Peptic ulcer.pptx

lecture notes for medical students

1. Tips on using my ppt. You can freely download, edit, modify and put your name etc. Don’t be concerned about number of slides. Half the slides are blanks except for the title. First show the blank slides (eg. Aetiology ) > Ask students what they already know about ethology of today's topic. > Then show next slide which enumerates aetiologies. At the end rerun the show – show blank> ask questions > show next slide. This will be an ACTIVE LEARNING SESSION x three revisions. Good for self study also. See notes for bibliography.

2. Introduction & History.

3. Introduction & History. Peptic ulcers are defects in the gastric or duodenal mucosa. Peptic - related to digestion Ulcer – Break in continuity of epithelium Sites- D1,Stomach,Stoma, Meckel’s diverticulum, which contains ectopic gastric epithelium. It is fundamental that any gastric ulcer should be regarded as being malignant

4. Pathophysiology

5. Pathophysiology Mucosal Defense mechanisms – Mucus gel layer Bicarbonate Prostaglandins of the E type (PGE) increases the production of both bicarbonate and the mucous layer. Tight intercellular junction, Mucosal blood flow, Cellular restitution, Epithelial renewal.

6. Pathophysiology Aggravating factors: H pylori   infection   Nonsteroidal anti-inflammatory drugs (NSAIDs ) Alcohol B ile salts Acid Pepsin

7. Aetiology

8. Aetiology Idiopathic Congenital/ Genetic Nutritional Deficiency/excess Traumatic Infections /Infestation Autoimmune Neoplastic (Benign/Malignant) Degenerative Iatrogenic

9. Etiology

10. Etiology H pylori  infection Lifestyle factors Severe physiologic stress Hyper secretary states (uncommon) Genetic factors

11. H pylori infection

12. H pylori infection Triad of H pylori  , Acid Pepsin Strong evidence Causes inflammation of mucosa .increased gastric acid secretion and reduced duodenal bicarbonate secretion 

13. Drugs

14. Drugs NSAIDs Corticosteroids NSAIDs concurrently. Diuretic- spironolactone Serotonin reuptake inhibitors  H pylori and NSAIDs are synergistic with respect to the development of peptic ulcer disease

15. Lifestyle factors

16. Lifestyle factors Tobacco smoking Diet Ethanol C affeine Evidence is inconclusive.

17. Severe physiologic stress

18. Severe physiologic stress Burns Central nervous system (CNS) trauma, surgery, S evere medical illness- Serious systemic illness Sepsis Hypotension R espiratory failure Polytrauma .  

19. Severe physiologic stress Cushing ulcers are associated with a brain tumor or injury Extensive burns are associated with Curling ulcers.

20. Physiological Factors

21. Physiological Factors Increased basal acid output (BAO) and maximal acid output (MAO ) A ccelerated gastric emptying

22. Hyper secretory states (uncommon)

23. Hyper secretory states (uncommon) Gastrinoma ( Zollinger -Ellison syndrome) or multiple endocrine neoplasia type I (MEN-I) Antral G cell hyperplasia Systemic mastocytosis Basophilic leukemias Cystic fibrosis Short bowel syndrome Hyperparathyroidism

24. Genetic factors

25. Genetic factors More than 20% of patients have a family history of duodenal ulcers, compared with only 5-10% in the control groups. Weak associations have been observed between duodenal ulcers and blood type O. Patients who do not secrete abo antigens in their saliva and gastric juices are known to be at higher risk A rare genetic association exists between familial hyperpepsinogenemia type I (a genetic phenotype leading to enhanced secretion of pepsin) and duodenal ulcers

26. Clinical Features

27. Clinical Features Demography Symptoms Signs Prognosis Complications

28. Demography

29. Demography 10% of the US population has evidence of a duodenal ulcer at some time. Incidence of duodenal ulcers and simple gastric ulcer has been decreasing over the past 3-4 decades Predominance in males has changed to similar occurrences in males and females. Declining rates in younger men,

30. Symptoms:

31. Symptoms: Epigastric pain Duodenal ulcer 2-3 hours after meals Food or antacids relieve the pain   Duodenal ulcer pain often awakens the patient at night. G astric ulcer S hortly after meals M inimal relief Pain with radiation to the back is suggestive of a posterior penetrating gastric ulcer complicated by pancreatitis.

32. Symptoms Dyspepsia, including belching, bloating, distention, and fatty food intolerance Heartburn, Chest discomfort Hematemesis or Rarely hematochezia . Symptoms of anemia ( eg , fatigue, dyspnea ) NSAID-induced gastritis or ulcers may be silent, especially in elderly patients. Only 20-25% of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer

33. Symptoms: Alarm features Bleeding or anemia Early satiety Unexplained weight loss Progressive dysphagia or odynophagia Recurrent vomiting Family history of gastrointestinal cancer

34. Signs \

35. Signs None

36. Prognosis \

37. Prognosis Prognosis is excellent if H. Pylori is eradicated and NSAID discontinued.

38. Complications \

39. Complications Perforation Hemorrhage Gastric outlet obstruction Gastric ulcers are also at risk of developing gastric malignancy Penetration Pancreatitis gastrocolic fistula

40. Investigations

41. Investigations Laboratory Studies Routine Special Imaging Studies Tissue diagnosis Cytology FNAC Histlogy

42. Laboratory Studies

43. Laboratory Studies Urea breath tests detect active  H pylori  infection Antibodies (immunoglobulin G [ IgG ]) to  H pylori can be measured in serum, plasma, or whole blood. Serum Gastrin Level Secretin Stimulation Test

44. Diagnostic Studies

45. Diagnostic Studies Imaging Studies X-Ray USG CT Angiography MRI Endoscopy Nuclear scan

46. Radiography  

47. Radiography  Chest radiograph  perforation  Upper gastrointestinal (GI) contrast study  Angiography may be necessary in patients with a massive GI bleed

48. Gas under diaphragm

49. Chest Radiograph

50. Endoscopy

51. Endoscopy Upper gastrointestinal (GI) endoscopy is the preferred diagnostic test Biopsy Brush cytology  Endoscopic or invasive tests for  H pylori  include a rapid urease test, histopathology, and culture.

52. Endoscopy: Duodenal ulcer

53. Benign gastric ulcer

54. Malignant gastric ulcer

55. Differential Diagnosis

56. Differential Diagnosis Nonulcer dyspepsia (NUD) or functional dyspepsia Crohn disease Zollinger -Ellison syndrome

57. Differential Diagnosis Acute Cholangitis Acute Coronary Syndrome Acute Gastritis Cholecystitis and Biliary Colic Inflammatory Bowel Disease Viral Hepatitis Chronic Gastritis Diverticulitis Gastroenteritis Esophageal Rupture and Tears Gastroesophageal Reflux Disease

58. Management

59. Management Antisecretory therapy Triple therapy for  H pylori infection Avoidance of nonsteroidal anti-inflammatory agents (NSAIDs) Antacids or a gastrointestinal (GI) cocktail (typically an antacid with an anesthetic such as viscous lidocaine and/or an antispasmodic

60. Operative Therapy

61. Operative Therapy Surgery has a very limited role in the management of PUD.   For refractory or complicated PUD- Vagotomy and pyloroplasty , Vagotomy and antrectomy with gastroduodenal reconstruction ( Billroth I) or gastrojejunal reconstruction ( Billroth II) Highly selective vagotomy .

62. Prevention

63. Prevention Indicated for long term NSAID Test for and eradicate h.Pylori  Changing to a cyclooxygenase (COX)-2 selective inhibitor Valdecoxib Celecoxib Rofecoxib PPI maintenance  therapy Naproxen+misoprostol  

64. Get this ppt in mobile Download microsoft powerpoint from playstore . Open google assistant Open google lens. Scan qr code from next slide.

65. Get this ppt in mobile Download Microsoft PowerPoint from play store. Open Google assistant Open Google lens. Scan qr code from next slide.

66. Get this ppt in mobile

67. Get my ppt collection https:// www.slideshare.net/drpradeeppande/edit_my_uploads https:// www.dropbox.com/sh/x600md3cvj85woy/AACVMHuQtvHvl_K8ehc3ltkEa?dl=0 https://www.facebook.com/doctorpradeeppande/?ref=pages_you_manage