Medical Nutrition Therapy of Gastrointestinal Disorder

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
• 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
• 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
• If etiology organic: soft food, low-fat diet, low
Gastritis & Peptic Ulcer Disease
Causes: disruption of mucosal integrity by infectious, chemical, neural
Helicobacter pylori: G- bacteria
with flagella. Resistant to acidic
medium of stomach.
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
– 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
Gastric & duodenal mucosa
protected from digestive acid &
pepsin by:
H. Pylori;
Stress; Alcohol;
• Mucus
• Bicarbonate
• Removal of XS acid by normal
blood flow
• Rapid renewal & repair or
epithelial cell injury
Peptic Ulcer
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
– Mostly within the 1st few centimeters of the duodenal bulb.
– Gastric outlet obstruction: common
– Duodenal ulcer related to H. pylori  gastric metaplasia may
– H2-receptor blockers or proton pump inhibitors for acid
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
• 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
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
Metabolic function of liver
• Carbohydrate, lipid and protein metabolism
• Storage and activation of vitamins and
• 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
•Urea cycle.
•Synthesis of non essensial amino acid
Company Logo
Acute liver disorders:
1. Anoreksia
2. Nausea
3. 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,
• 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
Company Logo
Nutritional therapy
Adequate energy intake
Malabsorption: specific nutrient
Adapted protein intake
Micronutrient supplementation
Company Logo
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
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
• Fat malabsorption: MCT
Company Logo
Related flashcards

41 Cards

Fast food

65 Cards


24 Cards


16 Cards

Create flashcards