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Peptic ulcer

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  2. 2. INTRODUCTION • Peptic ulcer occurs in that part of the gastrointestinal tract which is exposed to gastric acid and pepsin • The term ‘peptic ulcer’ describes a condition in which there is a discontinuity in the entire thickness of the gastric or duodenal mucosa that persists as a result of acid and pepsin in the gastric juice. • An ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation. Ulcers occur within the stomach and/or duodenum and are often chronic in nature. • A peptic ulcer is an abnormal area of mucosa that has been damaged by the pepsin and hydrochloric acid of gastric juice, with consequent inflammation of the underlying and surrounding tissue. • Most peptic ulcers occur either in the duodenum or in the stomach, where the pH is sufficiently low for peptic action, although ulcers may also occur in the lower oesophagus, as a result of refluxing of gastric contents
  3. 3. TYPES • There two different types of Peptic Ulcers. • Gastric ulcer, which form in the lining of the stomach • Duodenal ulcer, which forms in the upper small intestine
  4. 4. DIFFERENCESBETWEENGASTRICANDDUODENALULCER • Gastric ulcers occur in the stomach, located in the Atrum (submucosal or beyond ) • Gastric ulcers cause stomach pain 1-2 hours after eating • In Gastric Ulcers pain is worse during me meal • Associated with H.Pylori 70% • Gastric ulcers cause hematemesis or vomiting of blood • Duodenal ulcers occur in the duodenum bulb, portion of the duodenum which is closest to the stomach • Duodenal ulcers cause pain 3- 4 hours later • Eating can relieve stomach pain in duodenal ulcers • Associated with H.Pylori 95%
  5. 5. GASTRIC ANATOMY AND PHYSIOLOGY • PUD can be fully understood after anatomical study of the stomach, The gastric epithelial lining consists of rugae that contain microscopic gastric pits, each branching into four or five gastric glands made up of highly specialized epithelial cells • The majorities of gastric glands (75%) are found within the oxyntic mucosa and contain mucous neck, parietal, chief, endocrine, and enterochromaffin cells. Pyloric glands contain mucous and endocrine cells (including gastrin cells) and are found in the antrum. • A typical adult human stomach will secrete 2 or 3 liters of gastric acid daily. Gastric acid secretion happens in several steps. • It consists of: • Water and mineral salts secreted by gastric glands • Mucus secreted by mucous neck cells in the glands • Hydrochloric acid and intrinsic factor secreted by parietal cells in the gastric glands • Inactive enzyme precursors; pepsinogen secreted by chief cells • The benefits of gastric acid are to facilitate digestion of proteins and the absorption of calcium, iron, and vitamin B12. It also suppresses growth of bacteria, which can help prevent enteric infections and small intestinal bacterial overgrowth. • Mucus prevents mechanical injury to the wall by lubricating the contends
  6. 6. PROTECTIVEMECHANISMGASTRIC MUCOSA • Gastroduodenal Mucosal Defense - The gastric epithelium is under a constant assault by a series of endogenous noxious factors including HCl, pepsinogen/pepsin, and bile salts • In addition, a steady flow of exogenous substances such as medications, alcohol, and bacteria encounter the gastric mucosa. • The mucosal defense system can be envisioned as a three-level barrier, composed of preepithelial, epithelial, and subepithelial element.
  7. 7. REGULATION OF SECRETION • Gastric acid production is regulated by both the autonomic nervous system and by several hormones. The parasympathetic nervous system, via the vagus nerve, and the hormone gastrin stimulate the parietal cell to produce gastric acid, both directly acting on parietal cells and indirectly, through the stimulation of the secretion of the hormone histamine from enterochromaffine-like cells (ECL). • Vasoactive intestinal peptide, cholecystokinin, and secretin all inhibit production. Positive regulators and negative feedback mechanism regulate production of gastric acid in the stomach.
  8. 8. PATHOPHYSIOLOGYOFPEPTICULCERDISEASE • PUD encompasses both gastric and duodenal ulcers. Ulcers are defined as a break in the mucosal surface 5 mm in size, with depth to the submucosa. Duodenal ulcers (DUs) and gastric ulcers (GUs); share many common features in terms of pathogenesis, diagnosis, and treatment, but several factors distinguish them from one another.
  10. 10. EPIDEMIOLOGY • Peptic ulcers are common: it has been estimated that up to 10% of the population has an ulcer at some time, though many of these are asymptomatic, the annual incidence of symptomatic peptic ulcer being about 0.3%. Duodenal ulcers are four times as common as gastric ulcers and occur mainly in the duodenal cap . • DUODENAL ULCER: DUs are estimated to occur in 6 to 15% of the western population. The incidence of DUs declined steadily from 1960 to 1980 and has remained stable since then. The death rates, need for surgery, and physician visits have decreased by 50% over the past 30 years. • GASTRIC ULCER: GUs tends to occur later in life than duodenal lesions, with a peak incidence reported in the sixth decade. More than half of GUs occur in males and are less common than DUs,
  11. 11. ETIOLOGY • The etiology of peptic ulcer disease is multifactorial, the mechanisms normally operating to protect the mucosa from self-digestion by the acid and pepsin of gastric juice either failing or being overcome by a combination of injurious factors • The most common causes of peptic ulcer in are H. pylori infection and NSAID ingestion. • The old hypothesis that ulceration is caused simply by hyperacidity is not tenable, because about 70% of gastric ulcers and 50% of duodenal ulcers (i.e. about 55% of all ulcers) are not associated with abnormally high acid production • However, gastric ulcers occurring near the pylorus may be associated with combined H. pylori infection plus hyperacidity, as are many duodenal ulcers. • Heredity is also important: the development of duodenal ulcer at an early age tends to run in families. • Added to these naturally occurring factors are a number of social and environmental ones, the most important being smoking. The ingestion of some drugs, especially NSAIDs and alcohol, also promotes acute ulceration • Spicy foods do not cause ulceration, but may aggravate symptoms
  12. 12. H PYLORIAND ACIDPEPTICDISORDERS • Gastric infection with the bacterium H. pylori accounts for the majority of PUD. This organism also plays a role in the development of gastric mucosal-associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma. • The bacterium, initially named Campylobacter pyloridis, is a gram- negative microaerophilic rod found most commonly in the deeper portions of the mucous gel coating the gastric mucosa or between the mucous layer and the gastric epithelium • The first step in infection by H. pylori is dependent on the bacteria’s motility and its ability to produce urease. Urease produces ammonia from urea, an essential step in alkalinizing the surrounding pH
  13. 13. NSAID-INDUCED ULCER • NSAID use is a common cause of PUD. These drugs disrupt the mucosal permeability barrier, rendering the mucosa vulnerable to injury. • Prostaglandins play a critical role in maintaining gastroduodenal mucosal integrity and repair. It therefore follows that interruption of prostaglandin synthesis can impair mucosal defense and repair, thus facilitating mucosal injury via a systemic mechanism • NSAIDs act by inhibiting the enzyme cyclooxygenases (COX-1) which is a constitutive enzyme in the production of gastric mucosa
  14. 14. STRESS ULCER • Stressful conditions that may cause PUD include burns, CNS trauma, surgery, and severe medical illness. Serious systemic illness, sepsis, hypotension, respiratory failure, and multiple traumatic injuries increase the risk for secondary (stress) ulceration. • . Stress ulceration and upper-GI hemorrhage are complications that are increasingly encountered in critically ill children in the intensive care setting. Severe illness and a decreased gastric pH are related to an increased risk of gastric ulceration and hemorrhage
  15. 15. HYPERSECRETORY STATES (UNCOMMON) • The following are among hypersecretory states that may, uncommonly, cause PUD: • 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
  16. 16. SYMPTOMS OF PEPTIC ULCER • A number of symptoms are associated with Peptic ulcers. The severity of the symptoms depends on the severity of the ulcer. Each person’s symptoms may vary. In some cases ulcers don’t cause any symptoms. The most common symptom of peptic ulcers is abdominal pain. • The pain is usually in the upper middle part of the abdomen, above the belly button (navel) and below the breastbone. • The ulcer pain can feel like burning, or gnawing, and it may go through to the back. • Pain often comes several hours after a meal when the stomach is empty. • The pain is often worse at night and early morning. • It can last anywhere from a few minutes to several hours. • The ulcer pain may be relieved by food, antacids, or vomiting.
  17. 17. MANAGEMENT OF PUD • Treatment of peptic ulcers varies depending on the etiology and clinical presentation. The initial management of a stable patient with dyspepsia differs from the management of an unstable patient with upper GI hemorrhage. In the latter scenario, failure of medical management not uncommonly leads to surgical intervention. • Given the current understanding of the pathogenesis of PUD, most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance of NSAIDs, along with the appropriate use of antisecretory therapy.
  18. 18. PHARMACOTHERAPY The aims of pharmacotherapy are to: • • Relieve symptoms, by neutralizing acid or reducing acid secretion; • • Promote healing, by enhancing mucosal resistance, eliminating bacterial gastric infection and reducing acid secretion. • Ulcers are intrinsically self-healing if the imbalance between erosive and protective factors can be corrected. Healed ulcers are often found at postmortem examination in individuals with no prior ulcer history. With the exception of sucralfate and bismuth chelate, ‘ulcerhealing’ drugs do not actually heal or stimulate repair, but correct the imbalance and so promote natural healing. About one- third of ulcers remit spontaneously.
  19. 19. APPROACHESFOR TREATMENTOF PUD 1. REDUCING OF GASTRIC ACID SECRETION a. H2 antihistamines: Cimetidine, Ranitidine, Famotidine, Roxatidine b. Proton pump inhibitors: Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, Rabeprazole c. Anticholinergic: Pirenzipine, propantheline, Oxyphenonium d. Postaglandin analogue: Misoprostol 2. NEUTRALIZATION OF GASTRIC ACIDS (ANTACIDS) a. Systemic: sodium bicarbonate, sodium citrate b. Nonsystemic: magnesium hydroxide, mag. Trisilicate, Alluminium hydroxide 3. ULCER PROTECTIVES Sucralfate, colloidal bismuth subcitrate 4. Anti.H. PYLORI DRUGS Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline
  23. 23. DIET • A special diet is not indicated for patients with peptic ulcer. Its common sense approach to avoid any food or beverages that may aggravate symptoms. • Although the link between duodenal ulcers and alcohol is inconclusive, moderation of alcohol intake maybe recommended for other health reasons • AND YES AVOID SPICY FOOD
  24. 24. COMPLICATIONS OF PEPTIC ULCER • Refractory, symptomatic peptic ulcers, though rare after eradication of H pylori infection and the appropriate use of anti secretory therapy, are a potential complication of PUD • Patients with gastric ulcers are also at risk of developing gastric malignancy. • H pylori is associated with atropic gastritis, which in turn, predisposes to gastric cancer • H pylori is associated with gastric lymphoma or mucosa associated lymphoid tissue (MALT)