Git diseases presentn no. 2 applied nutrition

Dietary Management of GI Diseases

Jinky Harvey and Mah AsombangJinky Harvey and Mah Asombang

Topics

• DiarrheaDiarrhea

• Atonic constipationAtonic constipation

• Spastic constipationSpastic constipation

• Acute gastritisAcute gastritis

• Chronic gastritisChronic gastritis

• Peptic UlcerPeptic Ulcer

• Gastric UlcerGastric Ulcer

The Digestive system

• The digestive system is The digestive system is composed of the following composed of the following structures:structures:

-mouth-mouth

-esophagus-esophagus

-stomach-stomach

-small intestine-small intestine

-pancreas-pancreas

-liver-liver

-gallbladder-gallbladder

-large intestine (colon)-large intestine (colon)

-rectum-rectum

-anus-anus

What is the function of the digestive system?

• Digestion begins in the mouth, which grinds Digestion begins in the mouth, which grinds the food into smaller particles that are easier the food into smaller particles that are easier to digest. The enzyme, amylase (ptyalin) is to digest. The enzyme, amylase (ptyalin) is produced by the salivary glands. This produced by the salivary glands. This enzyme is responsible for the digestion of enzyme is responsible for the digestion of carbohydrates.carbohydrates.

• The esophagus enables the food to get from The esophagus enables the food to get from the mouth to the stomach via peristalsisthe mouth to the stomach via peristalsis


• Once the stomach receives the food, the Once the stomach receives the food, the mechanoreceptors/strecth receptorsmechanoreceptors/strecth receptors(via vagovagal reflex) stimulate the parietal (via vagovagal reflex) stimulate the parietal cells to secrete hydrochloric acid. This in cells to secrete hydrochloric acid. This in turn, enables the chief cells to begin the turn, enables the chief cells to begin the digestion of proteins via pepsin.digestion of proteins via pepsin.


• In response to acid entering from the In response to acid entering from the stomach secretin is released from the stomach secretin is released from the duodenum.duodenum.

• Secretin stimulates the pancreas to secrete Secretin stimulates the pancreas to secrete bicarbonate. This neutralizes the stomach bicarbonate. This neutralizes the stomach acid entering the duodenum. acid entering the duodenum.

• Cholecystokinin(CCK) is also released Cholecystokinin(CCK) is also released from the duodenum in response to the from the duodenum in response to the partially digested food (i.e. fats, amino partially digested food (i.e. fats, amino acids, peptides)acids, peptides)


• CCK also stimulates the pancreas to release CCK also stimulates the pancreas to release enzymes, such as; amylases, lipases, proteases. enzymes, such as; amylases, lipases, proteases. This enzyme is also responsible for gallbladder This enzyme is also responsible for gallbladder contraction and sphincter of Oddi relaxation.contraction and sphincter of Oddi relaxation.

• Bile salts are actively secreted by the liver. Once Bile salts are actively secreted by the liver. Once they become concentrated, they form micelles. they become concentrated, they form micelles. These water-soluble spheres with a lipid-soluble These water-soluble spheres with a lipid-soluble interior, providing a vehicle to transport lipid-interior, providing a vehicle to transport lipid-soluble materials in the aqueous medium of the soluble materials in the aqueous medium of the bile fluid and the small intestine.bile fluid and the small intestine.


• The small intestine functions to reabsorb The small intestine functions to reabsorb water and electrolytes with the help of the water and electrolytes with the help of the microvilli on the surface epithelial cells.microvilli on the surface epithelial cells.

• Most of the water and electrolytes must be Most of the water and electrolytes must be reabsorbed in the small intestine, or the reabsorbed in the small intestine, or the colon becomes overwhelmed. Although, the colon becomes overwhelmed. Although, the colon may reabsorb water and sodium colon may reabsorb water and sodium chloride. It mainly serves as a storage site. chloride. It mainly serves as a storage site.


• The high-amplitude propagated contractions The high-amplitude propagated contractions (HAPCS) transports the chyme through the (HAPCS) transports the chyme through the colon. colon.

• After meal ingestion, the colonic After meal ingestion, the colonic contractility increases , the initial phase is contractility increases , the initial phase is mediated by the vagus nerve and hormones mediated by the vagus nerve and hormones in response to mechanical distension of the in response to mechanical distension of the stomach.stomach.


• Distention of the rectum results in transient Distention of the rectum results in transient relaxation of the internal anal sphincter via relaxation of the internal anal sphincter via intrinsic and reflex sympathetic innervation. As intrinsic and reflex sympathetic innervation. As sigmoid and rectal contractions increase the sigmoid and rectal contractions increase the pressure with in the recutm, the rectosigmoid pressure with in the recutm, the rectosigmoid angle opens by 15 degrees.angle opens by 15 degrees.

• Voluntary relaxation of the external anal sphincter Voluntary relaxation of the external anal sphincter permits the evacuation of feces in response to the permits the evacuation of feces in response to the sensation produced by distention.sensation produced by distention.

Diarrhea

• the passage of abnormally liquid or the passage of abnormally liquid or unformed stools at an increased frequency. unformed stools at an increased frequency. The 24-hour stool weighs less than 250g The 24-hour stool weighs less than 250g and contains about 150ml of water. When and contains about 150ml of water. When daily stool weight exceeds 200g (approx. daily stool weight exceeds 200g (approx. 250 ml water). 250 ml water).

Four basic pathophysiologic causes of diarrhea

• Increased secretion of electrolytes and water into Increased secretion of electrolytes and water into the bowel lumenthe bowel lumen

• Increased osmotic load within the intestine, Increased osmotic load within the intestine, leading to water retention in the bowel lumenleading to water retention in the bowel lumen

• Inflammation leading to exudation of protein and Inflammation leading to exudation of protein and fluid from the intestinal mucosafluid from the intestinal mucosa

• Altered intestinal motility leading to rapid transit Altered intestinal motility leading to rapid transit timestimes

Classifications of diarrhea:organic diarrhea

functional diarrhea

Functional diarrhea

• less severe than organic diarrhealess severe than organic diarrhea

• May occur in people who are exposed to May occur in people who are exposed to irritants compromising the function of the irritants compromising the function of the intestineintestine

Major causes of functinoal diarrhea

• OvereatingOvereating• Eating the wrong Eating the wrong

foodsfoods• Fermentation caused Fermentation caused

by incomplete by incomplete digestion of starchdigestion of starch

• Putrefaction in the Putrefaction in the intestinal tractintestinal tract

• OvereatingOvereating• Eating the wrong Eating the wrong

foodsfoods• Fermentation caused Fermentation caused

by incomplete by incomplete digestion of starchdigestion of starch

• Putrefaction in the Putrefaction in the intestinal tractintestinal tract

Organic diarrhea

Organic diarrhea

• External poisonsExternal poisons• Amoebic dysenteryAmoebic dysentery• Bacillary dysentery or Bacillary dysentery or

shigellosisshigellosis• Enzyme deficiency Enzyme deficiency

(i.e. lactose (i.e. lactose intolerance)intolerance)

• External poisonsExternal poisons• Amoebic dysenteryAmoebic dysentery• Bacillary dysentery or Bacillary dysentery or

shigellosisshigellosis• Enzyme deficiency Enzyme deficiency

(i.e. lactose (i.e. lactose intolerance)intolerance)

Dietary management

• Fluid replacement such as; fruit juices that Fluid replacement such as; fruit juices that are high in potassium, oral rehydrating are high in potassium, oral rehydrating solution(ORS), in the absence of Oresol, a solution(ORS), in the absence of Oresol, a solution may be prepared at home using:solution may be prepared at home using:

¼ tsp crude rock salt + 1 tbsp sugar¼ tsp crude rock salt + 1 tbsp sugar

Dissolved in 1 glass of boiled water or teaDissolved in 1 glass of boiled water or tea

Dietary management cont’d

• The individual should return to their normal The individual should return to their normal diet gradually.diet gradually.

• Initially only fruit and vegetable juices Initially only fruit and vegetable juices should be consumed.should be consumed.

• Then creamed vegetable soup , and lastly Then creamed vegetable soup , and lastly selected whole cooked foods.selected whole cooked foods.

Dietary management cont’d

• If the fluid and electorlyte loss is critical, If the fluid and electorlyte loss is critical, intravenous fluids may be given.intravenous fluids may be given.

• Simple foods may be given such as; broth, gruel, Simple foods may be given such as; broth, gruel, dry toast and tea.dry toast and tea.

• Powdered milk or carbohydrates like glucose and Powdered milk or carbohydrates like glucose and lactose may be added to beverages.lactose may be added to beverages.

• Emulsified fats like butter and cream may be Emulsified fats like butter and cream may be added to foods as tolerated. added to foods as tolerated.

What is constipation?

• Constipation is a common complaint in clinical practice Constipation is a common complaint in clinical practice and usually refers to persistent, difficult, infrequent, or and usually refers to persistent, difficult, infrequent, or seemingly incomplete defecation. Because of the wide seemingly incomplete defecation. Because of the wide range of normal bowel habits, constipation is difficult to range of normal bowel habits, constipation is difficult to define precisely.define precisely.

• Most persons have at least three bowel movements per Most persons have at least three bowel movements per week; however, low stool frequency alone is not the sole week; however, low stool frequency alone is not the sole criterion for the diagnosis of constipation. Many criterion for the diagnosis of constipation. Many constipated patients have a normal frequency of defecation constipated patients have a normal frequency of defecation but complain of excessive straining, hard stools, lower but complain of excessive straining, hard stools, lower abdominal fullness, or a sense of incomplete evacuationabdominal fullness, or a sense of incomplete evacuation

Constipation

• Constipation occurs when the colon absorbs Constipation occurs when the colon absorbs too much water or if the colon’s muscle too much water or if the colon’s muscle contractions are slow or sluggish, causing contractions are slow or sluggish, causing the stool to move through the colon too the stool to move through the colon too slowly. As a result, stools can become hard slowly. As a result, stools can become hard and dry. and dry.

Classifications of constipation

Atonic ConstipationSpastic Constipation

Atonic constipation

• also known as “lazy colon”also known as “lazy colon”

• a lack of normal muscle tone or strength in a lack of normal muscle tone or strength in the colon. the colon.

Who is affected?

• Elderly people or individuals who lack Elderly people or individuals who lack physical activity.physical activity.

• Obese individuals.Obese individuals.

• Individuals recovering from a surgical Individuals recovering from a surgical operation.operation.

• During pregnancy or following childbirth.During pregnancy or following childbirth.

• Individuals with a diet low in fiber and high Individuals with a diet low in fiber and high in fatsin fats

Most Important causes

• Inadequate dietInadequate diet

• Irregular mealsIrregular meals

• Insufficient liquids and fibersInsufficient liquids and fibers

• Failure to establish a regular time for Failure to establish a regular time for defecationdefecation

Dietary Management

• High-fiber dietHigh-fiber diet

• Regularity of habit through bowel training Regularity of habit through bowel training programprogram

• Eating regular mealsEating regular meals

• Adequate fluidsAdequate fluids

• exerciseexercise

Dietary Management

Spastic constipation

• Also known as irritable colon syndrome.Also known as irritable colon syndrome.

• it is secondary to the overstimulationof the it is secondary to the overstimulationof the intestinal nerve endings resulting in the intestinal nerve endings resulting in the irregular contractions of the bowel. irregular contractions of the bowel.

Manifestations

• Uncoordinated Uncoordinated sigmoidal mobilitysigmoidal mobility

• Loss of rectal Loss of rectal sensibilitysensibility

• Abdominal painAbdominal pain• BelchingBelching• HeartburnHeartburn

• HeartburnHeartburn• Flatulence Flatulence • HeadacheHeadache• PalpitationPalpitation• nervousnessnervousness

Management

• A low fiber diet in order to avoid irritation of the A low fiber diet in order to avoid irritation of the mucous membrane of the intestinal tract. mucous membrane of the intestinal tract.

• Diet should consist of non-irritating foods, such Diet should consist of non-irritating foods, such as; milk, eggs, refined bread and cereals, butter, as; milk, eggs, refined bread and cereals, butter, oil, finely ground meat, fish, poultry .oil, finely ground meat, fish, poultry .

• Vitamin supplements are also recommended Vitamin supplements are also recommended during the period of a long restricted diet.during the period of a long restricted diet.

GASTRITIS• A term used to describe a group of A term used to describe a group of

condition with one thing in common: condition with one thing in common: inflammation of the stomach lininginflammation of the stomach lining

• Results from infection w/same bacterium Results from infection w/same bacterium that causes most stomach ulcersthat causes most stomach ulcers

• Other factors include traumatic injury & Other factors include traumatic injury & regular use of certain pain relievers, regular use of certain pain relievers, drinking too much alcohol can contribute to drinking too much alcohol can contribute to gastritisgastritis

Classification

Acute gastritis: Acute gastritis: is an inflammation of the is an inflammation of the gastric mucosa, occurs suddenly and gastric mucosa, occurs suddenly and sometimes violent in onset. sometimes violent in onset.

Chronic gastritis: Chronic gastritis: slowly develop over time slowly develop over time and it causes dull pain, feeling of fullness and it causes dull pain, feeling of fullness and loss of appetite.and loss of appetite.

• NormalNormal

• Increased AttackIncreased Attack HyperacidityHyperacidity

• Weak defenseWeak defense Helicobacter pyloriHelicobacter pylori Stress, drugs, smoking Stress, drugs, smoking

Signs and Symptoms

• Gnawing or burning pain in upper abdomen Gnawing or burning pain in upper abdomen • Loss of appetiteLoss of appetite• BloatingBloating• BelchingBelching• NauseaNausea• Vomiting Vomiting • Feeling of fullness after eating a mealFeeling of fullness after eating a meal• Weight lossWeight loss

Acute Gastritis Acute mucosal inflammatory process of a Acute mucosal inflammatory process of a

transient naturetransient nature Attacks follow after dietary indiscretions:Attacks follow after dietary indiscretions:

• OvereatingOvereating

• Eating too quicklyEating too quickly

• Eating while tired or stressedEating while tired or stressed

• Specific foodSpecific food

Other factors:Other factors:• Spoiled foods containing staphylococciSpoiled foods containing staphylococci

• Drugs (salicylates, ammonium chloride)Drugs (salicylates, ammonium chloride)

Management Dietary ManagementDietary Management

• Initial TreatmentInitial Treatment• Remove offending substance ASAP by emptying Remove offending substance ASAP by emptying

the stomach: induced vomiting and lavage or boththe stomach: induced vomiting and lavage or both• NPO for 24-48hrsNPO for 24-48hrs• Initiate IV fluidsInitiate IV fluids

• After fasting period:After fasting period:• Low fiber liquid diet can be given as toleratedLow fiber liquid diet can be given as tolerated• Milk, toast, cereal and cream soup are fed at an Milk, toast, cereal and cream soup are fed at an

interval of an hourinterval of an hour• Avoid highly seasoned and spicy foodsAvoid highly seasoned and spicy foods

Management Cont’d

• The amount of food and the number of The amount of food and the number of feedings are increased according to the feedings are increased according to the patient’s tolerance until eating a full regular patient’s tolerance until eating a full regular dietdiet

• Therapeutic diet: soft dietTherapeutic diet: soft diet

Chronic Gastritis Presence of chronic mucosal Presence of chronic mucosal

inflammatory changes such as erosions, inflammatory changes such as erosions, ulcerations, changes in the blood vessels, ulcerations, changes in the blood vessels, and the destruction of the surface cellsand the destruction of the surface cells

Same dietary indiscretions as acute Same dietary indiscretions as acute gastritisgastritis

Illness precedes development of organic Illness precedes development of organic gastritis lesionsgastritis lesions

Chief manifestation is painChief manifestation is pain

Chronic Gastritis Dietary ManagementDietary Management

• Provide adequate calories & nutrientsProvide adequate calories & nutrients• Start patient on soft dietStart patient on soft diet• Avoid highly seasoned foodsAvoid highly seasoned foods• Excess liquids during meals is avoided to Excess liquids during meals is avoided to

reduce discomfortreduce discomfort• Frequent small meals are recommended Frequent small meals are recommended • Anti-acid therapyAnti-acid therapy

Therapeutic Diet: Soft dietTherapeutic Diet: Soft diet

Peptic Ulcer Disease (PUD)

• One of the most common diseases affecting One of the most common diseases affecting the GITthe GIT

• It causes inflammatory injuries in the It causes inflammatory injuries in the gastric or duodenal mucosa with an gastric or duodenal mucosa with an extension to submucosa and into mucularis extension to submucosa and into mucularis mucosamucosa

• Acidic environment is believed to be the Acidic environment is believed to be the principal cause of PUDprincipal cause of PUD

Pathophysiology

The normal stomach maintains a balance The normal stomach maintains a balance between protective factors, such as mucus between protective factors, such as mucus secreted by the glands from the lower secreted by the glands from the lower esophagus to the upper duodenum and esophagus to the upper duodenum and sodium bicarbonate from the pancreas to sodium bicarbonate from the pancreas to neutralize HCL for the protection from its neutralize HCL for the protection from its strong acidic environmentstrong acidic environment

Pathophysiology

In alkaline environment, pepsin is inactivated In alkaline environment, pepsin is inactivated and cannot digest the duodenal mucosaand cannot digest the duodenal mucosa

Gastric ulcers develop when aggressive Gastric ulcers develop when aggressive factors overcome protective mechanismsfactors overcome protective mechanisms

Pathophysiology• The two major etiological factors for PUD The two major etiological factors for PUD

are are Helicobacter pyloriHelicobacter pylori infection and infection and nonsteroidal anti-inflammatory drug nonsteroidal anti-inflammatory drug (NSAID)(NSAID) consumption. Currently, 70% of consumption. Currently, 70% of all gastric ulcers occurring in the United all gastric ulcers occurring in the United States can be attributed to H pylori States can be attributed to H pylori infection.infection.

• Sanjeeb Shrestha, MD,Sanjeeb Shrestha, MD, Consulting Staff, Division of Gastroenterology, North West Arkansas Gastroenterology Clinic Consulting Staff, Division of Gastroenterology, North West Arkansas Gastroenterology ClinicDaryl Lau, MD, MPH, FRCP(C),Daryl Lau, MD, MPH, FRCP(C), Director of Translational Liver Research, Beth Israel Deaconess Medical Center; Associate Director of Translational Liver Research, Beth Israel Deaconess Medical Center; Associate Professor of Medicine, Harvard Medical SchoolProfessor of Medicine, Harvard Medical School

• Updated: Aug 24, 2009Updated: Aug 24, 2009

Pathophysiology

• Cigarette smoking can affect gastric Cigarette smoking can affect gastric mucosal defense adversely. Cigarette mucosal defense adversely. Cigarette smoking is believed to play a facultative smoking is believed to play a facultative role in role in H pyloriH pylori infection. People who infection. People who smoke tend to develop more frequent and smoke tend to develop more frequent and recurrent ulcers and their ulcers are more recurrent ulcers and their ulcers are more resistant to therapyresistant to therapy

PUD

Most common portion of the GIT affected by Most common portion of the GIT affected by PUD:PUD:

First portion of the duodenum First portion of the duodenum The antrum of the stomach The antrum of the stomach The gastroesophageal junction The gastroesophageal junction Ulcer is in the duodenum called duodenal Ulcer is in the duodenum called duodenal

ulcer (DU)ulcer (DU) Ulcer is found in the stomach called gastric Ulcer is found in the stomach called gastric

ulcer (GU)ulcer (GU)

H. Pylori

• A cytotoxin-associated gene (A cytotoxin-associated gene (cag Acag A) has ) has been isolated in approximately 65% of the been isolated in approximately 65% of the bacteria. The products of this gene are bacteria. The products of this gene are associated with more severe gastritis, associated with more severe gastritis, gastric ulcer, gastric cancer, and gastric ulcer, gastric cancer, and lymphoma. lymphoma.

H. Pylori

H pyloriH pylori infection also predisposes patients infection also predisposes patients to ulcer disease by disrupting mucosal to ulcer disease by disrupting mucosal integrity. The bacterium's spiral shape and integrity. The bacterium's spiral shape and flagella facilitate its penetration into the flagella facilitate its penetration into the mucous layer and its attachment to the mucous layer and its attachment to the epithelial layer. Subsequently, it releases epithelial layer. Subsequently, it releases phospholipase and proteases, which cause phospholipase and proteases, which cause further mucosal damage.further mucosal damage.

Duodenal Ulcer

More common than gastric ulcerMore common than gastric ulcer Usually appear within 3 cm of the Usually appear within 3 cm of the

pylorus an area where gastric acidity is pylorus an area where gastric acidity is high high

More prevalent in male than in femaleMore prevalent in male than in female Usually affect people who are tense, Usually affect people who are tense,

hardworking, and chronic worriershardworking, and chronic worriers

Duodenal Ulcer

Clinical feature: an intense burning epigastric Clinical feature: an intense burning epigastric pain 90 minutes to 3 hours after a meal pain 90 minutes to 3 hours after a meal

Aggravated at night and is usually relieved by Aggravated at night and is usually relieved by food food

Diagnosis of DU is done by endoscopy or Diagnosis of DU is done by endoscopy or upper GI barium radiography upper GI barium radiography

Increased acid load to the duodenum leads to Increased acid load to the duodenum leads to the development of DU the development of DU

Gastric Ulcer

Majority of gastric ulcers are situated in the Majority of gastric ulcers are situated in the antrum or the lesser curvature of the antrum or the lesser curvature of the stomach stomach

H. pylori is the primary cause for GU H. pylori is the primary cause for GU Gastric acid secretory rates with GU are Gastric acid secretory rates with GU are

normal or even decreased normal or even decreased Gastritis and chronic use of salicylate or Gastritis and chronic use of salicylate or

NSAIDs are other possible causes of GU NSAIDs are other possible causes of GU

Predisposing Factors• poor dietary habits poor dietary habits

• excessive smoking excessive smoking

• drinking of caffeine (coffee and sodas) and drinking of caffeine (coffee and sodas) and alcohol alcohol

• Rush through meals Rush through meals

• irregular mealtimesirregular mealtimes

• Hereditary Hereditary

• Physical and psychological stressesPhysical and psychological stresses

Objectives

• Relief pain Relief pain

• healing of the ulcer healing of the ulcer

• prevention of complications and prevention of complications and recurrences recurrences

• Suppression and eradication of H. pylori is Suppression and eradication of H. pylori is indicated for PUD indicated for PUD

• done by the use of triple or quadruple drug done by the use of triple or quadruple drug therapy therapy

Medical Treatment• antacids can be used to neutralize the antacids can be used to neutralize the

overload of acids (Tums, Maalox)overload of acids (Tums, Maalox)• Acid secretion may be subdued by the use of Acid secretion may be subdued by the use of

anticholinergics like Histamine 2 receptor anticholinergics like Histamine 2 receptor blockers (cimetidine, ranitidine, and blockers (cimetidine, ranitidine, and famotidine) w/c block the H2 receptor in the famotidine) w/c block the H2 receptor in the parietal cellsparietal cells

• Mucosal protectant: Bismuth or Sucralfate Mucosal protectant: Bismuth or Sucralfate can also be effective in healing gastric ulcer can also be effective in healing gastric ulcer

Medical Treatment

• Proton Pump Inhibitors (PPI): irreversibly Proton Pump Inhibitors (PPI): irreversibly inhibit the H/K ATPase pump effectively inhibit the H/K ATPase pump effectively inhibiting acid release (omeprazole, inhibiting acid release (omeprazole, lansoprazole, esomeprazole)lansoprazole, esomeprazole)

• H. Pylori eradication: triple therapy has H. Pylori eradication: triple therapy has consistently been shown to eradicate the consistently been shown to eradicate the organism more than 90% of the time.organism more than 90% of the time.

Drug therapy

• Bismuth Subsalicylate (2 tablets QID), plus Bismuth Subsalicylate (2 tablets QID), plus Metronidazole (250 mg tablet QID) plus Metronidazole (250 mg tablet QID) plus tetracycline (500 mg tablet QID). tetracycline (500 mg tablet QID).

• omeprazole (20 mg tablet OD), bismuth omeprazole (20 mg tablet OD), bismuth Subsalicylate (2 tablets QID), Subsalicylate (2 tablets QID), Metronidazole (250 mg tablet QID) and Metronidazole (250 mg tablet QID) and tetracycline (500 mg tablet QID) tetracycline (500 mg tablet QID)

Drug therapy Bismuth, metronidazole, and tetracycline qid with Bismuth, metronidazole, and tetracycline qid with

H2 blockers bidH2 blockers bid Bismuth, metronidazole, and tetracycline bid with Bismuth, metronidazole, and tetracycline bid with

a PPI (Helidac)a PPI (Helidac) Prevacid, amoxicillin, and clarithromycin bid Prevacid, amoxicillin, and clarithromycin bid

(PrevPac)(PrevPac) Prilosec, metronidazole, and clarithromycin bidPrilosec, metronidazole, and clarithromycin bid Ranitidine, bismuth, and clarithromycin with Ranitidine, bismuth, and clarithromycin with

amoxicillin, metronidazole, or tetracycline bid amoxicillin, metronidazole, or tetracycline bid

The 5 different regimens approved by AmericanCollege of Gastroenterology are as follows (all 5 The 5 different regimens approved by AmericanCollege of Gastroenterology are as follows (all 5 regimens are given for a total of 2 wk):regimens are given for a total of 2 wk):

Dietary Management

• The initial dietary management is to The initial dietary management is to consume adequate calories to maintain the consume adequate calories to maintain the desirable body weight of the patient desirable body weight of the patient

• High protein High protein • To promote healingTo promote healing

• To buffer acidsTo buffer acids

• To replace nitrogen lost from the ulcerTo replace nitrogen lost from the ulcer

Dietary Management

• Adequate carbohydrates Adequate carbohydrates

• High amounts of unsaturated fatsHigh amounts of unsaturated fats

– To inhibit gastric secretion and motility via To inhibit gastric secretion and motility via CholecystokininCholecystokinin

• Small frequent meals: Small frequent meals:

• To rest the organTo rest the organ

• To maintain constant neutralization of the acidTo maintain constant neutralization of the acid

• To minimize distention of the stomach, thus To minimize distention of the stomach, thus minimizing gastrin and HCl secretion minimizing gastrin and HCl secretion

Dietary Management

Limit fiber consumptionLimit fiber consumption

• To reduce motilityTo reduce motility Limit gastric secretagogues such as caffeine and Limit gastric secretagogues such as caffeine and

alcohol alcohol Limit Gas-forming foods like cabbage, baked Limit Gas-forming foods like cabbage, baked

beans, milk, onions, fried foods, spicy foods and beans, milk, onions, fried foods, spicy foods and orange juice orange juice

Avoidance of NSAIDs like salicylates and other Avoidance of NSAIDs like salicylates and other drugs known to affect GIT mucosadrugs known to affect GIT mucosa

References

Principles of Diet Therapy ManualPrinciples of Diet Therapy Manual http://digestive.niddk.nih.gov/ddiseases/pubs/constipation/ Sanjeeb Shrestha, MD,Sanjeeb Shrestha, MD, Consulting Staff, Division of Consulting Staff, Division of

Gastroenterology, North West Arkansas Gastroenterology Gastroenterology, North West Arkansas Gastroenterology ClinicClinic

Daryl Lau, MD, MPH, FRCP(C),Daryl Lau, MD, MPH, FRCP(C), Director of Director of Translational Liver Research, Beth Israel Deaconess Translational Liver Research, Beth Israel Deaconess Medical Center; Associate Professor of Medicine, Harvard Medical Center; Associate Professor of Medicine, Harvard Medical School, Updated: Aug 24, 2009Medical School, Updated: Aug 24, 2009

References

• Soll AH. Consensus conference. Medical treatment of Soll AH. Consensus conference. Medical treatment of peptic ulcer disease. Practice guidelines. Practice peptic ulcer disease. Practice guidelines. Practice Parameters Committee of the American College of Parameters Committee of the American College of Gastroenterology. Gastroenterology. JAMAJAMA. Feb 28 1996;275(8):622-9. . Feb 28 1996;275(8):622-9. [Medline]..

• Vaira D, Gatta L, Ricci C, et al. Peptic ulcer and Vaira D, Gatta L, Ricci C, et al. Peptic ulcer and Helicobacter pylori: update on testing and Helicobacter pylori: update on testing and treatment. treatment. Postgrad MedPostgrad Med. Jun 2005;117(6):17-22, 46. . Jun 2005;117(6):17-22, 46. [Medline]

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Git diseases presentn no. 2 applied nutrition