Dietary Management of GI

Diseases

Jinky Harvey and Mah Asombang

 Topics
• Diarrhea
• Atonic constipation
• Spastic constipation
• Acute gastritis
• Chronic gastritis
• Peptic Ulcer
• Gastric Ulcer
The Digestive system
• The digestive system is
composed of the following
structures:
-mouth
-esophagus
-stomach
-small intestine
-pancreas
-liver
-gallbladder
-large intestine (colon)
-rectum
-anus
 What is the function of the
digestive system?
• Digestion begins in the mouth, which grinds
the food into smaller particles that are easier
to digest. The enzyme, amylase (ptyalin) is
produced by the salivary glands. This
enzyme is responsible for the digestion of
carbohydrates.
• The esophagus enables the food to get from
the mouth to the stomach via peristalsis
 What is the function of the
digestive system?
• Once the stomach receives the food, the
mechanoreceptors/strecth receptors
(via vagovagal reflex) stimulate the parietal
cells to secrete hydrochloric acid. This in
turn, enables the chief cells to begin the
digestion of proteins via pepsin.
 What is the function of the
digestive system?
• In response to acid entering from the
stomach secretin is released from the
duodenum.
• Secretin stimulates the pancreas to secrete
bicarbonate. This neutralizes the stomach
acid entering the duodenum.
• Cholecystokinin(CCK) is also released
from the duodenum in response to the
partially digested food (i.e. fats, amino
acids, peptides)
 What is the function of the
digestive system?
• CCK also stimulates the pancreas to release
enzymes, such as; amylases, lipases, proteases.
This enzyme is also responsible for gallbladder
contraction and sphincter of Oddi relaxation.
• Bile salts are actively secreted by the liver. Once
they become concentrated, they form micelles.
These water-soluble spheres with a lipid-soluble
interior, providing a vehicle to transport lipid-
soluble materials in the aqueous medium of the
bile fluid and the small intestine.
 What is the function of the
digestive system?
• The small intestine functions to reabsorb
water and electrolytes with the help of the
microvilli on the surface epithelial cells.
• Most of the water and electrolytes must be
reabsorbed in the small intestine, or the
colon becomes overwhelmed. Although, the
colon may reabsorb water and sodium
chloride. It mainly serves as a storage site.
 What is the function of the
digestive system?
• The high-amplitude propagated contractions
(HAPCS) transports the chyme through the
colon.
• After meal ingestion, the colonic
contractility increases , the initial phase is
mediated by the vagus nerve and hormones
in response to mechanical distension of the
stomach.
 What is the function of the
digestive system?
• Distention of the rectum results in transient
relaxation of the internal anal sphincter via
intrinsic and reflex sympathetic innervation. As
sigmoid and rectal contractions increase the
pressure with in the recutm, the rectosigmoid
angle opens by 15 degrees.
• Voluntary relaxation of the external anal sphincter
permits the evacuation of feces in response to the
sensation produced by distention.
 Diarrhea

• the passage of abnormally liquid or

unformed stools at an increased frequency.
The 24-hour stool weighs less than 250g
and contains about 150ml of water. When
daily stool weight exceeds 200g (approx.
250 ml water).
 Four basic pathophysiologic
causes of diarrhea
• Increased secretion of electrolytes and water into
the bowel lumen
• Increased osmotic load within the intestine,
leading to water retention in the bowel lumen
• Inflammation leading to exudation of protein and
fluid from the intestinal mucosa
• Altered intestinal motility leading to rapid transit
times
Classifications of diarrhea:
organic diarrhea
functional diarrhea
 Functional diarrhea
• less severe than organic diarrhea
• May occur in people who are exposed to
irritants compromising the function of the
intestine
 Major causes of functinoal
diarrhea
• Overeating • Overeating
• Eating the wrong • Eating the wrong
foods foods
• Fermentation caused • Fermentation caused
by incomplete by incomplete
digestion of starch digestion of starch
• Putrefaction in the • Putrefaction in the
intestinal tract intestinal tract
Organic diarrhea
 Organic diarrhea
• External poisons • External poisons
• Amoebic dysentery • Amoebic dysentery
• Bacillary dysentery or • Bacillary dysentery or
shigellosis shigellosis
• Enzyme deficiency • Enzyme deficiency
(i.e. lactose (i.e. lactose
intolerance) intolerance)
 Dietary management
• Fluid replacement such as; fruit juices that
are high in potassium, oral rehydrating
solution(ORS), in the absence of Oresol, a
solution may be prepared at home using:
¼ tsp crude rock salt + 1 tbsp sugar
Dissolved in 1 glass of boiled water or tea
 Dietary management cont’d

• The individual should return to their normal

diet gradually.
• Initially only fruit and vegetable juices
should be consumed.
• Then creamed vegetable soup , and lastly
selected whole cooked foods.
 Dietary management cont’d
• If the fluid and electorlyte loss is critical,
intravenous fluids may be given.
• Simple foods may be given such as; broth, gruel,
dry toast and tea.
• Powdered milk or carbohydrates like glucose and
lactose may be added to beverages.
• Emulsified fats like butter and cream may be
added to foods as tolerated.
 What is constipation?
• Constipation is a common complaint in clinical practice and
usually refers to persistent, difficult, infrequent, or
seemingly incomplete defecation. Because of the wide range
of normal bowel habits, constipation is difficult to define
precisely.
• Most persons have at least three bowel movements per
week; however, low stool frequency alone is not the sole
criterion for the diagnosis of constipation. Many constipated
patients have a normal frequency of defecation but complain
of excessive straining, hard stools, lower abdominal
fullness, or a sense of incomplete evacuation
 Constipation
• Constipation occurs when the colon absorbs
too much water or if the colon’s muscle
contractions are slow or sluggish, causing
the stool to move through the colon too
slowly. As a result, stools can become hard
and dry.
Classifications of constipation

Atonic Constipation
Spastic Constipation
 Atonic constipation
• also known as “lazy colon”
• a lack of normal muscle tone or strength in
the colon.
 Who is affected?
• Elderly people or individuals who lack
physical activity.
• Obese individuals.
• Individuals recovering from a surgical
operation.
• During pregnancy or following childbirth.
• Individuals with a diet low in fiber and high
in fats
 Most Important causes
• Inadequate diet
• Irregular meals
• Insufficient liquids and fibers
• Failure to establish a regular time for
defecation
 Dietary Management
• High-fiber diet
• Regularity of habit through bowel training
program
• Eating regular meals
• Adequate fluids
• exercise
Dietary Management
 Spastic constipation
• Also known as irritable colon syndrome.
• it is secondary to the overstimulationof the
intestinal nerve endings resulting in the
irregular contractions of the bowel.
 Manifestations
• Uncoordinated • Heartburn
sigmoidal mobility • Flatulence
• Loss of rectal • Headache
sensibility • Palpitation
• Abdominal pain
• nervousness
• Belching
• Heartburn
 Management
• A low fiber diet in order to avoid irritation of the
mucous membrane of the intestinal tract.
• Diet should consist of non-irritating foods, such
as; milk, eggs, refined bread and cereals, butter,
oil, finely ground meat, fish, poultry .
• Vitamin supplements are also recommended
during the period of a long restricted diet.
 GASTRITIS
• A term used to describe a group of
condition with one thing in common:
inflammation of the stomach lining
• Results from infection w/same bacterium
that causes most stomach ulcers
• Other factors include traumatic injury &
regular use of certain pain relievers,
drinking too much alcohol can contribute to
gastritis
 Classification
 Acute gastritis: is an inflammation of the
gastric mucosa, occurs suddenly and
sometimes violent in onset.
 Chronic gastritis: slowly develop over time
and it causes dull pain, feeling of fullness
and loss of appetite.
• Normal

• Increased Attack
Hyperacidity

• Weak defense
Helicobacter pylori
Stress, drugs, smoking
 Signs and Symptoms
• Gnawing or burning pain in upper abdomen
• Loss of appetite
• Bloating
• Belching
• Nausea
• Vomiting
• Feeling of fullness after eating a meal
• Weight loss
 Acute Gastritis
 Acute mucosal inflammatory process of a
transient nature
 Attacks follow after dietary indiscretions:
• Overeating
• Eating too quickly
• Eating while tired or stressed
• Specific food
 Other factors:
• Spoiled foods containing staphylococci
• Drugs (salicylates, ammonium chloride)
 Management
 Dietary Management
• Initial Treatment
• Remove offending substance ASAP by emptying
the stomach: induced vomiting and lavage or both
• NPO for 24-48hrs
• Initiate IV fluids
• After fasting period:
• Low fiber liquid diet can be given as tolerated
• Milk, toast, cereal and cream soup are fed at an
interval of an hour
• Avoid highly seasoned and spicy foods
 Management Cont’d
• The amount of food and the number of
feedings are increased according to the
patient’s tolerance until eating a full regular
diet
• Therapeutic diet: soft diet
 Chronic Gastritis
 Presence of chronic mucosal
inflammatory changes such as erosions,
ulcerations, changes in the blood vessels,
and the destruction of the surface cells
 Same dietary indiscretions as acute
gastritis
 Illness precedes development of organic
gastritis lesions
 Chief manifestation is pain
 Chronic Gastritis
 Dietary Management
• Provide adequate calories & nutrients
• Start patient on soft diet
• Avoid highly seasoned foods
• Excess liquids during meals is avoided to
reduce discomfort
• Frequent small meals are recommended
• Anti-acid therapy
 Therapeutic Diet: Soft diet
 Peptic Ulcer Disease (PUD)
• One of the most common diseases affecting
the GIT
• It causes inflammatory injuries in the
gastric or duodenal mucosa with an
extension to submucosa and into mucularis
mucosa
• Acidic environment is believed to be the
principal cause of PUD
 Pathophysiology
The normal stomach maintains a balance
between protective factors, such as mucus
secreted by the glands from the lower
esophagus to the upper duodenum and
sodium bicarbonate from the pancreas to
neutralize HCL for the protection from its
strong acidic environment
 Pathophysiology
In alkaline environment, pepsin is inactivated
and cannot digest the duodenal mucosa
Gastric ulcers develop when aggressive
factors overcome protective mechanisms
 Pathophysiology
• The two major etiological factors for PUD
are Helicobacter pylori infection and
nonsteroidal anti-inflammatory drug
(NSAID) consumption. Currently, 70% of
all gastric ulcers occurring in the United
States can be attributed to H pylori
infection.

• Sanjeeb Shrestha, MD, Consulting Staff, Division of Gastroenterology, North West Arkansas Gastroenterology Clinic
Daryl Lau, MD, MPH, FRCP(C), Director of Translational Liver Research, Beth Israel Deaconess Medical Center; Associate
Professor of Medicine, Harvard Medical School
• Updated: Aug 24, 2009
 Pathophysiology
• Cigarette smoking can affect gastric
mucosal defense adversely. Cigarette
smoking is believed to play a facultative
role in H pylori infection. People who
smoke tend to develop more frequent and
recurrent ulcers and their ulcers are more
resistant to therapy
 PUD
Most common portion of the GIT affected by
PUD:
 First portion of the duodenum
 The antrum of the stomach
 The gastroesophageal junction
 Ulcer is in the duodenum called duodenal
ulcer (DU)
 Ulcer is found in the stomach called gastric
ulcer (GU)
 H. Pylori
• A cytotoxin-associated gene (cag A) has
been isolated in approximately 65% of the
bacteria. The products of this gene are
associated with more severe gastritis,
gastric ulcer, gastric cancer, and
lymphoma. 
 H. Pylori
 H pylori infection also predisposes patients
to ulcer disease by disrupting mucosal
integrity. The bacterium's spiral shape and
flagella facilitate its penetration into the
mucous layer and its attachment to the
epithelial layer. Subsequently, it releases
phospholipase and proteases, which cause
further mucosal damage.
 Duodenal Ulcer
 More common than gastric ulcer
 Usually appear within 3 cm of the
pylorus an area where gastric acidity is
high
 More prevalent in male than in female
 Usually affect people who are tense,
hardworking, and chronic worriers
 Duodenal Ulcer
 Clinical feature: an intense burning epigastric
pain 90 minutes to 3 hours after a meal
 Aggravated at night and is usually relieved by
food
 Diagnosis of DU is done by endoscopy or
upper GI barium radiography
 Increased acid load to the duodenum leads to
the development of DU
 Gastric Ulcer
 Majority of gastric ulcers are situated in the
antrum or the lesser curvature of the
stomach
 H. pylori is the primary cause for GU
 Gastric acid secretory rates with GU are
normal or even decreased
 Gastritis and chronic use of salicylate or
NSAIDs are other possible causes of GU
 Predisposing Factors
• poor dietary habits
• excessive smoking
• drinking of caffeine (coffee and sodas) and
alcohol
• Rush through meals
• irregular mealtimes
• Hereditary
• Physical and psychological stresses
 Objectives
• Relief pain
• healing of the ulcer
• prevention of complications and
recurrences
• Suppression and eradication of H. pylori is
indicated for PUD
• done by the use of triple or quadruple drug
therapy
 Medical Treatment
• antacids can be used to neutralize the
overload of acids (Tums, Maalox)
• Acid secretion may be subdued by the use of
anticholinergics like Histamine 2 receptor
blockers (cimetidine, ranitidine, and
famotidine) w/c block the H2 receptor in the
parietal cells
• Mucosal protectant: Bismuth or Sucralfate
can also be effective in healing gastric ulcer
 Medical Treatment
• Proton Pump Inhibitors (PPI): irreversibly
inhibit the H/K ATPase pump effectively
inhibiting acid release (omeprazole,
lansoprazole, esomeprazole)
• H. Pylori eradication: triple therapy has
consistently been shown to eradicate the
organism more than 90% of the time.
 Drug therapy
• Bismuth Subsalicylate (2 tablets QID), plus
Metronidazole (250 mg tablet QID) plus
tetracycline (500 mg tablet QID).
• omeprazole (20 mg tablet OD), bismuth
Subsalicylate (2 tablets QID),
Metronidazole (250 mg tablet QID) and
tetracycline (500 mg tablet QID)
 Drug therapy
 Bismuth, metronidazole, and tetracycline qid with
H2 blockers bid
 Bismuth, metronidazole, and tetracycline bid with a
PPI (Helidac)
 Prevacid, amoxicillin, and clarithromycin bid
(PrevPac)
 Prilosec, metronidazole, and clarithromycin bid
 Ranitidine, bismuth, and clarithromycin with
amoxicillin, metronidazole, or tetracycline bid  

The 5 different regimens approved by AmericanCollege of Gastroenterology are as follows (all 5

regimens are given for a total of 2 wk):
 Dietary Management
• The initial dietary management is to
consume adequate calories to maintain the
desirable body weight of the patient
• High protein
• To promote healing
• To buffer acids
• To replace nitrogen lost from the ulcer
 Dietary Management
• Adequate carbohydrates
• High amounts of unsaturated fats
– To inhibit gastric secretion and motility via
Cholecystokinin
• Small frequent meals:
• To rest the organ
• To maintain constant neutralization of the acid
• To minimize distention of the stomach, thus
minimizing gastrin and HCl secretion
 Dietary Management
 Limit fiber consumption
• To reduce motility
 Limit gastric secretagogues such as caffeine and
alcohol
 Limit Gas-forming foods like cabbage, baked
beans, milk, onions, fried foods, spicy foods and
orange juice
 Avoidance of NSAIDs like salicylates and other
drugs known to affect GIT mucosa
 References
 Principles of Diet Therapy Manual
 http://digestive.niddk.nih.gov/ddiseases/pubs/constipation/
 Sanjeeb Shrestha, MD, Consulting Staff, Division of
Gastroenterology, North West Arkansas Gastroenterology
Clinic
 Daryl Lau, MD, MPH, FRCP(C), Director of
Translational Liver Research, Beth Israel Deaconess
Medical Center; Associate Professor of Medicine, Harvard
Medical School, Updated: Aug 24, 2009
 References
• Soll AH. Consensus conference. Medical treatment of
peptic ulcer disease. Practice guidelines. Practice
Parameters Committee of the American College of
Gastroenterology. JAMA. Feb 28 1996;275(8):622-9. 
[Medline].
• Vaira D, Gatta L, Ricci C, et al. Peptic ulcer and
Helicobacter pylori: update on testing and
treatment. Postgrad Med. Jun 2005;117(6):17-22, 46. 
[Medline]
Thank You!