Peptic Ulcer_RDP
- 1. PEPTIC ULCER MRS.RISHITA D PATEL
- 2. Acute Peptic (Stress) Ulcers • Acute peptic ulcers or stress ulcers : are multiple, small mucosal erosions, seen most commonly in the stomach but occasionally involving the duodenum. • ETIOLOGY : These ulcers occur following severe stress. The causes are as follows: 1. Psychological stress 2. Physiological stress as in the following: i) Shock ii) Severe trauma iii) Septicaemia iv) Extensive burns (Curling’s ulcers in the posterior aspect of the first part of the duodenum). v) Intracranial lesions (Cushing’s ulcers developing from hyperacidity following excessive vagal stimulation). vi) Drug intake (e.g. aspirin, steroids, butazolidine, indomethacin). vii) Local irritants (e.g. alcohol, smoking, coffee etc)
- 4. • PATHOGENESIS It is not clear how the mucosal erosions occur in stress ulcers because actual hyper secretion of gastric acid is demonstrable in only Cushing’s ulcers occurring from intracranial conditions such as due to brain trauma, intracranial surgery and brain tumours. • In all other etiologic factors, gastric acid secretion is normal or below normal. In these conditions, the possible hypotheses for genesis of stress ulcers are as under: • 1. Ischemic hypoxic injury to the mucosal cells. • 2. Depletion of the gastric mucus ‘barrier’ rendering the mucosa susceptible to attack by acid-peptic secretions
- 5. Chronic Peptic Ulcers (Gastric and Duodenal Ulcers) • If not specified, chronic peptic ulcers would mean gastric and duodenal ulcers, the two major forms of ‘peptic ulcer disease’ of the upper GI tract in which the acid-pepsin secretions are implicated in their pathogenesis. • Peptic ulcers are common in the present-day life of the industrialized and civilized world. • Gastric and duodenal ulcers represent two distinct diseases as far as their etiology, pathogenesis and clinical features are concerned. However, morphological findings in both are similar and quite diagnostic.
- 6. • INCIDENCE • Peptic ulcers are more frequent in middle-aged adults. • The peak incidence for duodenal ulcer is 5th decade, while for gastric ulcer it is a decade later (6th decade). • Duodenal as well as gastric ulcers are more common in males than in females. • Duodenal ulcer is almost four times more common than gastric ulcer; the overall incidence of gastroduodenal ulcers being approximately 10% of the male population.
- 7. ETIOLOGY • The immediate cause of peptic ulcer disease is disturbance in normal protective mucosal ‘barrier’ by acid pepsin, resulting in digestion of the mucosa. • However, in contrast to duodenal ulcers, the patients of gastric ulcer have low-to-normal gastric acid secretions, though true achlorhydria in response to stimulants never occurs in benign gastric ulcer. • Besides, 10-20% patients of gastric ulcer may have coexistent duodenal ulcer as well. Thus, the etiology of peptic ulcers possibly may not be explained on the basis of a single factor but is multifactorial. These factors are discussed below but the first two—H. pylori gastritis and NSAIDs-induced injury are considered most important.
- 8. 1. Helicobacter pylori gastritis : About 15-20% cases infected with H. pylori in the antrum develop duodenal ulcer in their life time while gastric colonisation by H. pylori never develops ulceration and remain asymptomatic. • H. pylori can be identified in mucosal samples by histologic examination, culture and serology. 2. NSAIDs-induced mucosal injury Non-steroidal antiinflammatory drugs are most commonly used medications in the developed countries and are responsible for direct toxicity, endothelial damage and epithelial injury to both gastric as well as duodenal mucosa.
- 9. 3. Acid-pepsin secretions: There is conclusive evidence that some level of acid-pepsin secretion is essential for the development of duodenal as well as gastric ulcer. Peptic ulcers never occur in association with pernicious anemia in which there are no acid and pepsin-secreting parietal and chief cells respectively.
- 10. 4. Gastritis : Some degree of gastritis is always present in the region of gastric ulcer, though it is not clear whether it is the cause or the effect of ulcer. Besides, the population distribution pattern of gastric ulcer is similar to that of chronic gastritis. The term ‘gastritis’ is commonly employed for any clinical condition with upper abdominal discomfort like indigestion or dyspepsia in which the specific clinical signs and radiological abnormalities are absent. Th e condition is of great importance due to its relationship with peptic ulcer and gastric cancer.
- 11. • 5. Other local irritants : Pyloric antrum and lesser curvature of the stomach are the sites most exposed for longer periods to local irritants and thus are the common sites for occurrence of gastric ulcers. • Some of the local irritating substances implicated in the etiology of peptic ulcers are heavily spiced foods, alcohol, cigarette smoking, unbuffered aspirin. • 6. Dietary factors : Nutritional deficiencies have been regarded as etiologic factors in peptic ulcers e.g. occurrence of gastric ulcer in poor socioeconomic strata, higher incidence of duodenal ulcer in parts of South India. • However, malnutrition does not appear to have any causative role in peptic ulceration in European countries and the U.S.
- 12. • 7. Psychological factors : Psychological stress, anxiety, fatigue and ulcer-type personality may exacerbate as well as predispose to peptic ulcer disease. • 8. Genetic factors : People with blood group O appear to be more prone to develop peptic ulcers than those with other blood groups. • Genetic influences appear to have greater role in duodenal ulcers as evidenced by their occurrence in families, monozygotic twins and association with HLA-B5 antigen.
- 13. • 9. Hormonal factors : Secretion of certain hormones by tumours is associated with peptic ulceration e.g. elaboration of gastrin by islet-cell tumour in Zollinger-Ellison syndrome, endocrine secretions in hyperplasia and adenomas of parathyroid glands, adrenal cortex and anterior pituitary. • Peptic ulcer disease is uncommonly associated with pituitary adenoma when the latter is an isolated endocrine tumor, but frequently occurs with pituitary adenoma in association with polyglandular endocrine adenomatosis.
- 14. • 10. Miscellaneous Duodenal ulcers have been observed to occur in association with various other conditions such as • alcoholic cirrhosis, • chronic renal failure, • hyperparathyroidism, • chronic obstructive pulmonary disease, and • chronic pancreatitis
- 15. • PATHOGENESIS: There are distinct differences in the pathogenetic mechanisms involved in duodenal and gastric ulcers as under: • Duodenal ulcer : • There is conclusive evidence to support the role of high acid-pepsin secretions in the causation of duodenal ulcers. Besides this, a few other noteworthy features in the pathogenesis of duodenal ulcers are as follows: • 1. There is generally hypersecretion of gastric acid into the fasting stomach at night which takes place under the influence of vagal stimulation. There is high basal as well as maximal acid output (BAO and MAO) in response to various stimuli.
- 16. • 2. Patients of duodenal ulcer have rapid emptying of the stomach so that the food which normally buffers and neutralizes the gastric acid, passes down into the small intestine, leaving the duodenal mucosa exposed to the aggressive action of gastric acid.
- 17. • Helicobacter gastritis caused by H. pylori is seen in 95-100% cases of duodenal ulcers. The underlying mechanisms are as under: • i) Gastric mucosal defence is broken by bacterial elaboration of urease, protease, catalase and phospholipase. • ii) Host factors: H. pylori-infected mucosal epithelium releases pro Inflammatory cytokines such as IL-1, IL-6, IL-8 and tumour necrosis factor-, all of which incite intense inflammatory reaction. • iii) Bacterial factors: Epithelial injury is also induced by cytotoxin- associated gene protein (CagA), while vacuolating cytotoxin (VacA) induces elaboration of cytokines
- 18. Gastric ulcer • The pathogenesis of gastric ulcer is mainly explained on the basis of impaired gastric mucosal defenses against acid-pepsin secretions. Some other features in the pathogenesis of gastric ulcer are as follows: • 1. Hyperacidity may occur in gastric ulcer due to increased serum gastrin levels in response to ingested food in an atonic stomach.
- 19. • 2. However, many patients of gastric ulcer have low-to-normal gastric acid levels. Ulcerogenesis in such patients is explained on the basis of damaging influence of other factors such as gastritis, bile reflux, cigarette smoke etc. • 3. The normally protective gastric mucus ‘barrier’ against acid-pepsin is damaged in gastric ulcer. There is depletion in the quantity as well as quality of gastric mucus. • One of the mechanisms for its depletion is colonization of the gastric mucosa by H. pylori seen in 75-80% patients of gastric ulcer. • https://www.youtube.com/watch?v=E0IBMWQDEH4
- 20. COMPLICATIONS • Acute and subacute peptic ulcers usually heal without leaving any visible scar. • However, healing of chronic, larger and deeper ulcers may result in complications. • These are as follows: • 1. Obstruction: Development of fibrous scar at or near the pylorus results in pyloric stenosis. • Healed duodenal ulcers cause duodenal stenosis. Healed gastric ulcers along the lesser curvatures may produce ‘hourglass’ deformity due to fibrosis and contraction.
- 21. • 2. Haemorrhage : • Minor bleeding by erosion of small blood vessels in the base of an ulcer occurs in all the ulcers and can be detected by testing the stool for occult blood. • Chronic blood loss may result in iron deficiency anaemia. • Severe bleeding may cause ‘coffee ground’ vomitus or melaena. • A penetrating chronic ulcer may erode a major artery (e.g. left gastric, gastroduodenal or splenic artery) and cause a massive and severe hematemesis and sometimes death.
- 22. • 3. Perforation: • A perforated peptic ulcer is an acute abdominal emergency. • Perforation occurs more commonly in chronic duodenal ulcers than chronic gastric ulcers. • Following sequelae may result: • i) On perforation the contents escape into the lesser sac or into the peritoneal cavity, causing acute peritonitis. • ii) Air escapes from the stomach and lies between the liver and the diaphragm giving the characteristic radiological appearance of air under the diaphragm.
- 23. • iii) Subphrenic abscess between the liver and the diaphragm may develop due to infection. • iv) Perforation may extend to involve the adjacent organs e.g. the liver and pancreas.
- 24. • 4. Malignant transformation : • The dictum ‘cancers ulcerate but ulcers rarely cancerate’ holds true for most peptic ulcers. • A chronic duodenal ulcer never turns malignant, while less than 1% of chronic gastric ulcers may transform into carcinoma.