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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.

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medical nutrition therapy for gastrointestinal tract disorders

Medical Nutrition Therapy for Gastrointestinal Tract Disorders


Gaga Irawan Nugraha & Nur Fatimah

Department of Medical Nutrition

Faculty of Medicine, Unpad


Hepatic Disorder



Peptic Ulcer

indigestion dyspepsia
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
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 recomendation1
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
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


Medications: bismuth, antibiotics, antisecretory agents

gastritis peptic ulcer disease1
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 disease2
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
Peptic Ulcers


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 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 ulcers1
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 recommendation for ulcers
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 ulcers1
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 recommendation for ulcers2
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
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:

  • Anoreksia
  • Nausea
  • 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
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
Nutritional therapy
  • Adequate energy intake
  • Malabsorption: specific nutrient
  • Adapted protein intake
  • Micronutrient supplementation

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nutritional therapy1
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 therapy2
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 therapy3
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
Nutritional therapy with specific condition
  • Ascites: sodium restriction
  • Encephalopathy: BCAA
  • Glucose intolerance; adapted to blood glucose
  • Fat malabsorption: MCT

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