2 PEPTIC ULCER.pptx

PEPTIC ULCER

1. PEPTIC ULCER

2. Erosion of GI mucosa resulting from digestive action of HCl and pepsin. There are two main sites of peptic ulcer — 1. Gastric 2. Duodenal. Rare peptic ulcers may be seen in the ( i ) cardiac end of oesophagus ; (ii) Meckel’s diverticulum (due to presence of ectopic gastric mucosa); (iii) In any segment of bowel ( anastomotic ulcer) which has been surgically anastomosed to the gastric fundus . Peptic ulcers may be acute ulcers, which are shallow and multiple and chronic ulcers, which are single, deep and scirrhous .

3. AETIOLOGY AND PATHOGENESIS ACUTE PEPTIC ULCERS ( i ) About half the patients give history of ingestion of aspirin or butazolidin . (ii) Sometimes these acute ulcers may occur following stress, when they are called ‘stress ulcers’. This may occur following hypotension from haemorrhage , endotoxin shock or cardiac infarction, (iii) Sepsis is an important aetiologic factor. Undrained pus may be responsible for acute stress ulcers. Upper G.I. bleeding from these ulcers may be seen in critically ill patient and should be a signal to search for pus.

4. (iv) These acute ulcers may be seen after cerebral trauma or neurosurgical operations (Cushing’s ulcer). Higher rate of acid secretion and higher gastrin level suggest that patients with head injury may have increased vagal activity, (v) After major bums acute ulcers may be seen (Curling’s ulcer). Within first 48 hours multiple acute erosions may develop anywhere in the body and fundus of the stomach ( antrum and duodenum usually escape). During convalescent period of such bum cases, acute duodenal ulcer may occur which often become chronic, (vi) Patients on steroids may develop acute ulcers, known as ‘steroid ulcers’.

5. CHRONIC PEPTIC ULCERS.— 1.GASTRIC ULCER Gastric ulcer patients secrete either low normal or below normal amounts of acid. Only 5% of patients may demonstrate acid hypersecretion .

6. 1. DIMINISHED MUCOSAL RESISTANCE 2. PYLORODUODENAL REFLUX 3. DEFICIENT MUCOUS BARRIER 4. MUCOSAL TRAUMA 5. LOCAL ISCHAEMIA 6. ANTRAL STASIS 7. NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDs) 8. HELICOBACTER PYLORI

7. 1. DIMINISHED MUCOSAL RESISTANCE This has been incriminated as the cause of chronic gastric ulcer. This is due to lowering of the ability to resist the effect of acid pepsin digestion.

8. 2. PYLORODUODENAL REFLUX Regurgitated bile and other duodenal juices have been taken to be the prime cause of preulcerative superficial gastritis. Though such biliary reflux may account for a large number of gastric ulcer cases, it does not seem possible to explain all of them on this basis. Some gastric ulcers occur in the fundus or at the cardia where such biliary effects would seem least active.

9. 3. DEFICIENT MUCOUS BARRIER A surface layer of mucus protects normally from the digestive effect of the hydrochloric acid and pepsin. When this mucous barrier becomes deficient gastric ulcer may develop. But it is a matter of clinical observation that in most cases of gastric ulcer the stomach produces large quantities of mucus.

10. 4. MUCOSAL TRAUMA 85% of gastric ulcers occur along the lesser curve. This fact together with the observation that fluids tend to pass through the lesser curve of the stomach suggests that a mechanical factor might be involved. This part of the stomach is exposed to injurious effects of heat and trauma

11. 5. LOCAL ISCHAEMIA Microemboli artificially introduced into the gastric circulation of dogs or interference with blood supply by ligation of vessels or omental stripping would cause gastric erosions and ulcers todevelop . Arteriovenous shunts which are present in the submucosa of the stomach are under the control of sympatheticnervous system and excessive stress and strain may cause diminution of blood supply to the mucous membrane of the stomach leading to ulcer formation.

12. 6. ANTRAL STASIS This usually produces increased acid secretion and it is an accepted fact that the majority of patients with gastric ulcers have low acid content in the stomach. But it is seen that nearer the ulcer to the pylorus more is the acid secretion of the stomach.

13. 7. NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDs) Ingestion of these drugs in patients suffering from arthritis as a long term basis is a significant aetiologic factor at present time. The drugs of this group are often called ulcerogenic drugs. These drugs seem to disrupt the prostaglandin-driven support of the mucosal barrier. These prostaglandins are related to the production of mucosal gel layer in the stomach, which provides a protective barrier to the gastric and duodenal lining. So disruption of this mucosal barrier allows even minimal amount of acid to cause ulceration.

14. 8. HELICOBACTER PYLORI It is a spirochaetal bacterium which exists in the deep mucosal layer of the antrum mainly and duodenum rarely. Upto l/5th of normal population harbours this bacterium. In almost 100% of cases of duodenal ulcer patients H.pylori have been demonstrated. Eradication of this bacteria has led to decreased recurrence rate of ulcer cases. So presence of H.pylori clearly predisposes to peptic ulceration.

15. 2. Duodenal ulcer CAUSES 1. ACID HYPERSECRETION 2. GENETIC FACTORS 3. ENDOCRINE ORGAN DYSFUNCTION 4. LIVER DISEASE 5. EMOTIONAL FACTORS 6. DIET AND SMOKING 7. HELICOBACTER PYLORI 8. DECREASE IN BICARBONATE PRODUCTION

16. 1. ACID HYPERSECRETION Pathogenesis of duodenal ulceration is seemingly simplified at first sight by a clear relationship to over-production of hydrochloric acid by the stomach. In most collected series, the mean basal and maximal acid output of duodenal ulcer patients is approximately 2 times more than those of the control patients. It has also been shown that the stomachs of duodenal ulcer patients have almost twice the number of parietal cells (increased parietal cell mass) compared to normal stomachs. Serum group I pepsinogen level is also increased in duodenal ulcer patients.

17. It has got a direct relationship with the acid secretory potential of the stomach. Duodenal ulcer patients also show increased gastrin stimulation. They also show an increased rate of gastric emptying. Diminished acid inhibition of gastrin release is also noticed. Increased vagal excitation has also been assumed to underlie theduodenal ulcer diathesis.

18. 2. GENETIC FACTORS Diminished power of resistance of the mucosa has also been incriminated to cause duodenal ulcer. In a great number of cases the acid production may be within the high side of the normal range and in these cases ulceration cannot be explained except the diminished mucosal resistance to normal acid secretion. A genetic background can be well explained. There is a significant relationship between blood group ‘0’ and the development of duodenal ulcer. Persons of blood group ‘0’ who do not possess AB antigen are peculiarly apt to develop duodenal ulcers.

19. 3. ENDOCRINE ORGAN DYSFUNCTION In addition to the Zollinger -Ellison syndrome, in which there is over-production of gastrin by pancreatic tumour tissue with consequent hyperacidity and ulcer formation, other endocrine adenomata may be associated with duodenal ulcer. In Cushing’s syndrome, the high level of endogenous steroids may be responsible for duodenal ulcer. In parathyroid tumour hyperacidity may be either due to hypercalcaemia orother causes have been noticed. Some bronchial carcinomas do produce hyperacidity. Multiple adenoma syndrome, where adenoma in pituitary, adrenal, parathyroid and pancreas have been noticed, may cause hyperacidity.

20. 4. LIVER DISEASE Ulceration of both stomach and duodenum has co-existed with disease of the liver particularly cirrhosis. It may be due to increase in the blood supply to the gastric mucosa and over-production of histamine in the stomach wall to stimulate the parietal cells.

21. 5. EMOTIONAL FACTORS Anxiety, stress and strain have always been incriminated to cause peptic ulcer.

22. 6. DIET AND SMOKING Irregular diet, spicy food and excessive drinking of tea and coffee have always provoked formation of peptic ulcer. Opinions vary regarding alcohol. Some have found a clear relationship whereas others could not find any definite relation. Smoking does appear to predispose ulcer formation. Cigarette smoking has a definite relation with ulcer formation. The exact cause is not yet clearly understood, but it seems that smoking diminishes mucosal defence mechanism almost similar to NSAIDs

23. 7. HELICOBACTER PYLORI As mentioned in the aetiology of chronic gastric ulcer, H.pylori have been isolated in 100% of duodenal ulcer cases. Its irradication has definitely led to decrease in recurrence rate and this clearly indicates its importance in the aetiology of duodenal ulcer.

24. 8. DECREASE IN BICARBONATE PRODUCTION DECREASE IN BICARBONATE PRODUCTION by the stomach and/or duodenum leads to peptic ulceration. Those with decreased bicarbonate production cannot maintain a pH-neutral microlayer between the mucosal lining below and mucous gel layer above. That is why the drugs which increase bicarbonate production are being investigated to be used in the treatment of peptic ulcer disease.

25. PATHOLOGY Gastric ulcer is large in size, usually lies in the lesser curvature, its floor being formed by the muscular layer. Posteriorly it may penetrate into the pancreas; it may cause torrential bleeding by eroding left gastric (commonly) vessles or splenic vessels or vessels in the gastric ulcer wall. Anteriorly it may perforate or penetrate into the liver. It may lead into hour glass contracture, or tea-pot deformity.

26. Microscopically, it shows ulcer crater with chronic inflammatory cells and granulation tissue, endarteritis obliterans and epithelial proliferation.

27. Gastric ulcer >3 cm is called as giant gastric ulcer. It has got 6–23% chances to turn into malignancy. Incidence of perforation and bleeding is also very high. Endoscopy and biopsy should be done to rule out malignancy. Follow-up endoscopy is a must if drug therapy is used for treatment to confirm the complete healing of the ulcer. If complete remission has not occurred then partial gastrectomy should be done.

28. Grossly, margin of the benign gastric ulcer is clear; deep; near lesser curve; edge is not everted with gastric mucosal folds converging towards the base of the ulcer. Ninty -five per cent of benign gastric ulcer occurs towards lesser curve, as it takes more burden of passage of food and so more of wear and tear. Benign gastric ulcer is rare in greater curvature, fundus and cardia .

29. Acute ulcer: It is confined to mucosa and submucosa . It is commonly due to NSAIDs. Chronic ulcer: It penetrates muscularis layer of stomach.

30. Clinical Features Equal in both sexes. It is becoming more common in females. Common after the age of 40 years. Pain in epigastric region after taking food, lasting up to two hours. Pain is uncommon during night. It is relieved by vomiting or by inducing vomiting. Periodicity: Symptom free interval may be 2–6 months. Often with seasonal variation. Vomiting relieves pain and often it is induced by the patient for relief of pain.

31. Clinical Features Haematemesis and melaena : Haematemesis is more common. Appetite is good but hesitant to eat, because eating induces pain and that results in loss of weight. But once complications occur, appetite decreases. Aversion to spicy, fried foods occurs. On deep palpation, tenderness is felt in epigastric region.

32. Type &Location Type I: In the antrum , near the lesser curve. Type II: Combined gastric ulcer (in the body) with duodenal ulcer Type III: Prepyloric ulcer Type IV: Gastric ulcer in the proximal stomach or cardia

33. Investigations Barium meal X-ray to see niche and notch. Barium meal X-ray features of benign gastric ulcer: Niche on the lesser curve with notch on the greater curvature ™Ulcer crater projects beyond the lumen of the ulcer ™Regular/round margin of the ulcer crater— stomach spoke wheel pattern ™Overhanging mucosa at the margins of a benign gastric ulcer— projects inwards towards the ulcer Hamptom’s line ™Converging mucosal folds towards the base of the ulcer ™Symmetrical normal gastric mucosal folds

34. Gastroscopy is done to see the location, type of ulcer and also to take biopsy (10 biopsies). Ultrasound abdomen mainly to rule out other diseases and to confirm associated diseases. Multiple ulcers visualised on gastroscopy (A) Gastric ulcer in the body of the stomach; (B) Gastric ulcer in prepyloric region.

35. Treatment Drugs like H2 blockers, proton-pump inhibitors, carbenoxolone ( biogastrone , sucralfate , prostaglandins which coats the ulcer and so creates a mucosal barrier) helps in reducing or eliminating the symptoms. But asymptomatic ulcer may exist silently and may turn into malignancy.

36. So surgery is the preferred line of treatment. Partial gastrectomy and Billroth I gastroduodenal anastomosis is done. Type IV proximal gastric ulcer is difficult to manage. It is treated by subtotal gastrectomy . Often distal gastrectomy with selective sleeve like extension cut along the lesser curve to remove the ulcer is done— Pauchet’s procedure.

37. 3. HSV with excision of ulcer. 4. Kelling Madlener procedure: It is antrectomy and excision of proximal gastric ulcer Type IV. 5. Csendes procedure: It is subtotal gastrectomy with sleeve extended resection along the lesser curve for type IV proximal gastric ulcer.

38. Complications of Gastric Ulcer Hour glass contracture

39. Tea-pot deformity (Hand-bag stomach) Complications of Gastric Ulcer

40. Complications of Gastric Ulcer Perforation Penetration posteriorly into pancreas, anteriorly into liver. Malignant transformation usually into adenocarcinoma of stomach.

41. DUODENAL ULCER

42. Aetiology Common in people with blood group O + ve . Stress, anxiety—‘ hurry, worry, curry’. Helicobacter pylori infection is an important aetiology for duodenal ulcer (90%). NSAIDs, steroids. Endocrine causes: Zollinger -Ellison syndrome, MEN syndrome, hyperparathyroidism. Other causes: Alcohol, smoking, vitamin deficiency. “No acid – No ulcer”.

43. Pathology Ulcer occurs in the first part of duodenum, usually with in the first inch,involving the muscular layer. Sites: a. In the bulb (bulbar)—95%. b. Post-bulbar (5%). Eventually it shows cicatrisation causing pyloric stenosis . Serosa overlying the site of duodenal ulcer shows petechial haemorrhages with speckled red dots, appearing like sprinkled cayenne pepper.

44. Microscopically, ulcer with chronic inflammation with granulation tissue, gastric metaplasia of duodenal mucosa, endarteritis obliterans are visualised. Sometimes two opposing ulcers, i.e. over anterior and posterior surfaces of duodenum are present and are called as kissing ulcers. An anterior ulcer perforates commonly, posterior ulcer bleeds or penetrates commonly.

45. Clinical Features In India, ratio of duodenal ulcer (DU) to gastric ulcer is 30 : 1. A very high incidence. It is common in all socioeconomic group, more with stressed professionals (Type A personality).

46. Pain is more before food, in early morning and decreases after taking food. It is classically called as hunger pain as it is relieved by taking food. Night pains are common. Common in males. Periodicity is more common than in chronic gastric ulcer with seasonal variation. Water-brash, heart burn, vomiting may be present. Melaena is more common, haematemesis also can occur.

47. Appetite is good and there is gain in weight. It decreases once stenosis develops. Eats more frequently without any restriction. Chronic duodenal ulcer can be uncomplicated or complicated.

48. Complications of Duodenal Ulcer 1. Pyloric stenosis : Due to scarring and cicatrisation of first part of the duodenum. 2. Bleeding (10%). 3. Perforation (5%). Both acute and chronic ulcers can perforate. Anterior ulcers perforate. 4. Residual abscess. 5. Penetration to pancreas.

49. NOTE Chronic duodenal ulcer will not turn into malignancy. Ulcer which is more than 2 cm is called as giant duodenal ulcer.

50. Investigations x Barium meal X-ray shows deformed or absence of duodenal cap (because of spasm). Appearance of ‘trifoliate’ duodenum is due to secondary duodenal diverticula which occurs as a result of scarring of ulcer.

51. Gastroscopy reveals the type, location of ulcer, narrowing if any. Biopsy also can be taken to look for the presence of Helicobacter pylori. Usually biopsies are taken from duodenum, pylorus, antrum , body, fundus , and confirmed by rapid urease test or C13 or C14 breath tests. Estimation of serum gastrin level, serum calcium level.

52. Differential diagnosis Carcinoma stomach (pylorus) ™. Dyspepsia due to other causes –– Hiatus hernia –– Oesophagitis –– Cholecystitis –– Chronic pancreatitis

53. Treatment Aim of therapy : To relieve symptoms; to heal ulcer; to prevent recurrence. I. General measures: Avoid alcohol, NSAIDs, smoking, spicy foods. Have more frequent food. II. Specific measures: Intragastric pH should be maintained above 5.

54. Drugs 1 . H2 Blockers 2 . Proton-pump inhibitors 3. Antacids 4. Sucralfate 5. Anti-Helicobacter pylori regime 6. Colloid bismuth sulphate 7. Misoprostol

55. Surgery for Uncomplicated Duodenal Ulcer Indications for surgical intervention for chronic DU (Uncomplicated DU): 1. Uncomplicated DU, not responding to drug therapy of 8–12 weeks —intractable duodenal ulcer 2. Repeated recurrences Presently most of the uncomplicated DU does not require surgery

56. Highly selective vagotomy (HSV). Selective vagotomy with pyloroplasty (SV + P). Truncal vagotomy with gastrojejunostomy (TV + GJ). Posterior truncal vagotomy with anterior seromyotomy . Vagotomy with antrectomy Posterior truncal vagotomy with HSV without drainage procedure (Kim’s) often through laparoscopy is also done. Linear gastrectomy with posterior truncal vagotomy through laparoscopy.

57. HOMOEOPATHIC TREATMENT

58. Argentum nitricum  . For abdominal bloating with belching and pain. Arsenicum album  . For ulcers with intense burning pains and nausea; especially for people who cannot bear the sight or smell of food and are thirsty. Kali bichromicum  . For burning or shooting abdominal pain that is worse in the hours after midnight. Lycopodium  . For bloating after eating with burning that lasts for hours; especially for people who feel hungry soon after eating and wake up hungry.

59. Nitric acid  . For sharp, shooting pain that worsens at night and is accompanied by feelings of hopelessness and even fear of dying. Nux vomica  . For digestive disturbances (including heartburn and indigestion) that worsen after eating; particularly for those who crave alcohol, coffee, and tobacco. Phosphorus  . For burning stomach pain that worsens at night; those for whom this remedy is appropriate tend to feel very thirsty, craving cold beverages. Pulsatilla  . For symptoms that vary (that is, change abruptly) and pain that gets worse from fatty foods; appropriate people are distinctly not thirsty.