PEPTIC ULCER DISEASE.pptx
- 2. INTRODUCTION • Peptic Ulcer is a lesion in the lining (mucosa) of the digestive tract, typically in the stomach or duodenum, caused by the digestive action of pepsin and stomach acid. • Lesion may subsequently occur into the lamina propria and submucosa to cause bleeding. - • Most of peptic ulcer occur either in the duodenum, or in the stomach. • Ulcer may also occur in the lower esophagus due to reflexing of gastric content
- 4. • Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury.
- 5. ETIOLOGY RISK FACTORS • Lifestyle • Smoking • Acidic drinks • Medications • • H. Pylori infection • - 90% have this bacterium • Passed from person to person (fecal-oral route or oral-oral route) • Age • Duodenal 30-40 • Gastric over 50 • Gender • Duodenal: are increasing in older women • Genetic factors • More likely if family member has HX • Other factors: stress can worsen
- 9. INVESTIGATION/DIAGNOSTIC TEST • Stool examination for fecal occult blood. • Complete blood count (CBC) for decrease in blood cells • DIAGNOSTIC TEST -Esophagogastrodeodenoscopy (EGD) • Endoscopic procedure-Visualizes ulcer Ability to take tissue biopsy to R/O cancer and diagnose H. pylori - Upper gastrointestinal series (UGI) • • Barium swallow • X-ray that visualizes structures of the upper GI tract • Urea Breath Testing • Used to detect H.pylori • Client drinks a carbon-enriched urea solution • Exhaled carbon dioxide is then measured.
- 10. Complications of Peptic Ulcers • Hemorrhage • Blood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wall • Coffee ground vomitus or occult blood in tarry stools • Perforation • An ulcer can erode through the entire wall • Bacteria and partially digested food spill into peritoneum=peritonitis • Narrowing and obstruction (pyloric) • Swelling and scarring can cause obstruction of food leaving stomach=repeated vomiting
- 11. Management • LIFE STYLE MODIFICATION • HYPOSECRETORY DRUG THERAPY • H. pylori ERADICATION THERAPY • SURGERY • 1- LIFE STYLE MODIFICATION • Discontinue NSAIDs • Smoking cessation. • Alcohol cessation. • Stress reduction
- 12. 2-HYPOSECRETORY DRUG THERAPY Proton Pump Inhibitors • Suppress acid production H2-Receptor Antagonists • Block histamine-stimulated gastric secretions • Zantac, Pepcid Antacids • Neutralizes acid and prevents formation of pepsin (Maalox, Mylanta) Give 2 hours after meals and at bedtime Prostaglandin Analogs • Reduce gastric acid and enhances mucosal resistance to injury • Cytotec Mucosal barrier fortifiers • Forms a protective coat • Carafate/Sucralfate
- 13. 3-H. pylori ERADICATION THERAPY • H. pylori Eradication Therapy:Triple therapy: • Proton pump inhibitor • > 2 Antibiotics: • Metronidazole + Clarithromycin. • Clarithromycin + Amoxicillin. 4-SURGICAL TREATMENT Indications: Failure of medical treatment. • Development of complications • High level of gastric secretion and combined duodenal and gastric ulcer. • Principle: Reduce acid and pepsin……. • Types of Surgical Procedures • ANTRECTOMY/ SUBTOTAL GASTRECTOMY • Lower half of stomach (antrum) makes most of the acid • Removing this portion (antrectomy) decreases acid production • SUBTOTAL GASTRECTOMY • Removes ½ to 2/3 of stomach • Remainder must be reattached to the rest of the bowel • Billroth I-Distal portion of stomach removed and anastomosed with duodenum • Billroth II-Lower portion of stomach is removed and anastomosed with jejunum
- 14. H.pylori • Epidemiology-More than half the world's population is infected. • Africa has the highest pooled prevalence (70.1%); Northern America (37.1%) and Oceania (24.4%) have the lowest prevalence • H. pylori prevalence differs by ethnicity in the U.S.: • Non-Hispanic whites: 18.4 - 26.2% • Nonwhites: 34.5 - 61.6% • Native American / Alaskan Native: 75.0% • H. pylori prevalence reflects the level of urbanization, sanitation, access to clean water and varied socioeconomic status • In children, the most frequent transmission route is from mother to child
- 16. • Sites Organisms colonize the antrum first by binding to gastric mucins (TFF1) in a pH dependent manner; the organisms have affinity for gastric mucous cells but do not attach to small intestinal or other gastric epithelial cell types • Ideal pH for bacteria survival: 4 - 8 • Ideal pH for bacterial growth: 6 - 8
- 17. Pathophysiology • Major virulence factors: CagA (cytotoxin associated gene A) and its pathogenicity island (Cag PAI) and VacA (vacuolating cytotoxin A) • CagA and Cag PAI: • Translocates to the host cytoplasm and binds to the inner surface of the cell membrane • Major effects: disrupts tight junctions, provokes proinflammatory and mitogenic response • VacA: • Cytochrome c release and activation of proapoptotic factor leading to apoptosis • Gastric inflammation is a result of H. pylori infection mediated upregulation of cytokines; most significant are: • CagA PAI mediated induction of NFκB and IL8 secretion • Reactive oxygen species and reactive nitrogen species produced by host gastric epithelial cells
- 18. Etiology Pathogenic species in humans: • Helicobacter pylori, Helicobacter heilmannii • Taxonomy: • Campylobacterales (order); Helicobacteraceae (family); Helicobacter (genus) • Characteristic features: • Gram negative • Helical or spiral shaped • Flagellate • 3 physiologic states or forms of H. pylori: • Vegetative / proliferative: S shaped, culturable and viable, capable of replication • Dormant: C / U shaped, reversible state, not obviously viable but culturable, transformation induced at low pH (< 6) • Coccoid: nonviable
- 19. Clinical features • Asymptomatic or mild self limited dyspeptic symptoms with transient hypochlorhydria - acute gastritis • Abdominal pain seen with chronic gastritis with or without peptic ulcer disease • Extragastrointestinal manifestations: iron deficiency anemia, idiopathic thrombocytopenic purpura, vitamin B12 deficiency
- 20. Diagnosis
- 21. Laboratory • Invasive (endoscopic) and noninvasive techniques: • Endoscopic diagnosis: • Biopsy urease test: sensitivity and specificity, 90% and 95% • Histology: sensitivity and specificity, 95% and 98% • Bacterial culture and sensitivity test: high specificity, low sensitivity as H. pylori is difficult to culture • Noninvasive testing: • Urea breath test: sensitivity and specificity, 88 - 95% and 95 - 100% • Stool antigen test: sensitivity and specificity, 94% and 97% • Serology: sensitivity and specificity, 85% and 79% • Eradication confirmation recommended; tests recommended: urea breath test, stool antigen testing or endoscopy based testing • Other infrequently used tests: • 13C urea assay: serodiagnostic test using a 13C urea assay • Polymerase chain reaction: used to detect low bacterial loads and identify specific mutations associated with antimicrobial resistanc
- 22. • Treatment • Bismuth quadruple (PPI, bismuth subcitrate, tetracycline and metronidazole) or levofloxacin triple (PPI, levofloxacin, amoxicillin), rifabutin triple (PPI, rifabutin and amoxicillin • Decision made based on risk factors for macrolide resistance and the presence of a penicillin allergy
- 23. STAINS • Easily recognized on routine H&E stain, upfront H. pylori immunohistochemistry not recommended • Immunohistochemistry and special stains: histochemical stains do not distinguish H. pylori from other bacteria and immunohistochemical antibodies against H. pylori cross react with H. heilmanni • Immunohistochemistry: most common, associated with low false positive rare, also stains coccoid forms • Silver based stains: Warthin-Starry, Steiner, El-Zimaity dual stain, Genta • Nonsilver based stains: Diff-Quik, Giemsa, Leung Alcian yellow • Gastrointestinal Pathology Society (GIPS) offers recommendations for ancillary stains in detecting H. pylori when evaluating gastric biopsies
- 24. TYPHOID • INTRODUCTION • Enteric fever, also known as typhoid fever. • Typhoid fever is an acute illness associated with fever caused by the Salmonella typhi bacteria. It can also be caused by Salmonella paratyphi, a related bacterium that usually causes a less severe illness. • Major cause morbidity and mortality. • Food water borne disease. • The bacteria are deposited in water or food by a human carrier and then spread to other people
- 25. CAUSES • BACTERIA • Cause by Bacteria - Salmonella Typhi. • Family-Enterobacteriacea. • Gram negative bacilii. • Best grows at 37 C. • TRANSMISSION • faecal-oral route. • close contact with patients or carriers. • contaminated water and food. • flies and cockroaches.
- 26. PATHOPHYSIOLOGY
- 29. COMPLICATION • BOWEL • Perforation • Hemorrhage • SEPTICAEMIC FOCI • Bone and joint infection • Meningitis • Cholecystitis • TOXIC PHENOMENA • Myocarditis • Nephritis • CHRONIC CARRIAGE • Persistent Gallbladder Carriage
- 34. TYPHOID ULCER • One of the complication of typhoid fever There are several obvious lesions, which are shaped like Peyer's patches. The organism, Salmonella typhi, accumulates in lymphoid tissue in Peyer's patches and causes the patches to become inflamed and ulcerated. • Why are typhoid ulcers longitudinal? • Necrosis of the overlying mucosa causes linear ulcers which are oriented parallel to the longitudinal axis of the ileum. Following the primary enteric phase of the disease, bacteremia occurs with subsequent involvement of the reticuloendothelial elements of the spleen, lymph nodes, liver, skin and gall- bladder.
- 35. • How is typhoid ulcer diagnosed? • On colonoscopy, typhoid fever-related gastrointestinal ulcers appear as multiple, ovoid, variable-sized punched out lesions. The edges are soft, swollen and irregular . Intestinal perforation occurs commonly near the ileo-caecal valve, where the ulcers become deeper than elsewhere.