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Peptic Ulcer - Diagnosis and Management


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Acid Peptic Disorders are common and often remains un-diagnosed. The symptoms are often vague. Let us have a look of symptoms, signs, diagnostic criteria and management.

Published in: Health & Medicine
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  • This presentation is presented by an Ayurvedic scholar so the concept of Ayurveda regarding 'peptic ulcer' should be mentioned here though your science also has lots of information regarding the disease as well as its own basic principle, so you should not be forgot it.
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Peptic Ulcer - Diagnosis and Management

  1. 1. Karol Bagh New Delhi – 110005 (University of Delhi) Directed By :- Presented By :- Dr. P.K. Chaudhary (M.S.) Monika Sharma 2004 - 05
  3. 3. DEFINITION An ulcer is defined as disruption of the mucosal integrity so ‘peptic ulcer’ refers to an ulcer in the lower oesophagus, stomach or duodenum, in jejunum after surgical anastomosis to stomach or rarely in the ileum adjacent to muckel’s diverticulum leading to local defect or excavation due to active inflammation.
  4. 4. INCIDENCE Although the prevalence of peptic ulcer is decreasing in many western countries it still affects approximately 10% of all adults at some time in their lives. The male to female ratio for duodenal ulcers varies from 5:1 to 2:1 whilist for gastric ulcers is 2:1 or less.
  5. 5. GASTRIC PHYSIOLOGY Despite the constant attack on gastroduodeual mucosa by a host of noxious agents (acid, pepsin, bile, acids, pancreatic enzymes, drugs & bacteria) integrity is maintained by an intricate system that provides mucosal defense & repair.
  6. 6. GASTRIC ANATOMY Gastric epithelium consists of rugae with microscopic gastric pits haring each four - five branching gastric glands. Majority of gastric glands (75%) found with in oxyntic mucosa & contain mucous neck, parietal, chief endocrine & entero chromaffin cells. Pylori glands contain mucous & endocrine cells & are found in antrum.
  7. 7. GASRIC MUCOSAL DEFENSE Defense system consist of 3 level barriers: 1. 2. 3. Figure : Components involved in providing gastroduodenal mucosal defense and repair. Pre – epithelial Epithelial Sub-epithelial elements
  8. 8. First line of defense Consist of mucous – bicarbonate layer. Some as a physiochemical barrier. Mucous secreted from surface epithelial cells Act as non-stirred water layer Impend diffusion of ions & molecules Bicarbonate :- Secretes by surface epithelial cells into mucons gel. Raise the PH gradient at gastric luminal surface.
  9. 9. II line of defense Epithelial element defense by : Mucous production. Epithelial cell ionic transport maintains intra cellular pH. Bicarbonate production. Intra cellular tight junctions. On breaching of first line of defense gastric epithelial calls bordering a site of injury can migrate to restore a damaged region.
  10. 10. III rd line of defense :An elaborate microvascular system with in gastric sub mucosal layer key component of sub epithelial defense system. Rich submucosal circulatory bed. Provide HCO3 - + provide micronutrients + O2 Neutralizes acid remove toxic metabolic by – product PROSTA GLANDIS plays important role in defense system regulate release of mucosal bicarbonate & mucus, inhibit parietal cells secretion & epithelial cell restitution.
  11. 11. AETIOLOGY & PATHOGENESIS PUD encompasses both gastric and duodenal ulcers.
  12. 12. Acute peptic ulcer Ingestion of Aspirin or butazolidin. By stress (Stress ulcer):- May be following endotoxic shock : Hypotension, Haemorrhage or Cardiac infarction.
  13. 13. Acute peptic ulcer The size of peptic ulcer Sepsis. After trauma or neurosurgical operations (Curling’s ulcers). After burns (curling’s ulcers). Patient on steroids (Steroids ulcers).
  14. 14. CHRONIC PEPTIC ULCERS GASTRIC ULCERS 1. Decrease mucosal resistance. 2. Pyloroduodenal reflex. 3. Deficient mucous barriers. 4. Mucosal trauma. 5. Local Ischaemia. 6. Antral stasis. 7. NSAIDs. 8. Helicobacter pylori.
  15. 15. CHRONIC PEPTIC ULCERS DUODENAL ULCER 1. 2. 3. 4. 5. 6. 7. 8. Acid hyper secretion. Genetics factor. Endocrine organ dysfunction. Liver abscess. Emotional factors. Diet & smoking. Helicobacter pylori. Decrease in bicarbonate production.
  16. 16. Pathogenesis Related with NSAIDs NSAIDs migrate across lipid membrane of epithelial cells. Trapped in an ionized form. Cell injury. Topical NSAIDs. Alter surface mucous layer. Peronits back diffusion of H+ & Pepsin. Further cell damage.
  17. 17. Figure shows machanisms by which NSAIDs may induce nucosal injury :
  18. 18. Risk factors for NSAID – induced Gastroduodenal ulcers Established Advanced age. History of ulcer. Concomitant use of glucocorticoids. High dose of NSAIDs. Multiple NSAIDs. Concomitant use of anticoagulants serious or multi system disease. Possible Concomitant infection with H. pylori. Cigarette smoking. Alcohol consumption.
  19. 19. Related to H. Pylori Factors predisposing to higher colonization rate includes :Poor socio – economic status. Less education. Transmission : Oral-oral.  Fecal-oral route.
  20. 20. Bacterial factors Produces surface factors chemo tactic for neutrophils & monocytes contributing to epithelial cell injury. Make proteases & phospholipase one breaking down glycoprotein of mucous gel, reducing efficacy of first line of defense. Expresses adhesions facilitating attachment of bacteria to gastric epithelial cells. LPS of bacteria help in infection.
  21. 21. Host Factors  Inflammatory response contributing epithelial cell damage.  H. Pylori antral infection. Increase acid production. Increase duodenal acid & mucosal injury.  H. pylori infection. Increase Basal & stimulated gastrin. Decrease somatostain – secreting D-cells.  It associates with decrease duodenal mucosal bicarbonate production.
  22. 22. Clinical feature Symptoms :- Acute peptic ulcers Symptoms of short duration. Ulcers recognized when they cause haematemesis. May perforate particularly when all in wall of duodenum. May progress to an ulceration. Chronic Peptic ulcers Main symptom :- Pain in upper abdomen.
  23. 23. Chronic gastric ulcers Age - Usually middle aged. Sex - Males more. Chronic Duodenal ulcers Chronic Duodenal ulcers Males but not so much. Constitution Thin & anaemic patient with ‘J’ shaped hypotonic stomach. Healthy males with steer-horn stomach, which is high in position. Periodicity Less marked Attack lasts for several weeks followed by interval of freedom from symmetrical for 2 – 6 Well marked Attack lasts for several wks with interval of freedom from 2 – 6 months usually appears in spring & antrum. Continued….
  24. 24. Chronic gastric ulcers Pain Strictly epigastric. Boring /pricking natures pain. On ulcer penetration pain radiate to back. Site Mid – epigastrium / slightly to its left. Chronic Duodenal ulcers Pain more severe & spasmodic innature. Pain on transpyloric plane about 1 inch to right of midline. Continued…..
  25. 25. Chronic gastric ulcers Chronic Duodenal ulcers Relation with food Almost immediately or any time up to 1½ hr. after meal as food irritates ulcer. Starts usually 2½ - 3 hr. after food.When stomach pushes chyme into duodenum & irritate ulcer. Pain not felt empty stomach. Felt empty stomach ‘Hunger – Pain’. Pain not felt at night. At dead of night, pain is characteristic. Food relieves pain. Food aggravates pain. Continued…
  26. 26. Chronic gastric ulcers Vomiting  Noticeable in half cases.  Occur after food.  Relieves pain.  May be self induces. Appetite  Good.  Patient afraid to take food. Diet  Patient avoids fried & spicy food. Chronic Duodenal ulcers  Rare.  Quite good.  Eat frequently to around pain.  No particular food initiates pain. Continued…
  27. 27. Chronic gastric ulcers Weight Chronic Duodenal ulcers  Patient Losses weight.  Patient gains the weight Hemorrhage  Less common.  More common.  Haematemesis is more –  Malena more common than than malena. haematemesis. On Examination  Tenderness in midepigastric / slightly to left of it.  Tenderness at ‘duodenal pt’ situated on transpyloric with plane 1 inch to midline.
  28. 28. SPECIAL INVESTIGETIONS 1) Examination of blood. 2) Examination of stool. 3) Gastric function test 4) Radiological investigations. 5) Endoscopy. 6) USG.
  29. 29. USG, Endoscopy and radiology examination of PUD :
  30. 30. Treatment Basic Treatment  Rest.  Diet (avoid spicy food, use balance diet, no alcohol and smoking).
  31. 31. Medical Treatment Antacids. H2 receptor antagonistic. Proton pump inhibitors. Cytoprotective agents. Bismuth – containing preparations. Prostaglandin analogues.
  32. 32. Drugs used in Treatment of PUD Drug Eg. Dose Acid suppressing drug ‘Antacids’. Mylanta 100 – 140 mg / L/ Maalox, Tums, 3 hr. after meal. Gaviscon Hs. Cimetidine 800 mg hs. Renitidine 300 mg hs. Famotidine 400 mg hs. Nizatidine 300 mg hs. H2 receptor antagonists.
  33. 33. Drugs used in Treatment of PUD Drug Eg. Dose Proton pump inhibitors. Omeprazol 20 mg / d Lansoprazol Rabeprazol Pantoprazol 30 mg / d 20 mg / d 40 mg / d Sucralfatet Misoprostol 1g qid. 200 mcg. qid. Bismuth subsalicylate (BSS) 2 tablet qid. Mucosal protective agents. Sucralfate. Prostaglandis analogus. Bismuth – containing compounds.
  34. 34. Regimens recommended for eradication of H. pylori : Drug Dose Triple therapy 1. 2. 3. Bismuth sub salicylate plus. Metronidagole plus. Tetracycline. Ranitidine Bismuth Citrate plus. Tetracycline plus. Clarithromycin or Metronidazole. Omeprazole plus. Clarithromycin plus. Metronidazole or Amoxicillin. 2 tab qid 250mg qid 500mg qid 400mg bd 500mg bd 500mg bd 20mg bd 250mg bd 500mg bd 1g bd
  35. 35. Regimens recommended for eradication of H. pylori : Quadruple therapy : Drug Dose Omeprazole. Bismuth subsalicylate. Metronidazole. Tetracyline. 20mg daily 2 Tab qid 250mg qid 500mg qid
  36. 36. RECOMMENDED TREATMENT FOR NSAID – RELATED MUCOSAL INJURY : Active ulcer NSAID discontinued. NSAID Continued. Prophylactic therapy. H2 receptor antagonist or PPI. Misoprostol. PPI Selective Cox – 2 inhibitor. H. Pylori infection. Eradication if active ulcer present or there is a past history of PUD.
  37. 37. Surgical therapy Indications When ulcer fails to heal with medical management (2 months for gastric ulcer & 6 month for duodenal ulcers). Patient in need of quick relief. Long-standing non – healing ulcer. Ulcer producing obstruction. Haemorrhagic ulcers. Perforation of ulcers. Suspicion of malignancy. Continued…
  38. 38. Surgical therapy Surgical procedures • • • HSV Billroth I Billroth II - (Highly selective vagetomy) Continued…
  39. 39. Surgical therapy Complications • • • • • • Perforation. Haemorrhage (Haematemesis, Maloena). Stenosis. Penetration into neighboring viscera. Carcinoma. Residual absence.