Nutritional Therapy of Gastrointestinal Diseases

Medical Nutrition
Dra. Tiongson
January 27, 2008
ORAL DISEASES
Dental Caries
- An oral infectious disease in which organic acid metabolites produced
by the metabolism of oral microorganisms lead to gradual
demineralization of tooth enamel followed by rapid proteolytic
destruction of the tooth structure
Pathophysiology
- Depends on the following factors
- Susceptible host or tooth surface
- Microorganisms in the dental plaque
- Streptococcus mutans xylitol act against it
- Lactobacillus casein
- Streptococcus sanguis
- Fermentable carbohydrates in the diet
- Acids produced case a drop in pH (<5.5) creating an
environment for decay
- Fermentable carbohydrates are found in:
- Grains crackers, chips, pretzels cereals,
breads
- Fruits fresh, dried, canned
- Dairy products sweetened with fructose and
sucrose
- Dietary forms of sugar sucrose, maltose
- Time of exposure to bacterial fermentation
Cariogenic Foods
- Contain fermentable carbohydrates
- Can cause a drop in salivary pH to <5.5
- Stimulate the caries process
Cariostatic foods
- Do not contribute to decay
- Not metabolized in plaque
- Do not cause a drop in salivary pH to 5.5 or less within 30 minutes
- Examples:
- Protein foods eggs, meat, fish, poultry
- Most vegetables
- Fats
- Sugarless gum
- Non-CHO sweeteners aspartame, saccharin, cyclamate
Anticariogenic Foods
- Prevent plaque from recognizing an acidogenic food when it is eaten
first
- Xylitol
- Not hydrolyzed by salivary amylase and not subjected to
bacterial degradation
- Antimicrobial activity against Streptococcus mutans
- Increases saliva production
- e.g. Trident
Factors Affecting Food Cariogenicity
- Frequency of consumption of fermentable carbohydrates
- Small frequent meals high in carbohydrate increase the
cariogenicity of a diet more than three square meals and
minimal snacks
- Food form
- Liquids are rapidly cleared from the mouth and have low
adherence capabilities
- Solids stick between the interproximal spaces between the
teeth and have high adherence capabilities
- Chewy food stimulate saliva production such as gum drops and
marshmallows although have high in sugar content, stimulate
saliva production and have lower adherence potential than
solid, stick foods such as pretzels, crackers and chips
- High fiber foods such as popcorn and raw vegetables are
cariostatic
- Sequence of eating foods and beverages
- Cheese and milk have good buffering capacity and are
desirable to eat at the end of a meal reduces cariogencity of
fermentable carbohydrates
- Caries-promoting activity by fermentable carbohydrates is
initiated within 5 to 15 minutes and lasts up to 30 minutes

- Nutrient composition of foods and beverages

- Calcium and Phosphorus buffering potential of dairy products
- Cheddar cheese has anticariogenic properties and stimulate an
alkaline saliva
- Nuts, protein foods and fats are cariostatic
- Protein foods along with other fats are cariostatic
- Combination of foods
- Bananas have less cariogenic potential when eaten with cereal
and milk
- Crackers eaten with cheese are less cariogenic than when
eaten alone
- Duration of exposure to teeth of food and beverages
- Simple carbohydrate-based foods that adhere to the tooth
surfaces are retained for longer periods of time
- Simple carbohydrates-based food and dessert foods (e.g.
potato chips, pretzels, cookies, cakes and doughnuts) provide
gradually increasing oral sugar concentrations for a longer
period of time because these foods adhere to the tooth
surfaces and are retained for longer periods of time than hard
candies
The Decay Process
- Carious process begins with the production of acid as a by-product of
bacterial metabolism taking place in the dental plaque
- Plaque sticky colorless mass of microorganisms and
polysaccharides that forms around the tooth and adheres to
teeth and gums
- Plaque shields the tooth from buffering and remineralization
- Plaque combines with calcium to form calculus
- Softdrinks, sports beverages, citrus juices and vitamin C supplements
can contribute to an acidic pH
- Critical pH (<5.5) acid begins to dissolve tooth enamel
- The acidic pH persists for 30-120 minutes until the buffering
effect of saliva neutralizes plaque acidity
Saliva Function
- HCO3, H2CO3 and PO4 buffer neutralizes bacterial acid metabolism
- Supersaturated with Calcium and Phosphorus once buffering
action has restored plaque pH above the critical point,
remineralization can occur
- Chewing promotes saliva production
- Conditions that decrease salivary production:
- Sjogrens syndrome
- Fasting
- Radiation therapy to the head and neck
- Certain medications
Caries Pattern
- Caries pattern describe the location and surfaces of the teeth affected
- Root caries, occurring on the root surfaces of teeth secondary to
gingival recession affect a large portion of the older population
- Lingual caries (occurring on the surface next to or toward the tongue)
of the anterior teeth are seen in persons with bulimia or anorexiabulimia. It can also be seen in persons with GERD as a result of
repeated episodes of acid regurgitation
Fluoride
- Primary anticaries agent
- Mechanism of action:
- Forms fluoroapatite in enamel and dentin with Ca and P
- Promotes repair and remineralization
- Deters harmful effects of bacteria in the oral cavity by
interfering with formation and function of the microorganisms
Caries Prevention Guidelines
- Brush your teeth twice daily, preferably after meals
- Rinse your mouth
- Chew sugarless gum
- Floss twice daily
- Use fluoridated toothpaste
- Pair cariogenic with cariostatic foods
- Snack on cariostatic and anticariostatic foods
- Limit in-between meal eating and drinking of fermentable
carbohydrates
Periodontal Disease
- Inflammation of the gingival with destruction of the tooth attachment
apparatus

Pathophysiology
- The primary etiologic factor in the development of PD is plaque.
Plaque in the gingival sulcus, a shallow V-shaped space around the
tooth, produces toxins that destroy tissue and permit loosening of the
teeth
Nutritional Care
- Nutritional and dietary management of the patient with PD follow
many of the guidelines fro caries prevention
- Before and after periodontal surgery, a diet with adequate nutrients
are needed to regenerate tissue and maintain an immune response to
prevent infection
Early Childhood Caries (ECC) and Baby-Bottle Tooth Decay (BBTD)
- Caries pattern in the maxillary anterior teeth of infants and younger
children
- Prolonged bottle feeding
- Pooling of liquid around the maxillary incisors
Pathophysiology
- ECC occurs secondary to prolonged bottle-feeding, especially at night
of juice, milk formula or other sweetened beverages
- The extended contact time with fermentable carbohydrates, coupled
with the position of the tongue against the nipple, which causes
pooling of the liquid around the maxillary incisors
Nutritional Care
- Remove bedtime bottles
- Modify frequency and content of daytime bottles
- Clean teeth and gums after bottle feeding
- Wean from bottle by 1 year of age
Tooth Loss and Dentures
- Significant impact on dietary habits, mastication, olfaction and
nutrition
- Decreased intake of whole grains, fruits, and vegetables due to
decreased masticatory function
Nutritional Care
- Simple guidelines should be provided for cutting and preparing fruits
and vegetables to minimize the need for biting and reduce the amount
of chewing
- Foods should be cooked to a softer consistency and meat and
vegetables can be cut across the fibers in to bite-size pieces to make
eating easier
- Avoid sticky foods such as soft white bread, caramels, chewing gums
and chewy candies
Oral Manifestations of Systemic Diseases
- Acute as well as chronic diseases are characterized by oral
manifestations that may alter the diet and nutritional status
- Impact of oral infections:
Location
Problem
Effect
Dietary
Management
Oral Cavity
Candidiasis,
Pain, infection,

Increase Kcal
Kaposis
lesions, altered
and protein
sarcoma,
ability to eat
intake
Herpes

Administer
stomatitis
oral
supplements

Provide caries
risk reduction
education
Xerostomia
Increase caries
Moist, soft, nonrisk, pain, no
spicy foods,
moistening
smooth
power, tendency cool/warm foods
of food to stick
and fluids
Esophagus
Candidiasis,
Dysphagia,
Try oral
Herpes, KS
odynophagia
supplementation
first. If
unsuccessdul,
initiate NGT
feeding or PEG
Cytomegalovirus Dysphagia, food PEG
+ ulceration
accumulation

Upper Gastrointestinal Diseases

- Dietary habits and specific food types can play a significant role in the
onset, treatment, and prevention of many GI disorders. In many
cases, diet can also play a role in improving patients sense of wellbeing and quality of life and decreasing pain, suffering and the costs
associated with GI disease
Upper GI Disorders and Nutritional Consequences
GI Condition
Common Symptoms
Possible Nutritional
Consequences
Esophagitis and

Reflux of gastric
Possible discomfort
esophageal reflux
contents
during and after eating
disease (GERD)

Burning sensation to or change in eating
habits especially in
upper middle of chest
(heartburn); increased
evening; reduced
intake
belching and painful
spasm
Esophageal stricture or
Swallowing sold food Possible weight loss if
tumor
intake is chronically
causes discomfort;
liquids are tolerated
inadequate
Possible discomfort
Hiatal Hernia

Asymptomatic or
after eating especially
prolonged heartburn
after a meal, bending
large meals and with
over or reclining after a position changes; may
meal
worsen GERD
symptoms
Cancer of oral cavity or
Asymptomatic or
May lead to surgical
esophagus
epigastric pain when
procedure, radiation
eating (more likely with therapy,
gastric tumor); difficulty chemotherapy;
chewing or swallowing
difficulty in chewing

Delayed gastric
and swallowing;
emptying
change in food
textures; weight loss
May require enteral
feeding
Indigestion/Dyspepsia/
GI discomfort after
Abdominal discomfort;
Gastritis
eating
altered diet; decreased
overall intake;
increased food
intolerance
Duodenal Ulcer

Pain 2-5 hours after
Abdominal discomfort,
a mean; pain relief
altered diet, decreased
after eating
overall intake,
increased food
intolerance
Gastric Ulcer
Vague epigastric
Abdominal discomfort
discomfort or pain
that may lead to
when eating
lowered food intake
and weight loss
Gastrectomy; partial
Early satiety or
Smaller, more frequent
gastrectomy
symptoms of nausea,
meals, decreased
bloating or diarrhea
lactose intolerance;
after eating (dumping
altered composition of
syndrome)
foods; possible weight
loss; malabsorption
and diarrhea

DISORDERS OF THE ESOPHAGUS (Chapter 29 pp 687-692)

Gastroesophageal Reflux Disease (GERD) and Esophagitis
- Acute causes:
- Ingestion of irritating agents
- Viral infection
- Intubation
- Chronic causes
- Reduced LES
- Increased abdominal pressure
- Recurrent vomiting
- Hiatal hernia
- Increased belching and painful spasm
- Possible discomfort during and after eating
- Change in eating habits especially in the evening
- Reduced food intake
- Burning sensation (heartburn)
Pathophysiology
- Reflux of gastric acid or intestinal content through the LES and into
the esophagus

Medical and Surgical Management

- Proton pump inhibitors (PPI)
- H2 receptor antagonists
- Antacid
- Antibiotics
- Prokinetic agents
- Fundoplication
Nutritional Management
- Prevent esophageal reflux
- Avoid dietary fat, alcohol, carminatives (herbal medicine that
can dispel gas from the intestine)
- Decrease acidity of gastric beverages
- Avoid coffee, fermented alcoholic beverages
- Prevent pain and irritation
- Avoid acidic and highly spiced foods
Behavioral Modification
- Avoid
- Eating within 3 hours of retiring
- Lying down after meals
- Cigarette smoking
- Tight-fitting garments
Hiatal Hernia
- Incomplete attachment of the esophagus to the hiatal ring
- Esophagus or portion of the stomach moves above the diaphragm
- Asymptomatic or prolonged heartburn after a meal, bending over, or
reclining after a meal
- Possible discomfort after eating and position changes
- May worsen GERD symptoms
Nutritional Management
- Aim is to decrease the symptoms in those who have reflux or
esophagitis
- Consume smaller, low fat meals
- Avoid food that may increase gastric secretions or reduce LES
pressure
Cancer and Surgery
- Nutritional deficits may be compounded by the treatment
- Often affect chewing, swallowing, salivation and taste acuity
- Chemotherapy may be expected to produce nausea, vomiting, and
anorexia
- Extensive dental decay, osteoradionecrosis and infections may occur
Nutritional Management
- For patients who are unable to eat:
- Gastrostomy feedings if the remainder of the GI tract is
functional
- If oral feeding is possible after surgery:
- Liquids, soft-textures, moist foods for easy mastication and
swallowing
- Small, frequent meals of relatively high caloric density
- Complex carbohydrates preferred over simple sugars
- After extensive surgery:
- Oral nutrition support in liquid form
- Surgeries within the pharynx (ex. Tonsillectomy)
- Cold, mild-flavored, soft, moist foods (ice cream) can
provide comfort and protection against unexpected bleeding in
surgical area
DISORDERS OF THE STOMACH
Indigestion and Dyspepsia
- Vague abdominal pain, bloating, nausea, regurgitation, belching
- Dietary indulgences excessive volumes of food, high intake of fat,
sugar, caffeine, spices, alcohol commonly implicated in dyspepsia
Nutritional Management
- Eat slowly
- Chew thoroughly
- Dont eat or drink excessively
- Take it easy to withstand life stress
Gastritis and PUD
- Erosion through muscularis mucosa into submucosa or muscularis
propria
- Vague epigastric pain or discomfort when eating
- Lowered food intake
- Weight loss

Causes
- Aspirin and other NSAIDS
- Helicobacter pylori
- Stress
- Gastritis
Gastric Ulcer
- Can occur anywhere along the lesser curvature of the stomach
- Inflammatory involvement of acid-producing cells, and atrophy of
these cells with advancing age
- Gastric ulcer may develop despite a low acid output
Duodenal Ulcer
- Increased acid secretion, nocturnal acid secretion, and decreased
HCO3 secretion
- Occurs in the first few centimeter of the duodenal bulb
- Gastric outlet obstruction more common with duodenal ulcers than
with gastric ulcers
- Pain 2-5 hours after a meal
- Pain relief after eating
Medical Management (Gastritis and PUD)
- Reduce or withdraw use of NSAIDS
- Use antibiotics, sucralfate, antacids
- Acid secretion suppression- PPI
- Evaluation of Vitamin B12 status
Nutrional Mangement
- Decrease consumption of :
- Alcohol may cause superficial mucosal damage
- Coffee (regular and decaf) irritant to mucosal cells
- Red and black pepper irritant to mucosal cells
- Milk stimulate gastrin and pepsin
- Increase intake of -3 and -6 fatty acids which may have a
protective effect
- Good nutritional status help decrease H. pylori
Behavioral Management
- Avoid:
- Tobacco products may cause duodenal ulcer and may
delay ulcer healing
- Stress may worsen the pain or indigestion associated with
ulcer
While ulcer is bleeding:
- No food is allowed
- IV feeding of dextrose and amino acids
- Full liquid to regular diet as condition progresses
- Omission of irritant
- Prudent diet
Gastric Carcinoma
- Malnutirition due to:
- Excessive blood and protein loss
- Obstruction or mechanical interference with food intake (more
common)
- Risk factors:
- Chronic H. pylori infection
- Smoking
- Heavy alcohol intake
- Diet low in fibrous foods
- Foods inadequate in micronutrients junk foods
- Smoked, pickled or highly salted foods
Nitrates

Nitrites
Bacteria

Nitrites + amines

Nitrosoamines

Nutritional Management
- Advanced inoperable cancer:
- Diet to provide comfort any food preferences unless
contraindicated are granted, patient should be made as
comfortable as possible
- Liquid diet
- Parenteral nutrition
- After gastric surgery
- Oral intake of food is suspended until GI tract function returns
- Water (ice cold or tepid) first type of fluid allowed
- Soft, starchy and low-fat protein foods
- Small, frequent meals or snacks
3

Dumping syndrome
- Complex physiological response to large amounts of food and liquid in
the proximal small intestine
- Result of gastrectomy, pyloric manipulation or fundoplication
- Loss of normal regulation of gastric emptying and gastrointestinal and
systemic responses to a meal
- 10-20 minutes after eating a meal (first stage)
- Abdominal fullness and nausea due to small bowel
distention and fluid shift into small intestine which is due to the
result of foods becoming hypertonic from the action of
digestive enzymes
- 20 minutes to 1 hour (intermediate stage)
- Bloating, flatulence, crampy abdominal pain and diarrhea
- Colonic Symptoms due to increased malabsorption of
carbohydrates and other foodstuffs and subsequent
fermentation in the colon
- 1 to 3 hours (late stage)
- Alimentary hypoglycemia due to rapid absorption of
carbohydrates which produces an exaggerated rise in insulin
level with a subsequent decline in blood glucose level
Nutritional Care Guidelines
- Small meals spread throughout the day improved net absorption
and less dramatic fluid shifts
- High protein (20%)
- Moderate- fat foods (35-45%) has to have sufficient calories for
weight gain or maintenance
- Complex carbohydrates
- Fibrous food slow upper GI transit and increase viscosity caution
must be exercised to avoid obstruction
- Lying down and avoiding activity one hour after eating may help slow
gastric emptying
- Adequate liquids, small amounts at a time
- Only small amounts of hypertonic, concentrated sweets (unless made
with sugar substitute)
- Avoid lactose containing foods especially ice cream may be poorly
tolerated due to rapid transit
- Give cheese and yogurt instead for calcium requirements
LOWER GASTROINTESTINAL DISORDERS
Common Intestinal Problems (Chapter 30 pp 705-720)
Intestinal Gas and Flatulence
- Aerophagia swallowing air (primary reason)
- Increased gas production due to bacterial fermentation particularly
with consumption of carbohydrates
- Consumption of large amounts of
- Dietary fiber
- Resistant starches
- Lactose (among lactose-deficient)
- Fructose and sorbitol
Nutritional Management
Eat slowly, chew with mouth closed, refrain use of drinking straws
to avoid aerophagia
Reduce carbohydrate foods that are likely to be malabsorbed and
fermented legumes, soluble fibers, resistant starches and
simple sugars such as fructose and alcohol
Legumes contain stachyose and raffinose carbohydrates
that are only partially digested in the small intestine
Constipation
- Having infrequent and difficult (sometimes painful) passage of small
amounts of dry hard stools
- Symptom, not a disease
- Causes:
- Systemic/Neurogenic/Metabolic
- Side effect of medication
- Metabolic and endocrine abnormalities such as
hypothyroidism, uremia and hypercalcemia
- Lack of exercise
- Ignoring urge to defecate
- Vascular disease of the large bowel
- Systemic neuromuscular disease leading to deficiency
of voluntary muscles
- Poor diet, low in fiber
- Pregnancy
- Gastrointestinal
- Cancer
- Diseases of the upper GIT
- Diseases of the large bowel resulting in:

- Failure of propulsion along he colon (colonic

inertia
- Failure of passage through anorectal strictures
(outlet obstruction)
- Irritable bowel syndrome
- Anal fissure or hemorrhoids
- Laxative abuse
Nutritional Management
- Adequate consumption of soluble and insoluble dietary fiber
Fiber
- Edible plant materials not digested by enzymes in the upper digestive
tract
- Cellulose, hemicellulose, pectins, gums, lignin
- Prebiotics starchy material and oligosaccharides partially resistant
to digestive enzymes
- Increases colonic fecal fluid, microbial mass, stool weight
- Increases frequency and rate of colonic transit
- Softens stools and makes them easier to pass
High Fiber Diet
- 6-11 servings/day
- Whole grain breads and products
- 5-8 servings/day
- Vegetables, legumes, fruits, nuts, seeds
- High-fiber cereals and granolas need to bring fiber intake to 25g or
more daily
- At least 2L fluids daily
Diarrhea
- Frequent evacuation of liquid stools, usually exceeding 300 ml
- Excessive loss of fluids and electrolytes
- Ostmotic diarrhea when osmotically active solutes are present in
the intestinal tract and are poorly absorbed
- Dumping syndrome, lactase deficiency
- Secretory diarrhea secretion of electrolytes and water by the
intestinal epithelium
- Bacterial toxins, intestinal hormone secretion
- Exudative diarrhea
- Mucosal damage
- Outpouring of mucus, fluid, blood and plasma proteins with a
net accumulation of electrolytes and water in the gut
- Causes:
- Inflammatory disease
- Bacterial, viral and fungal infections
- Medications
- Overconsumption of sugars
- Insufficient or damaged mucosal absorptive surface
- Malnutrition
Nutritional Management
- For adults:
- Replace fluids and electrolytes loss with broths and electrolyte
solutions
- Minimum residue diet
- Limit intake of sugar alcohols, lactose, fructose, sucrose to
prevent worsening osmotic diarrhea
- Limit caffeine which increase GI secretions and colonic motility
- Limit alcohol
- Modest amount of prebiotics e.g. pectin, oligosaccharides,
inulin, oats favor the maintenance of the so called friendly
lactobacillus and bifidus microbes and may prevent overgrowth
of potentially pathogenic organisms
- Ingestion of probiotics sources of bacteria used to
reestablish beneficial gut flora e.g. Yakult, yoghurt
- For infants and children:
- Immediate and aggressive replacement of fluid and electrolytes
Steatorrhea
- Excessive fat in stool
- Consequence of disease, excessive resection of organs involved in
lipid digestion and absorption
- Causes:
- Inadequate bile secretion secondary to liver disease or biliary
obstruction
- Blind loop syndrome
- Pancreatic insufficiency

Nutritional Management
- Introduce medium chain triglycerides (MCT) into the diet
- Directly absorbed in the absence of bile acids
- Enter the portal venous blood to the liver without resynthesis
into TAGs in the intestinal cells
INTESTINAL BRUSH-BORDER ENZYME DEFICIENCY
Lactose Maldigestion and Intolerance (Chapter 30 pp 718-720)
- Lactase deficiency enzyme that hydrolyzes lactose to galactose
and glucose in the upper small intestine
- If lactose passes to the colon, bacteria in the colon ferment lactose to
SCFAs and gasses, CO2, and H2 gas
Nutritional Management
- Reduce consumption of lactose-containing foods
- Calcium supplements
- Introduce cheese or other cultured dairy products (low lactose content
and slow gastric emptying)
- Most lactose-maldigesters can consume some lactose (upto 12g)
without major symptoms especially when taken with meals
Inflammatory Bowel Disease (IBD) (Chapter 30 pp 721-727)
- Genetic predisposition or unknown irritant (viral, bacterial,
autoimmune) leads to abnormal activation of the mucosal immune
system and secondary systemic response
- Damage to cells with malabsorption, ulceration and stricture
-

DISORDERS OF THE LARGE INTESTINE

Irritable Bowel Syndrome (Chapter 30 pp 727-730)
- Altered intestinal motility increased GI tract sensitivity, and increased
responsiveness of the viscera to enteral and external stimuli
- Excess use of laxatives and other over the counter medications
- Antibiotics
- Caffeine
- Previous GI illness
- Lack of regularity in sleep, rest and fluid intake
- Alternating diarrhea and constipation with abdominal pain
Nutritional Management
- Adequate nutrient intake
- Guide the patient to a diet that would not likely to produce symptoms
- Limit dietary fats, caffeine, sugars, large meals, and alcohol
- Increase dietary fiber to 25 g/day to help normalize bowel habits
- Psyllium if patient cannot consume fiber from food sources or does
not respond adequately
- Prebiotic food to maintain the healthy microflora and resistance to
pathogenic infections
- Foods with fiber, resistant starches and oligosaccharides
- Calming reassurance and gradual return to a good diet with limitations
of only item that likely will exacerbate symptoms will often greatly
improve the quality of life
Diverticular Disease (Chapter 30 pp 727-730)
- Sac-like herniations (diverticula) of the colonic wall, thought to result
from long-term constipation and increased colonic pressures
Nutritional Management
- High fiber diet (30-60 g) for soft bulky stools, and lowered intracolonic
pressures
- Adequate fluid intake (2-3 L daily) to facilitate effectiveness of the
high-fiber levels
- Switch to low-residue diet for acute flare-up of diverticulitis
Colon Cancer and Polyps (Chapter 30 pp 727-730)

Ulcerative colitis

Crohns disease

Potential Nutrition-related Problems

- Anemias due to blood loss and poor food intake
- GI narrowing and strictures
- Inflammation and surgical resection
- Diarrhea and malabsorption
- Increased GI secretions
- Abdominal pain, nausea, vomiting, bloating
- Food aversion
- Association of food with adverse symptoms
- Drug- nutrient interactions
- True and perceived food allergens
- Dietary restrictions
- Growth failure, weight loss, micronutrient deficiencies, CHON-calorie
malnutrition
Medical Management
- To induce and maintain remission and to maintain nutritional status
- Cortocosteroids
- Anti-inflammatory agents
- Immunosuppressants
- Antibiotics
- Anticytokine medications
Nutritional Management
- Set dietary goals that are adequate for the nutritional needs
- Minimize stress on the bowl
- Foods with sufficient calories, protein, vitamins and minerals
Diet Modifications
- Bowel rest and parenteral nutrition during acute flare-up of Crohns
disease but not a major requirement for achieving remission
- Oral and enteral feedings for those unable to tolerate food. In some,
enteral nutrition is found to be more successful at inducing remission
than parenteral nutrition
- High energy allowance (2500-3000 kcal/day) for weight gain
- Increase protein intake (100g/day) for tissue synthesis and healing
and replacement of losses
- Vitamin B complex, Vitamin E, Zinc necessary
- Mineral residue diet in acute stages or when lumen is narrowed
- MCT when fat malabsorption is likely

Risk of Colorectal Cancer

- Family history
- Occurrence of IBD
- Familial polyposis
- Adenomatous polyps
- Diet
- Polyps
Dietary Risk Factors
- Increased mead and fat intake
- Red meats, such as beef, pork, lamb
- Food preparation may also influence the carcinogenic potential of
meats and fatty foods
- Inadequate intake of micronutrients
Protection and Prevention
- Fruits, vegetables, phytochemicals
- High fiber grains
- Omega-3 FAs
- Carotenoids
- Vitamins D, E, Folate
- Ca, Zn, Selenium
- Use of pre and probiotics
- Alters colonic flora
- Induces GSH transferase
- Increases butyrate content of the stool
- Reduces toxic and genotoxic compounds
- Reduces precancerous lesions in animal models
- Aspirin, NSAIDS, exercise
- Maintenance of acceptable weight
Medical Nutrition and Mangement
- Improve the diet based on dietary guidelines
- The recommendations promote the consumption of adequate
micronutrient intake, and reasonable amounts of omega-3 fatty acids
along with adequate exercise
Short Bowel Syndrome (SBS) (pp. 730-732)
- Fluid and nutrient malabsorption associated with significant resections
of the small intestine (3-5 feet)

Consequence of ileal resection

- Rapid transit of intestinal contents
- Decrease fluid absorptive area
- Malabsorption of vitamin B12/ intrinsic factor
- Malabsorption and loss of bile salts inadequate bile salts for lipid
digestion leading to loss of fat and fat-soluble nutrients; loss of bile
salts because of decreased reabsorption
- Formulation of hydroxyl fatty acids by colonic bacteria from
malabsorbed fats
- Formation of insoluble soaps from malabsorbed Ca, Mg, Zn and
FFA
- Increased formation of oxalate stones due to increased absorption
of oxalate, which normally binds Ca, Mg and Zn
Nutritional Management
- First Stage after surgery
- Parenteral means to restore and maintain nutritional status
- Second Stage
- Gradual change from parenteral to enteral nutrition:
- Avoid lactose and sucrose
- Start with liquid diet until bowel adapts
- Ca, Mg, Zn, Fat-soluble vitamins
- Vitamin B12 status
- Medical control of diarrhea and intestinal transit time
- Third Stage
- 5 months post-bowel resection:
- More food into the diet
- Avoid alcohol and coffee
- 6 to 8 small meals per day
- Recommended diet modifications
- Low-fat, high calorie, fluid and electrolyte replacement
Ileostomy and Colostomy (pp 733-735)
- Ileostomy
- Removal of entire colon, rectum, anus
- Liquid consistency
- Weakly acidic odor
- Colostomy
- Removal of only the rectum and anus
- Mushy to well-formed in consistency
Medical Nutrition Therapy
- To prevent malodorous stools, determine which foods to eliminate
- Legumes, onions, garlic, cabbage, highly spiced foods, fish,
antibiotics, some vitamin and mineral supplements
- Patients with ileostomies have increased need for salt and water to
compensate for excessive losses instool
- Vitamin C, B12 and Folate supplementation
- Avoid very fibrous foods
DISEASES OF THE LIVER
Alcoholic Liver Disease (Chapter 31 pp. 742-743)
- Stages:
- Hepatic steatosis
- Alcoholic hepatitis
- Cirrhosis
Hepatic Steatosis
- Causes:
- Increase in the mobilization of fatty acids from adipose tissue
- Increase in hepatic synthesis of fatty acids
- Decrease in fatty acid oxidation
- Increase in TAG production
- Trapping of TAG in the liver
Alcoholic Hepatitis
- Hepatomegaly
- Modest elevation of transaminases
- Increased bilirubin
- Normal or depressed albumin
- Anemia thrombocytopenia
Alcoholic Cirrhosis
- Ascites
- GI bleeding
- Portal HPN
- Hepatic encephalopathy
Malnutrition in Alcoholics
- Metabolic consequences of Alcohol Consumption p743
- Clinical Insight p746

Hepatitis (Viral and Precirrhotic)

Nutritional Management
- Provide 2500 to 3000 kcal/day to meet energy demands for tissue
regeneration and to compensate for losses resulting from fever and
general disability, as well as to renew strength and recuperative
powers
- Allow a high protein diet which provides 1.5 grams of protein or more
per KBW/day in order to meet increased protein needs or replace
proteins lost from the body and to promote liver tissue repair
- Encourage high carbohydrate intake (about 50% of the TCA) to
restore protective glycogen reserves and to meet the energy
demands of the disease process
- Feedings may be in liquid form initially, using concentrated formulas
- Fat intake should be modified according to the tolerance
Cirrhosis (pp748-755)
- Malnutrition
- Major role in the pathogenesis of liver injury
- Profound negative impact on prognosis
- Causes of Malnutrition:
- Anorexia (inadequate oral intake)
- Maldigestion and malabsorption
- Early satiety or dysgeusia
- Nausea and vomiting
- Altered metabolism
- Restricted diets
Major Complications of ESLD
- Malnutrition
- Ascites
- Hyponatremia
- Hepatic encephalopathy
- Glucose alterations
- Fat malabsorption
- Hepatorenal syndrome
- Osteopenia
SGA parameters for Nutritional Evalutaion of Liver Disease Patients
- History
- Physical
- Existing Conditions
- Nutritional Rating
*Box 31-1 p 749
Nutrient Requirement
- Energy
- For patient with ESLD and without ascites are about 120-140%
of the resting energy expenditure (REE Mc Cullough et al
1998)
- 150-175% of REE if ascites, infection or malabsorption is
present or if nutritional repletion is necessary
- 25 to 35 calories per Kg
- Carbohydrate
- Liver failure reduces CHO production and peripheral glucose
utilization
- Decreased rate of gluconeogenesis with preference for lipids
and amino acids for energy
- Lipid
- FFA, glycerol, and ketone bodies are increased in the fasting
state
- Recommended 25-40% calories as fat
- Protein
- Increased protein breakdown and inadequate resynthesis
- Depletion of visceral protein stores and muscle wasting
Ascites
- Early satiety is a frequent complaint
- Smaller frequent feedings are better tolerated than 3 traditional meals
- Fasting hypoglycemia
- Hypoglycemia after alcohol consumption
Hyponatremia
- Decreased ability to excrete water
- Daily fluid restriction
- 1 to 1.5 L/day depending on severity of edema and ascites
Glucose intolerance in Cirrhosis
- Due to insulin resistance in peripheral tissues
- Hyperinsulinism may also occur
Fat Malabsorption
- Decreased salt secretion: Pancreatic enzyme insufficiency
6

Nutrient Requirement
- Increase energy intake via small frequent meals
- Sodium restriction for fluid retention
- Fluid restriction for hyponatremia
- CHO- controlled diets for hyperglycemia
- Vitamin and mineral supplements
- Oral liquid supplements or enteral feeding
Nutritional Therapy in Cirrhosis
- Objectives:
- Maintain and improve nutritional status through provision of
adequate energy and nutrients
- Prevent and ameliorate hepatic encephalopathy
- Prevent degeneration and enable regeneration
- Dietary modifications:
- High energy diet (35-45 kcal/kg/day)
- 300-400 g/day complex carbohydrates to spare available
protein
- In the absence of encephalopathy, increase protein intake to
1.5 g/kgDBW
Hepatic Encephalopathy (pp 753-755)
- Ammonia is an important etiologic factor
- Fundamental principle of nutritional therapy is the removal of the
source of excess ammonia
Nutritional Therapy
- Protein
- Reduce dietary intake of protein to approx 0.8-1.0 g/Kg/day
- Maintain positive nitrogen balance
- In situations of stress 1.5 g/Kg/day
- Reduce blood ammonia by:
- Oral neomycin to destroy gut flora
- Lactulose removed intestinal contents by inducing
ammonia and also lowers intestinal pH
- Branched-chain amino acids (BCAA) to supplement protein
intake
- Vegetable proteins have lower methoinine and aromatic amino
acids and higher BCAA better tolerated
- If neurologically clear after 1 week on low protein
- Increase protein intake in 10-15 g increments each
week until 1 g/Kg/day
- Fat
- Lower dietary fat to 25% of total Kcal
- Use of MCTG
- 4-7 g of linoleic acid especially if only MCT are used in
exclusion of other dietary fat
- If MCT is ineffective, total fat reduction may make food
unpalatable. Thus 40-70 g fat or about 25-30% if total
kilocalories is recommended to increase the energy content of
diet
- Vitamins
- Folate, thiamine and vitamin B12 should be prescribed
- Vitamins A, D and E may be necessary with steatorrhea
- Vitamin K should be prescribed with hypoprothombinemia
- Calcium supplement is needed with hypocalcemia in the
presence of steatorrhea
- Copper excess often requires chelation with D-penicillamine
and low-copper diet
- Supplementation with zinc will be necessary with evidence of
abnormalities of dark adaptation or taste acuity
- Reduce fluid accumulation in ascites
- Restrict Na to 500-2000 mg/day depending on the rate of
diuresis and patient tolerance
- Maintain food palatability Na should be given as high as
allowable
- Diuretics are also given, usually spironolactone
- Adjust fluid intake based on weight and serum electrolytes
- Weigh daily and palpate abdomen for fluid retention
- Watch out for hypokalemia, hyperkalemia, azotemia,
hyponatremia and precipitation of hepatorenal syndrome
- Serve attractive and appetizing food
- 6 to 8 small feedings per day
- Major part of intake should be given in the morning

DISEASES OF THE GALLBLADDER (pp 757-760)

Cholecystitis and Cholelithiasis
Nutritional Therapy
- Surgery is the preferred treatment
- Low- fat diet to decrease gallbladder stimulation
- Oral feelings discontinued during acute attacks
Low-Fat Diet
- Fat restricted diet no more than 15% of total calories
- 30 g of fat or 1800kcal of fat
- Increasing allowance for fruit, rice exchanges or sugar
- One medium fat exchange (egg)
- Less restricted diet 20-30% of total calories
- Increasing fat exchanges calories maintained by reducing
the amount of rice and sugar in the plan
- Fat-soluble vitamins (Vitamin A) supplementation is desirable
- In an acute attack of cholecystitis, oral feedings are discontinued,
parenteral nutrition may be indicated if the patient is malnourished
and it is anticipated that he or she will not be taking anything orally for
a prolonged period
Food Group
Vegetables

Fat

Allowed
All, cooked without
added fat or with fat
allowance only
All
Whole/evaporated cows
milk in allowed amounts
only, skimmed or non-fat
as desired
All cereals, roots, tubers
pan de sal, noodles
except those avoided,
macaroni spaghetti
Fish, lean meat, chicken
without skin and fat,
broiled/baked, boiled;
egg cooked in any way
except fried; mature
bean products like
tokwa, tofu, taho
Allowed amounts only

Sugar/sweets

All except those avoided

Desserts

Gelatin, fruit ices, dietary

sherbets, puddings with
skimmed milk,
meringue, angel cake,
sponge cake

Beverage

Coffee, tea

Soups

Clear, fat free

Fruits
Milk

Rice/Substitute

Meat/Fish/Substiture

Avoided
Fried, buttered, creamed
or cooked with fat in
excess of allowance
Carabaos milk,
condensed milk

Mami, miqui, breads like

croissants, sweet rolls,
muffins, biscuits,
pancakes waffles
Meat/poultry with visible
fat/cooked with fat; fish
canned in oil;
processed/canned meat,
fried eggs, nuts,
peanuts, whole milk or
cream cheese
Cream, butter, oil,
mayonnaise, bacon
except as allowed;
chicharon, fried foods
Chocolate bars, creamfilled sweets
Pies, pastries, cookies,
butter, chiffon cakes,
butter and cream icings,
doughnuts, yema, leche
flan, desserts with
coconutmilk
Soda fountain
beverages as milk
shakes, malted milk,
chocolate drinks
Cream soups, fatty
broths

DISEASES OF THE EXOCINRE PANCREAS (pp 760-765)

Pancreatitis
- Upper abdominal pain
- Symptoms may worsen with the ingestion of food
- Ransons criteria to classify the severity of pancreatitis
Acute Pancreatitis
- Pain is partially related to the secretory mechanisms of the pancreatic
enzymes and bile
- Nutritional therapy adjusted to provide minimal stimulation of these
systems
Medical Management
- Without oral feedings pancreas is put to rest
- Give IV fluids
- Administer H2-receptor antagonists to decrease HCl production

Nutritional Management
- If oral nutrition cannot be initiated in 5 to 7 days, start nutrition support
- For less severe cases of prolonged acute pancreatitis, tube feeding
can be initiated beyond the ligament of Treitz using a defined formula
diet
- For severe acute pancreatitis, PN should be initiated:
- If TGs are <400 mg/dl before PN initiation, use a 3-in-1 solution
and monitor TG levels
- If TGs are >400 mg/dl, use a dextrose based solution, monitor
glucose frequently and treat as needed with insulin
- Once oral nutrition is started, provide
- Easily digestible food + low fat diet + 6 small meals
- Adequate protein intake + increased calories
Hypocalcemia
- Hypoalbuminemia
- Soap formation
Location of tube feeding
Composition of the formula

Chronic Pancreatitis
- Increased risk of developing protein calorie malnutrition
- Deficiency of pancreatic protease necessary to cleave VitaminB12
from its carrier protein
- Objective Treatment
- Prevent further damage to the pancreas
- Decrease the number of acute inflammation
- Alleviate pain
- Decrease steatorrhea
- Correct malnutrition
Medical Management
- Manage intestinal pH with:
- Antacids
- H2 receptor antagonists
- PPI
- Administer insulin for glucose intolerance
- Provide oral diet as in acute phase
- TF can be used when oral diet is inadequate
- Supplement pancreatic enzymes
- Supplement fat-soluble vitamins and Vitamin B12

- Osmolality
- General purpose formulas have osmolalities between 300-500
mOsm close to the osmolality of body fluids
Parenteral Nutrition
- For malnourished or will become malnourished
- No sufficient GI function to restore or maintain nutrition needs
- Administered though subclavian vein
- Protein (3-15%)
- Essential and non-essential crystalline amino acids
- Specialized solutions with adjusted amino acid content for
patients with hypermetabolism or renal/liver disease
- Carbohydrate (5-70%)
- Dextrose monohydrate
- To ensure sparing of protein, prevent protein catabolism
- Lipid (10-20%)
- Aqueous suspensions of soybean or safflower oil with egg yolk
phospholipid as emulsifier
- Gycerol added to emulsion (lecithin) to provide osmolarity
- Linoleic Acid (2-4%) to prevent EFA deficiency
Refeeding syndrome
- After aggressive IV administration of nutrition
- Proliferation of new tissue required increased amounts of glucose,
potassium, phosphorus, magnesium and other nutrients for tissue
growth
- Low levels of electrolytes (specifically phosphorus) hallmark of
refeeding syndrome when they are not supplied in sufficient amounts
to keep up with tissue growth
- Insulin after rapid CHO administration reduces salt and water
excretion and increases chance of cardiac and pulmonary
complications from fluid overload
Transcribed by: Tin Ramos
Fred Monteverde
Notes from: Caprice Yang
Emy Onishi

ENTERAL AND PARENTERAL NUTRITIONAL SUPPORT (pp 537-549)

Enteral Nutrition
- At least 2-3 feet of functional GI tract
- Who are or will become malnourished
- Inadequate oral intake
- Enteral access
- Nasogastric route
- Short-term enteral feeding
- Normal GI function and gag reflex
- Administered by bolus injection or intermittent or
continuous infusions
- Percutaneous endoscopic gastrostomy (PEG) or jejunostomy
- Nonsurgical technique for placing a tube directly into
the stomach through the abdominal wall
- For > 3-4 weeks of tube feeding because short time
required for insertion, limited need for anesthesia and
minimal wound complications
Enteral Formula Composition
- Protein (4-32% of total Kcal)
- Biologically complete, intact proteins such as caseinate,
lactalbumin, beef and soy protein isolate
- Caseinate, lactalbumin, beef and soy protein isolate
- Peptide fragments and amino acids for maldigestion or
malabsorption
- Carbohydrates (40-90% of total Kcal)
- Pureed fruits and vegetables, corn syrup solids, maltodextrin,
sucrose, fructose, glucose
- Lactose is not used as carbohydrate source in most formulas
because lactase deficiency common among acutely ill
- Lipids (1.5-55% of total Kcal)
- General-purpose formulas have 30-40% of their total kcal
provided by lipids, usually from corn, soy, sunflower or
safflower oils
- Linoleic Acid (2-4%) to prevent EFA deficiency
- Fluids
- 1 ml of water/kcal or 30-35 ml/Kg BW
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