History

Fact Explanation
Gender of the patient According to epidemiological data available, male sex is a risk factor for developing gastric ulcer disease. Lifetime cumulative incidence for males is 10% and for females is lower at 4%. The peak incidence males is in their 40s, while for females it is more common in their 50s and 60s. [1]
Epigastric burning[4][5] / gnawing type pain associated with fullness/ bloating sensation, heartburn, chest discomfort, nausea and vomitting This can radiate to neck, back or to the lower abdomen. Pain comes from the ulcer itself when gastric acid contact with it and irritate it. Duration of pain will be varies from few minutes to few hours and usually during the daytime. Pain will exaggerate shortly after meals and it usually does not respond to antacids. Some peoples will feel exaggeration of the symptoms with fatty/ chilled foods and some may gain relief of the pain with vomiting.
Vomiting of blood/ passage of dark colour stools might be associated with anemic symptoms such as easy fatiguability, lethargy, dyspnea These symptoms are related with complications of gastric ulcer(31- 67%)[6]. When the ulcer erodes into a blood vessel bleeding can be occur. This may present either as hematemesis, melena or other features of anaemia (easy fatigability, lethargy, dyspnea). Very rarely profusely bleeding ulcer can be present as hematochezia. Melena may be multiple episodes in a single day or intermittent over several days.
Sudden onset genaralized abdominal pain, fever, ill health, dizziness Perforation[7][8][9][10] of gastric ulcer releases the content of the stomach to the abdomen leading to peritonitis. Peritonitis will present as sudden illness and may leads to bacteremia/ sepsis.
Recurrent vomiting, bloating sensation after meal, early satiety, weight loss Gastric outlet obstruction[3][11] following gastric ulcer( due to fibrosis during healing) may present with those symptoms. Symptoms will depend on the site and degree of the obstruction. Vomiting is intermittent, non bilious and occurs one hour after meals containing undigested foods.
Early satiety, unexplained weight loss, loss of appetite, progressive dysphagia, gradually worsening symptoms of gastric outlet obstruction Gastric cancer is another complication in gastric ulcer disease[12]. For gastric carcinoma there is evidence of a strong association with H pylori infection. [1][13] According to current data old age, non-white ethnicity and male sex has strong,independent risk factors for non-cardiac gastric cancers. [14]
Past history of gastric ulcer disease/ recurrent attacks of gastritis, history of chronic renal failure[1], history of chronic obstructive pulmonary disease[1] Past medical history of gastric ulcer disease[16] and recurrent attacks of gastritis is important as there is an increased risk of recurrence with H. pylori infection( this was found as the only risk factor for the recurrence)[16][17]. Patients with chronic renal failure are at high risk of developing gastric ulcers. Among them-patients receiving in-patient care, haemodialysis and patients on NSAIDs are at higher risk. [18] Patients with chronic obstructive pulmonary disease are also at risk of developing gastric ulcer disease[19]. Reason is due to the common etiological agent: tobacco smoking. [20]
A family history of gastric ulcer disease[1] Family history of gastric ulcer disease is a risk factor[1][21] as there are some genetic predispositions to develop the disease, but there is no genetic relationship in developing H. pylori infection. Some research results suggest that there is a significant association between genetic polymorphism at the PGC-RFLP gene locus and gastric body ulcer[21].
Drug history[1][22] Non steroidal anti inflammatory drugs (NSAIDs) interfere with the mucosal defense in the stomach via direct toxic effects in addition to cyclooxygenase inhibition and then depletion of endogenous prostaglandins[23]. Usually 30-50% of all gastric ulcers are due to NSAIDs. Among drugs diclofenac and aspirin[24] are the most commonly associated drugs. NSAID-induced gastritis/ ulcers may be silent, especially in elderly patients.
Dietary history Skipping of meals allows gastric acid to directly act on surface mucosa of the stomach causing recurrent irritation which ultimately leads to gastric ulcers. Gastric ulcers cause abdominal pain which aggravate with meals[25]. So this goes as a cycle leading to increase morbidity.
Social history: alcohol, smoking, stress Consumption of alcohol and smoking are risk factors. [1][26][27] Chronic alcohol disturbs gastric mucosal barrier by inhibiting COX 1 receptor enzymes which reduce the production of cytoprotective prostaglandin. Cigarette smoking causes reduction of circulating epidermal growth factor and increase free radical production in gastric mucosa. The free radicals present in smoke together with produced free radicals leads to reduction of mucosal constitutive nitric oxide synthase activity. Also it affects the normal gastric mucosal blood flow, angiogenesis and the suppression of cell proliferation causing delay in ulcer healing in cigarette smokers. Occupation and related stress/ any other stressful conditions at present also need to be assessed [1]. In a stressful situation there is an acute threat to homeostasis( causing reduction in blood supply to superficial mucosa of the stomach) and this evokes an adaptive or allostatic response by this stress may play a role in the onset/modulation of acute/chronic gastric ulcer disease. [2]
References
  1. SCHWARTZ MD. Dyspepsia, peptic ulcer disease, and esophageal reflux disease West J Med [online] 2002 Mar, 176(2):98-103 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071675
  2. CHOUNG RS, TALLEY NJ. Epidemiology and clinical presentation of stress-related peptic damage and chronic peptic ulcer. Curr Mol Med [online] 2008 Jun, 8(4):253-7 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/18537633
  3. ARAúJO MB, BORINI P, GUIMARãES RC. ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past? Arq Gastroenterol [online] 2014 Apr, 51(2):155-61 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/25003270
  4. NAJM WI. Peptic ulcer disease. Prim Care [online] 2011 Sep, 38(3):383-94, vii [viewed 29 July 2014] Available from: doi:10.1016/j.pop.2011.05.001
  5. RAMAKRISHNAN K, SALINAS RC. Peptic ulcer disease. Am Fam Physician [online] 2007 Oct 1, 76(7):1005-12 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17956071
  6. HOLSTER IL, KUIPERS EJ. Update on the Endoscopic Management of Peptic Ulcer Bleeding Curr Gastroenterol Rep [online] 2011 Dec, 13(6):525-531 [viewed 29 July 2014] Available from: doi:10.1007/s11894-011-0223-7
  7. WILSON-MACDONALD J, MORTENSEN NJ, WILLIAMSON RC. Perforated gastric ulcer. Postgrad Med J [online] 1985 Mar, 61(713):217-220 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2418177
  8. WYSOCKI A, BIESIADA Z, BEBEN P, BUDZYNSKI A. Perforated gastric ulcer. Dig Surg [online] 2000, 17(2):132-7 [viewed 29 July 2014] Available from: doi:18815
  9. MCCREERY JA. PERFORATED GASTRIC AND DUODENAL ULCER Ann Surg [online] 1938 Mar, 107(3):350-358 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1386854
  10. SCHIETROMA M, PICCIONE F, CARLEI F, SISTA F, CECILIA EM, AMICUCCI G. Peritonitis from perforated peptic ulcer and immune response. J Invest Surg [online] 2013 Oct, 26(5):294-304 [viewed 29 July 2014] Available from: doi:10.3109/08941939.2012.762073
  11. GIBSON JB, BEHRMAN SW, FABIAN TC, BRITT LG. Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg [online] 2000 Jul, 191(1):32-7 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10898181
  12. MOLLOY RM, SONNENBERG A. Relation between gastric cancer and previous peptic ulcer disease. Gut [online] 1997 Feb, 40(2):247-252 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1027057
  13. HANSSON LE, NYRéN O, HSING AW, BERGSTRöM R, JOSEFSSON S, CHOW WH, FRAUMENI JF JR, ADAMI HO. The risk of stomach cancer in patients with gastric or duodenal ulcer disease. N Engl J Med [online] 1996 Jul 25, 335(4):242-9 [viewed 29 July 2014] Available from: doi:10.1056/NEJM199607253350404
  14. MOLLOY RM, SONNENBERG A. Relation between gastric cancer and previous peptic ulcer disease. Gut [online] 1997 Feb, 40(2):247-52 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9071940
  15. HEPPELL J, BESS MA, MCILRATH DC, DOZOIS RR. Surgical treatment of recurrent peptic ulcer disease. Ann Surg [online] 1983 Jul, 198(1):1-4 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1352921
  16. KIM JJ, KIM N, LEE BH, KANG JM, SEO P, LIM MK, KWON JH, SONG BJ, LEE JW, LEE SH, PARK YS, HWANG JH, KIM JW, JEONG SH, LEE DH, JUNG HC, SONG IS. [Risk factors for development and recurrence of peptic ulcer disease]. Korean J Gastroenterol [online] 2010 Oct, 56(4):220-8 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20962557
  17. MACARTHUR C, SAUNDERS N, FELDMAN W. Helicobacter pylori, gastroduodenal disease, and recurrent abdominal pain in children. JAMA [online] 1995 Mar 1, 273(9):729-34 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/7853632
  18. LIANG CC, MUO CH, WANG IK, CHANG CT, CHOU CY, LIU JH, YEN TH, HUANG CC, CHUNG CJ. Peptic Ulcer Disease Risk in Chronic Kidney Disease: Ten-Year Incidence, Ulcer Location, and Ulcerogenic Effect of Medications PLoS One [online] , 9(2):e87952 [viewed 29 July 2014] Available from: doi:10.1371/journal.pone.0087952
  19. HUANG KW, LUO JC, LEU HB, LIN HC, LEE FY, CHAN WL, LIN SJ, CHEN JW, CHANG FY. Chronic obstructive pulmonary disease: an independent risk factor for peptic ulcer bleeding: a nationwide population-based study. Aliment Pharmacol Ther [online] 2012 Apr, 35(7):796-802 [viewed 29 July 2014] Available from: doi:10.1111/j.1365-2036.2012.05028.x
  20. SIVA R, BIRRING SS, BERRY M, ROWBOTTOM A, PAVORD ID. Peptic ulceration, Helicobacter pylori seropositivity and chronic obstructive pulmonary disease. Respirology [online] 2013 May, 18(4):728-31 [viewed 29 July 2014] Available from: doi:10.1111/resp.12075
  21. OHTAKI Y, AZUMA T, KONISHI J, ITO S, KURIYAMA M. Association between genetic polymorphism of the pepsinogen C gene and gastric body ulcer: the genetic predisposition is not associated with Helicobacter pylori infection Gut [online] 1997 Oct, 41(4):469-474 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891520
  22. COLIN-JONES DG. Drug-induced gastrointestinal ulceration: a review. J R Soc Med [online] 1980 Jan, 73(1):46-47 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440055
  23. SCHEIMAN JM. NSAID-induced peptic ulcer disease: a critical review of pathogenesis and management. Dig Dis [online] 1994 Jul-Aug, 12(4):210-22 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/7851000
  24. HAWTHORNE AB, MAHIDA YR, COLE AT, HAWKEY CJ. Aspirin-induced gastric mucosal damage: prevention by enteric-coating and relation to prostaglandin synthesis. Br J Clin Pharmacol [online] 1991 Jul, 32(1):77-83 [viewed 01 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1368496
  25. HARJU E. The complaints and dietary habits of the patients with gastritis and undefined abdominal pain. Chir Ital [online] 1985 Feb, 37(1):29-36 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/3995661
  26. KO JK, CHO CH. Alcohol drinking and cigarette smoking: a "partner" for gastric ulceration. Zhonghua Yi Xue Za Zhi (Taipei) [online] 2000 Dec, 63(12):845-54 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11195134
  27. MA L, CHOW JY, CHO CH. Effects of cigarette smoking on gastric ulcer formation and healing: possible mechanisms of action. J Clin Gastroenterol [online] 1998:S80-6 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9872502

Examination

Fact Explanation
Mild epigastric tenderness[1] This is a common but non specific symptom. Anatomical location of stomach leads to this sign.
Hematemesis, melena, hematochezia and pallor These signs are related with complications of gastric ulcer (31- 67%)[1][2]. When the ulcer erodes into a blood vessel bleeding can be occur. This may present either as hematemesis( blood stain vomitus), melena( occult blood passage with stools) or pallor (anaemia associated with blood loss). Very rarely profuse bleeding ulcer can be present as hematochezia( passage of fresh blood with stool). In profuse bleeding blood irritates the bowel mucosa causing diarrhoea with reduction of transporting time and fresh blood will pass along with feces.
Ill health, dehydration, pallor, emaciated, non bilious vomit, containing food particles, visible peristalsis and succussion splash Gastric outlet obstruction[3][4] leads to these signs. Recurrent vomiting usually with in an hour after meals leads to ill health, dehydration, wasting and anaemia. On abdominal examination visible peristalsis may or may not be present and on auscultation of the abdomen succussion splash may be present[5].
On general examination: signs of shock such as tachycardia, hypotension and reduced urine output.[1]On abdominal examination, generalized tenderness, rebound tenderness, guarding and muscle rigidity -bowel sounds are diminished/ absent. Perforation[6][7][8][9] of a gastric ulcer releases the contents of the stomach to the abdomen leading to peritonitis. Peritonitis will present as sudden illness and may leads to bacteremia/ sepsis giving those signs.
Loss of weight, palllor, ill health These symptoms are associated with a clinical history of early satiety, unexplained weight loss, loss of appetite, progressive dysphagia, gradually worsening symptoms of gastric outlet obstruction may be suggestive of gastric carcinoma[10].
References
  1. SCHWARTZ MD. Dyspepsia, peptic ulcer disease, and esophageal reflux disease West J Med [online] 2002 Mar, 176(2):98-103 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071675
  2. HOLSTER IL, KUIPERS EJ. Update on the Endoscopic Management of Peptic Ulcer Bleeding Curr Gastroenterol Rep [online] 2011 Dec, 13(6):525-531 [viewed 29 July 2014] Available from: doi:10.1007/s11894-011-0223-7
  3. ARAúJO MB, BORINI P, GUIMARãES RC. ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past? Arq Gastroenterol [online] 2014 Apr, 51(2):155-61 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/25003270
  4. GIBSON JB, BEHRMAN SW, FABIAN TC, BRITT LG. Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg [online] 2000 Jul, 191(1):32-7 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10898181
  5. WICHENDU PN, DODIYI-MANUEL A. Gastric Outlet Obstruction from Duodenal Lipoma in an Adult Niger J Surg [online] 2013, 19(2):79-81 [viewed 30 July 2014] Available from: doi:10.4103/1117-6806.119239
  6. WILSON-MACDONALD J, MORTENSEN NJ, WILLIAMSON RC. Perforated gastric ulcer. Postgrad Med J [online] 1985 Mar, 61(713):217-220 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2418177
  7. WYSOCKI A, BIESIADA Z, BEBEN P, BUDZYNSKI A. Perforated gastric ulcer. Dig Surg [online] 2000, 17(2):132-7 [viewed 29 July 2014] Available from: doi:18815
  8. MCCREERY JA. PERFORATED GASTRIC AND DUODENAL ULCER Ann Surg [online] 1938 Mar, 107(3):350-358 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1386854
  9. SCHIETROMA M, PICCIONE F, CARLEI F, SISTA F, CECILIA EM, AMICUCCI G. Peritonitis from perforated peptic ulcer and immune response. J Invest Surg [online] 2013 Oct, 26(5):294-304 [viewed 01 August 2014] Available from: doi:10.3109/08941939.2012.762073
  10. MOLLOY RM, SONNENBERG A. Relation between gastric cancer and previous peptic ulcer disease. Gut [online] 1997 Feb, 40(2):247-252 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1027057

Differential Diagnoses

Fact Explanation
Acute Coronary Syndrome[3][4] Patients typically present with deep, tightening type, localized chest pain that is exacerbated by activity or emotional stress and relieved by rest, nitroglycerin, or both. Symptoms will depend on site and degree of myocardial ischemia. Pain can arise from substernal(epigastric) area and may radiates to the neck, jaw, left shoulder, and left arm. The chest pain is usually associated with dyspnea, nausea/ vomiting, sweating, palpitations and syncope.
Duodenal ulcer[5][6] This also gives epigastric pain which can radiate to the back. Pain typically occurs over several weeks, timing is usually nocturnal or early in the morning. The pain related to hunger and relieves after meals.
Crohn disease[7][8] Crohn ulceration can occur in any part of the GI tract from the buccal mucosa to the rectum. Isolated Crohn ulceration of the stomach is usually rare but it may cause duodenal or ileal ulcerations. These ulcers may give rise to similar symptoms.
Abdominal aortic aneurysm[9][10] Majority of abdominal aortic aneurysms are asymptomatic. When symptomatic aneurysms present they appear as back, abdominal, buttock, groin, testicular, or leg pain requiring urgent surgical attention. On examination there will be a pulsatile abdominal lump.
Gastritis[11][12] This also give rise to epigastric pain associated with nausea, vomiting and dyspeptic symptoms. Presentation is very much similar to gastric ulcer disease other than associated complications with ulcer.
Cholangitis[13][14] Fever, abdominal (right upper quadrant) pain, and jaundice are the classical triad of symptoms. patient can complain of an epigastric pain as well.
Cholecystitis[15] Frequently the pain in the epigastric region localises to the right upper quadrant.pain associated with nausea, vomiting.
Biliary Colic[16] This is penetrating aching severe pain located in the epigastrium. It develops suddenly and lasts for 15 minutes to several hours and then resolves suddenly. Pain may be referred to posterior scapula or right shoulder area. This may be associated with nausea, vomiting, Jaundice and pruritus.
Acute Diverticulitis[17] Here the typical pain occurs in left lower quadrant pain. Pain is often a crampy in nature and may be associated with changes in bowel habits. Other symptoms are nausea and vomiting, constipation, diarrhea, flatulence, and bloating. In mild diverticulitis may give non specific symptoms similar to gastric ulcer disease. diverticular hemorrhage may lead to malena.
Esophagitis[19] Patients may be assymptomatic but may have symptoms of dysphagia, heartburn, retrosternal discomfort or pain, nausea, vomiting, abdominal pain, epigastric pain, hematemesis (occasionally), anorexia, weight loss, cough
Gastroesophageal Reflux Disease[20] This is associated with heartburn, chest pain, regurgitation, and dysphagia.
Zollinger-Ellison syndrome[21] This is a rare disorder which can cause gastric or duodenal ulcers from excessive acid secretion. This should be considered if a patient has severe peptic ulceration, kidney stones, watery diarrhea, or malabsorption.
Nonulcer dyspepsia (NUD)/ functional dyspepsia[1][2] Functional dyspepsia is diagnosed after excluding other causes of chronic persistent epigastric pain. Patients may have epigastric pain, dyspepsia, or postprandial bloating without any organic cause.
References
  1. BRUN R, KUO B. Functional dyspepsia Therap Adv Gastroenterol [online] 2010 May, 3(3):145-164 [viewed 30 July 2014] Available from: doi:10.1177/1756283X10362639
  2. BRUN R, KUO B. Functional dyspepsia Therap Adv Gastroenterol [online] 2010 May, 3(3):145-164 [viewed 30 July 2014] Available from: doi:10.1177/1756283X10362639
  3. KUMAR A, CANNON CP. Acute Coronary Syndromes: Diagnosis and Management, Part I Mayo Clin Proc [online] 2009 Oct, 84(10):917-938 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755812
  4. FINDLAY IN, CUNNINGHAM AD. Definition of acute coronary syndrome Heart [online] 2005 Jul, 91(7):857-859 [viewed 30 July 2014] Available from: doi:10.1136/hrt.2004.052795
  5. NAJM WI. Peptic ulcer disease. Prim Care [online] 2011 Sep, 38(3):383-94, vii [viewed 30 July 2014] Available from: doi:10.1016/j.pop.2011.05.001
  6. FORD AC, DELANEY BC, FORMAN D, MOAYYEDI P. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev [online] 2006 Apr 19:CD003840 [viewed 30 July 2014] Available from: doi:10.1002/14651858.CD003840.pub4
  7. FUJIMURA Y, KAMOI R, IIDA M. Pathogenesis of aphthoid ulcers in Crohn's disease: correlative findings by magnifying colonoscopy, electron microscopy, and immunohistochemistry. Gut [online] 1996 May, 38(5):724-32 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/8707119
  8. REHBERGER A, PüSPöK A, STALLMEISTER T, JURECKA W, WOLF K. Crohn's disease masquerading as aphthous ulcers. Eur J Dermatol [online] 1998 Jun, 8(4):274-6 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9649656
  9. SAKALIHASAN N, LIMET R, DEFAWE OD. Abdominal aortic aneurysm. Lancet [online] 2005 Apr 30-May 6, 365(9470):1577-89 [viewed 30 July 2014] Available from: doi:10.1016/S0140-6736(05)66459-8
  10. UPCHURCH GR JR, SCHAUB TA. Abdominal aortic aneurysm. Am Fam Physician [online] 2006 Apr 1, 73(7):1198-204 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16623206
  11. NORDENSTEDT H, GRAHAM DY, KRAMER JR, RUGGE M, VERSTOVSEK G, FITZGERALD S, ALSARRAJ A, SHAIB Y, VELEZ ME, ABRAHAM N, ANAND B, COLE R, EL-SERAG HB. Helicobacter pylori-negative gastritis: prevalence and risk factors. Am J Gastroenterol [online] 2013 Jan, 108(1):65-71 [viewed 30 July 2014] Available from: doi:10.1038/ajg.2012.372
  12. OHATA H, KITAUCHI S, YOSHIMURA N, MUGITANI K, IWANE M, NAKAMURA H, YOSHIKAWA A, YANAOKA K, ARII K, TAMAI H, SHIMIZU Y, TAKESHITA T, MOHARA O, ICHINOSE M. Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer. Int J Cancer [online] 2004 Mar, 109(1):138-43 [viewed 30 July 2014] Available from: doi:10.1002/ijc.11680
  13. HIRSCHFIELD GM, KARLSEN TH, LINDOR KD, ADAMS DH. Primary sclerosing cholangitis. Lancet [online] 2013 Nov 9, 382(9904):1587-99 [viewed 30 July 2014] Available from: doi:10.1016/S0140-6736(13)60096-3
  14. BOEY JH, WAY LW. Acute cholangitis. Ann Surg [online] 1980 Mar, 191(3):264-270 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1344694
  15. SCHIRMER BD, WINTERS KL, EDLICH RF. Cholelithiasis and cholecystitis. J Long Term Eff Med Implants [online] 2005, 15(3):329-38 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16022643
  16. RéGENT D, LAURENT V, MEYER-BISCH L, BARBARY-LEFèVRE C, CORBY-CIPRIAN S, MATHIAS J. [Biliary colic: imaging diagnosis]. J Radiol [online] 2006 Apr, 87(4 Pt 2):413-29 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16691173
  17. STOLLMAN N, RASKIN JB. Diverticular disease of the colon. Lancet [online] 2004 Feb 21, 363(9409):631-9 [viewed 30 July 2014] Available from: doi:10.1016/S0140-6736(04)15597-9
  18. STOLLMAN N, RASKIN JB. Diverticular disease of the colon. Lancet [online] 2004 Feb 21, 363(9409):631-9 [viewed 30 July 2014] Available from: doi:10.1016/S0140-6736(04)15597-9
  19. FURUTA GT, LIACOURAS CA, COLLINS MH, GUPTA SK, JUSTINICH C, PUTNAM PE, BONIS P, HASSALL E, STRAUMANN A, ROTHENBERG ME, FIRST INTERNATIONAL GASTROINTESTINAL EOSINOPHIL RESEARCH SYMPOSIUM (FIGERS) SUBCOMMITTEES. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology [online] 2007 Oct, 133(4):1342-63 [viewed 30 July 2014] Available from: doi:10.1053/j.gastro.2007.08.017
  20. PATRICK L. Gastroesophageal reflux disease (GERD): a review of conventional and alternative treatments. Altern Med Rev [online] 2011 Jun, 16(2):116-33 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21649454
  21. WILCOX CM, HIRSCHOWITZ BI. Treatment strategies for Zollinger-Ellison syndrome. Expert Opin Pharmacother [online] 2009 May, 10(7):1145-57 [viewed 30 July 2014] Available from: doi:10.1517/14656560902887035

Investigations - for Diagnosis

Fact Explanation
H pylori Testing[4] H pylori is a gram-negative, urease-producing bacterium that colonizes gastric mucosa and produces chronic, superficial antral gastritis. Prevalence is 70% to 80% in the developing world. H pylori is the major cause of chronic gastritis[1]. Endoscopic/ invasive tests for H pylori includes: the rapid urease test, histopathology and culture. Urea breath tests detect active H pylori infection. The bacteria convert urea into carbon dioxide and the test involves swallowing of radioactive carbon (C14) and testing the air exhaled from the lungs. Obtain a biopsy( upper GI endoscopy guided) from the lesion and look for histopathology helps to establish a diagnosis of H pylori infection Serological tests for antibodies (immunoglobulin G [IgG]) to H.pylori can be measured in serum/ plasma/ whole blood.
Upper GI endoscopy[1] and biopsy[1][5] This allows for biopsies( from healing ulcers, from base with slough, adherent clots) and cytologic brushings in gastric ulcers. Multiple biopsy should be taken from all lesions( single biopsy- 70% and 7 biopsy- 99% accuracy in diagnosing gastric cancer) This helps to to: differentiate a benign ulcer from a malignant lesion. Giemsa staining examination allows demonstration of the bacteria[1]. If patient is having acute bleeding gastric biopsies obtained after the bleeding was controlled[1]
Barium meal[6][7] Barium containing liquid is given to drink and an x-ray is performed. This shows the stomach lining helping to identify gastric ulcers/ malignant growths due to filling defects. Test is not diagnostic but may be useful where endoscopy is unavailable.
Angiography[3][8] In patients presenting with a massive GI bleeding and endoscopy cannot be performed, angiography is helpful. When there is ongoing bleeding in a rate of 0.5 mL/min or more, angiography is able to accurately identify the bleeding source and it useful to provide needed therapy (vasoconstrictive agents as a direct injection/ angiographic embolization).
Chest radiograph[2] This may be useful in detecting complicated gastric ulcer with perforation. In a perforation, gas under the diaphragm will be visible. Upper GI contrast study with water-soluble contrast will show extravasation.
References
  1. ARAúJO MB, BORINI P, GUIMARãES RC. ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past? Arq Gastroenterol [online] 2014 Apr, 51(2):155-61 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/25003270
  2. WILSON-MACDONALD J, MORTENSEN NJ, WILLIAMSON RC. Perforated gastric ulcer. Postgrad Med J [online] 1985 Mar, 61(713):217-220 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2418177
  3. CHEUNG FK, LAU JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am [online] 2009 Jun, 38(2):231-43 [viewed 29 July 2014] Available from: doi:10.1016/j.gtc.2009.03.003
  4. RICCI C, HOLTON J, VAIRA D. Diagnosis of Helicobacter pylori: invasive and non-invasive tests. Best Pract Res Clin Gastroenterol [online] 2007, 21(2):299-313 [viewed 30 July 2014] Available from: doi:10.1016/j.bpg.2006.11.002
  5. LV SX, GAN JH, WANG CC, LUO EP, HUANG XP, XIE Y, HUANG Y. Biopsy from the base of gastric ulcer may find gastric cancer earlier. Med Hypotheses [online] 2011 Feb, 76(2):249-50 [viewed 30 July 2014] Available from: doi:10.1016/j.mehy.2010.10.011
  6. STEVENSON G. The distribution of gastric ulcers: double contrast barium meal and endoscopy findings. Clin Radiol [online] 1977 Nov, 28(6):617-24 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/589916
  7. MOUNTFORD RA, BROWN P, SALMON PR, ALVARENGA C, NEUMANN CS, READ AE. Gastric cancer detection in gastric ulcer disease. Gut [online] 1980 Jan, 21(1):9-17 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1419578
  8. CHEUNG FK, LAU JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am [online] 2009 Jun, 38(2):231-43 [viewed 31 July 2014] Available from: doi:10.1016/j.gtc.2009.03.003
  9. SURAPANENI S, S R, REDDY A. VB. The Perforation-Operation time Interval; An Important Mortality Indicator in Peptic Ulcer Perforation J Clin Diagn Res [online] 2013 May, 7(5):880-882 [viewed 31 July 2014] Available from: doi:10.7860/JCDR/2013/4925.2965
  10. ALCAIDE N, HERRERO C, BARRIO J, ATIENZA R, HERRANZ MT, PéREZ SABORIDO B, PéREZ-MIRANDA M, CARO-PATóN A. [Massive gastrointestinal bleeding due to gastric ulcer in a patient with amyloidosis]. Gastroenterol Hepatol [online] 2011 Jun-Jul, 34(6):411-4 [viewed 31 July 2014] Available from: doi:10.1016/j.gastrohep.2011.03.018
  11. CHEUNG FK, LAU JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am [online] 2009 Jun, 38(2):231-43 [viewed 31 July 2014] Available from: doi:10.1016/j.gtc.2009.03.003

Investigations - Fitness for Management

Fact Explanation
Full Blood Count In assessing the patients with gastric ulcer disease most of them are have anaemia.[1] White Blood Cells (neutrophils) count will be increased with peritonitis[2].
Serum electrolytes[3], blood urea and serum creatinine This is helpful in patients with recurrent vomiting in patients with gastric outlet obstruction and in patients suspected to have peritonitis/ septicaemia. Recurrent vomiting causes- loss of chloride in excess of sodium causes severe alkalosis, hypochloremia and hypokalaemia. Hypoperfusion of kidneys due to dehydration in recurrent vomiting, peritonitis, massive gastric bleeding leads to acute renal failure[4] causing increase in serum creatinine and blood urea levels.
APTT, PT, and INR[5] aPTT, PT, and INR is used in assessing the patient's bleeding tendency in patients with active bleeding( to exclude any clotting defects) and if they are on anticoagulant medication.
References
  1. ZHU A, KANESHIRO M, KAUNITZ JD. Evaluation and Treatment of Iron Deficiency Anemia: A Gastroenterological Perspective Dig Dis Sci [online] 2010 Mar, 55(3):548-559 [viewed 31 July 2014] Available from: doi:10.1007/s10620-009-1108-6
  2. KOULAOUZIDIS A, BHAT S, KARAGIANNIDIS A, TAN WC, LINAKER BD. Spontaneous bacterial peritonitis Postgrad Med J [online] 2007 Jun, 83(980):379-383 [viewed 31 July 2014] Available from: doi:10.1136/pgmj.2006.056168
  3. LANS HS, STEIN IF JR, MEYER KA. Electrolyte Abnormalities in Pyloric Obstruction Resulting from Peptic Ulcer or Gastric Garcinoma Ann Surg [online] 1952 Apr, 135(4):441-453 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1802494
  4. FRY AC, FARRINGTON K. Management of acute renal failure Postgrad Med J [online] 2006 Feb, 82(964):106-116 [viewed 31 July 2014] Available from: doi:10.1136/pgmj.2005.038588
  5. OPARTKIATTIKUL N. Standardization of coagulation tests. Southeast Asian J Trop Med Public Health [online] 1999:79-85 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10926265

Investigations - Followup

Fact Explanation
Endoscopy[2] Required in followup for documenting the healing of gastric ulcers and in ruling out gastric cancer. Endoscopy is usually done on the 6 to 8th week after the initial diagnosis of Peptic Ulcer Disease (PUD).
Full blood count[1] and serum electrolytes In patients with bleeding and recurrent vomiting these tests are helpful to assess general condition during follow up.
References
  1. ZHU A, KANESHIRO M, KAUNITZ JD. Evaluation and Treatment of Iron Deficiency Anemia: A Gastroenterological Perspective Dig Dis Sci [online] 2010 Mar, 55(3):548-559 [viewed 31 July 2014] Available from: doi:10.1007/s10620-009-1108-6
  2. ARAúJO MB, BORINI P, GUIMARãES RC. ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past? Arq Gastroenterol [online] 2014 Apr, 51(2):155-61 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/25003270

Investigations - Screening/Staging

Fact Explanation
Screening for gastric cancer by endoscopy and biopsy [2]. History of gastric ulcer disease is a risk factor for gastric carcinoma [1]. If an individual presents with non specific symptom like weight loss, loss of appetite, easy fatigability, progressive dysphagia and a history of peptic ulcer disease, the patient should be screened for gastric cancer. Adenocarcinoma is more often associated with H. Pylori infection [3].
References
  1. LIU CY, WU CY, LIN JT, LEE YC, YEN AM, CHEN TH. Multistate and multifactorial progression of gastric cancer: results from community-based mass screening for gastric cancer. J Med Screen [online] 2006:S2-5 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17227633
  2. PARK JM, JANG YJ, KIM JH, PARK SS, PARK SH, KIM SJ, MOK YJ, KIM CS. Gastric cancer histology: clinicopathologic characteristics and prognostic value. J Surg Oncol [online] 2008 Dec 1, 98(7):520-5 [viewed 31 July 2014] Available from: doi:10.1002/jso.21150
  3. HU B, EL HAJJ N, SITTLER S, LAMMERT N, BARNES R, MELONI-EHRIG A. Gastric cancer: Classification, histology and application of molecular pathology J Gastrointest Oncol [online] 2012 Sep, 3(3):251-261 [viewed 31 July 2014] Available from: doi:10.3978/j.issn.2078-6891.2012.021

Management - General Measures

Fact Explanation
Improvement of sanitary conditions H.pylori infection prevalence is higher in underdeveloped and developing countries and it is shown that the incidence has reduced with the eradication therapy and with improvement of sanitary conditions [1].
Dietary advise [2][3][4] A special diet is not indicated for patients with gastric ulcers. Better to avoid foods that may aggravate symptoms (fatty foods, spicy foods, coffee). The major goal of diet is to avoid extreme elevations of gastric acid secretion and the direct irritation of gastric mucosa. Now the frequent milk ingestion is not encouraged due to significant gastric acid secretion effect of milk. No special recommendation for small frequent feedings but patients are advised to avoid extra feeding and large meals. Advised to take three meals per day at regular intervals without skipping meals.
Stop smoking and minimize alcohol intake [5][6][7] As described in the history section both of these are risk factors for both occurrence and prolongation of healing of gastric ulcers. Thus it is, important to avoid alcohol and cigarette smoking.
References
  1. ARAúJO MB, BORINI P, GUIMARãES RC. ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past? Arq Gastroenterol [online] 2014 Apr, 51(2):155-61 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/25003270
  2. MAROTTA RB, FLOCH MH. Diet and nutrition in ulcer disease. Med Clin North Am [online] 1991 Jul, 75(4):967-79 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/2072799
  3. REESE RE, ANDREWS FM. Nutrition and dietary management of equine gastric ulcer syndrome. Vet Clin North Am Equine Pract [online] 2009 Apr, 25(1):79-92, vi-vii [viewed 31 July 2014] Available from: doi:10.1016/j.cveq.2008.11.004
  4. Diets for peptic ulcer. Br Med J [online] 1965 Oct 9, 2(5466):834 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1846340
  5. MA L, CHOW JY, CHO CH. Effects of cigarette smoking on gastric ulcer formation and healing: possible mechanisms of action. J Clin Gastroenterol [online] 1998:S80-6 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9872502
  6. SCHWARTZ MD. Dyspepsia, peptic ulcer disease, and esophageal reflux disease West J Med [online] 2002 Mar, 176(2):98-103 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071675
  7. KO JK, CHO CH. Alcohol drinking and cigarette smoking: a "partner" for gastric ulceration. Zhonghua Yi Xue Za Zhi (Taipei) [online] 2000 Dec, 63(12):845-54 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11195134

Management - Specific Treatments

Fact Explanation
Triple-therapy regimens 14 days[1][2][3] The National Institutes of Health Consensus Conference in 1994 concluded that ulcer disease was an infectious disease that could be cured by bacterial eradication [2]. Triple therapy is consist of: a Proton Pump Inhibitor [2], a combination of two antimicrobials[2] such as Amoxicillin and Clarithromycin.
Alternative triple-therapy regimens This used in patients who are allergic to penicillin, as an alternative for amoxicillin in triple therapy, here Metronidazole 500 mg PO bd is used. According to available statistical data triple therapy with pantoprazole, metronidazole and clarithromycin provides efficient eradication of H. pylori infection[3].
Quadruple therapy[7][8][9] Quadruple therapies for H pylori infection is used in patients whom the standard course of treatment has failed. It includes: a Proton pump inhibitor (PPI), Bismuth, Metronidazole and Tetracycline. These drugs are administered for 14 days.
Treatment for NSAID induced gastric ulcer disease[6][10][11] In a case of NSAID induced gastric ulcer disease or in patients with positive H pylori test results, NSAIDs should be immediately discontinued. In a patients who must continue NSAIDs, one option is changing the drug to a COX-2 selective inhibitor if possible. If same drug should be continued, PPI maintenance is recommended in preventing recurrences even after the eradication of H pylori infection. Treatment with a prostaglandin analogue or a PPI is helpful in patients with bleeding ulcers and 6-8 weeks of treatment is needed for complete healing.
Emergency management of a massive Upper GI bleed A massive gastric bleed is an emergency which will need resuscitation. Those who with significant or potentially significant hemorrhages hospitalization is required In patients with chronic bleeding. Anaemia should be treated with oral Iron therapy.
Surgical care for perforated peptic ulcer [13][14][15] Surgical care for perforated peptic ulcer should include the following: emergency laparotomy in peritonitis, the surgery will include simple closure, truncal vagotomy and pyloroplasty and gastrectomy.
Management of Gastric Outlet Obstruction [16] Endoscopic balloon dilatation, endoscopic incision have circumvented the use of surgery. Surgery is the gold standard for management of gastric outlet obstruction. Newer modalities like biodegradable stents also plays a role in the management.
Gastric carcinoma[17] Surgery is the only curative treatment. Aim of surgery is to remove all grossly visible tumor tissue and to obtain histologically tumour free surgical margins. Endoscopic (submucosal resection (EMR) or dissection (ESD), minimally invasive surgery, and open gastrectomy are the three major approaches in surgery.
References
  1. FELDMAN M, PETERSON WL. Helicobacter pylori and peptic ulcer disease. West J Med [online] 1993 Nov, 159(5):555-559 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1022344
  2. ARAúJO MB, BORINI P, GUIMARãES RC. ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past? Arq Gastroenterol [online] 2014 Apr, 51(2):155-61 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/25003270
  3. ELLENRIEDER V, FENSTERER H, WAURICK M, ADLER G, GLASBRENNER B. Influence of clarithromycin dosage on pantoprazole combined triple therapy for eradication of Helicobacter pylori. Aliment Pharmacol Ther [online] 1998 Jul, 12(7):613-8 [viewed 29 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9701524
  4. HOLSTER IL, KUIPERS EJ. Update on the Endoscopic Management of Peptic Ulcer Bleeding Curr Gastroenterol Rep [online] 2011 Dec, 13(6):525-531 [viewed 29 July 2014] Available from: doi:10.1007/s11894-011-0223-7
  5. CHEUNG FK, LAU JY. Management of massive peptic ulcer bleeding. Gastroenterol Clin North Am [online] 2009 Jun, 38(2):231-43 [viewed 29 July 2014] Available from: doi:10.1016/j.gtc.2009.03.003
  6. MCCARTHY DM. Nonsteroidal antiinflammatory drug-induced ulcers: management by traditional therapies. Gastroenterology [online] 1989 Feb, 96(2 Pt 2 Suppl):662-74 [viewed 30 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/2642451
  7. PAI CG, THOMAS CP, BISWAS A, RAO S, RAMNARAYAN K. Quadruple therapy for initial eradication of Helicobacter pylori in peptic ulcer: comparison with triple therapy. Indian J Gastroenterol [online] 2003 May-Jun, 22(3):85-7 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/12839378
  8. MANTZARIS GJ, PETRAKI K, ARCHAVLIS E, AMBERIADIS P, CHRISTOFORIDIS P, KOURTESSAS D, CHIOTAKAKOU E, TRIANTAFYLLOU G. Omeprazole triple therapy versus omeprazole quadruple therapy for healing duodenal ulcer and eradication of Helicobacter pylori infection: a 24-month follow-up study. Eur J Gastroenterol Hepatol [online] 2002 Nov, 14(11):1237-43 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/12439119
  9. FENG LY, YAO XX, JIANG SL. Effects of killing Helicobacter pylori quadruple therapy on peptic ulcer: a randomized double-blind clinical trial. World J Gastroenterol [online] 2005 Feb 21, 11(7):1083-6 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/15742421
  10. ROSTOM A, DUBE C, WELLS G, TUGWELL P, WELCH V, JOLICOEUR E, MCGOWAN J. Prevention of NSAID-induced gastroduodenal ulcers. Cochrane Database Syst Rev [online] 2002:CD002296 [viewed 31 July 2014] Available from: doi:10.1002/14651858.CD002296
  11. MURAKAMI K, OKIMOTO T, KODAMA M, TANAHASHI J, YASAKA S, INOUE K, UCHIDA M, ANAN J, MIZUKAMI K, ABE T, WATADA M, FUJIOKA T. Helicobacter pylori and NSAID-induced gastric ulcer in a Japanese population. J Gastroenterol [online] 2009:40-3 [viewed 31 July 2014] Available from: doi:10.1007/s00535-008-2259-5
  12. ALCAIDE N, HERRERO C, BARRIO J, ATIENZA R, HERRANZ MT, PéREZ SABORIDO B, PéREZ-MIRANDA M, CARO-PATóN A. [Massive gastrointestinal bleeding due to gastric ulcer in a patient with amyloidosis]. Gastroenterol Hepatol [online] 2011 Jun-Jul, 34(6):411-4 [viewed 31 July 2014] Available from: doi:10.1016/j.gastrohep.2011.03.018
  13. JORDAN GL JR, DEBAKEY ME, DUNCAN JM JR. Surgical management of perforated peptic ulcer. Ann Surg [online] 1974 May, 179(5):628-633 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1356038
  14. WILSON-MACDONALD J, MORTENSEN NJ, WILLIAMSON RC. Perforated gastric ulcer. Postgrad Med J [online] 1985 Mar, 61(713):217-220 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2418177
  15. HOLSTER IL, KUIPERS EJ. Update on the Endoscopic Management of Peptic Ulcer Bleeding Curr Gastroenterol Rep [online] 2011 Dec, 13(6):525-531 [viewed 31 July 2014] Available from: doi:10.1007/s11894-011-0223-7
  16. APPASANI S, KOCHHAR S, NAGI B, GUPTA V, KOCHHAR R. Benign gastric outlet obstruction--spectrum and management. Trop Gastroenterol [online] 2011 Oct-Dec, 32(4):259-66 [viewed 31 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22696905
  17. DIKKEN JL, VAN DE VELDE CJ, COIT DG, SHAH MA, VERHEIJ M, CATS A. Treatment of resectable gastric cancer Therap Adv Gastroenterol [online] 2012 Jan, 5(1):49-69 [viewed 31 July 2014] Available from: doi:10.1177/1756283X11410771