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Peptic ulcer disease

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This ppt is mainly from Sabiston's textbook. Hope it helps :)

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Peptic ulcer disease

  1. 1. Peptic ulcer disease Nomin-Erdene. D SOM-531
  2. 2. Learning objectives  Stomach gross anatomy  PUD  Epidemiology  Pathogenesis  Clinical manifestation  Diagnosing  Treatment  Complicated ulcer disease  Surgical procedures
  3. 3. Divisions  Stomach begins as a dilation in the tubular embryonic foregut during the fifth week of gestation.
  4. 4. Stomach parts & location
  5. 5. Blood supply
  6. 6. Lymphatic drainage Four zones of LN Celiac group node Thoracic duct
  7. 7. Innervation
  8. 8. Peptic ulcer disease  Peptic ulcers are defined as erosions in the gastric or duodenalmucosa that extend through the muscularis mucosae.  Lifetime Prevalence = 10% of Americans develop PUD  >10% of ER patients with abdominal pain diagnosed with PUD  Prevalence decreasing over last 30yrs  Male-to-female ratio of PUD = 2:1  4000 deaths caused by PUD each year.
  9. 9. Pathogenesis Increased aggressive factors HCl acid secretion Ethanol ingestion, smoking NSAID H.PYLORI Decreased defensive factors mucosal bicarbonate secretion mucus production Cell renewal blood flow
  10. 10. H.Pylori infection  80% to 95% of duodenal ulcers  75% of gastric ulcers are associated with H. pylori infection. Production of toxin (urease) Local mucosal immune response Gastrin increased Acid secretion D cell reduction Gastric metaplasia
  11. 11. NSAID NSAID absorption COX inhibition Prostaglandin synthesis decreased Mucosal protection failure
  12. 12. Ulcer Duodenal ulcer Gastric ulcer
  13. 13. Clinical manifestation  The most common symptom is midepigastric abdominal pain.  The pain is generally tolerable  Frequently relieved by food.  The pain may be episodic, worse during periods of emotional stress.  Many patients do not seek medical attention.  Constant pain - deeper ulcer penetration. Referral of  Pain to the back - penetration into the pancreas.  Diffuse peritoneal irritation - free perforation.
  14. 14. Diagnosis History & PE Laboratory test Upper GI radiography Flexible upper endoscopy H.Pylori testing Invasive test - Urease - Culture Noninvasive - Serology -Urea breath test -Stool antigen
  15. 15. Radiography  Less expensive  Require barium  Most ulcer (90%) diagnosed accurately  Double contrast > single contrast
  16. 16. Flexible upper endoscopy  Most reliable method  Visual diagnosis  Provide to sample tissue  H.pylori testing – mucosal biopsy
  17. 17. Urease assay  With endoscopy  From the gastric body and the antrum  Sensitivity in diagnosing infection is greater than 90%, and specificity is 95% to 100%  Sensitivity of the test is lowered in patients who are taking PPIs, H2 antagonists, or antibiotics.
  18. 18. Histology H.pylori  Silver stain
  19. 19. Noninvasive tests  Serology  Sensitivity 90%  Specificity 76- 96%  Check IgG antibodies of H.pylori  Urea breath test  Sensitivity 90%  Specificity 86- 92%  Recommended  discontinue antibiotics for 4 weeks  PPIs for 2 weeks to ensure optimal test accuracy.  Stool antigen  H.pylori are present in stool  Sensitivity 90%  Specificity 86-92%  Most cost effective method
  20. 20. Treatment Targeted agianst H.pylori To reduce acid level Increase the mucosal barrier
  21. 21. Treatment  Antacids  Sucralfate  H2 receptor antagonist  PPI  Treatment of H.pylori infection  lifestyle changes,  smoking cessation  discontinuing NSAIDs and aspirin  avoiding coffee and alcohol
  22. 22. Complicated Ulcer disease
  23. 23. Endoscopic approach  Evaluating by Forrest classification  High-risk patients - injection of a vasoconstrictor at the site of bleeding  Guidelines for endoscopic control of bleeding 2010: use of epinephrine plus an additional method or monotherapy with either thermocoagulation or clipping,  But discourage the use of epinephrine alone.
  24. 24. Nonsurgical control of bleeding  Catheter-directed angiography and endovascular embolization
  25. 25. Perforation  Typically complain of sudden-onset, frequently severe epigastric pain  Highest mortality rate of any complication of ulcer disease  Graham patch repair is performed
  26. 26. If Perforation >3cm
  27. 27. Gastric outlet obstruction Acute inflammation of the duodenum Mechanical obstruction Delayed gastric emptying, anorexia, nausea, and vomiting Antrectomy and reconstruction along with vagotomy.
  28. 28. Surgical procedures Truncal vagotomy Selective vagotomy Parietal vagotomy Truncal vagotomy and antrectomy
  29. 29. Truncal vagotomy  Most common operation performed for duodenal ulcer disease  Pyloric relaxation is mediated by vagal stimulation, and a vagotomy without a drainage procedure can cause delayed gastric emptying.
  30. 30. Classic truncal vagotomy, in combination with a Heineke-Mikulicz pyloroplasty
  31. 31. Antrectomy
  32. 32. Post-operative outcome
  33. 33. Gastric ulcer  Most ulcers are the consequence of H. pylori infection or NSAID usage.  Usually manifest on the lesser curvature  Peak incidence: 55 to 65 years old  More likely to occur in individuals in:  a lower socioeconomic class  common in the nonwhite than white population
  34. 34. Johnson classification
  35. 35. Quick difference Duodenal Gastric Incidence More common Less common Anatomy First part of duodenum – wall Lesser curvature of stomach Duration Acute or chronic Chronic Malignancy Rare Benign or malignant Food intake Relieved by food Worsened by food
  36. 36. Type 1 gastric ulcer Wedge resection – pathology examination Gastrectomy w/out vagotomy Type 2&3 gastric ulcer Ulcer + increased gastric acid Gastrectomy w/ vagotomy Type 4 gastric ulcer Difficult to manage Gastectomy / Rouxen Y/gastroduodenostomy
  37. 37. Zollinger-Ellison syndrome Severe PUD
  38. 38. Diagnosing ZES  Secretin-stimulated gastrin level  Serum gastrin samples are measured before and after IV secretin (2 U/kg) administration at 5-minute intervals for 30 minutes.  An increase in the serum gastrin level of greater than 200 pg/mL is specific for gastrinoma.
  39. 39. Diagnosing  Localize the gastrinoma is either CT or MRI of the abdomen.  However, these imaging modalities have a relatively low sensitivity in detecting tumors that are less than 1 cm in diameter as well as small liver metastases.  Somatostatin receptor scintigraphy uses radionucleotide labeled octreotide, which binds to the ZES tumor cells and can detect hepatic metastases in 85% to 95% of patients
  40. 40. Treatment  Resection of tumor  Patients with tumor recurrence or metastatic disease are treated with chemotherapy (streptozotocin with 5- fluorouracil or doxorubicin or both).
  41. 41. THANK YOU Because I already told you what I know only if you had listened to me 
  43. 43. Question #1  The consistently largest artery to the stomach is the  A. Right gastric  B. Left gastric  C. Right gastroepiploic  D. Left gastroepiploic
  44. 44. Answer  Answer: B  The consistently largest artery to the stomach is the left gastric artery, which usually arises directly rom the celiac trunk and divides into an ascending and descending branch along the lesser gastric curvature
  45. 45. Question #2  Which of the following inhibits gastrin secretion?  A. Histamine  B. Acetylcholine  C. Amino acids  D. Acid
  46. 46.  Answer: D  Luminal peptides and amino acids are the most potent stimulants o gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion.
  47. 47. Question #3  Helicobacter pylori infection primarily mediates duodenal ulcer pathogenesis via  A. Antral alkalinization leading to inhibition of somatostatin release  B. Direct stimulation of gastrin release  C. Local infammation with autoimmune response  D. Upregulation of parietal cell acid production
  48. 48.  Answer: A  Helicobacter pylori possess the enzyme urease, which converts urea into ammonia and bicarbonate, thus creating an environment around the bacteria that buffers the acid secreted by the stomach. H. pylori infection is associated with decreased levels of somatostatin, Production of toxin (urease) Local mucosal immune response Gastrin increased Acid secretion D cell reduction Gastric metaplasia
  49. 49. Question #4 Which of the following is the preoperative imaging study of choice for gastrinoma?  A. CT scan  B. Magnetic resonance imaging (MRI)  C. Endoscopic ultrasound (EUS)  D. Angiographic localization  E. Somatostatin receptor scintigraphy
  50. 50.  Answer: E  Currently, the preoperative imaging study of choice for gastrinoma is somatostatin-receptor scintigraphy (the octreotide scan). When the pretest probability of gastrinoma is high, the sensitivity and specificity o this modality approach 100%