medical nutrition therapy for gastrointestinal tract disorders by gaga irawan nugraha & nur...

Medical Nutrition Therapy for Gastrointestinal Tract Disorders

By

Gaga Irawan Nugraha & Nur FatimahDepartment of Medical Nutrition

Faculty of Medicine, Unpad

Dyspepsia/indigestion

Gastritis

Peptic Ulcer

Hepatic Disorder

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

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

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

Gastritis & Peptic Ulcer Disease

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

Patho-physiology 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 pepsin-producing cells

– Antral hypomotility, gastric stasis, and duodenal reflux gastric injury severity

– Higher hemorrhage and overall mortality than with duodenal ulcer.

• 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

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

• 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

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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

THANK YOU....