Peptic ulcer. rubel ppt

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Peptic ulcer. rubel ppt

  1. 1. Peptic Ulcer Disease PROFESSOR A. M. S. M. SHARFUZZAMANSunday, November 18, 2012 DR. RUBEL, SSMC 1 PROFESSOR OF SURGERY
  2. 2. Learning Objectives To be able to decide on the most appropriatetechniques to use in the investigation of patients withcomplaints relating to the stomach and duodenum. To understand the critical importance of gastritis andHelicobacter pylori in upper gastrointestinal disease. To be able to investigate and treat peptic ulcerdisease and its complications.Sunday, November 18, 2012 DR. RUBEL, SSMC 2
  3. 3. DefinitionPeptic Ulcer Disease is defined as an ulceroccurring in a region that touches gastric acidand pepsin and usually refers to gastric ulcer orduodenal ulcer.Sites:Duodenum, ……(80%)Stomach ……….(19%)Duodenum and Stomach……(4%)G-E junctionGastro-jejunostomy site (1%)Meckel’s diverticulumSunday, November 18, 2012 DR. RUBEL, SSMC 3
  4. 4. Erosion : a superficial lesion caused bydenudation of the surface epithelium Ulcer : a mucosal defect extending into the muscularis mucosaSunday, November 18, 2012 DR. RUBEL, SSMC 4
  5. 5. Epidemiology of peptic ulcerationFrequencyUnited States:One-year point prevalence is 1.8%. Lifetime prevalence is approximately 10%.PUD affects approximately 4.5 million people annually.Internationally:The prevalence of H pylori infection in developing countries is as high as 50-100%. The prevalence of PUD is increasing in developing countries.SexThere is a 3 to 1 male to female ratio for GU and 4 to 1 for DU. Prevalence hasshifted from predominance in males to similar occurrences for both sexes.Lifetime prevalence is approximately 11-14% for men and 8-11% for women.AgeThe peak age for DU is increasing(25-50 years worldwide but higher indeveloped countries), GU occurs in older age groups>50 Sunday, November 18, 2012 DR. RUBEL, SSMC 5
  6. 6. Mucosal defences against peptic ulcerationEXTRAMUCOSAL Mucous cap; a hydrophobic gel layer secreted by the mucus cells, Buffer layer; hydrogen carbonate is trapped in the mucous cap buffering the acid, Bicarbonate secretion: leads to a pH gradient from 2 in the lumen to 7 on the epithelial surface.MUCOSAL Luminal cells resistance to acid. Mucosal integrity(prostaglandin helps to maintain this so is reduced when taking NSAIDs; other growth factors also help and are inhibited by alcohol) Tight cell junctions.MICROVASCULAR The microcirculation neutralises acid and removes toxic substances; smoking-related microvascular disease reduces this blood flow. Sunday, November 18, 2012 DR. RUBEL, SSMC 6
  7. 7. Pathogenesis; Normal Increased Attack Hyperacidity Weak defense Helicobacter pylori Stress, drugs, smoking Sunday, November 18, 2012 DR. RUBEL, SSMC 7
  8. 8. Pathogenesis;Damaging forces: - Acid - PepsinDefensive forces:*Surface mucous, *Bicarbonate ion in mucous, *Mucosal blood Flow, *Apical surface membrane transport, *Epithelial regeneration, *Prostaglandins Sunday, November 18, 2012 DR. RUBEL, SSMC 8
  9. 9. Etiology; H.Pylori Urease – Ammonia stimulates gastrin release, increases acid secretion Protease – breaks glycoprotein of mucous Lipopolysaccharide – attracts neutrophils Hyperacidity Zollinger – Ellison Syndrome multiple endocrine neoplasia (MEN-I) Antral G cell hyperplasia Systemic mastocytosis Basophilic leukemias Drugs No effect of NSAIDS Corticosteroids genetics and Systemic stresses spicy foods Cigarette smoking, Alcohol Rapid gastric emptying Personality and stress Sunday, November 18, 2012 DR. RUBEL, SSMC 9
  10. 10. Helicobacter pylori: Most common infection in the world (20%) 10% of men, 4% women develop PUD Positive in 70-100% of PUD patients. H.pylori related disorders: Chronic gastritis – 90% Peptic ulcer disease – 95-100% Gastric carcinoma – 70% Gastric lymphoma Reflux Oesophagitis. Non ulcer dyspepsia Sunday, November 18, 2012 DR. RUBEL, SSMC 10
  11. 11. H. pylori – silver stainSunday, November 18, 2012 DR. RUBEL, SSMC 11
  12. 12. H. pylori – giemsa stainSunday, November 18, 2012 DR. RUBEL, SSMC 12
  13. 13. H. pylori – H & E stainSunday, November 18, 2012 DR. RUBEL, SSMC 13
  14. 14. H. Pylori S-shaped gram negative rod, flagella Produces urease, protease, cytotoxin Alters acid secretory function Binds to mucosal blood group antigen Colonization rate increases with age: up to 50% in persons >50 years Sunday, November 18, 2012 DR. RUBEL, SSMC 14
  15. 15. Risk factors for H.Pylori infection; Birth in a developing country Low socioeconomic status Crowded living conditions Large families Unsanitary living conditions Unclean food or water Presence of infants in the home Exposure to gastric contents of infected individualsSunday, November 18, 2012 DR. RUBEL, SSMC 15
  16. 16. Pathogenetic qualities of H.pylori; Adheres to gastric epithelium Lives within mucous gel layer overlying gastric epithelium Penetrates intercellular junctions Invades gastric glands and canaliculi of parietal cells Secretes urease to produce ammonia, which protects it from gastric acid Produces cytotoxins that may play role in pathogenicity Induces epithelial cytolysis and disrupts intercellular junctions Increases permeability of mucous layer to hydrogen ions and pepsin Enables gastric acid and pepsin to create ulcer craters Evades host immune defenses Damages tissue. Sunday, November 18, 2012 DR. RUBEL, SSMC 16
  17. 17. Peptic Ulcer Size – variable; 0.3 – 4 cm in diameter Shape - round to oval Sharply demarcated, clean-cut, punched-out area with clean base Margins are usually level with surrounding mucosa or slightly elevated due to edema; the mucosa is undermined at the edges Radiating mucosal rugae 80% are solitary, 80% occur in the duodenum, of which 90% in the first part of the duodenum on the anterior wall’ within a few centimeter of the pyloric ring. 19% occur in the stomach(usually at the lesser curvature at the border of the body and antrum. Sunday, November 18, 2012 DR. RUBEL, SSMC 17
  18. 18. Gastric Ulcer- Endoscopic Appearance Sunday, November 18, 2012 DR. RUBEL, SSMC 18
  19. 19. Gastric Ulcer- Gross Appearance Sharply punched-out Large, mucosal defect or ulcer Radiating mucosal folds Sunday, November 18, 2012 DR. RUBEL, SSMC 19
  20. 20. Acute Gastric Ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 20
  21. 21. Giant gastric ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 21
  22. 22. Gastric Ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 22
  23. 23. Duodenal Peptic Ulcers- Gross Sunday, November 18, 2012 DR. RUBEL, SSMC 23
  24. 24. Duodenal Peptic Ulcer-Gross Sunday, November 18, 2012 DR. RUBEL, SSMC 24
  25. 25. Microscopy: Overhanging gastric mucosal margins (A) A B Necrotic fibrinoid C, D debris (B) Acute inflammatory infiltrate (C) Granulation tissue (D) E Fibrotic scarred base (E) Sunday, November 18, 2012 DR. RUBEL, SSMC 25
  26. 26. Ulcer Base Superficial thin layer of necrotic fibrinoid debris Zone of inflammatory infiltrate with neutrophils Zone of granulation tissue with dilated blood vessels and lymphocytes Zone of fibrous scarringSunday, November 18, 2012 DR. RUBEL, SSMC 26
  27. 27. H. Pylori - Lab Studies HP fecal antigen test Monoclonal antibody immunochromatography of stool samples. Very specific (98%) and sensitive (94%). 13 Carbon-urea breath test HP serology – IgG Biopsy/Histopathology CLO test, Culture Sunday, November 18, 2012 DR. RUBEL, SSMC 27
  28. 28. PUD - Diagnosis Endoscopy upper GIT Barium meal – contrast x-ray Biopsy – bacteria & malignancy H.Pylori: CLO test Endoscopy cytology Biopsy – Special stains Culture - difficult 13/14 Carbon-Urea Breath test. H.pylori serology Sunday, November 18, 2012 DR. RUBEL, SSMC 28
  29. 29. Endoscopy upper GITSunday, November 18, 2012 DR. RUBEL, SSMC 29
  30. 30. Video-endoscopy upper GIT Sunday, November 18, 2012 DR. RUBEL, SSMC 30
  31. 31. Video-endoscopy upper GIT Sunday, November 18, 2012 DR. RUBEL, SSMC 31
  32. 32. Typical radiographic features ofa duodenal ulcer; Sunday, November 18, 2012 DR. RUBEL, SSMC 32
  33. 33. Typical radiographic features of duodenal ulcer. Thisduodenal bulb ulcer is associated with marked edema,resulting in the appearance of radiating folds to the ulcercrater. The bulb is also distorted secondary to previouslyexisting ulceration Sunday, November 18, 2012 DR. RUBEL, SSMC 33
  34. 34. Typical radiographic features ofa benign gastric ulcer; A large well- circumscribed ulcer is seen on the angularis Sunday, November 18, 2012 DR. RUBEL, SSMC 34
  35. 35. Urease production test(CLO Test) Sunday, November 18, 2012 DR. RUBEL, SSMC 35
  36. 36. Acute Esophagitis & Gastritis Sunday, November 18, 2012 DR. RUBEL, SSMC 36
  37. 37. Acute Gastritis Sunday, November 18, 2012 DR. RUBEL, SSMC 37
  38. 38. Gastric erosionsSunday, November 18, 2012 DR. RUBEL, SSMC 38
  39. 39. Typical endoscopic appearance of a benign gastric ulcer. The ulcer ison the angularis, the most common location for a gastric ulcer, and iswell circumscribed without any associated mass effect. Thesurrounding mucosa is mildly erythematous and without nodularity. Sunday, November 18, 2012 DR. RUBEL, SSMC 39
  40. 40. A posterior duodenal ulcerSunday, November 18, 2012 DR. RUBEL, SSMC 40
  41. 41. Erosions in the duodenal bulb and aposterior duodenal ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 41
  42. 42. Clinical presentation of PUDSymptoms:Abdominal pain located in the epigastric area burning in quality occurred on an empty stomach 2 to 4 hours after meals and/or at night (nocturnal pain); relieved by antacids and/or meals tend to wax and wane over months “acid dyspepsia”Sunday, November 18, 2012 DR. RUBEL, SSMC 42
  43. 43. Abdominal pain(cont.) the majority of patients (approximately 70%) with epigastric distress (“dyspepsia”) do not have evidence of active ulcer disease; conversely up to 40% of patients with an active ulcer crater deny abdominal pain; patients can present with an ulcer-related complication, particularly hemorrhage, without antecedent symptomsSunday, November 18, 2012 DR. RUBEL, SSMC 43
  44. 44. Abdominal pain(cont.)Despite being both insensitive andnon-specific, the symptom ofepigastric abdominal pain, particularlyburning after meals and at night andrelieved with food or antacid,suggests the possibility of ulcerdisease. Sunday, November 18, 2012 DR. RUBEL, SSMC 44
  45. 45. Other symptoms gastro esophageal reflux including upright and supine reflux and non-cardiac chest pain symptoms of indigestion occurring with or shortly after eating and characterized by epigastric fullness and discomfort belching bloating nausea early satiety and specific food intolerances.Sunday, November 18, 2012 DR. RUBEL, SSMC 45
  46. 46. Signs;Physical examination is of limited valuein patients with uncomplicated ulcer.For epigastric tenderness on deeppalpation, the sensitivity and specificityare all approximately 50% or less.Furthermore, many patients with non-ulcer diseases also have epigastrictenderness on physical examination. Sunday, November 18, 2012 DR. RUBEL, SSMC 46
  47. 47. Signs(cont.) In patients with free perforation or ulcer penetration into the pancreas, findings of peritonitis are usually present. In patients with gastric retention who have been fasting for a few hours, a succussion splash (produced by auscultating the abdomen while rocking the patient back and forth), suggests retained gastric contents.Sunday, November 18, 2012 DR. RUBEL, SSMC 47
  48. 48. Complications:Hemorrhage The most common complication of ulcer disease (in approximately 15% of patients) manifest as haematemesis and melena.Perforation Duodenal ulcers: perforate anteriorly Gastric ulcers: perforate along the anterior wall of the lesser curvature of the stomach.Penetration Mainly to posterior structure as pancreas.Scarring and stenosis Stomach: tea-pot deformity, hour-glass contracture. Duodenum: pyloric stenosis as GOO. Sunday, November 18, 2012 DR. RUBEL, SSMC 48
  49. 49. HemorrhageThe most common complication of ulcer disease (inapproximately 15% of patients) manifest ashaematemesis and melena. Bleeding: Uppergastrointestinal (UGI) bleeding secondary to pepticulcer is a common medical condition that results inhigh patient morbidity UGI bleeding commonlypresents with hematemesis (vomiting of blood orcoffee-ground like material) and/or melena (black,tarry stools).Sunday, November 18, 2012 DR. RUBEL, SSMC 49
  50. 50. D.U-Hemorrhage Sunday, November 18, 2012 DR. RUBEL, SSMC 50
  51. 51. Perforated peptic ulcer.Duodenal, antral, and gastric body ulcers account for 60, 20 and20percent of perforations due to peptic ulcer, respectively . One-thirdto one-half of perforated ulcers are associated with NSAID use; theseusually occur in elderly patients Sunday, November 18, 2012 DR. RUBEL, SSMC 51
  52. 52. Penetration Is similar pathologically to perforation, except that the ulcer crater burrows through the entire wall of the intestine, and instead of leaking digestive contents into the peritoneal cavity, the crater bores into an adjacent organ. Gastric ulcers most commonly penetrate into the left lobe of the liver, while duodenal ulcers penetrate posteriorly into the adjacent pancreas, sometimes leading to pancreatitis. Rarely, gastric ulcers may penetrate into the colon, resulting in a gastrocolic fistula Sunday, November 18, 2012 DR. RUBEL, SSMC 52
  53. 53. Gastric outlet obstruction (gastric retentionor pyloric stenosis); Gastric outlet obstruction is the least frequent ulcer complication. Most cases are associated with duodenal or pyloric channel ulceration, with gastric ulceration accounting for only 5 percent of cases. functional impairment of antral motility due to the effects of acute inflammation and edema; mechanical obstruction due to scarring near the gastroduodenal junction; manifest as gastroesophageal reflux, early satiety, weight loss, abdominal pain, and vomiting; As the degree of retention increases, the quantity of vomitus also increases, often containing food ingested 12 or more hours previously. Sunday, November 18, 2012 DR. RUBEL, SSMC 53
  54. 54. Barium upper gastrointestinal studydemonstrates the size of the stomach. Pyloric stenosis Sunday, November 18, 2012 DR. RUBEL, SSMC 54
  55. 55. Endoscopy demonstrates the pyloricobstruction with an active ulcer crater seenin the pyloric channel. Sunday, November 18, 2012 DR. RUBEL, SSMC 55
  56. 56. Malignant transformation (Gastric ulcer )Sunday, November 18, 2012 DR. RUBEL, SSMC 56
  57. 57. Malignant transformation (Gastric ulcer )Sunday, November 18, 2012 DR. RUBEL, SSMC 57
  58. 58. Malignant transformation (Gastric ulcer )Sunday, November 18, 2012 DR. RUBEL, SSMC 58
  59. 59. TREATMENT;Medical treatment Given the current understanding of the pathogenesis of PUD, most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance of NSAIDs, along with the appropriate use of antisecretory therapy. A number of treatment options exist for patients presenting with symptoms suggestive of PUD or ulcerlike dyspepsia, including empiric antisecretory therapy, empiric triple therapy for H pylori infection, endoscopy followed by appropriate therapy based on findings, and H pylori serology followed by triple therapy for patients who are infected. Breath testing for active H pylori infection may be used. Sunday, November 18, 2012 DR. RUBEL, SSMC 59
  60. 60. Medical treatment(cont.) Computer models have suggested that obtaining H pylori serology followed by triple therapy for patients who are infected is the most cost-effective approach; however, no direct evidence from clinical trials provides confirmation. Perform endoscopy early in patients older than 45-50 years and in patients with associated so-called alarm symptoms, such as dysphagia, recurrent vomiting, weight loss, or bleeding. Sunday, November 18, 2012 DR. RUBEL, SSMC 60
  61. 61. Surgical Care With the success of medical therapy, surgery has a very limited role in themanagement of PUD.Potential indications for surgery include refractory disease. Complications ofPUD include the following: Refractory, symptomatic peptic ulcers, though rare with the cure of H pylori infection and the appropriate use of antisecretory therapy, are a potential complication of PUD. Perforation usually is managed emergently with surgical repair.However, this is not mandatory for all patients. Obstruction can complicate PUD, particularly if PUD is refractory to aggressive antisecretory therapy, H pylori eradication, or avoidance of NSAIDs. Obstruction may persist or recur despite endoscopic balloon dilation. Sunday, November 18, 2012 DR. RUBEL, SSMC 61
  62. 62. Surgical Care(cont.) Penetration, particularly if not walled off or if a gastrocolic fistula develops, is a potential complication of PUD. Bleeding can complicate PUD, particularly in patients with massive hemorrhage and hemodynamic instability, recurrent bleeding on medical therapy, and failure of therapeutic endoscopy to control bleeding. The appropriate surgical procedure depends on the location and nature of the ulcer. Many authorities recommend simple oversewing of the ulcer with treatment of the underlying H pylori infection or cessation of NSAIDs for bleeding PUD. Additional surgical options for refractory or complicated PUD include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly selective vagotomy. Sunday, November 18, 2012 DR. RUBEL, SSMC 62
  63. 63. DietNo special diet is required.MedicationTreat all patients with peptic ulcers and associated H pylori infection with protonpump inhibitor (PPI)-based triple therapy, which results in a cure rate ofinfection and healing in approximately 85-90% of cases. Ulcers can relapse inthe absence of successful H pylori eradication.Dual therapies, which are alternative regimens for treating H pylori infection,are usually not recommended as first-line therapy because of a variable curerate that is significantly less than the cure rate achieved with triple therapy.Active ulcers associated with NSAID use are treated with an appropriate courseof PPI therapy and the cessation of NSAIDs. For patients with a known historyof ulcer, and in whom NSAID use is unavoidable, the lowest possible dose andduration of the NSAID and co-therapy with a PPI or misoprostol arerecommended Sunday, November 18, 2012 DR. RUBEL, SSMC 63
  64. 64. Medication(contd.)PPI-based triple therapies for H pylori are considered the first-line therapies forthe treatment of H pylori in the United States with a cure rate of 85-90%. Theseregimens consist of a PPI, amoxicillin, and clarithromycin for 7-14 days. Alonger duration of treatment (14 d vs 7 d) appears to be more affective and iscurrently the recommended duration of treatment. Amoxicillin should only besubstituted by metronidazole in penicillin-allergic patients because of the highrate of metronidazole resistance.In the setting of active ulcers caused by H pylori, treatment with a PPI beyondthe 14-day course of antibiotics and until the confirmation for the eradication ofH pylori is recommended for complicated ulcers.. Sunday, November 18, 2012 DR. RUBEL, SSMC 64
  65. 65. PPI-based triple therapies consist of a 14-day treatment of thefollowing: Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30 mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole (Nexium): 40 mg PO qd Plus: Clarithromycin (Biaxin): 500 mg PO bid and Amoxicillin (Amoxil): 1 g PO bidThe alternative combination therapy consists of the followingtreatments administered for 14 days: Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30 mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole (Nexium): 40 mg PO qd Plus: Clarithromycin (Biaxin): 500 mg PO bid and Metronidazole (Flagyl): 500 mg PO bid Sunday, November 18, 2012 DR. RUBEL, SSMC 65
  66. 66. Quadruple therapiesfor H pylori infection are generally reserved for patientswho have failed a course of treatment and are administeredfor 14 days. The treatment includes the following drugs:PPI PO bid andBismuth 525 mg PO qid andMetronidazole 500 mg PO qid andTetracycline 500 mg PO qid Sunday, November 18, 2012 DR. RUBEL, SSMC 66
  67. 67. Further Outpatient Care Endoscopy is required to document healing of gastric ulcers and to rule out gastric cancer. This usually is performed 6-8 weeks after the initial diagnosis of PUD. Documentation of H pylori cure with a noninvasive test, such as the urea breath test or fecal antigen test, is appropriate in patients with complicated ulcersIn/Out Patient Meds Consider maintenance therapy with half standard doses of H2-receptor antagonists at bedtime in patients with recurrent, refractory, or complicated ulcers, particularly if cure of H pylori has not been documented or if an H pylori-negative ulcer is present. Sunday, November 18, 2012 DR. RUBEL, SSMC 67
  68. 68. PREVENTION Primary prevention of NSAID-induced ulcers includes the following: Avoid unnecessary use of NSAIDs. Use acetaminophen or nonacetylated salicylates when possible. Use the lowest effective dose of an NSAID and switch to less toxic NSAIDs, such as the newer NSAIDs or cyclooxygenase-2 (COX-2) inhibitors, in high-risk patients without cardiovascular disease. Consider prophylactic or preventive therapy for the following patients: Patients with NSAID-induced ulcers who require chronic, daily NSAID therapy Patients older than 60 years Patients with a history of PUD or a complication such as gastrointestinal bleeding Patients taking concomitant steroids or anticoagulants or patients with significant comorbid medical illnesses Sunday, November 18, 2012 DR. RUBEL, SSMC 68
  69. 69. Prognosis When the underlying cause is addressed, the prognosis is excellent. Most patients are treated successfully with the cure of H pylori infection, avoidance of NSAIDs, and the appropriate use of antisecretory therapy. Cure of H pylori infection changes the natural history of the disease, with a decrease in the ulcer recurrence rate from 60-90% to approximately 10-20%. However, this is a higher recurrence rate than previously reported, suggesting an increased number of ulcers not caused by H pylori infection.Patient Education Stop smoking. Avoid NSAID and aspirin use. Avoid heavy alcohol use. Stress reduction counseling might be helpful in individual cases but is not needed routinely. . DR. RUBEL, SSMC 69 Sunday, November 18, 2012
  70. 70. Summary Most PU are caused by H. pylori or NSAIDs and changes inepidemiology mirror changes in these principle etiologicalfactors. DU are more common than GU, but the symptoms areindistinguishable. GU may become malignant and an ulcerated GU may mimica benign ulcer. Gastric antisecretory agents and H. pylori eradication therapyare the mainstay of treatment, and elective surgery is not nowcommonly performed. The common complication of peptic ulcer are perforation,bleeding and stenosis. The treatment of the perforated PU is primarily surgical,although some patients may be managed conservatively. Sunday, November 18, 2012 DR. RUBEL, SSMC 70
  71. 71. Sunday, November 18, 2012 DR. RUBEL, SSMC 71

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