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Medical Nutrition Therapy for Gastrointestinal Tract Disorders
By
Gaga Irawan Nugraha & Nur FatimahDepartment of Medical Nutrition
Faculty of Medicine, Unpad
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Dyspepsia/indigestion
Gastritis
Peptic Ulcer
Hepatic Disorder
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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
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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
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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
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Gastritis & Peptic Ulcer Disease
Causes: disruption of mucosal integrity by infectious, chemical, neural abnormalities
Chronic inflammation of the gastric mucosa; gastric and duodenal ulcers; some forms of atrophic gastritis & gastric cancer
Helicobacter pylori: G- bacteria with flagella. Resistant to acidic medium of stomach.
Infection chronic inflammatory state + damage by cytotoxins produced by the organism
Treatment:
Medications: bismuth, antibiotics, antisecretory agents
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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
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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
Gastritis & Peptic Ulcer Disease
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Peptic UlcersPathophysiology
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
H. Pylori; NSAIDs; Corticosteroids; Stress; Alcohol; Tobacco
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Patho-physiology Algorithm: Peptic Ulcer
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A.Stomach and Duodenum with Eroded Lesions
B.Gastric Ulcer
C.Duodenal Ulcer
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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.
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• 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
Gastric vs. Duodenal Ulcers
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Nutrition Recommendation for 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
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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.
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Nutrition Recommendation for 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
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NUTRITIONAL MANAGEMENT IN HEPATIC DISORDERS
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Metabolic function of liver
• Carbohydrate, lipid and protein metabolism• Storage and activation of vitamins and
mineral• Formation and excretion of bile• Metabolism of steroids
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Intermediate metabolism of carbohydrate
•Heksose isomerization•Maintain blood glucose (glycogenesis/lysis)•Gluconeogenesis (from lactate, glucogenic amino acid)
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Intermediate metabolism of lipid
•Synthesis acetyl CoA from fatty acid•Synthesis and hydrolysis triglycerides, phospholipids, cholesterol and lipoproteins•Synthesis of bile
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Intermediate metabolism of protein
•Synthesis of visceral protein (albumin, transferin, ceruloplasmin), coagulation factor, apolipoprotein•Gluconeogenesis •Urea cycle.•Synthesis of non essensial amino acid
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Acute liver disorders:1. Anoreksia2. Nausea 3. Vomitus
Depletion of glycogen storage
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Chronic liver disorder:
• Maldigestion, malabsorption• Energy metabolism • Hypoalbuminemia
• Malnutrition • Vitamin deficiency
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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
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• Laboratory assessment:– Liver function– nutritional status:
• nitrogen balance, visceral protein, immunologic parameter.
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Nutritional therapy
• Adequate energy intake• Malabsorption: specific nutrient• Adapted protein intake• Micronutrient supplementation
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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
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Nutritional therapy
• Composition:– Protein:
• Branch chain amino acid (valine, leucine, isoleucine)– Lipid :
• Medium chain fatty acid (MCT)– Carbohydrates :
• complex carbohydrates
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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
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Nutritional therapy with specific condition
• Ascites: sodium restriction• Encephalopathy: BCAA• Glucose intolerance; adapted to blood
glucose• Fat malabsorption: MCT
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THANK YOU....