510 likes | 1.16k Views
Medical Nutrition Therapy for Gastrointestinal Tract Disorders. By Gaga Irawan Nugraha & Nur Fatimah Department of Medical Nutrition Faculty of Medicine, Unpad. Hepatic Disorder. Dyspepsia/indigestion. Gastritis. Peptic Ulcer. Indigestion & Dyspepsia.
E N D
Medical Nutrition Therapy for Gastrointestinal Tract Disorders By Gaga Irawan Nugraha & Nur Fatimah Department of Medical Nutrition Faculty of Medicine, Unpad
Hepatic Disorder Dyspepsia/indigestion Gastritis Peptic Ulcer
Indigestion & Dyspepsia • Dyspepsia refers to persistent upper abdominal discomfort or pain • The discomfort may be related to organic causes such as esophageal reflux, gastri- tis, or peptic ulcer, gallbladder disease, or other identifiable pathology. • Functional dyspepsia is a term that de- scribes unexplained persistent or recurrent upper GI discomfort. It may also be described as non-ulcer dyspepsia • Symptoms of functional dyspepsia are reported in about 15%-20% of adults over a year's time and may include vague abdominal discomfort, bloating, early satiety, nausea, and belching. • May be caused by diet, stress, other lifestyle factors
Nutritional Recomendation • Use of well-cooked foods • Adequate amount • Small meals best tolerated • Eat slowly • Chew thoroughly • Avoid excesses: • Excess volumes of food • High fat intake • Sugar, caffeine, spices, alcohol • Stress management
Nutritional Recomendation • If etiology psychogenic: removing the cause often results in the disappearance of the dyspepsia • If etiology organic: soft food, low-fat diet, low fiber
Gastritis & Peptic Ulcer Disease Causes: disruption of mucosal integrity by infectious, chemical, neural abnormalities Infection chronic inflammatory state + damage by cytotoxins produced by the organism Helicobacter pylori: G- bacteria with flagella. Resistant to acidic medium of stomach. Chronic inflammation of the gastric mucosa; gastric and duodenal ulcers; some forms of atrophic gastritis & gastric cancer Treatment: Medications: bismuth, antibiotics, antisecretory agents
Gastritis & Peptic Ulcer Disease Gastritis • Nausea, vomiting, malaise, anorexia, hemorrhage, epigastric pain • Atrophy & loss of stomach parietal cells, with loss of HCl secretion(achlorhydria)and intrinsic factor. • Patients may have serum B12 levels
Gastritis & Peptic Ulcer Disease Medical Treatment • Endoscopy to identify problems • Eradication of pathogenic organisms • Withdrawal of provoking agents • Antibiotics, antacids, H2-receptor antagonists, proton pump inhibitors Nutritional Recommendation • Lack of acid & intrinsic factor B12 malabsorption • Evaluate vitamin B12 status
Peptic Ulcers Pathophysiology H. Pylori; NSAIDs; Corticosteroids; Stress; Alcohol; Tobacco • Gastric & duodenal mucosa protected from digestive acid & pepsin by: • Mucus • Bicarbonate • Removal of XS acid by normal blood flow • Rapid renewal & repair or epithelial cell injury Peptic Ulcer
Stomach and Duodenum with Eroded Lesions • Gastric Ulcer • Duodenal Ulcer
Gastric vs. Duodenal Ulcers • Gastric ulcers: • Mostly along the lesser curvature of the stomach • Widespread gastritis, inflammatory involvement of oxyntic (acid-producing) cells, & atrophy of acid- and pepsin-producing cells • Antral hypomotility, gastric stasis, and duodenal reflux gastric injury severity • Higher hemorrhage and overall mortality than with duodenal ulcer.
Gastric vs. Duodenal Ulcers • Duodenal ulcer: • Acid secretion, nocturnal acid secretion, & bicarbonate secretion. • Mostly within the 1st few centimeters of the duodenal bulb. • Gastric outlet obstruction: common • Duodenal ulcer related to H. pylori gastric metaplasia may occur • H2-receptor blockers or proton pump inhibitors for acid suppression
Nutrition Recommendationfor Ulcers • Protein foods: • Stimulate gastrin & pepsin secretion • Food pH: • Little importance unless presence of lesions of mouth or esophagus (normal gastric pH = 1-3) • Alcohol: • May cause superficial mucosal damage. • Beers & wines gastric secretions Avoid • Coffee& caffeine: • Stimulate acid secretion and may LES pressure • Spices: • Very large doses acid secretion; small superficial erosions; mucosal lining inflammation; altered GI permeability or motility. • Spicy foods not shown to cause or affect the healing of peptic ulcer
Nutrition Recommendation for Ulcers • Prostaglandins from -3 & -6 FAs: • Conflicting studies: protective or harmful effects of -3 & -6 FAs. • -3: antiinflammatory properties, protective against mucosal injury by drugs and H. pylori. • Ideal dose or form of lipids in the diet has not been established. • Malnutrition: • Micronutrient deficiencies or protein-calorie malnutrition • Affect rapidly dividing cells such as in GI tract • Avoid deficiencies protection from PUD + may help in wound healing. • Meal frequency: • Frequent small meals: comfort, acid reflux, & stimulate gastric blood flow – BUT – may net acid output. • Avoid large meals esp. before bed to latent increases in acid secretion.
Nutrition Recommendationfor Ulcers • Use small feeding and frequent • High protein foods and vitamin C • Avoid personal intolerance • Limit gastric stimulant: • Caffeine • Alcohol • Pepermint, garlic, black peppr, cloves, chili • Use fewer saturated fat and more polyunsaturated fat • Supplement with vitamin C-rich foods or oral supplement. Citrus foods may not be tolareated • High intake vitamin A, vitamin C, fruits and vegetables, Soluble fiber reduce the risk • Refined sugar a risk
Metabolic function of liver • Carbohydrate, lipid and protein metabolism • Storage and activation of vitamins and mineral • Formation and excretion of bile • Metabolism of steroids Company Logo
Intermediate metabolism of carbohydrate • Heksose isomerization • Maintain blood glucose (glycogenesis/lysis) • Gluconeogenesis (from lactate, • glucogenic amino acid) Company Logo
Intermediate metabolism of lipid • Synthesis acetyl CoA from fatty acid • Synthesis and hydrolysis triglycerides, • phospholipids, cholesterol and lipoproteins • Synthesis of bile Company Logo
Intermediate metabolism of protein • Synthesis of visceral protein (albumin, transferin, • ceruloplasmin), coagulation factor, apolipoprotein • Gluconeogenesis • Urea cycle. • Synthesis of non essensial amino acid Company Logo
Acute liver disorders: • Anoreksia • Nausea • Vomitus • Depletion of glycogen storage Company Logo
Chronic liver disorder: • Maldigestion, malabsorption • Energy metabolism • Hypoalbuminemia • Malnutrition • Vitamin deficiency Company Logo
Subjective global assessment for nutrition management in live disease • History: • Weight change • apetite • Persistent GI problem (nausea, vomitus, diarrhea, constipation) • Physical: • Edema, ascites, muscle wasting. • Existing condition: • Hepatic encephalopathy, GI bleeding, renal insufficiency, infection Company Logo
Laboratory assessment: • Liver function • nutritional status: • nitrogen balance, visceral protein, immunologic parameter. Company Logo
Nutritional therapy • Adequate energy intake • Malabsorption: specific nutrient • Adapted protein intake • Micronutrient supplementation Company Logo
Nutritional therapy • Energy intake need: • Basal metabolic rate: • Harris Benedict formula: • Men : 66 + (13,7 x BW kg) + (5 x BH cm) – (6,8 x age) • Women : 665 + (9,6 x BW kg) + (1,7 x BH cm) – (4,7 x age) • Correction factor: • Thermogenic effect of food (10% BMR) • Physical activity • Stress factor TEE = BEE + PA + SDA (TEF) + stress factor Company Logo
Nutritional therapy • Composition: • Protein: • Branch chain amino acid (valine, leucine, isoleucine) • Lipid : • Medium chain fatty acid (MCT) • Carbohydrates : • complex carbohydrates Company Logo
Nutritional therapy • Consistency : • Adapted to liver capacity • Step by step to increase consistency. • Frequency: • Small frequent • Methods : • Intake >60%: per oral • Intake <60%: enteral • Contra indication via GI: parenteral Company Logo
Nutritional therapy with specific condition • Ascites: sodium restriction • Encephalopathy: BCAA • Glucose intolerance; adapted to blood glucose • Fat malabsorption: MCT Company Logo