Unit 5 Research Gastroesophageal Reflux Disease

Unit 5 research gastroesophageal reflux disease (GERD)?
1. GERD.COM
Gastroesophageal reflux disease, or GERD, is a condition that affects millions of

people, and can cause significant health problems. ...
www.gerd.com
What is GERD?
Your stomach is filled with acid. Its purpose is to help digest the food you eat. Believe it or not, this acid is the same
acidity as battery acid. Your stomach is built to handle the acid it produces. However, your esophagus isn’t. So when
acid backs up into your esophagus, it can cause the burning sensation known as heartburn.
Almost everyone has occasional heartburn. But if these symptoms occur two or more days a week for at least three
months, you may have GERD, or acid reflux disease. Acid reflux occurs when the lower esophageal sphincter (the
valve separating the esophagus and stomach) does not close properly, allowing acid to back up into the esophagus.
GERD is a chronic condition and may lead to more serious medical conditions, but is treatable. In this section, you’ll
learn about the causes and common symptoms of GERD, a disease that is more common than you might think
How is GERD Treated?

GERD is a treatable medical condition. If you are experiencing symptoms of GERD, you should schedule an
appointment with your health care provider to discuss your symptoms and receive an official diagnosis. In order to
appropriately diagnose you, your doctor may recommend lifestyle changes, a trial of a specific medical treatment, or
diagnostic tests. In this section, our experts discuss lifestyle changes that can help you manage symptoms, tests that
are used to diagnose GERD, and common treatment options.
Diagnosing GERD
Common Treatment Options
Lifestyle Changes
What Can I Do?

If you are concerned that you may have GERD, you should arrange to visit your doctor as soon as possible. GERD is
a chronic medical condition that may lead to more serious problems, but it is treatable, and can be effectively
managed through diet and lifestyle changes along with medical treatments. In this section, you will find advice that
will assist you before, during, and after your doctor visit.
Helpful Tools
A symptom diary helps to make the most of the time you have with your doctor. Enter symptoms into the diary
starting one to two weeks before you see the doctor. Write down what you felt in the diary. An example is, “I had a
burning sensation halfway down my chest.” Another example is, “I had difficulty swallowing.” Note how long the
feeling lasted. Write about what you were doing that might have brought on the discomfort. If the discomfort seemed
to be related to something you ate, write that down too. Keeping track of how your heartburn symptoms affect your
life will help you and your doctor decide if your treatment is working.
Heartburn-Friendly Recipes
Heartburn can be caused by ordinary foods most of us eat every day. But limiting these food triggers from your diet
doesn’t mean you have to sacrifice delicious meals! Remember to eat small meals… portion control is key. Here you
can find recipes for flavorful dishes that limit ingredients known to trigger heartburn. We hope you will savor these
flavors!
Take The Assessment
Use this tool to help your doctor determine whether you have acid reflux disease, also known as GERD
(gastroesophageal reflux disease).This tool may help you and your doctor find appropriate treatment.
Glossary
A|B|C|D|E|F|G|H|I|J|K|L|M|N|O|P|Q|R|S|T|U|V|W|X|Y|Z
Antacids
Drugs used for indigestion and heartburn that neutralize stomach acid.
Barium Esophagram (upper GI)

A test in which the patient swallows a chalky, nonradioactive liquid containing barium. The barium coats the digestive
tract and emphasizes the contours on x-ray. It can show narrowing of the esophagus and other structural
abnormalities.
Barrett’s Epithelium/Esophagus
An abnormality of the cells lining the esophagus (esophageal epithelium) in which they are altered so that they
become columnar, thus resembling the lining of the stomach.
Dysphagia
Difficulty in swallowing.
Endoscopy
A diagnostic test in which a thin, flexible tube carrying a fiberoptic cable is swallowed by the patient to allow the
physician to directly inspect the lining of the upper gastrointestinal tract.
Epithelium
The purely cellular layer covering all the free surfaces of the body: cutaneous (skin), mucous, and serous.
Erosion
A shallow break in the esophagus limited to the mucosa.
Esophageal pH monitoring
This test determines the severity of acid reflux, including the amount of acidity and the time acid remains in the
esophagus. There are two types of pH montoring tests. In the first, a tiny tube is inserted through the nose and into
the esophagus. An acid monitor at the end of the tube measures and records the acid levels in the esophagus for 24
hours. In the second, a pH monitor is clipped into the esophagus by endoscopy and records the pH up to a 48-hour
period.
Esophagitis
Inflammation of the esophagus.
Esophagus
The tube that carries food from your throat to your stomach.
Gastroenterologist
A doctor who specializes in treating problems and diseases of the esophagus, stomach, small intestines, colon, liver,
and pancreas.
Gastroesophageal Reflux
Regurgitation of the stomach contents into the esophagus.
GERD (Gastroesophageal Reflux Disease)

Chronic symptoms or mucosal damage produced by abnormal reflux of gastric contents into the esophagus.
Heartburn
A burning sensation, usually centered in the middle of the chest near the sternum, caused by the reflux of acidic
stomach fluids that enter the lower end of the esophagus. Also called acid reflux, cardialgia, pyrosis.
Histamine2-Receptor Antagonist (H2-RA)

A class of medications that decrease stomach acid by preventing histamine from stimulating the stomach to produce
acid.
LES
The lower esophageal sphincter. The muscular ring where the esophagus meets the stomach. Its function is to keep
stomach juices from flowing up into the esophagus.
Mucosal
The inner lining of a tubular structure or hollow organ.
Mucosal Protective Agents

Medications that create a protective barrier on the lining of the esophagus to protect it from stomach acid.
Parietal Cell
A cell found within the stomach lumen that secretes hydrochloric acid.
Pepsin
The principal digestive enzyme of the gastric juices.
Peristalsis (Esophageal)
The movement of the esophagus, induced by swallowing, in which waves of alternate circular contraction and
relaxation propel the contents onward.
Primary Peristalsis (Esophageal)
Peristalsis that occurs in response to a swallow, and usually travels the full length of the esophagus.
Promotility Agent
Medications that increase the lower esophageal sphincter pressure, increase stomach emptying, and stimulate the
esophagus to contract more often and with more power.
Proton Pump Inhibitor

A class of medications that block the final step in stomach acid production.
Reflux
The backflow of stomach acid into the esophagus.
Regurgitation
The backflow of swallowed food or drink into the throat or mouth.
Secondary Peristalsis (Esophageal)

Peristalsis that originates in the esophagus in response to esophageal stimulation (distention or irritation), as
opposed to that initiated by swallowing. The wave of contractions originates at the site of stimulation and extends to
the lower esophageal sphincter (LES).
Sphincter
A ring-like band of muscle that can tighten to narrow or close off a tube or an orifice.
Ulcer
A slow-healing open sore in which tissue breaks down.
Water Brash
Vagally mediated excessive salivation that results from esophageal acidification during reflux.
Site References
1. Klauser AG, Schindlebeck NE, Muller-Lissner SA. Symptoms in gastro-
oesophageal reflux disease. Lancet . 1990;335:205-208.
2. Jacob P, Kahrilas PJ, Vanagunas A. Peristaltic dysfunction associated

with non-obstructive dysphagia in reflux disease. Dig Dis Sci.
1990;35(8):939-942.
3. Helm JF, Dodds WJ, Hogan WJ. Salivary Response to Esophageal Acid
in Normal Subjects and Patients with Reflux Esophagitis.
Gastroenterology. 1987;93(6):1393-1397.
4. Richter JE. Extraesophageal presentations of gastroesophageal reflux

disease: an overview. Am J Gastroenterol . 2000;95(8 suppl):S1-S3.
5. Richter JE. Gastroesophageal Reflux Disease. In: Yamada T, Alpers
DH, Kaplowitz N, et al., eds. Textbook of Gastroenterology . 2003;
Lippincott Williams & Wilkins: pp.
6. Dent J, Brun J, Fendrick AM, et al. An evidence-based appraisal of

reflux disease management: The Genval Workshop Report. Gut.
1999;44 (Suppl 2): S1-S16.
7. American Gastroenterological Association. The Burden of

Gastrointestinal Diseases. American Gastroenterological Association.
Bethesda, MD. 2001.
8. DeVault KR, Castell DO. Updated Guidelines for the Diagnosis and
Treatment of Gastroesophageal Reflux Disease. Am J Gastroenterol .
1999;94 (6):1434-1442.
9. Ward EM, DeVault KR, Bouras EP, et al. Successful oesophageal pH

monitoring with a catheter-free system. Aliment Pharmacol Ther.
2004;19(4):449-454.
10. Maton PN. Profile and assessment of GERD pharmacotherapy. Cleve

Clin J Med. 2003;70(suppl 5):S51-S70.
11. Hameeteman W, van de Boomgaard DM, Dekker W, et al. Sucralfate

versus cimetidine in reflux esophagitis: single-blind multicenter study. J
Clin Gastroenterol. 1987;9(4):390-394.
12. Simon B, Ravelli G-P, Goffin H. Sucralfate gel versus placebo in patient
with non-erosive gastro-oesophageal reflux disease. Aliment Pharmacol
Ther. 1996;10(3):441-446.
13. Lambert JR, Korman MG, Nicholson L, et al. In-vivo anti-reflux and raft
properties of alginates. Aliment Pharmacol Ther. 1990;4(6):615-622.
14. Ramirez B, Richter J. Review article: promotility drugs in the treatment

of gastro-oesophageal reflux disease.Aliment Pharmacol Ther.
1993;7(1):5-20.
15. Smith JL, Opekun AR, Larkai E, et al. Sensitivity of the esophageal
mucosa to pH in gastroesophageal reflux disease. Gastroenterology.
1989;96(3):683-689
16. Stein HJ, Barlow AP, DeMeester TR, et al. Complications of

gastroesophageal reflux disease. Role of the lower esophageal
sphincter, esophageal acid and acid/alkaline exposure, and
duodenogastric reflux. Ann Surg. 1992;216(1):35-43.
17. Kahrilas PJ. Gastroesophageal reflux disease. JAMA. 1996;276:983-

988.
18. Lipsy RJ, Fennerty B, Fagan TC. Clinical review of histamine2 receptor
antagonists. Arch Intern Med. 1990;150(4):745-751.
19. Howden CW, Henning JM, Huang B, et al. Management of heartburn in

a large, randomized, community-based study; comparison of four
therapeutic strategies. Am J Gastroenterol. 2001;96(6):1704-1710.
20. Hatlebakk JG, Berstad A Gastro-oesophageal reflux during 3 months of

therapy with ranitidine in reflux oesophagitis. Scand J Gastroenterol.
1996;31:954-958.
21. Frislid K, Berstad A. Prolonged influence of a meal on the effect of

ranitidine.Scand J Gastroenterol. 1984;19:429-432.
22. Klinkenberg-Knol E, Nelis F, Dent J, et al. Long-term omeprazole

treatment in resistant gastroesophageal reflux disease.
Gastroenterology. 2000;118:661-669.
23. Bardhan KD, Morris P, Thompson M, et al. Omeprazole in the treatment

of erosive esophagitis refractory to high dose of cimetidine and
ranitidine. Gut. 1990. 31(7):745-749.
24. Huang JQ, Hunt RH. Meta-analysis of comparative trials for healing
erosive esophagitis (EE) with proton pump inhibitors (PPIs) and H2-
receptor antagonists (H2RAs). Gastroenterology. 1998;114(4):A154
(abstract G0633).
25. Richter JE, Campbell DR, Kahrilas PJ et al. Lansoprazole compared

with ranitidine for the treatment of nonerosive gastroesophageal reflux
disease. Arch Intern Med. 2000;160:1803-1809.
26. Robinson M, Sahba B, Avner D et al. A comparison of lansoprazole and

ranitidine in the treatment of erosive esophagitis. Aliment Pharmacol
Ther. 1995;9:25-31.
27. Oberg S, Clark GW, DeMeester TR. Barrett’s esophagus. Update of

pathophysiology and management. Hepatogastroenterology.
1998;45(23):1348-1356.
28. Bell NJV, Burget D, Howden CW, et al. Appropriate acid suppression for
the management of gastro-oesophageal reflux disease. Digestion.
1992;51(suppl 1):59-67.
29. Castell DO, Richter JE, Robinson M, et al. Efficacy and safety of
lansoprazole in the treatment of erosive reflux esophagitis. The
Lansoprazole Group. Am J Gastroenterol. 1996;91(9):1749-1757.
30. Dekkers CP, Beker JA, Thjodleifsson B, et al. Double-blind comparison

[correction of Double-blind, placebo controlled comparison] of
rabeprazole 20 mg vs.omeprazole 20 mg in the treatment of erosive or
ulcerative gastro-oesophageal reflux disease. The European
Rabeprazole Study Group. Aliment Pharmacol Ther. 1999;13(1):49-57.
31. Mossner J, Holscher AH, Herz R, et al. A double-blind study of

pantoprazole and omeprazole in the treatment of reflux oesophagitis; a
multicentre trial. Aliment Pharmacol Ther. 1995;9(3):321-326.
32. Caro JJ, Salas M, Ward A. Healing and Relapse Rates in

Gastroesophageal Reflux Disease Treated with the Newer Proton-Pump
Inhibitors Lansoprazole, Rabeprazole, and Pantoprazole Compared with
Omeprazole, Ranitidine, and Placebo: Evidence from Randomized
Clinical Trials. Clin Ther. 2001;23(7):998-1017.
33. Vigneri S, Termini R, Leandro G, et al.: A comparison of five

maintenance therapies for reflux esophagitis. N Engl J Med.
1995;333:1106-1110.
34. Katzka DA, Castell DO. Successful elimination of reflux symptoms does
not ensure adequate control of acid reflux in patients with Barrett's
esophagus. Am J Gastroenterol. 1994;89(7):989-991.
35. Vaezi MF, Richter JE. Role of acid and duodenogastroesophageal reflux
in gastroesophageal reflux disease. Gastroenterology. 1996;111:1192-
1199.
36. Marshall REK, Anggiansah A, Manifold DK, et al. Effect of omeprazole

20 mg twice daily on duodenogastric and gastro-oesophageal bile reflux
in Barrett's esophagus. Gut. 1998;43(5):603-606.
37. Harris RA, Kuppermann M, Richter JE. Prevention of recurrences of

erosive reflux esophagitis: a cost-effectiveness analysis of maintenance
proton pump inhibition. Am J Med. 1997;102(1):78-88.
38. Goeree R, O’Brien B, Hunt R, et al. Economic evaluation of long-term
management strategies for erosive oesophagitis. Pharmacoeconomics.
1999;16(6):679-697.
39. Harris RA, Kuppermann M, Richter JE. Proton pump inhibitors or

histamine-2 receptor antagonists for the prevention of recurrences of
erosive reflux esophagitis: a cost-effective analysis. Am J Gastroenterol.
1997;92(12):2179-2187.
40. Ladas SD, Tassios PS, Raptis SA. Selection of patients for successful
maintenance treatment of esophagitis with low-dose omeprazole: use of
24-hour gastric pH monitoring. Am J Gastroenterol. 2000;95(2):374-380.
41. Inadomi JM, Jamal R, Murata GH, et al. Step-down management of

gastroesophageal reflux disease. Gastroenterology. 2001;121(5):1095-
1100.
42. Katz PO, Anderson C, Khoury R, et al. Gastro-oesophageal reflux

associated with nocturnal gastric acid breakthrough on proton pump
inhibitors. Aliment Pharmacol Ther. 1998;12(12):1231-1234.
43. Paoletti V, Karvois D, Greski-Rose P, et al. Lansoprazole is superior to

omeprazole in increasing both 24-hour and nighttime intragastric pH in
"omeprazole failure" GERD patients. Am J Gastroenterol.
1997;92:1621(Abstract).
Treatment of Gastroesophageal Reflux Disease. Am J Gastroenterol.
2005 (100):190-200.
45. Bell NJV, Burget DW, Howden CW, et al. Healing of gastro-esophageal
reflux disease: regression analysis of the role of gastric acid suppression
[abstract]. Am J Gastroenterol. 1992;87(9):1253 Abs 46. (Data on file)
46. Schindlbeck NE, Ippisch H, Klauser AG, et al. Which pH threshold is

best in esophageal pH monitoring? Am J Gastroenterol. 1991;86:1138-
1141. (Data on file)
47. Schindlbeck NE, Heinrich C, Konig A, et al. Optimal thresholds,

sensitivity, and specificity of long-term pH metry for the detection of
gastroesophageal reflux disease. Gastroenterology. 1987;93:85-90.
(Data on file)
Patient Education
Patients with heartburn or other gastrointestinal reflux disease (GERD) symptoms will come to you for diagnosis and
treatment. Many will have already tried over the counter remedies such as antacids, alginic acid, and low-dose
histamine-2 receptor antagonists (H2RAs). Providing them with a good understanding of acid reflux disease, its
causes, symptoms, and treatment, may be helpful in assuring patient compliance with the treatment regimen you
prescribe.
What patients want to know
Patients will want information on a number of issues including:
• What is GERD?
• What causes GERD?
• What are the sequelae of GERD?
• How can they get relief from their symptoms?
• What tests will they need?
• How often will they need to be seen by you for their GERD?
What educational materials can you give them?
Providing your patients with fact sheets will allow them to review the information you discuss during the visit, assist
them in complying more fully with instructions, and formulate questions for the next visit.
Acid Reflux Disease discusses, in a language patients can understand, the symptoms and cause of GERD.
Symptoms described include heartburn, acid reflux, and dysphagia. The basis of GERD is explained with text and
anatomic diagrams.
Heartburn Facts emphasizes that GERD is a real disease and gives some epidemiological information so that
patients know that this is a common disease.
Heartburn Tips is a list of lifestyle modifications that they can make, including keeping a symptom diary.
Food Triggers and Tips will help to remind them of foods they should avoid, to not lie down after eating, and to keep a
food diary.
Doctor Visits is a list of tips for patients to assist them in making the most of their visit. They are encouraged to come
prepared with a list of questions to ask them at the beginning of the visit. They should be specific, keep the diary and
bring it with them, and repeat instructions back to you to be sure they understand them.
A Symptom Diary will aid in establishing an effective individualized regimen for each patient.
Educational Web Sites
For those of you who have patients who want to know more about GERD, the following are some Web sites you
could consider recommending:
Medline Plus
www.nlm.nih.gov/medlineplus/
This Web site is produced by the National Library of Medicine and the National Institutes of Health. It is a health
information center for consumers. Patients can read about health topics, access a medical encyclopedia, read about
medications, and get health news.
Mayo Clinic Consumer Health

www.mayoclinic.com
This is a consumer health Web site produced by the Mayo Clinic. It provides information on diseases and conditions,
suggestions for a healthier lifestyle, information on medications, health assessment tools, books, newsletters, essays,
and more.
Accent Health
www.accenthealth.com
This Web site has information on a variety of health and wellness topics, articles, tips, interactive tools, and support
groups.
GERD Diet
www.gicare.com/pated/edtgs03.htm
This site provides good, detailed information about diet and lifestyle changes that may help GERD symptoms.
Health A to Z
www.healthatoz.com
This site gives information on a variety of diseases. The digestive disease library provides information, a glossary,
and suggestions for healthier eating habits.
iVillage
www.allhealth.com
This is a general health site. There is a medical encyclopedia, special site areas for certain conditions, daily health
news, chat rooms, and information on current research.
Resources
Between 4.6 and 18.6 million people in the United States have GERD.7 GERD can have a significant impact on
quality of life; because of this, a great deal of information is available both on the Internet, in textbooks, and in
journals on this common disease.
Textbooks
A number of excellent gastroenterology textbooks are available:
Yamada T, Alpers DH, Laine L, et al. Atlas of Gastroenterology. 2003 Lippincott Williams and Wilkins. ISBN 0-
7817-3081-3. 1100 pages, 3087 illustrations.
http://www.lww.com/products/?0-7817-3081-3.
Yamada T, Alpers DH, Laine L, et al. Atlas of Gastroenterology, Third Edition and Gastroenterology CD-ROM,
package. 2003 Lippincott Williams and Wilkins. ISBN 0-7817-4720-1. 1100 pages, 3087 illustrations.
Yamada T, Alpers DH, Laine L, et al. Textbook of Gastroenterology, Fourth Edition and Gastroenterology CD-
ROM. 2003 Lippincott Williams and Wilkins. ISBN 0-7817-4719-8. 3900 pages, 2000 illustrations.
Links to Internet Web Sites

The National Institute of Diabetes and Digestive and Kidney Diseases
www.niddk.nih.gov
This site offers disease information on a variety of diseases, statistics on digestive diseases in the United States, and
links to other useful government Web sites. It also provides information about clinical trials and practice guidelines.
NIDDK publications can be ordered from the Web site.
PubMed
www.pubmed.com
A service of the National Library of Medicine, includes over 14 million citations for biomedical articles back to the
1950's. These citations are from MEDLINE and additional life science journals. PubMed includes links to many sites
providing full text articles and other related resources.
eMedicine.com, Inc.
www.emedicine.com
The eMedicine Clinical Knowledge Base contains articles on 7,000 diseases and disorders (including many with CME
credit). The evidence-based content is updated daily and provides the latest practice guidelines in 62 medical
specialties. eMedicine's professional content undergoes four levels of physician peer review plus an additional review
by a PharmD. The Clinical Knowledge Base contains 30,000 multimedia files and features the largest online
repository of medical education credits for physicians, nurses, pharmacists, and optometrists.
Medscape
www.medscape.com
This Web site provides medical information for physicians and other health care professionals. There are sections for
news, treatment updates, clinical management, practice guidelines, CME, and conference information. A daily,
specialty-specific e-mail newsletter is available.
The Cleveland Clinic Medical Education Web Site

www.clevelandclinicmeded.com
This Web site offers access to CME including Selected Topics in Gastrotherapy. The Disease Management project
provides current information on treating 120 commonly seen diseases. The “One Minute Consult” comprises brief
answers to questions on current clinical controversies. The site also offers information on pharmaceuticals, a
pharmacy newsletter, and more.
MDlinx
www.mdlinx.com
MDlinx has both a professional and a patient section. The professional section is a network of 34 medical specialty
Web sites, including a GI Web site, http://www.mdlinx.com/GILinx/ . There are daily updates on specialty news, daily
e-mail newsletters for each specialty, e-mail discussion lists, and CME. MDlinx will also help you set up your own
Web site for free.
Doctor’s Guide
www.docguide.com
Doctor's Guide is a comprehensive source for peer-reviewed literature, case studies, Webcasts/CME, and more. It
provides a daily update on news and can be customized for your personal interests.
Feldman’s GastroAtlas
www.gastroatlas.com
Feldman’s GastroAtlas is the ultimate online gastroenterology image resource. It contains over 4,000 clinical,
radiologic, pathologic, and histologic images. You can create and maintain your own named files of slides based on
the Feldman Atlas image collection. These files become part of the central GastroAtlas database and can be
accessed, on login, from any computer anywhere in the world.
The Visible Human Project

www.nlm.nih.gov/research/visible/visible_human.html
The Visible Human Project® is an outgrowth of the National Library of Medicine's 1986 Long-Range Plan. It is the
creation of complete, anatomically detailed, three-dimensional representations of the normal male and female human
bodies. Acquisition of transverse CT, MR, and cryosection images of representative male and female cadavers has
been completed. Information on the site includes how to get image data, an update of the Virtual Human’s initiatives,
information on other National Library of Medicine initiatives, information from the contractors for the Project
proceedings from project conferences, and publications.
MediClicks
www.MediClicks.net
MediClicks is a free e-mail medical newsletter sent every two weeks. It provides information about the latest trends in
technology and how they relate to the field of medicine. Insights about health care as it relates to the Internet are
provided, as are tips on how to use the Internet, computers, and other electronic devices. There is an original cartoon
that illustrates the lighter side of medicine with each issue.
For links to medical journals including GI-specific journals, professional organizations Web sites, and CME sites click
here.
GERD Articles
The American Gastroenterological Society’s Report on the Burden of Gastrointestinal Disease:(Membership is
required to view the articles)
http://www.gastro.org/clinicalRes/burdenReport.html.
The American Gastroenterological Society’s GERD monograph:(Membership is required to view the articles)
http://www.gastro.org/edu/GERDmonograph.pdf.
The American College of Gastroenterology’s Updated Guidelines for the Diagnosis and Treatment of
Gastroesophageal Reflux Disease available at: http://www.acg.gi.org/physicians/guidelines/GERDTreatment.pdf
Site References
1. Klauser AG, Schindlebeck NE, Muller-Lissner SA. Symptoms in gastro-
oesophageal reflux disease. Lancet . 1990;335:205-208.
2. Jacob P, Kahrilas PJ, Vanagunas A. Peristaltic dysfunction associated

with non-obstructive dysphagia in reflux disease. Dig Dis Sci.
1990;35(8):939-942.
3. Helm JF, Dodds WJ, Hogan WJ. Salivary Response to Esophageal Acid
in Normal Subjects and Patients with Reflux Esophagitis.
Gastroenterology. 1987;93(6):1393-1397.
4. Richter JE. Extraesophageal presentations of gastroesophageal reflux

disease: an overview. Am J Gastroenterol . 2000;95(8 suppl):S1-S3.
5. Richter JE. Gastroesophageal Reflux Disease. In: Yamada T, Alpers

DH, Kaplowitz N, et al., eds. Textbook of Gastroenterology . 2003;
Lippincott Williams & Wilkins: pp.
6. Dent J, Brun J, Fendrick AM, et al. An evidence-based appraisal of
reflux disease management: The Genval Workshop Report. Gut.
1999;44 (Suppl 2): S1-S16.
7. American Gastroenterological Association. The Burden of

Gastrointestinal Diseases. American Gastroenterological Association.
Bethesda, MD. 2001.
Treatment of Gastroesophageal Reflux Disease. Am J Gastroenterol .
1999;94 (6):1434-1442.
9. Ward EM, DeVault KR, Bouras EP, et al. Successful oesophageal pH

monitoring with a catheter-free system. Aliment Pharmacol Ther.
2004;19(4):449-454.
10. Maton PN. Profile and assessment of GERD pharmacotherapy. Cleve

Clin J Med. 2003;70(suppl 5):S51-S70.
11. Hameeteman W, van de Boomgaard DM, Dekker W, et al. Sucralfate

versus cimetidine in reflux esophagitis: single-blind multicenter study. J
Clin Gastroenterol. 1987;9(4):390-394.
12. Simon B, Ravelli G-P, Goffin H. Sucralfate gel versus placebo in patient
with non-erosive gastro-oesophageal reflux disease. Aliment Pharmacol
Ther. 1996;10(3):441-446.
13. Lambert JR, Korman MG, Nicholson L, et al. In-vivo anti-reflux and raft
properties of alginates. Aliment Pharmacol Ther. 1990;4(6):615-622.
14. Ramirez B, Richter J. Review article: promotility drugs in the treatment

of gastro-oesophageal reflux disease.Aliment Pharmacol Ther.
1993;7(1):5-20.
15. Smith JL, Opekun AR, Larkai E, et al. Sensitivity of the esophageal
mucosa to pH in gastroesophageal reflux disease. Gastroenterology.
1989;96(3):683-689
16. Stein HJ, Barlow AP, DeMeester TR, et al. Complications of

gastroesophageal reflux disease. Role of the lower esophageal
sphincter, esophageal acid and acid/alkaline exposure, and
duodenogastric reflux. Ann Surg. 1992;216(1):35-43.
17. Kahrilas PJ. Gastroesophageal reflux disease. JAMA. 1996;276:983-

988.
18. Lipsy RJ, Fennerty B, Fagan TC. Clinical review of histamine2 receptor
antagonists. Arch Intern Med. 1990;150(4):745-751.
19. Howden CW, Henning JM, Huang B, et al. Management of heartburn in

a large, randomized, community-based study; comparison of four
therapeutic strategies. Am J Gastroenterol. 2001;96(6):1704-1710.
20. Hatlebakk JG, Berstad A Gastro-oesophageal reflux during 3 months of

therapy with ranitidine in reflux oesophagitis. Scand J Gastroenterol.
1996;31:954-958.
21. Frislid K, Berstad A. Prolonged influence of a meal on the effect of

ranitidine.Scand J Gastroenterol. 1984;19:429-432.
22. Klinkenberg-Knol E, Nelis F, Dent J, et al. Long-term omeprazole

treatment in resistant gastroesophageal reflux disease.
Gastroenterology. 2000;118:661-669.
23. Bardhan KD, Morris P, Thompson M, et al. Omeprazole in the treatment

of erosive esophagitis refractory to high dose of cimetidine and
ranitidine. Gut. 1990. 31(7):745-749.
24. Huang JQ, Hunt RH. Meta-analysis of comparative trials for healing
erosive esophagitis (EE) with proton pump inhibitors (PPIs) and H2-
receptor antagonists (H2RAs). Gastroenterology. 1998;114(4):A154
(abstract G0633).
25. Richter JE, Campbell DR, Kahrilas PJ et al. Lansoprazole compared

with ranitidine for the treatment of nonerosive gastroesophageal reflux
disease. Arch Intern Med. 2000;160:1803-1809.
26. Robinson M, Sahba B, Avner D et al. A comparison of lansoprazole and

ranitidine in the treatment of erosive esophagitis. Aliment Pharmacol
Ther. 1995;9:25-31.
27. Oberg S, Clark GW, DeMeester TR. Barrett’s esophagus. Update of

pathophysiology and management. Hepatogastroenterology.
1998;45(23):1348-1356.
28. Bell NJV, Burget D, Howden CW, et al. Appropriate acid suppression for
the management of gastro-oesophageal reflux disease. Digestion.
1992;51(suppl 1):59-67.
29. Castell DO, Richter JE, Robinson M, et al. Efficacy and safety of
lansoprazole in the treatment of erosive reflux esophagitis. The
Lansoprazole Group. Am J Gastroenterol. 1996;91(9):1749-1757.
30. Dekkers CP, Beker JA, Thjodleifsson B, et al. Double-blind comparison

[correction of Double-blind, placebo controlled comparison] of
rabeprazole 20 mg vs.omeprazole 20 mg in the treatment of erosive or
ulcerative gastro-oesophageal reflux disease. The European
Rabeprazole Study Group. Aliment Pharmacol Ther. 1999;13(1):49-57.
31. Mossner J, Holscher AH, Herz R, et al. A double-blind study of

pantoprazole and omeprazole in the treatment of reflux oesophagitis; a
multicentre trial. Aliment Pharmacol Ther. 1995;9(3):321-326.
32. Caro JJ, Salas M, Ward A. Healing and Relapse Rates in

Gastroesophageal Reflux Disease Treated with the Newer Proton-Pump
Inhibitors Lansoprazole, Rabeprazole, and Pantoprazole Compared with
Omeprazole, Ranitidine, and Placebo: Evidence from Randomized
Clinical Trials. Clin Ther. 2001;23(7):998-1017.
33. Vigneri S, Termini R, Leandro G, et al.: A comparison of five

maintenance therapies for reflux esophagitis. N Engl J Med.
1995;333:1106-1110.
34. Katzka DA, Castell DO. Successful elimination of reflux symptoms does
not ensure adequate control of acid reflux in patients with Barrett's
esophagus. Am J Gastroenterol. 1994;89(7):989-991.
35. Vaezi MF, Richter JE. Role of acid and duodenogastroesophageal reflux
in gastroesophageal reflux disease. Gastroenterology. 1996;111:1192-
1199.
36. Marshall REK, Anggiansah A, Manifold DK, et al. Effect of omeprazole

20 mg twice daily on duodenogastric and gastro-oesophageal bile reflux
in Barrett's esophagus. Gut. 1998;43(5):603-606.
37. Harris RA, Kuppermann M, Richter JE. Prevention of recurrences of

erosive reflux esophagitis: a cost-effectiveness analysis of maintenance
proton pump inhibition. Am J Med. 1997;102(1):78-88.
38. Goeree R, O’Brien B, Hunt R, et al. Economic evaluation of long-term

management strategies for erosive oesophagitis. Pharmacoeconomics.
1999;16(6):679-697.
39. Harris RA, Kuppermann M, Richter JE. Proton pump inhibitors or
histamine-2 receptor antagonists for the prevention of recurrences of
erosive reflux esophagitis: a cost-effective analysis. Am J Gastroenterol.
1997;92(12):2179-2187.
40. Ladas SD, Tassios PS, Raptis SA. Selection of patients for successful
maintenance treatment of esophagitis with low-dose omeprazole: use of
24-hour gastric pH monitoring. Am J Gastroenterol. 2000;95(2):374-380.
41. Inadomi JM, Jamal R, Murata GH, et al. Step-down management of

gastroesophageal reflux disease. Gastroenterology. 2001;121(5):1095-
1100.
42. Katz PO, Anderson C, Khoury R, et al. Gastro-oesophageal reflux

associated with nocturnal gastric acid breakthrough on proton pump
inhibitors. Aliment Pharmacol Ther. 1998;12(12):1231-1234.
43. Paoletti V, Karvois D, Greski-Rose P, et al. Lansoprazole is superior to

omeprazole in increasing both 24-hour and nighttime intragastric pH in
"omeprazole failure" GERD patients. Am J Gastroenterol.
1997;92:1621(Abstract).
Treatment of Gastroesophageal Reflux Disease. Am J Gastroenterol.
2005 (100):190-200.
45. Bell NJV, Burget DW, Howden CW, et al. Healing of gastro-esophageal
reflux disease: regression analysis of the role of gastric acid suppression
[abstract]. Am J Gastroenterol. 1992;87(9):1253 Abs 46. (Data on file)
46. Schindlbeck NE, Ippisch H, Klauser AG, et al. Which pH threshold is

best in esophageal pH monitoring? Am J Gastroenterol. 1991;86:1138-
1141. (Data on file)
47. Schindlbeck NE, Heinrich C, Konig A, et al. Optimal thresholds,

sensitivity, and specificity of long-term pH metry for the detection of
gastroesophageal reflux disease. Gastroenterology. 1987;93:85-90.
(Data on file)
48. Reflux Laryngitis

...throat clearing, swallowing problems, asthma, chronic cough, and more. Typical
symptoms of reflux laryngitis include heartburn,...MD Why does reflux laryngitis occur?
What are the typical symptoms of...
Source: MedicineNet
Medical Author: John P. Cunha, DO, FACOEP
Medical Editor: Jay W. Marks, MD
• Why does reflux laryngitis occur?

• What are the typical symptoms of reflux laryngitis?
• How are reflux laryngitis evaluated?
• What is the conservative therapy of reflux?
• What types of medications are used to treat reflux?
• What are the difficulties in diagnosing reflux laryngitis?
• Reflux Laryngitis At A Glance
Why does reflux laryngitis occur?
Reflux is caused by weakness in the muscle at the junction of the esophagus with the stomach. Normally, this
muscular valve, or sphincter, functions to keep food and stomach acid from moving upward from the stomach to the
esophagus and larynx. This valve opens to allow food into the stomach and closes to keep the stomach's contents
from coming back up. The backward movement of stomach contents (gastric contents) up into the esophagus is
referred to as gastroesophageal reflux.
Additionally, any increase in abdominal pressure (such as obesity), which can push acid back from the stomach up
the esophagus, or a patient with a hiatal hernia, will have an increased risk for reflux. When it causes symptoms, it is
referred to as gastroesophageal reflux disease (or GERD). When the acid backs up into the voice box (larynx), the
condition is referred to as reflux laryngitis.
Stomach acid can cause irritation of the lining of the esophagus, larynx, and throat. This can lead to:
• erosion of the lining of the esophagus (erosive esophagitis),
• narrowing of the esophagus (stricture),
• chronic hoarseness,
• chronic throat clearing,
• difficulty swallowing,
• foreign body sensation in the throat,
• asthma or cough,
• spasms of the vocal cords,
• sinusitis, and
• growths on the vocal cords (granulomas).

Rarely, reflux can lead to cancers of the esophagus or larynx.
Gastroesophageal Reflux Disease (GERD) (cont.)
In this Article
• What is GERD (acid reflux)?

• What causes GERD?
• What are the symptoms of uncomplicated GERD?
• What are the complications of GERD?
• How is GERD diagnosed and evaluated?
• How is GERD treated?
• What is a reasonable approach to the management of GERD?
• What are the unresolved issues in GERD?
• GERD At A Glance
• Patient Discussions: GERD - Proton Pump Inhibitors
• Gastroesophageal Reflux Disease (GERD) Glossary
• Gastroesophageal Reflux Disease (GERD) Index
How is GERD treated?
Life-style changes
One of the simplest treatments for GERD is referred to as life-style changes, a combination of several changes in
habit, particularly related to eating.
As discussed above, reflux of acid is more injurious at night than during the day. At night, when individuals are lying
down, it is easier for reflux to occur. The reason that it is easier is because gravity is not opposing the reflux, as it
does in the upright position during the day. In addition, the lack of an effect of gravity allows the refluxed liquid to
travel further up the esophagus and remain in the esophagus longer. These problems can be overcome partially by
elevating the upper body in bed. The elevation is accomplished either by putting blocks under the bed's feet at the
head of the bed or, more conveniently, by sleeping with the upper body on a wedge. These maneuvers raise the
esophagus above the stomach and partially restore the effects of gravity. It is important that the upper body and not
just the head be elevated. Elevating only the head does not raise the esophagus and fails to restore the effects of
gravity.
Elevation of the upper body at night generally is recommended for all patients with GERD. Nevertheless, most
patients with GERD have reflux only during the day and elevation at night is of little benefit for them. It is not possible
to know for certain which patients will benefit from elevation at night unless acid testing clearly demonstrates night
reflux. However, patients who have heartburn, regurgitation, or other symptoms of GERD at night are probably
experiencing reflux at night and definitely should use upper body elevation. Reflux also occurs less frequently when
patients lie on their left rather than their right sides.
GERD Diet
Several changes in eating habits can be beneficial in treating GERD. Reflux is worse following meals. This probably
is so because the stomach is distended with food at that time and transient relaxations of the lower esophageal
sphincter are more frequent. Therefore, smaller and earlier evening meals may reduce the amount of reflux for two
reasons. First, the smaller meal results in lesser distention of the stomach. Second, by bedtime, a smaller and earlier
meal is more likely to have emptied from the stomach than is a larger one. As a result, reflux is less likely to occur
when patients with GERD lie down.
Certain foods are known to reduce the pressure in the lower esophageal sphincter and thereby promote reflux. These
foods should be avoided and include:
• chocolate,
• peppermint,
• alcohol, and
• caffeinated drinks.
Fatty foods (which should be decreased) and smoking (which should be stopped) also reduce the pressure in the
sphincter and promote reflux.
In addition, patients with GERD may find that other foods aggravate their symptoms. Examples are spicy or acid-
containing foods, like citrus juices, carbonated beverages, and tomato juice. These foods should also be avoided.
One novel approach to the treatment of GERD is chewing gum. Chewing gum stimulates the production of more
bicarbonate-containing saliva and increases the rate of swallowing. After the saliva is swallowed, it neutralizes acid in
the esophagus. In effect, chewing gum exaggerates one of the normal processes that neutralizes acid in the
esophagus. It is not clear, however, how effective chewing gum actually is in treating heartburn. Nevertheless,
chewing gum after meals is certainly worth a try.
Antacids
Despite the development of potent medications for the treatment of GERD, antacids remain a mainstay of treatment.
Antacids neutralize the acid in the stomach so that there is no acid to reflux. The problem with antacids is that their
action is brief. They are emptied from the empty stomach quickly, in less than an hour, and the acid then re-
accumulates. The best way to take antacids, therefore, is approximately one hour after meals or just before the
symptoms of reflux begin after a meal. Since the food from meals slows the emptying from the stomach, an antacid
taken after a meal stays in the stomach longer and is effective longer. For the same reason, a second dose of
antacids approximately two hours after a meal takes advantage of the continuing post-meal slower emptying of the
stomach and replenishes the acid-neutralizing capacity within the stomach.
Antacids may be aluminum, magnesium, or calcium based. Calcium-based antacids (usually calcium carbonate),
unlike other antacids, stimulate the release of gastrin from the stomach and duodenum. Gastrin is the hormone that is
primarily responsible for the stimulation of acid secretion by the stomach. Therefore, the secretion of acid rebounds
after the direct acid-neutralizing effect of the calcium carbonate is exhausted. The rebound is due to the release of
gastrin, which results in an overproduction of acid. Theoretically at least, this increased acid is not good for GERD.
Acid rebound, however, has not been shown to be clinically important. That is, treatment with calcium carbonate has
not been shown to be less effective or safe than treatment with antacids not containing calcium carbonate.
Nevertheless, the phenomenon of acid rebound is theoretically harmful. In practice, therefore, calcium-containing
antacids such as Tums and Rolaids are not recommended. The occasional use of these calcium carbonate-
containing antacids, however, is not believed to be harmful. The advantages of calcium carbonate-containing
antacids are their low cost , the calcium they add to the diet, and their convenience as compared to liquids.
Aluminum-containing antacids have a tendency to cause constipation, while magnesium-containing antacids tend to
cause diarrhea. If diarrhea or constipation becomes a problem, it may be necessary to switch antacids or alternately
use antacids containing aluminum and magnesium.
Histamine antagonists
Although antacids can neutralize acid, they do so for only a short period of time. For substantial neutralization of acid
throughout the day, antacids would need to be given frequently, at least every hour.
The first medication developed for more effective and convenient treatment of acid-related diseases, including GERD,
was a histamine antagonist, specifically cimetidine (Tagamet). Histamine is an important chemical because it
stimulates acid production by the stomach. Released within the wall of the stomach, histamine attaches to receptors
(binders) on the stomach's acid-producing cells and stimulates the cells to produce acid. Histamine antagonists work
by blocking the receptor for histamine and thereby preventing histamine from stimulating the acid-producing cells.
(Histamine antagonists are referred to as H2 antagonists because the specific receptor they block is the histamine
type 2 receptor.)
Because histamine is particularly important for the stimulation of acid after meals, H2 antagonists are best taken 30
minutes before meals. The reason for this timing is so that the H2 antagonists will be at peak levels in the body after
the meal when the stomach is actively producing acid. H2 antagonists also can be taken at bedtime to suppress
nighttime production of acid.
H2 antagonists are very good for relieving the symptoms of GERD, particularly heartburn. However, they are not very
good for healing the inflammation (esophagitis) that may accompany GERD. In fact, they are used primarily for the
treatment of heartburn in GERD that is not associated with inflammation or complications, such as erosions or ulcers,
strictures, or Barrett's esophagus.
Four different H2 antagonists are available by prescription, including cimetidine (Tagamet), ranitidine (Zantac),
nizatidine (Axid), and famotidine, (Pepcid). All four are also available over-the-counter (OTC), without the need for a
prescription. However, the OTC dosages are lower than those available by prescription.
Proton pump inhibitors
The second type of drug developed specifically for acid-related diseases, such as GERD, was a proton pump inhibitor
(PPI), specifically, omeprazole (Prilosec). A PPI blocks the secretion of acid into the stomach by the acid-secreting
cells. The advantage of a PPI over an H2 antagonist is that the PPI shuts off acid production more completely and for
a longer period of time. Not only is the PPI good for treating the symptom of heartburn, but it also is good for
protecting the esophagus from acid so that esophageal inflammation can heal.
PPIs are used when H2 antagonists do not relieve symptoms adequately or when complications of GERD such as
erosions or ulcers, strictures, or Barrett's esophagus exist. Five different PPIs are approved for the treatment of
GERD, including omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix), and
esomeprazole (Nexium). A fifth PPI product consists of a combination of omeprazole and sodium bicarbonate
(Zegerid). PPIs (except for Zegarid) are best taken an hour before meals. The reason for this timing is that the PPIs
work best when the stomach is most actively producing acid, which occurs after meals. If the PPI is taken before the
meal, it is at peak levels in the body after the meal when the acid is being made.
Pro-motility drugs
Pro-motility drugs work by stimulating the muscles of the gastrointestinal tract, including the esophagus, stomach,
small intestine, and/or colon. One pro-motility drug, metoclopramide (Reglan), is approved for GERD. Pro-motility
drugs increase the pressure in the lower esophageal sphincter and strengthen the contractions (peristalsis) of the
esophagus. Both effects would be expected to reduce reflux of acid. However, these effects on the sphincter and
esophagus are small. Therefore, it is believed that the primary effect of metoclopramide may be to speed up
emptying of the stomach, which also would be expected to reduce reflux.
Pro-motility drugs are most effective when taken 30 minutes before meals and again at bedtime. They are not very
effective for treating either the symptoms or complications of GERD. Therefore, the pro-motility agents are reserved
either for patients who do not respond to other treatments or are added to enhance other treatments for GERD.
Foam barriers
Foam barriers provide a unique form of treatment for GERD. Foam barriers are tablets that are composed of an
antacid and a foaming agent. As the tablet disintegrates and reaches the stomach, it turns into foam that floats on the
top of the liquid contents of the stomach. The foam forms a physical barrier to the reflux of liquid. At the same time,
the antacid bound to the foam neutralizes acid that comes in contact with the foam. The tablets are best taken after
meals (when the stomach is distended) and when lying down, both times when reflux is more likely to occur. Foam
barriers are not often used as the first or only treatment for GERD. Rather, they are added to other drugs for GERD
when the other drugs are not adequately effective in relieving symptoms. There is only one foam barrier, which is a
combination of aluminum hydroxide gel, magnesium trisilicate, and alginate (Gaviscon).
Surgery
The drugs described above usually are effective in treating the symptoms and complications of GERD. Nevertheless,
sometimes they are not. For example, despite adequate suppression of acid and relief from heartburn, regurgitation,
with its potential for complications in the lungs, may still occur. Moreover, the amounts and/or numbers of drugs that
are required for satisfactory treatment are sometimes so great that drug treatment is unreasonable. In such
situations, surgery can effectively stop reflux.
The surgical procedure that is done to prevent reflux is technically known as fundoplication and is called reflux
surgery or anti-reflux surgery. During fundoplication, any hiatal hernial sac is pulled below the diaphragm and stitched
there. In addition, the opening in the diaphragm through which the esophagus passes is tightened around the
esophagus. Finally, the upper part of the stomach next to the opening of the esophagus into the stomach is wrapped
around the lower esophagus to make an artificial lower esophageal sphincter. All of this surgery can be done through
an incision in the abdomen (laparotomy) or using a technique called laparoscopy. During laparoscopy, a small
viewing device and surgical instruments are passed through several small puncture sites in the abdomen. This
procedure avoids the need for a major abdominal incision.
Surgery is very effective at relieving symptoms and treating the complications of GERD. Approximately 80% of
patients will have good or excellent relief of their symptoms for at least 5 to 10 years. Nevertheless, many patients
who have had surgery—perhaps as many as half—will continue to take drugs for reflux. It is not clear whether they
take the drugs because they continue to have reflux and symptoms of reflux or if they take them for symptoms that
are being caused by problems other than GERD. The most common complication of fundoplication is swallowed food
that sticks at the artificial sphincter. Fortunately, the sticking usually is temporary. If it is not transient, endoscopic
treatment to stretch (dilate) the artificial sphincter usually will relieve the problem. Only occasionally is it necessary to
re-operate to revise the prior surgery.
Endoscopy
Very recently, endoscopic techniques for the treatment of GERD have been developed and tested. One type of
endoscopic treatment involves suturing (stitching) the area of the lower esophageal sphincter, which essentially
tightens the sphincter.
A second type involves the application of radio-frequency waves to the lower part of the esophagus just above the
sphincter. The waves cause damage to the tissue beneath the esophageal lining and a scar (fibrosis) forms. The scar
shrinks and pulls on the surrounding tissue, thereby tightening the sphincter and the area above it.
A third type of endoscopic treatment involves the injection of materials into the esophageal wall in the area of the
LES. The injected material is intended to increase pressure in the LES and thereby prevent reflux. In one treatment
the injected material was a polymer. Unfortunately, the injection of polymer led to serious complications, and the
material for injection is no longer available. Another treatment involving injection of expandable pellets also was
discontinued. Limited information is available about a third type of injection which uses gelatinous
polymethylmethacrylate microspheres.
Endoscopic treatment has the advantage of not requiring surgery. It can be performed without hospitalization.
Experience with endoscopic techniques is limited. It is not clear how effective they are, especially long-term. Because
the effectiveness and the full extent of potential complications of endoscopic techniques are not clear, it is felt
generally that endoscopic treatment should only be done as part of experimental trials.
Prevention of transient LES relaxation
Transient LES relaxations appear to be the most common way in which acid reflux occurs. Although there are
available drugs that prevent relaxations, they have too many side effects to be generally useful. Much attention is
being directed at the development of drugs that prevent these relaxations without accompanying side effects
1. Discussion 2Digestive System
Digestive System. KidsHealth> Teens> Diseases &

Conditions> Body Basics Library> Digestive System ... The
digestive system is made up of the alimentary canal ...
kidshealth.org/teen/.../body_basics/digestive_system.html
Food Is the Body's Fuel Source
What's the first step in digesting food? Believe it or not, the digestive process starts even before you
put food in your mouth. It begins when you smell something irresistible or when you see a favorite
food you know will taste good. Just by smelling that homemade apple pie or thinking about how
delicious that ice cream sundae is going to taste, you begin to salivate — and the digestive process
kicks in, preparing for that first scrumptious bite.
If it's been a while since your last meal or if you even think about something tasty, you feel hungry.
You eat until you're satisfied and then go about your business. But for the next 20 hours or so, your
digestive system is doing its job as the food you ate travels through your body.
Food is the body's fuel source. The nutrients in food give the body's cells the energy and other
substances they need to operate. But before food can do any of these things, it has to be digested into
small pieces the body can absorb and use.
Almost all animals have a tube-type digestive system in which food

enters the mouth, passes through a long tube, and exits as feces (poop) through the anus. The
smooth muscle in the walls of the tube-shaped digestive organs rhythmically and efficiently moves the
food through the system, where it is broken down into tiny absorbable nutrients.
During the process of absorption, nutrients that come from the food (including carbohydrates,
proteins, fats, vitamins, and minerals) pass through channels in the intestinal wall and into the
bloodstream. The blood works to distribute these nutrients to the rest of the body. The waste parts of
food that the body can't use are passed out of the body as feces.
What Is the Digestive System and What Does It Do?
Every morsel of food we eat has to be broken down into nutrients that can be absorbed by the body,
which is why it takes hours to fully digest food. In humans, protein must be broken down into amino
acids, starches into simple sugars, and fats into fatty acids and glycerol. The water in our food and
drink is also absorbed into the bloodstream to provide the body with the fluid it needs.
The digestive system is made up of the alimentary canal and the other abdominal organs that play a
part in digestion, such as the liver and pancreas. The alimentary canal (also called the digestive
tract) is the long tube of organs — including the esophagus, the stomach, and the intestines — that
runs from the mouth to the anus. An adult's digestive tract is about 30 feet long.
Digestion Begins in the Mouth
The process of digestion starts well before food reaches the stomach. When we see, smell, taste, or
even imagine a tasty snack, our salivary glands, which are located under the tongue and near the
lower jaw, begin producing saliva. This flow of saliva is set in motion by a brain reflex that's triggered
when we sense food or even think about eating. In response to this sensory stimulation, the brain
sends impulses through the nerves that control the salivary glands, telling them to prepare for a meal.
As the teeth tear and chop the food, saliva moistens it for easy swallowing. A digestive enzyme called
amylase (pronounced: ah-meh-lace), which is found in saliva, starts to break down some of the
carbohydrates (starches and sugars) in the food even before it leaves the mouth.
Swallowing, which is accomplished by muscle movements in the tongue and mouth, moves the food
into the throat, or pharynx. The pharynx (pronounced: fair-inks), a passageway for food and air, is
about 5 inches long. A flexible flap of tissue called the epiglottis (pronounced: ep-ih-glah-tus)
reflexively closes over the windpipe when we swallow to prevent choking.
From the throat, food travels down a muscular tube in the chest called the esophagus (pronounced:
ih-sah-fuh-gus). Waves of muscle contractions called peristalsis (pronounced: per-uh-stall-sus)
force food down through the esophagus to the stomach. A person normally isn't aware of the
movements of the esophagus, stomach, and intestine that take place as food passes through the
digestive tract.
BackContinue

Continue
digestive tract.
BackContinue
The Stomach
At the end of the esophagus, a muscular ring called a sphincter (pronounced: sfink-ter) allows food
to enter the stomach and then squeezes shut to keep food or fluid from flowing back up into the
esophagus. The stomach muscles churn and mix the food with acids and enzymes, breaking it into
much smaller, more digestible pieces. An acidic environment is needed for the digestion that takes
place in the stomach. Glands in the stomach lining produce about 3 quarts of these digestive juices
each day.
Most substances in the food we eat need further digestion and must travel into the intestine before
being absorbed. When it's empty, an adult's stomach has a volume of one fifth of a cup, but it can
expand to hold more than 8 cups of food after a large meal.
By the time food is ready to leave the stomach, it has been processed into a thick liquid called chyme
(pronounced: kime). A walnut-sized muscular tube at the outlet of the stomach called the pylorus
(pronounced: py-lore-us) keeps chyme in the stomach until it reaches the right consistency to pass
into the small intestine. Chyme is then squirted down into the small intestine, where digestion of food
continues so the body can absorb the nutrients into the bloodstream.
The Small Intestine
The small intestine is made up of three parts:
1. the duodenum (pronounced: due-uh-dee-num), the C-shaped first part
2. the jejunum (pronounced: jih-ju-num), the coiled midsection
3. the ileum (pronounced: ih-lee-um), the final section that leads into the large intestine
The inner wall of the small intestine is covered with millions of microscopic, finger-like projections
called villi (pronounced: vih-lie). The villi are the vehicles through which nutrients can be absorbed
into the body.

Continue

digestive tract.
BackContinue
The Stomach
At the end of the esophagus, a muscular ring called a sphincter (pronounced: sfink-ter) allows food
to enter the stomach and then squeezes shut to keep food or fluid from flowing back up into the
esophagus. The stomach muscles churn and mix the food with acids and enzymes, breaking it into
much smaller, more digestible pieces. An acidic environment is needed for the digestion that takes
place in the stomach. Glands in the stomach lining produce about 3 quarts of these digestive juices
each day.
Most substances in the food we eat need further digestion and must travel into the intestine before
being absorbed. When it's empty, an adult's stomach has a volume of one fifth of a cup, but it can
expand to hold more than 8 cups of food after a large meal.
By the time food is ready to leave the stomach, it has been processed into a thick liquid called chyme
(pronounced: kime). A walnut-sized muscular tube at the outlet of the stomach called the pylorus
(pronounced: py-lore-us) keeps chyme in the stomach until it reaches the right consistency to pass
into the small intestine. Chyme is then squirted down into the small intestine, where digestion of food
continues so the body can absorb the nutrients into the bloodstream.
The Small Intestine
The small intestine is made up of three parts:
1. the duodenum (pronounced: due-uh-dee-num), the C-shaped first part
2. the jejunum (pronounced: jih-ju-num), the coiled midsection
3. the ileum (pronounced: ih-lee-um), the final section that leads into the large intestine
The inner wall of the small intestine is covered with millions of microscopic, finger-like projections
called villi (pronounced: vih-lie). The villi are the vehicles through which nutrients can be absorbed
into the body.
BackContinue
The Liver
The liver (located under the ribcage in the right upper part of the abdomen), the gallbladder (hidden
just below the liver), and the pancreas (beneath the stomach) are not part of the alimentary canal,
but these organs are still important for healthy digestion.
The pancreas produces enzymes that help digest proteins, fats, and carbohydrates. It also makes a
substance that neutralizes stomach acid. The liver produces bile, which helps the body absorb fat. Bile
is stored in the gallbladder until it is needed. These enzymes and bile travel through special channels
(called ducts) directly into the small intestine, where they help to break down food.
The liver also plays a major role in the handling and processing of nutrients. These nutrients are
carried to the liver in the blood from the small intestine.
The Large Intestine
From the small intestine, food that has not been digested (and some water) travels to the large
intestine through a valve that prevents food from returning to the small intestine. By the time food
reaches the large intestine, the work of absorbing nutrients is nearly finished. The large intestine's
main function is to remove water from the undigested matter and form solid waste that can be
excreted. The large intestine is made up of three parts:
1. The cecum (pronounced: see-kum) is a pouch at the beginning of the large intestine that
joins the small intestine to the large intestine. This transition area allows food to travel
from the small intestine to the large intestine. The appendix, a small, hollow, finger-like
pouch, hangs off the cecum. Doctors believe the appendix is left over from a previous time
in human evolution. It no longer appears to be useful to the digestive process.
2. The colon extends from the cecum up the right side of the abdomen, across the upper
abdomen, and then down the left side of the abdomen, finally connecting to the rectum.
The colon has three parts: the ascending colon and transverse colon, which absorb water
and salts, and the descending colon, which holds the resulting waste. Bacteria in the colon
help to digest the remaining food products.
3. The rectum is where feces are stored until they leave the digestive system through the
anus as a bowel movement.
Things That Can Go Wrong With the Digestive System
Nearly everyone has a digestive problem at one time or another. Some conditions, such as indigestion
or mild diarrhea, are common; they result in mild discomfort and get better on their own or are easy
to treat. Others, such as inflammatory bowel disease (IBD), can be long lasting or troublesome. A
doctor who specializes in the digestive system and who can be helpful when dealing with these
conditions is called a GI specialist or gastroenterologist.
Conditions Affecting the Esophagus
Conditions affecting the esophagus may be congenital (meaning people are born with them) or
noncongenital (meaning people can develop them after birth).
Some examples include:
1. Tracheoesophageal fistula (pronounced: tray-kee-oh-ih-saf-uh-jee-ul fish-chuh-luh) and

esophageal atresia (pronounced: ih-saf-uh-jee-ul uh-tree-zhuh) are both examples of congenital
conditions. Tracheoesophageal fistula is where there is a connection between the esophagus and the
trachea (windpipe) where there shouldn't be one. In babies with esophageal atresia, the esophagus
comes to a dead end instead of connecting to the stomach. Both conditions are usually detected soon
after a baby is born — sometimes even beforehand. They require surgery to repair.
2. Esophagitis (pronounced: ih-saf-uh-jeye-tus) or inflammation of the esophagus, is an

example of a noncongenital condition. Esophagitis is usually caused by gastroesophageal reflux
disease (GERD), a condition in which the esophageal sphincter (the tube of muscle that connects the
esophagus with the stomach) allows the acidic contents of the stomach to move backward up into the
esophagus. GERD can sometimes be corrected through lifestyle changes, such as adjusting the types
of things a person eats. Sometimes, though, it requires treatment with medication. Occasionally,
esophagitis can be caused by infection or certain medications.
Conditions Affecting the Stomach and Intestines
Almost everyone has experienced diarrhea or constipation at some point in their lives. With diarrhea,
muscle contractions move the contents of the intestines along too quickly and there isn't enough time
for water to be absorbed before the feces are pushed out of the body. Constipation is the opposite:
The contents of the large intestines do not move along fast enough and waste materials stay in the
large intestine so long that too much water is removed and the feces become hard.
Other common stomach and intestinal disorders include:
1. Celiac disease is a digestive disorder caused by the abnormal response of the immune
system to a protein called gluten, which is found in certain foods. People with celiac disease have
difficulty digesting the nutrients from their food because eating things with gluten damages the lining
of the intestines over time. Some of the symptoms are diarrhea, abdominal pain, and bloating. The
disease can be managed by following a gluten-free diet.
2. Irritable bowel syndrome (IBS) is a common intestinal disorder that affects the colon.
When the muscles in the colon don't work smoothly, a person can feel the abdominal cramps,
bloating, constipation, and diarrhea that may be signs of IBS. There's no cure for IBS, but it can be
managed by making some dietary and lifestyle changes. Occasionally, medications may be used as
well.
3. Gastritis and peptic ulcers. Under normal conditions, the stomach and duodenum are
extremely resistant to irritation by the strong acids produced in the stomach. Sometimes, though, a
bacterium called Helicobacter pylori or the chronic use of certain medications weakens the protective
mucous coating of the stomach and duodenum, allowing acid to get through to the sensitive lining
beneath. This can irritate and inflame the lining of the stomach (a condition known as gastritis) or
cause peptic ulcers, which are sores or holes that form in the lining of the stomach or the duodenum
and cause pain or bleeding. Medications are usually successful in treating these conditions.
4. Inflammatory bowel disease (IBD) is chronic inflammation of the intestines that affects
older kids, teens, and adults. There are two major types: ulcerative colitis, which usually affects just
the rectum and the large intestine, and Crohn's disease, which can affect the whole gastrointestinal
tract from the mouth to the anus as well as other parts of the body. They are treated with
medications, but in some cases, surgery may be necessary to remove inflamed or damaged areas of
the intestine.
Disorders of the Pancreas, Liver, and Gallbladder
Conditions affecting the pancreas, liver, and gallbladder often affect the ability of these organs to
produce enzymes and other substances that aid in digestion.
These include:
1. Cystic fibrosis is a chronic, inherited illness where the production of abnormally thick mucus
blocks the ducts or passageways in the pancreas and prevents its digestive juices from entering the
intestines, making it difficult for a person to properly digest proteins and fats. This causes important
nutrients to pass out of the body unused. To help manage their digestive problems, people with cystic
fibrosis can take digestive enzymes and nutritional supplements.
2. Hepatitis is a viral infection in which the liver becomes inflamed and can lose its ability to
function. Some forms of viral hepatitis are highly contagious. Mild cases of hepatitis A can be treated
at home; however, serious cases involving liver damage may require hospitalization.
3. The gallbladder can develop gallstones and become inflamed — a condition called
cholecystitis (pronounced: ko-lee-sis-teye-tus). Although gallbladder conditions are uncommon in
teens, they can occur when a teen has sickle cell anemia or is being treated with certain long-term
medications.
The kinds and amounts of food a person eats and how the digestive system processes that food play
key roles in maintaining good health. Eating a healthy diet is the best way to prevent common
digestive problems.
Reviewed by: Steven Dowshen, MD

Date reviewed: April 2007

Unit 5 Research Gastroesophageal Reflux Disease

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Unit 5 Research Gastroesophageal Reflux Disease

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Unit 5 research gastroesophageal reflux disease (GERD)?

Gastroesophageal reflux disease, or GERD, is a condition that affects millions of

How is GERD Treated?

What Can I Do?

Take The Assessment

Barium Esophagram (upper GI)

GERD (Gastroesophageal Reflux Disease)

Histamine2-Receptor Antagonist (H2-RA)

Mucosal Protective Agents

Proton Pump Inhibitor

Secondary Peristalsis (Esophageal)

2. Jacob P, Kahrilas PJ, Vanagunas A. Peristaltic dysfunction associated

4. Richter JE. Extraesophageal presentations of gastroesophageal reflux

6. Dent J, Brun J, Fendrick AM, et al. An evidence-based appraisal of

7. American Gastroenterological Association. The Burden of

9. Ward EM, DeVault KR, Bouras EP, et al. Successful oesophageal pH

10. Maton PN. Profile and assessment of GERD pharmacotherapy. Cleve

11. Hameeteman W, van de Boomgaard DM, Dekker W, et al. Sucralfate

14. Ramirez B, Richter J. Review article: promotility drugs in the treatment

16. Stein HJ, Barlow AP, DeMeester TR, et al. Complications of

17. Kahrilas PJ. Gastroesophageal reflux disease. JAMA. 1996;276:983-

19. Howden CW, Henning JM, Huang B, et al. Management of heartburn in

20. Hatlebakk JG, Berstad A Gastro-oesophageal reflux during 3 months of

21. Frislid K, Berstad A. Prolonged influence of a meal on the effect of

22. Klinkenberg-Knol E, Nelis F, Dent J, et al. Long-term omeprazole

23. Bardhan KD, Morris P, Thompson M, et al. Omeprazole in the treatment

25. Richter JE, Campbell DR, Kahrilas PJ et al. Lansoprazole compared

26. Robinson M, Sahba B, Avner D et al. A comparison of lansoprazole and

27. Oberg S, Clark GW, DeMeester TR. Barrett’s esophagus. Update of

30. Dekkers CP, Beker JA, Thjodleifsson B, et al. Double-blind comparison

31. Mossner J, Holscher AH, Herz R, et al. A double-blind study of

32. Caro JJ, Salas M, Ward A. Healing and Relapse Rates in

33. Vigneri S, Termini R, Leandro G, et al.: A comparison of five

36. Marshall REK, Anggiansah A, Manifold DK, et al. Effect of omeprazole

37. Harris RA, Kuppermann M, Richter JE. Prevention of recurrences of

39. Harris RA, Kuppermann M, Richter JE. Proton pump inhibitors or

41. Inadomi JM, Jamal R, Murata GH, et al. Step-down management of

42. Katz PO, Anderson C, Khoury R, et al. Gastro-oesophageal reflux

43. Paoletti V, Karvois D, Greski-Rose P, et al. Lansoprazole is superior to

46. Schindlbeck NE, Ippisch H, Klauser AG, et al. Which pH threshold is

47. Schindlbeck NE, Heinrich C, Konig A, et al. Optimal thresholds,

What patients want to know

Patients will want information on a number of issues including:

• What causes GERD?

• What are the sequelae of GERD?

• How can they get relief from their symptoms?

• What tests will they need?

What educational materials can you give them?

Educational Web Sites

Mayo Clinic Consumer Health

Links to Internet Web Sites

The Cleveland Clinic Medical Education Web Site

The Visible Human Project

2. Jacob P, Kahrilas PJ, Vanagunas A. Peristaltic dysfunction associated

4. Richter JE. Extraesophageal presentations of gastroesophageal reflux

5. Richter JE. Gastroesophageal Reflux Disease. In: Yamada T, Alpers

7. American Gastroenterological Association. The Burden of

9. Ward EM, DeVault KR, Bouras EP, et al. Successful oesophageal pH

10. Maton PN. Profile and assessment of GERD pharmacotherapy. Cleve

11. Hameeteman W, van de Boomgaard DM, Dekker W, et al. Sucralfate

14. Ramirez B, Richter J. Review article: promotility drugs in the treatment

16. Stein HJ, Barlow AP, DeMeester TR, et al. Complications of