© 2007 Thomson - Wadsworth Upper Gastrointestinal Tract Chapter 16

© 2007 Thomson - Wadsworth Upper GI – A&P GI tract – long tube ~ 15 ft. Upper GI – mouth, pharynx, esophagus, stomach Accessory organs – pancreas, biliary system, liver Four basic functions: motility, secretion, digestion, absorption

© 2007 Thomson - Wadsworth

Upper GI – A&P Motility - movement of food by propulsion and contractions Secretions – water, electrolytes, enzymes, bile salts, mucus Digestion – complex molecules converted to simplest form Absorption – basic molecules, electrolytes, water, vitamins & minerals provide nutrients to the cells

© 2007 Thomson - Wadsworth Upper GI – A&P Regulated through neurotransmitter secretion e.g. acetylcholine, substance P, serotonin, dopamine, CCK, somatostatin etc. See Table 16.1 for others Parasympathetic impulses carried by vagus nerve

© 2007 Thomson - Wadsworth

Upper GI – A&P Oral Cavity Motility Mastication Oral Cavity Secretions Saliva from 3 sets of salivary glands Water Electrolytes - sodium chloride, bicarbonate, potassium Proteins - enzymes, mucus, lysozymes

© 2007 Thomson - Wadsworth Upper GI – A&P Saliva – functions Moistening/lubrication Initial digestion of CHO Antibacterial protection Enhances taste Serves as a buffer Oral hygiene Assisting speech

© 2007 Thomson - Wadsworth Upper GI – A&P Esophagus Sphincters at either end Four layers of tissue: mucosa, submucosa, muscle, adventitia Chief function is motility Swallow phases: Oral preparatory phase Oral Pharyngeal Esophageal

© 2007 Thomson - Wadsworth Upper GI – A&P Esophagus Peristalsis begins after swallow Lower esophageal sphincter (LES) controls release of bolus into stomach Nitric oxide and VIP inhibit closure (relax LES)

© 2007 Thomson - Wadsworth Upper GI – A&P Stomach - Motility Filling, storage, mixing, emptying 50 mL empty – stretches to 1000 mL Pyloric sphincter

© 2007 Thomson - Wadsworth Upper GI – A&P Stomach – Secretions 1-3 L of gastric juices Water, mucus, HCL, enzymes, electrolytes Mucus protects lining of stomach Chief cells - zymogen, pepsinogen, gastric lipase Parietal cells – HCL and intrinsic factor Cells in pylorus – histamine, gastrin, somatostatin

© 2007 Thomson - Wadsworth Upper GI – A&P Stomach – control of secretions Acetylcholine, histamine, gastrin - stimulate gastric secretions Somatostatin - inhibits gastric secretion

© 2007 Thomson - Wadsworth

Upper GI – A&P Stomach – release of secretions Phases: Cephalic - release of HCL and pepsinogen stimulated by tasting, smelling, seeing food Gastric - when food enters the stomach Intestinal - inhibitory; slows gastric secretions and prepares small intestine for receipt of acidic chyme

© 2007 Thomson - Wadsworth

Upper GI – A&P Stomach – release of secretions Inhibit action of chief and parietal cells decreasing gastric juices CCK & secretin – slow gastric motility Somatostatin

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Upper GI – A&P Stomach – Digestion & Absorption Mechanical and chemical HCL denatures protein structure and converts pepsinogen to pepsin Pepsin cleaves proteins Absorption is limited except for alcohol & aspirin

© 2007 Thomson - Wadsworth Pathophysiology – Oral Cavity Oral disease – can lead to nutritional deficits Dental caries, periodontal disease Inflammatory conditions such as gingivitis, stomatitis, glossitis, cheilosis Altered salivary gland function Xerostomia resulting from surgery or radiation or blockage Sjogrens syndrome Dehydration Medications

© 2007 Thomson - Wadsworth

Pathophysiology - Oral Cavity Surgical procedures Tongue, palate, pharynx MMF – “wiring the jaw” – intake limited to liquids and blenderized foods Impaired taste (dysgeusia) or ageusia Chemotherapy, radiation, nervous system diseases Medications

© 2007 Thomson - Wadsworth Pathophysiology - Oral Cavity Nutrition Implications/Therapy Inability to maintain oral intake, difficulty swallowing Texture modifications – soft, moist, liquids, or blenderized Increase kcal and protein density Modular supplements Liquid supplements Increase fat intake

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Pathophysiology - Oral Cavity Nutrition Therapy/Evaluation Increase frequency of meals Bland foods served at room temp. Liberal use of fluids Preference for cold and frozen foods Oral hygiene Monitor using food diary, observation, or kcal count Monitor weight gain or maintenance

© 2007 Thomson - Wadsworth Pathophysiology - Esophagus GERD - reflux of gastric contents into the esophagus Incompetence of LES Increased secretion of gastrin, estrogen, progesterone Hiatal hernia Cigarette smoking Use of medications Foods high in fat, chocolate, spearmint, peppermint, alcohol, caffeine

© 2007 Thomson - Wadsworth Pathophysiology - Esophagus GERD - symptoms Dysphagia Heartburn Increased salivation Belching Pain radiating to back, neck, or jaw Aspiration Ulceration Barrett’s esophagus

© 2007 Thomson - Wadsworth Pathophysiology - Esophagus GERD - Treatment Medical management Modify lifestyle factors Medications – 5 classes – see Table Surgery Fundoplication Stretta procedure

© 2007 Thomson - Wadsworth

Pathophysiology - Esophagus GERD - Nutrition Therapy Identify foods that worsen symptoms Assess food intake esp. those that reduce LES pressure, or increase gastric acidity Assess smoking and physical activity Small, frequent meals Weight loss if warranted See Table 16.12

© 2007 Thomson - Wadsworth Pathophysiology - Esophagus Dysphagia – difficulty swallowing Potential causes – see Table Drooling, coughing, choking Weight loss, generalized malnutrition Aspiration to aspiration pneumonia Treatment requires health care team dg by bedside swallowing, videofluoroscopy, barium swallow

© 2007 Thomson - Wadsworth

Pathophysiology - Esophagus Dysphagia – Nutrition Therapy Use acceptable textures to develop adequate menu National Dysphagia Diet 1,2,3 – see Table Use of thickening agents and specialized products Monitor weight, hydration, and nutritional parameters

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Pathophysiology - Esophagus Achalasia – motility disorder with absence of peristalsis Elevated LES pressure Impaired relaxation of LES Primary and secondary Treatment includes medications and invasive procedures

© 2007 Thomson - Wadsworth

Pathophysiology - Esophagus Achalasia – nutritional intervention Dysphagia, vomiting, substernal pain Body of esophagus loses muscle tone causing it to stretch – poor oral intake, weight loss Texture modification Increased kcal and protein density Avoid extreme temp. or spicy foods Small, more frequent meals

© 2007 Thomson - Wadsworth Hiatal Hernia

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Indigestion – dyspepsia Abdominal pain, fullness, gas, bloating, belching, nausea, reflux Nausea & Vomiting Caused by drugs, toxins, metabolic conditions, stress or extreme emotions Treat underlying cause Medications or antiemetics

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Severe Vomiting Rupture Hematemesis Dehydration Acid-base imbalances Malnutrition Aspiration pneumonia

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Nausea & Vomiting – Nutrition May lead to learned food aversions Minimize symptoms and discomfort See Table for suggestions Monitor hydration status

© 2007 Thomson - Wadsworth

Pathophysiology - Stomach Gastritis Inflammation of the gastric mucosa Primary cause: H. pylori bacteria Alcohol, food poisoning, NSAIDs Symptoms: belching, anorexia, abdominal pain, vomiting Type A - automimmune Type B – H. pylori Increases with age, achlorhydria Treat with antibiotics and medications

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Peptic ulcer disease - ulcerations of the gastric mucosa that penetrate submucosa Gastric or duodenal H. pylori NSAIDS, alcohol, smoking Certain foods, genetic link Increased risk of gastric cancer

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Peptic Ulcer Disease Symptoms: epigastric pain relieved or worsened by abdominal pain, burning sensation Relieved with eating or antacids Rebound gastrin release – more pain Presence of blood in the stool or vomit Treatment: triple/quadruple therapy of meds, surgery

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Peptic Ulcer Disease - Nutrition Restrict only those foods known to increase acid secretion Black and red pepper, caffeine, coffee, alcohol, individually non-tolerated foods Consider timing and size of meal Do not lie down after meals Small, frequent meals

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Gastric Surgery With complications: hemorrhage, perforation, obstruction Vagotomy Vagotomy with pyloroplasty Billroth I & II, Roux-en-Y See Fig. 16.9

© 2007 Thomson - Wadsworth

Pathophysiology - Stomach Gastric Surgery - Nutrition Implications Reduced capacity Changes in gastric emptying & transit time Components of digestion altered or lost Decreased oral intake, maldigestion, malabsorption

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Gastric Surgery - Dumping Syndrome Increased osmolar load enters small intestine too quickly from stomach Release of hormones, enzymes, other secretions altered Food “dumps” into small intestine

© 2007 Thomson - Wadsworth

Pathophysiology - Stomach Gastric Surgery - Dumping Syndrome Early dumping – min.; diarrhea, dizziness, weakness, tachycardia Intermediate min.; fermentation of bacteria produces gas, abdominal pain, etc. Late dumping hrs.; hypoglycemia

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Gastric Surgery - Dumping Syndrome Other nutritional concerns: vitamin and mineral deficiencies, lack of intrinsic factor, iron deficiency, osteoporosis

© 2007 Thomson - Wadsworth Pathophysiology - Stomach Dumping Syndrome - Nutrition “Anti-dumping” diet Slightly higher in protein & fat Avoid simple sugars & lactose Calcium & vitamin D Liquid between meals Small, frequent meals Lie down after meals Assess for weight loss, malabsorption, and steatorrhea

© 2007 Thomson - Wadsworth

Other Conditions Stress ulcers Caused by sepsis, shock, burns, head injuries Infusion of H2 blockers, liquid antacids Zollinger-Ellison syndrome Gastric acid hypersecretion Symptoms similar to PUD but unresponsive to therapy