Medical Nutrition Therapy for Gastrointestinal Tract Disorders

Medical Nutrition Therapy for Gastrointestinal Tract Disorders

ByGaga Irawan Nugraha & Nur Fatimah

Department of Medical NutritionFaculty 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, gastritis, 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


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 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 UlcerC.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


• 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.


• 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


Intermediate metabolism of carbohydrate

•Heksose isomerization•Maintain blood glucose (glycogenesis/lysis)•Gluconeogenesis (from lactate, glucogenic amino acid)


Intermediate metabolism of lipid

•Synthesis acetyl CoA from fatty acid•Synthesis and hydrolysis triglycerides, phospholipids, cholesterol and lipoproteins•Synthesis of bile


Intermediate metabolism of protein

•Synthesis of visceral protein (albumin, transferin, ceruloplasmin), coagulation factor, apolipoprotein•Gluconeogenesis •Urea cycle.•Synthesis of non essensial amino acid


Acute liver disorders:1. Anoreksia2. Nausea 3. Vomitus

Depletion of glycogen storage


Chronic liver disorder:

• Maldigestion, malabsorption• Energy metabolism • Hypoalbuminemia

• Malnutrition • Vitamin deficiency


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


• Laboratory assessment:– Liver function– nutritional status:

• nitrogen balance, visceral protein, immunologic parameter.


Nutritional therapy

• Adequate energy intake• Malabsorption: specific nutrient• Adapted protein intake• Micronutrient supplementation


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


Nutritional therapy

• Composition:– Protein:

• Branch chain amino acid (valine, leucine, isoleucine)– Lipid :

• Medium chain fatty acid (MCT)– Carbohydrates :

• complex carbohydrates


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


Nutritional therapy with specific condition

• Ascites: sodium restriction• Encephalopathy: BCAA• Glucose intolerance; adapted to blood

glucose• Fat malabsorption: MCT

THANK YOU....

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Medical Nutrition Therapy for Gastrointestinal Tract Disorders

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