Peptic Ulcer

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Peptic Ulcer

  1. 1. <ul><li>Peptic ulcer disease By Dr. Osman Bukhari </li></ul>
  2. 2. <ul><li>Site: </li></ul><ul><li>1- Stomach </li></ul><ul><li>2- Duodenum </li></ul><ul><li>3- Lower esophagus </li></ul><ul><li>4- Jejunum after gastrojejunostomy </li></ul><ul><li>5- Terminal ileum adjacent to Mekels </li></ul><ul><li>diverticulum which contains ectopic </li></ul><ul><li>gastric mucosa </li></ul>
  3. 3. <ul><li>Types </li></ul><ul><li>1- Acute: superficial </li></ul><ul><li>2- Chronic: deep to muscularis mucosa </li></ul><ul><li>Fibrosis </li></ul><ul><li>Epidemiology 1- Prevalence of PU is 3-4%. </li></ul><ul><li>2- 10% of male & 8% of female suffer PU </li></ul><ul><li>in their lifetime. </li></ul><ul><li>3- DU > GU (3:1) </li></ul>
  4. 4. <ul><li>4- Male: Female </li></ul><ul><li>4:1-2:1 in DU </li></ul><ul><li>2:1 or less in GU 5- Geographical variation. </li></ul><ul><li>6- Age </li></ul><ul><li>DU : 20 ـــ 50 years </li></ul><ul><li>GU : > 40 years </li></ul><ul><li>Aeteology </li></ul><ul><li>1- H. pylori in 90% with DU & 70% with GU </li></ul>
  5. 5. <ul><li>2- Acid pepsin VS mucosal barrier </li></ul><ul><li>- DU occurs in acid hypersecreter. </li></ul><ul><li>- GU is never found in achlorhydrics e.g </li></ul><ul><li>pernicious anaemia. ** Severe ulceration occur in Zollenger Ellison syndrome characterized by high acid out put and hyper parathyroidism (Hyperclcaemia stimulates acid secretion) </li></ul><ul><li>**Aspirin & NSAID affect the mucosal barrier and may cause GU. </li></ul>
  6. 6. <ul><li>*Bile and intestinal secretions damage gastric mucosal barrier and may cause GU. </li></ul><ul><li>3- Smoking depresses gastric mucosal barrier and may cause GU 4- Hereditary : DU is common in blood </li></ul><ul><li>group O. FH in DU. </li></ul><ul><li>Pathology </li></ul><ul><li>1- Break in surface epithelium penetrating </li></ul><ul><li>to za muscularis mucosa. </li></ul>
  7. 7. <ul><li>2- Chronic GU are usually single & occur in lesser curvature of antrum in 90% </li></ul><ul><li>3- DU more common in the bulb with surrounding duodenitis & 50% occur in the anterior wall </li></ul><ul><li>4- DU & GU coexist in 10% </li></ul><ul><li>5- 10-15% of DU & 10% of GU are multiple </li></ul>
  8. 8. <ul><li>Clinical features </li></ul><ul><li>1- Natural history is that of remissions </li></ul><ul><li>and relapses. </li></ul><ul><li>2- Epigastric pain </li></ul><ul><li>- Episodic </li></ul><ul><li>- Sharply localized </li></ul><ul><li>- Induced by hunger in DU </li></ul><ul><li>- Nocturnal & before meal in DU </li></ul><ul><li>- Relieved by food, milk & anti acids in </li></ul><ul><li>DU and by vomiting in GU </li></ul>
  9. 9. <ul><li>3- Anorexia, nausea & weigh loss in GU </li></ul><ul><li>4- Heart burn & water brush in DU . </li></ul><ul><li>5- Vomiting in 40% . Persistent vomiting is suspicious of G.L.O obstruction . </li></ul><ul><li>6- Persistent pain indicate ulcer penetration </li></ul><ul><li>7- Finger pointing </li></ul><ul><li>8- Epigastric tenderness </li></ul><ul><li>9- 20-25% are asymptomatic & may present with complications . e.g. bleeding . </li></ul>
  10. 10. <ul><li>Diagnosis </li></ul><ul><li>1- Clinical suspicion </li></ul><ul><li>2- Endoscopy is the gold standard investigation </li></ul><ul><li>- It is simple, safe & sensitive </li></ul><ul><li>- Detects associated pathology e.g. GORD </li></ul><ul><li>and Ca </li></ul><ul><li>- GUs biopsed & repeated after treatment </li></ul><ul><li>- H. pylori infection is identified in antral </li></ul><ul><li>biopsies </li></ul>
  11. 11. <ul><li>3- Ba meal +_ double contrast less used now </li></ul><ul><li>4- Measurement of gastric acid secretion & serum gastrin levels in Z. Ellison syndrom </li></ul><ul><li>5- Ulcer like symptoms in less 40 year do serology or urea breath test for H. pylori and if positive give eradication therapy. Endoscope if symptoms persist after eradication therapy. </li></ul><ul><li>6- Ulcer like symptoms for the first time in patients over 40 years should always be endoscoped . </li></ul>
  12. 12. <ul><li>Management of PU </li></ul><ul><li>Aim of management : </li></ul><ul><li>a- Relief of pain in short term. </li></ul><ul><li>b- Induce healing in long term </li></ul><ul><li>c- Prevent complications </li></ul><ul><li>* Most ulcers heal in 4-6 weeks </li></ul><ul><li>* Prevention of relapse needs H. pylori eradication, maintenance therapy or surgery </li></ul><ul><li>* H. pylori eradication is the cornerstone of therapy in PU & successfully prevents relapse and may eliminate the need for long term therapy in the majority of patients . </li></ul>
  13. 13. <ul><li>Short term management </li></ul><ul><li>1 - General managements </li></ul><ul><li>- Stop smoking . Smoking delays healing, interferes with H2RA & increase relapse rate </li></ul><ul><li>- Stop NSAID (which delay healing, increases relapse rate & complications </li></ul><ul><li>- Stop alcohol . </li></ul><ul><li>- No special diet </li></ul><ul><li>- Anti acids for symptomatic relief . In large dose therapy they induce healing in 4-6 weeks </li></ul>
  14. 14. <ul><li>2 - PU associated with H. pylori : </li></ul><ul><li>- PPI based triple therapy 90% healing rate & prevents relapse (usually given for 1/52) </li></ul><ul><li>- PPI or H2RA often continued for 4-6 weeks to ensure ulcer healing </li></ul><ul><li>- If symptoms persist perform urea breath test & if + give further course of eradication using different antibiotics </li></ul><ul><li>3 - PU not associated with H. pylori (usually due to NSAID ingestion) </li></ul><ul><li>- Withdraw NSAID </li></ul>
  15. 15. <ul><li>- Acid suppression using PPI & H2RA </li></ul><ul><li>Proton pump inhibitor (PPI) </li></ul><ul><li>1- Omeprazole (20mg) </li></ul><ul><li>2- Lansoprazole (30mg </li></ul><ul><li>3- Pantoprazole (40mg) </li></ul><ul><li>4- Esomeprazole (40mg) </li></ul><ul><li>*PPI has higher ulcer healing rate than H2RA & better tolerated than misoprostol </li></ul><ul><li>but may induce hypergastrinaemia and interact with phenytoin & warfarin </li></ul>
  16. 16. <ul><li>H2 receptor antagonists </li></ul><ul><li>1- Cimetidine (200,400 & 800mg tab) </li></ul><ul><li>2- Ranitidine (150 & 300mg tab) </li></ul><ul><li>3- Famotidine (20 & 40mg tab) </li></ul><ul><li>4- Nizatidine (300mg tab) not recommended for maintenance therapy *Treatment is for 4-6 weeks & is prolonged in smokers, following complication & in patient with GU. </li></ul>
  17. 17. <ul><li>Misoprostol </li></ul><ul><li>- Synthetic prostaglandin analogue </li></ul><ul><li>- In low dose used for cytoprotection in patients on NSAID </li></ul><ul><li>- In high dose (200microg × 3) it is acid suppression </li></ul><ul><li>- Contraindicated in female in child bearing age </li></ul><ul><li>- Abdominal pain diarrhoea are the main side effects </li></ul>
  18. 18. <ul><li>Sucralfate </li></ul><ul><li>- Basic aluminum salt of sucrose octasulphate </li></ul><ul><li>- Forms adherent complex with protiens at ulcer base </li></ul><ul><li>- Non absorable </li></ul><ul><li>- Dose 2gm 12 homly - Dose not suppress acid </li></ul><ul><li>- Not recommended for long term therapy </li></ul>
  19. 19. <ul><li>Colloid bismuth </li></ul><ul><li>- It is tripotassium dicitiato bismuthate </li></ul><ul><li>- It binds with protiens in ulcer base in acid PH - Effective agent against H. pylori </li></ul><ul><li>- Not recommended for maintenance therapy </li></ul><ul><li>- Dose 240mg × 2 </li></ul><ul><li>*Pirenzepine : antimuscarinic. </li></ul><ul><li>* Carbenoxolone : leads to HT & Na retention & no longer used. </li></ul>
  20. 20. <ul><li>Long term management of PU: </li></ul><ul><li>- Continuous long term therapy is not necessary in the majority of patients after successful H. pylori eradication </li></ul><ul><li>- Further management will depend on </li></ul><ul><li>a- Age of patient </li></ul><ul><li>b- Rate of relapse </li></ul><ul><li>c- Occurrence of complications </li></ul><ul><li>d- Presence of other serous medical </li></ul><ul><li>disease. </li></ul>
  21. 21. <ul><li>1- Intermittent treatment : if relapses are less than 4 per year </li></ul><ul><li>2 - Maintenance treatment : 80% will remain in remission as long as treatment is maintained. It is given for: </li></ul><ul><li>a- Frequent relapse interfering with quality of life </li></ul><ul><li>b- History of life thertening complication </li></ul><ul><li>c- In elderly d- patient with serous medical disease when the risk of future complications </li></ul>
  22. 22. <ul><li>or surgery must be avoided </li></ul><ul><li>3- Surgery :- with recent advance in medical treatment surgery is rarely necessary except for complications. </li></ul><ul><li>Surgery can relieve symptoms and prevent complications </li></ul><ul><li>Indications for surgery </li></ul><ul><li>1- Complication of PU </li></ul><ul><li>2- Recurrent ulcer after surgery </li></ul><ul><li>3- Failure to comply with medical TR . </li></ul>
  23. 23. <ul><li>4- Failure of medical therapy specially in young with FH of PU. </li></ul><ul><li>5- Previous complications </li></ul><ul><li>6- Relapse while on medical treatment </li></ul><ul><li>Types of surgery </li></ul><ul><li>1- Bill Roth in GU </li></ul><ul><li>2- Vagotomy & drainage procedure in </li></ul><ul><li>DU </li></ul>
  24. 24. <ul><li>Complications of PU </li></ul><ul><li>Bleeding (15-20%) </li></ul><ul><li>- Present with haematemesis & melaena </li></ul><ul><li>- Amount of blood lost is assessed </li></ul><ul><li>- Hb% is not a good indicator of acute </li></ul><ul><li>bleeding. </li></ul><ul><li>- All patients with significant bleeding within the previous 48 hours should be admitted </li></ul>
  25. 25. <ul><li>- Bleeding stops within 48 hours in 85% of patients </li></ul><ul><li>Factors affecting managing : </li></ul><ul><li>1- Age </li></ul><ul><li>2- Amount of blood loss </li></ul><ul><li>3- Shock </li></ul><ul><li>4- Evidence of chronic liver disease or other co morbidities. </li></ul>
  26. 26. <ul><li>- Immediate management A- Urgent resuscitation in shocked patients </li></ul><ul><li>1- I.V. canulae </li></ul><ul><li>2-Take blood for grouping & cross matching, Hb, urea, electrolytes & liver biochemistry 3- Assess the patients & monitor pulse & BP frequently </li></ul><ul><li>4- Rapid restoration of blood volume </li></ul>
  27. 27. <ul><li>Guide lines for BT </li></ul><ul><li>1- Clinical shock </li></ul><ul><li>2- PR >100 </li></ul><ul><li>3- SBP >100 </li></ul><ul><li>4- Hb <10gm/dl in patients with active bleeding or recent bleed </li></ul><ul><li>Blood volume is restored : </li></ul><ul><li>1- Initially with volume expanders </li></ul><ul><li>2- blood transfusion as soon as </li></ul><ul><li>possible . </li></ul><ul><li>3- avoid overload by using CVP line </li></ul>
  28. 28. <ul><li>B- Urgent endoscopy after resuscitation in patient with shock patients, liver disease or continuing bleeding </li></ul><ul><li>- If there is bleeding ulcer: </li></ul><ul><li>a- Inject adrenaline or sclerosing agent </li></ul><ul><li>b- Heat, laser or argon coagulation </li></ul><ul><li>c- If bleeding is uncontrolled ligate the bleeding artery surgically. </li></ul><ul><li>* Mortality in bleeding PU is 10-15%. More </li></ul><ul><li>in elderly. </li></ul>
  29. 29. <ul><li>Perforation </li></ul><ul><li>- More in DU than GU </li></ul><ul><li>- May be precipitated by NSAID </li></ul><ul><li>- Incidence decreased with better medical care </li></ul><ul><li>-There may be a history of PU or perforation may be the first presentation of PU </li></ul><ul><li>- Gastric contents lead to peritonitis </li></ul><ul><li>- There is severe Abdomenal pain & vomiting. </li></ul>
  30. 30. <ul><li>- Signs of peritonitis </li></ul><ul><li>- Shock </li></ul><ul><li>- Decreased liver dullness </li></ul><ul><li>- Gas under the diaphragm on radiology is diagnostic </li></ul><ul><li>- Exclude other causes of acute abdomen </li></ul><ul><li>Management </li></ul><ul><li>1- Admission </li></ul><ul><li>2- Nil by mouth. </li></ul>
  31. 31. <ul><li>3- N-G suction </li></ul><ul><li>4- I.V.fluids </li></ul><ul><li>5- Anti biotics </li></ul><ul><li>6- Surgery:- drainage, oversewing +/- </li></ul><ul><li>vagotomy. </li></ul>
  32. 32. <ul><li>Gastric out flow obstruction </li></ul><ul><li>( Pyloric stenosis) </li></ul><ul><li>Due to:- </li></ul><ul><li>a- Fibrosis of DU </li></ul><ul><li>b- Edema & spasm of active ulcer </li></ul><ul><li>Diff. Diagnosis </li></ul><ul><li>a- Ca antrum </li></ul><ul><li>b- External pressure </li></ul><ul><li>c- gastro paresis </li></ul><ul><li>d- Adult hypertrophic pyloric stenosis </li></ul>
  33. 33. <ul><li>Clinical feature & management </li></ul><ul><li>1- Long history of DU </li></ul><ul><li>2- Persistent vomiting </li></ul><ul><li>- Large & projectile </li></ul><ul><li>- Contain previous food elements </li></ul><ul><li>3- Epigastric fullness, visible peristalsis and succussion splash </li></ul><ul><li>4- Dehydration & electrolyte disturbances </li></ul><ul><li>5- Metabolic alkalosis and tetany. </li></ul>
  34. 34. <ul><li>6- Wasting & malnutrition. </li></ul><ul><li>7- High fasting gastric juice </li></ul><ul><li>8- Ba meal rarely advised (gastro graffin) </li></ul><ul><li>9- Endoscopy </li></ul><ul><li>10 - Correct fluid & electrolytes disturbance and improve nutrition </li></ul><ul><li>Treatment opntions include balloon dilation +_stenting, but surgery with drainage procedure is usually the final answer . </li></ul>
  35. 35. <ul><li>Zollinger Ellison syndrome </li></ul><ul><li>Triad of: </li></ul><ul><li>1- Gastrinoma (non beta cell islet tumour of pancreas) </li></ul><ul><li>2- Gastric acid hypersecretion 3- severe peptic ulceration </li></ul><ul><li>- 0.1% of cases of PU - age 30-50y. </li></ul><ul><li>*Gastrinoma stimulates parietal cells to max and increases parietal cell mass . </li></ul><ul><li>*Acid reaches small bowel & lowers PH inactivating lipase& precipitating bile acids leading to diarrhoea & steatorrhoea . </li></ul>
  36. 36. <ul><li>Pathology </li></ul><ul><li>- 90% of tum. in head of panc.%. </li></ul><ul><li>- 50% multiple - 1/2-2/3 are slow growing malig. tumours - 20-60% have MEA1 </li></ul><ul><li>Clinically : history is usually short. </li></ul><ul><li>- PUs are severe, multiple, recurrent & at unusual sites, poor response to standard ulcer therapy & more complications </li></ul><ul><li>- Diarrhoea in 1/3 . </li></ul>
  37. 37. <ul><li>Diagnosis </li></ul><ul><li>Suspected in pat. with severe PU , specially if Ba.shows abn. coarse gastric folds. </li></ul><ul><li>- Gastric acid studies show high basal </li></ul><ul><li>acid output little affected by pentagastrin </li></ul><ul><li>- Grossly elevated ser. gastrin confirms </li></ul><ul><li>the diag. </li></ul><ul><li>- Tum. localised by CT, E- US and </li></ul><ul><li>scanning after Octreotide taken by the </li></ul><ul><li>tumour. </li></ul>
  38. 38. <ul><li>Management </li></ul><ul><li>- 30% of tum . are small & single and resectable ( curable) . Many are multifocal and some present with metastasis & surgery is inappropriate. </li></ul><ul><li>- Higher doses of PPI to suppress sympt </li></ul><ul><li>- Octreotide s/c reduces gastrin secretion and is useful. </li></ul><ul><li>- 5 year survival is 60-80% </li></ul><ul><li>- Pats die of malig tum rather than PU if </li></ul><ul><li>if the tum is not resectable </li></ul><ul><li>- All patients should be monitored for later development of MEA1. </li></ul>
  39. 39. <ul><li>Problem 1: Epigastric pain </li></ul><ul><li>- Ali is a 40 years old business man who used to smoke heavily & drink alcohol regularly for the last 15 years. He was seen by za MO in </li></ul><ul><li>medical out patient dept. with periodic epigastric pain for 3years. As he said, za pain is </li></ul><ul><li>burning in character & used to awake him in za early hours of za morning & relieved by drinking milk. Ali recalls an episode of haematemesis and melaena 2 years ago. </li></ul>
  40. 40. <ul><li>- Clinical examination was normal a part from </li></ul><ul><li>marked epigastric tenderness. The Dr. made </li></ul><ul><li>a provisional diagn & requested an investigation </li></ul><ul><li>for definite diagnosis </li></ul><ul><li>Q1: What was za provisional diagn? </li></ul><ul><li>Q2: What was za investigation requested ? </li></ul><ul><li>Q3: Discuss za aetiology & pathogenesis of this </li></ul><ul><li>disease? </li></ul><ul><li>- Ali reported next day wz severe epigastric pain </li></ul><ul><li>which started at 8 oo a.m & in due time </li></ul><ul><li>became generalized wz persistent vomiting . </li></ul>
  41. 41. <ul><li>- On exam. Ali was in severe pain & shocked. The abdomen was rigid & silent on auscultation. </li></ul><ul><li>CXR in za erect position explained Ali,s problem. </li></ul><ul><li>Q4: What complication happened to Ali? </li></ul><ul><li>Q5: What was the diagnostic X- ray finding? </li></ul><ul><li>Q6: Mention 3 differential diagn? </li></ul><ul><li>Q7: What za immediate line of management? </li></ul><ul><li>- Ali was taken to za theatre after za initial </li></ul><ul><li>management for definite TR & had a successful </li></ul>
  42. 42. <ul><li>recovery from za surgery. </li></ul><ul><li>Q8: What surgical operation had been done </li></ul><ul><li>Ali? </li></ul><ul><li>- Ali was discharged from za surgical ward and </li></ul><ul><li>referred to za physician for specific TR of the </li></ul><ul><li>original disease. </li></ul><ul><li>Q9: What are za components of this disease? </li></ul><ul><li>Q10: What advice will you offer to Ali concerning </li></ul><ul><li>life style modification? </li></ul>

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