation, and is associated with additional complications of H. pylori infection.The incidence and number of surgical procedures related to peptic ulcers has decreased markedly in the past 3 decades because of recognition of symptoms and risk factors, and earlier screening for H. pylori. Peptic ulcers normally involve two major regions: gastric and duodenal. Uncomplicated peptic ulcers in either region may present with signs similar to those associated with dyspepsia and gastritis.6/12/2020Dr. Abdulaziz Abbas54

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56. Abdominal discomfort is the most common symptom of duodenal and gastric ulcers. Felt anywhere between the navel and the breastbone, this discomfort usually is a dull or burning pain, occurs when the stomach is empty—between meals or during the night, may be briefly relieved by eating food, in the case of duodenal ulcers, or by taking antacids. In both types of peptic ulcers the symptoms last for minutes to hours and come and go for several days or weeks. Other symptoms include bloating, burping, nausea, vomiting, poor appetite, and weight loss. Some people experience only mild symptoms or none at all. Peptic ulcers also may have “emergency symptoms,” in which medical assistance should be sought immediately. 6/12/2020Dr. Abdulaziz Abbas56

57. These include sharp, sudden, persistent, and severe stomach pain, bloody or black stools (melena), bloody vomit (hematemesis), or vomit that looks like coffee grounds. These symptoms could be signs of a serious problem, such as acute or chronic GI bleeding—when acid or the peptic ulcer breaks a blood vessel; perforation—when the peptic ulcer burrows completely through the stomach or duodenal wall potentially penetrating an adjacent organ (e.g., pancreas); or obstruction—when the peptic ulcer blocks the path of food trying to leave the stomach. Complications of hemorrhage and perforation contribute significantly to the morbidity and mortality of peptic ulcers.6/12/2020Dr. Abdulaziz Abbas57

58. Gastric versus Duodenal UlcersPathophysiologyAlthough gastric ulcers can occur anywhere in the stomach, most occur along the lesser curvature (Figure 27-5). Gastric ulcers typically are associated with widespread gastritis, inflammatory involvement of parietal cells, and atrophy of acid- and pepsin-producing cells occurring with advancing age. In some cases gastric ulceration develops despite relatively low acid output. Antral hypomotility, gastric stasis, and increased duodenal reflux are associated commonly with gastric ulcers, and when present, may increase the severity of the gastric injury. The incidence of hemorrhage and overall mortality is higher with a gastric ulcer than a duodenal ulcer.6/12/2020Dr. Abdulaziz Abbas58

59. A duodenal ulcer is characterized by increased acid secretion throughout the entire day accompanied with decreased bicarbonate secretion. Most duodenal ulcers occur within the first few centimeters of the duodenal bulb, in an area immediately below the pylorus. Gastric outlet obstruction occurs more commonly with duodenal ulcers than with gastric ulcers, and gastric metaplasia (e.g., replacement of duodenal villous cells with gastric-type mucosal cells) may occur with duodenal ulcer related to H. pylori.6/12/2020Dr. Abdulaziz Abbas59

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61. Medical and Surgical Management of UlcersRegardless of the type of ulcer, the first intervention is to evaluate the patient endocopically and resuscitate as needed. Control acute bleeding if present.Peptic Ulcers. H. pylori is the primary cause of gastritis and peptic ulcers, thus its diagnosis if present, and treatment, should be the first medical intervention. At the first endoscopy, diagnostic biopsies should be taken for H. pylori. Treatment of H. pylori infection entails eradication of this organism with the appropriate antibiotic and acid suppressive regimen. Although surgical intervention is less prevalent, emergent and elective procedures and surgeries are still required for peptic ulcer complications. Interventions can range from endoscopic, open, and laparoscopic procedures to treat individual lesions, to partial gastrectomy and occasionally selective vagotomies.6/12/2020Dr. Abdulaziz Abbas61

62. In addition to traditional medical treatments, several complementary medicine interventions have been investigated. Use of foods or their extracts (e.g., phenolic fractions of ginger and ginger hydrolysed phenolic fractions of ginger, Zingiber officinale) that contain phenolic antioxidants have been found to be potent inhibitors of proton potassium ATPase activity and H. pylori growth.Although certain species of probiotics (e.g., Lactobacillus acidophilus, Lactobacillus salivarius, Lactobacillus rhamnosus, and Bifidobacterium bifidum) have been shown to exert direct inhibitory effects on H. pylori in in-vitro and in-vivo animal models, these effects have not consistently been found in humans, leaving probiotic supplementation for this purpose controversial. 6/12/2020Dr. Abdulaziz Abbas62

63. Systematic reviews of the literature have shown that various probiotic species (including Lactobacillus spp., Bifidobacterium spp., Saccharomyces spp., and Bacillus spp.) can help diminish eradication-related side effects, including diarrhea, nausea, dyspepsia, and dysgeusia, thus increasing tolerability and therefore compliance. 6/12/2020Dr. Abdulaziz Abbas63

64. Stress Ulcers. Stress ulcers may occur as a complication of metabolic stress caused by trauma, burns, surgery, shock, renal failure, or radiation therapy. A primary concern with stress ulceration is the potential for significant GI hemorrhage. Although stress ulcerations usually occur in the fundus and body of the stomach, they also may develop in the antrum, duodenum, or distal esophagus. Typically shallow and causing oozing of blood from superficial capillary beds, stress ulcer lesions also may occur deeper, eroding into the submucosa, causing massive hemorrhage or perforation.Stress ulcers that bleed can be a significant cause of morbidity in the critically ill patient. Although current prevention and treatment include sucralfate, acid suppressives, and antibiotics as needed, high-quality evidence to guide clinical practice in effective treatments is limited. 6/12/2020Dr. Abdulaziz Abbas64

65. Medical Nutrition TherapyIn persons with atrophic gastritis, vitamin B12 status should be evaluated because of lack of intrinsic factor and gastric acid results in malabsorption of this vitamin. Low acid states may influence absorption of iron, calcium, and other nutrients because gastric acid enhances bioavailability. In the case of iron deficiency anemia, other causes may be the presence of H. pylori and gastritis. Eradication of H. pylori has resulted in improved absorption of iron and increased ferritin Levels. For several decades dietary factors have gained or lost favor as a significant component in the cause and treatment of dyspepsia, gastritis, and peptic ulcer disease. 6/12/2020Dr. Abdulaziz Abbas65

66. There is little evidence that specific dietary factors cause or exacerbate gastritis or peptic ulcer disease. Protein foods temporarily buffer gastric secretions, but they also stimulate secretion of gastrin, acid, and pepsin. Milk or cream, which in the early days of peptic ulcer management was considered important in coating the stomach, is no longer considered medicinal.6/12/2020Dr. Abdulaziz Abbas66

67. The pH of a food has little therapeutic importance, except for patients with existing lesions of the mouth or the esophagus. Most foods are considerably less acidic than the normal gastric pH of 1 to 3. The pH of orange juice and grapefruit is 3.2 to 3.6, and the pH of commonly used soft drinks ranges from approximately 2.8 to 3.5. On the basis of their intrinsic acidity and the amount consumed, fruit juices and soft drinks are not likely to cause peptic ulcers or appreciably interfere with healing. Some patients express discomfort with ingestion of acidic foods, but the response is not consistent among patients, and in some, symptoms may be related to heartburn. The dietary inclusion of “acidic foods” should be individualized based on the patient’s perception of their effect.6/12/2020Dr. Abdulaziz Abbas67

68. Coffee and caffeine stimulate acid secretion and also may decrease LES pressure; however, neither has been strongly implicated as a cause of peptic ulcers outside of the increased acid secretion and discomfort associated with their consumption. When very large doses of certain spices are fed orally or placed intragastrically without other foods, they increase acid secretion and cause small, transient superficial erosions, inflammation of the mucosal lining, and altered GI permeability or motility. Most often incriminated are chili, cayenne, and black peppers. 6/12/2020Dr. Abdulaziz Abbas68

69. Small amounts of chili pepper or its pungent ingredient, capsicum, may increase mucosal protection by increasing production of mucus. However, large amounts may cause superficial mucosal damage, especially when consumed with alcohol. Another spice, curcumin, through its antiinflammatory activity that inhibits the NF-KB pathway activation may be a chemopreventative candidate against H. pylori–related cancer .The synergy of food combinations may inhibit the growth of H. pylori. Food provides an interesting alternative to therapies that include antibiotics, PPIs and bismuth salts .Studies suggest that green tea, broccoli sprouts, black currant oil, and kimchi (fermented cabbage) help with H. pylori eradication. Probiotics species (Lactobacillus, Bifidobacterium) also have been studied for prevention, management, and eradication of H. pylori .6/12/2020Dr. Abdulaziz Abbas69

70. Omega-3 and omega-6 fatty acids are involved in inflammatory, immune, and cytoprotective physiologic conditions of the GI mucosa, but they have not yet been found to be effective for treatment. Long-term clinical trials have not been performed. Overall, a high-quality diet without nutrient deficiencies may offer some protection and may promote healing. Persons being treated for gastritis and peptic ulcer disease should be advised to avoid foods that exacerbate their symptoms and to consume a nutritionally complete diet with adequate dietary fiber from fruits and vegetables.6/12/2020Dr. Abdulaziz Abbas70

71. Carcinoma of the StomachAlthough the incidence and mortality have fallen dramatically over the last 50 years in many regions, gastric cancer is still the second most common cause of cancer death worldwide, with varying incidence in different parts of the world and among various ethnic groups. Despite advances in diagnosis and treatment, the 5-year survival rate of stomach cancer is only 20%.EtiologyThe cause of gastric cancer is multifactorial, but more than 80% of cases have been attributed to H. pylori infection. In addition, diet, lifestyle, genetic, socioeconomic, and other factors contribute to gastric carcinogenesis. A Western diet, high in processed meats, fat, starches, and simple sugars, is associated with an increased risk of gastric cancer compared with a diet high in fruits and vegetables. 6/12/2020Dr. Abdulaziz Abbas71

72. Other factors that may increase the risk of gastric cancer include alcohol consumption, excess body weight, smoking, intake of highly salted or pickled foods, or inadequate amounts of micronutrients. Certain cooking practices also are associated with increased risk of gastric cancer including broiling of meats, roasting, grilling, baking, and deep frying in open furnaces, sun drying, salting, curing, and pickling, all of which increase the formation of carcinogenic N-nitroso compounds. Polycyclic aromatic hydrocarbons such as benzo[a]pyrene formed in smoked food have been incriminated in many areas of the world. 6/12/2020Dr. Abdulaziz Abbas72

73. Medical and Surgical ManagementMost cancers of the stomach are treated by surgical resection; thus part of the nutritional considerations includes partial or total resection of the stomach, a gastrectomy. Some patients may experience difficulties with nutrition after surgery.Medical Nutrition TherapyThe dietary regimen for carcinoma of the stomach is determined by the location of the cancer, the nature of the functional disturbance, and the stage of the disease. The patient with advanced, inoperable cancer should receive a diet that is adjusted to his or her tolerances, preferences, and comfort. Anorexia is almost always present from the early stages of disease. In the later stages of the disease, the patient may tolerate only a liquid diet. If a patient is unable to tolerate oral feeding, consideration should be given to using an alternate route, such as a gastric or intestinal enteral tube feeding, or if this is not tolerated or feasible, parenteral feeding. The nutritional support for the patient should be in accordance with the patient’s goals of care. 6/12/2020Dr. Abdulaziz Abbas73

74. Dumping SyndromeEtiologyThe dumping syndrome is a complex GI and vasomotor response to the presence of large quantities of hypertonic foods and liquids in the proximal small intestine. Dumping syndrome usually occurs as a result of surgical procedures that allow excessive amounts of liquid or solid foods to enter the small intestine in a concentrated form. Milder forms of dumping may occur to varying degrees in persons without surgical procedures, and most of the symptoms can be reproduced in normal individuals by infusing a loading dose of glucose into the jejunum. Dumping may occur as a result of total or partial gastrectomy, manipulation of the pylorus, fundoplication, vagotomy, and some gastric bypass procedures for obesity. 6/12/2020Dr. Abdulaziz Abbas74

75. PathophysiologySymptoms can be divided into two stages of dumping of solids and liquids into the small intestine: early (within 10 to 30 minutes postprandially) and late (1-3 hrs postprandially). Characteristics and severity of symptoms vary between patients. Early dumping is characterized by GI and vasomotor symptoms, which include abdominal pain, bloating, nausea, vomiting, diarrhea, headache, flushing, fatigue, and hypotension.6/12/2020Dr. Abdulaziz Abbas75

76. These early symptoms likely occur because of the rapid influx of hyperosmolar contents into the duodenum or small intestine. A subsequent fluid shift from the intravascular compartment to the intestinal lumen occurs resulting in small intestine distention potentially causing cramps and bloating. Late symptoms are predominantly vasomotor and include perspiration, weakness, confusion, shakiness, hunger, and hypoglycemia. Late dumping is likely the result of reactive hypoglycemia. Rapid delivery, as well as hydrolysis and absorption of carbohydrates, produces an exaggerated rise in insulin level and a subsequent decline in blood glucose. The rapid changes in blood glucose and the secretion of gut peptides, glucose insulinotropic polypeptide, and glucagon-like polypeptide-1 appear to be at least partly responsible for the late symptoms.6/12/2020Dr. Abdulaziz Abbas76

77. Medical ManagementMedical intervention typically involves dietary changes as the initial treatment, and they are usually effective. However, in 3% to 5% of patients, severe dumping persists despite dietary change. In these patients, medications may be used to slow gastric emptying and delay transit of food through the GI tract. Some, such as acarbose, inhibit alpha glycoside hydrolase and interfere with carbohydrate absorption, and octreotide, a somatostatin analog, inhibits insulin release (see Table 27-3 for common medications). Rarely, surgical intervention is used to treat dumping syndrome.6/12/2020Dr. Abdulaziz Abbas77

78. Medical Nutrition TherapyPatients with dumping syndrome may experience weight loss and malnutrition caused by inadequate intake, malabsorption, or a combination of both. The prime objective of nutrition therapy is to restore nutrition status and quality of life. Because they are digested more slowly, proteins and fats are better tolerated than carbohydrates, particularly simple carbohydrates. Simple carbohydrates such as lactose, sucrose, fructose, glucose and dextrose are hydrolyzed rapidly and should be limited, but complex carbohydrates (starches) can be included in the diet. Liquids leave the stomach and enter the jejunum rapidly; thus some patients have trouble tolerating liquids with meals. Patients with severe dumping may benefit from limiting the amount of liquids taken with meals and drinking liquids between meals without solid food. Reclining (approximately 30 degrees) after meals may also minimize severity of symptoms. 6/12/2020Dr. Abdulaziz Abbas78

79. The use of fiber supplements, particularly pectin or gums (e.g., guar) can be beneficial in managing dumping syndrome because of fiber’s ability to form gels with carbohydrates and fluids and delay GI transit. Patients may need to be taught about portion sizes of foods, especially of carbohydrate foods such as juices, soft drinks, desserts, and milk. The exchange list given in Appendix 27 can be used to calculate carbohydrate intake and teach about carbohydrate control.Postgastrectomy patients often do not tolerate lactose, but small amounts (e.g., 6 g or less per meal) may be tolerated at one time. Patients typically do better with cheeses or unsweetened yogurt than with fluid milk. Vitamin D and calcium supplements may be needed when intake is inadequate. 6/12/2020Dr. Abdulaziz Abbas79

80. When steatorrhea (greater than 7% of dietary fat in the stool) exists, reduced fat formulas or pancreatic enzymes may be beneficial. Box 27-5 provides general nutrition guidelines for patients with dumping syndrome after gastric surgery; however, each diet must be adjusted based on a careful dietary and social history from the patient.6/12/2020Dr. Abdulaziz Abbas80

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