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
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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
Helicobacter pylori: G- bacteria
with flagella. Resistant to acidic
medium of stomach.
Treatment:
Medications: bismuth, antibiotics,
antisecretory agents
Infection  chronic inflammatory
state + damage by cytotoxins
produced by the organism
Chronic inflammation of the gastric
mucosa; gastric and duodenal
ulcers; some forms of atrophic
gastritis & gastric cancer
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
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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
Gastric & duodenal mucosa
protected from digestive acid &
pepsin by:
H. Pylori;
NSAIDs;
Corticosteroids;
Stress; Alcohol;
Tobacco
• Mucus
• Bicarbonate
• Removal of XS acid by normal
blood flow
• Rapid renewal & repair or
epithelial cell injury
Peptic Ulcer
Pathophysiology
Algorithm:
Peptic Ulcer
A.Stomach and
Duodenum with
Eroded Lesions
B.Gastric Ulcer
C.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 pepsinproducing 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 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
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 Ulcers
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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
NUTRITIONAL MANAGEMENT IN HEPATIC
DISORDERS
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. Anoreksia
2. 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
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Adequate energy intake
Malabsorption: specific nutrient
Adapted protein intake
Micronutrient supplementation
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Nutritional therapy
• Energy intake need:
TEE = BEE + PA + SDA (TEF) + stress factor
– Basal metabolic rate:
• Harris Benedict formula:
– Men
– Women
: 66 + (13,7 x BW kg) + (5 x BH cm) – (6,8 x age)
: 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
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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....