Peptic Ulcer (a).pdf

Layers of stomach wall Ulcer spit blood Removed with stool Malena: = dark stool look About 15% of patients with active PUD Bleeding About 7% of patients with active PUD Major complications of PUD Perforation About 6% - 10% Mortality from acute bleeding Mortality is a gram negative, flagella...

Layers of stomach wall Ulcer spit blood Removed with stool Malena: = dark stool look About 15% of patients with active PUD Bleeding About 7% of patients with active PUD Major complications of PUD Perforation About 6% - 10% Mortality from acute bleeding Mortality is a gram negative, flagellated bacteria. Found in About 95% of those with duodenal ulcers Helicobacter pylori (HP): Found in About 80% of those with gastric ulcers Above 60 > 50-60% and Children <12 years 10-15%. Approx. 30- 40% of the U.S. population is infected About 15% of those infected will develop PUD. Helicobacter Pylori (HP)Associated PUDs HP catalyzes urea -> ammonia is produced -> ammonia erodes the mucous barrier and causes epithelial damage ⬆ Physiology of Acid secretion superficial, does not penetrate the mucosa Erosions less than 2 weeks, Acute deeper lesions, penetrates beyond the muscularis mucosa Ulcers Classification of Peptic Lesions not associated with any fibrotic reaction in the submucosa more than 2 weeks Chronic and associated with fibrosis and formation of granulation tissue Inflammation Gastric cancer? 3rd leading cause death Ulcerative disorders of the upper gastrointestinal tract Peptic ulcers: Intro: involving principally the most proximal portion of the: duodenum stomach (posterior) Duodenal Ulcer (intestine) Major types Gastric Ulcer (stomach) Most common form of PUD It is 3 times more common than gastric ulcers Visuals: -> H+ ions are liberated and cause cellular damage. at gastric pH – cross into gastric epithelial cells Reduction in gastric and mucosal blood flow Decrease in mucous and bicarbonate secretion Usually located in the duodenal bulb of the small intestine Duodenal Ulcer: Most commonly occurs in people between the ages of 30 and 50 NSAIDs are weak acids and are non-ionized NSAIDs inhibit cyclooxygenase activity and therefore decrease prostaglandin production which results in a: Overview: Less common than duodenal ulcers Especially in the absence of chronic NSAID use Decrease in cellular repair and replication Gastric Ulcer: (cause gastric ulcer) antrum of the stomach (high in here) Most commonly located in the lesser curvature of the but can appear in body More common in people greater than 60 years old Acid (HCL) Pepsin (active -> pepsinogen/ inactive) Aggressive factors: Bile Mechanisms: NSAID-Induced PUD Helicobacter pylori Aspirin , NSAID Pathogenesis of Peptic Ulcer Disease: Gastric mucus Peptic Ulcer (a) Mucus Gel layer Bicarbonate Visuals: Mucosal blood flow Endogenous PGs Age > than 60 years old With a prior history of PUD What can we give? HIgh dose NSAIDs or multiple NSAIDs. even low dose aspirin Cell restitution The come over (not turn over) mechanism – Helicobacter pylori (H.pylori) infection Risk of developing an NSAIDrelated complications is greater in patients: – Nonsteroidal Antiinflammatory Drugs (NSAIDs) Common causes of PUD – Critical illness (stress-related mucosal damage-SRMD) Corticosteroids Concurrent medications Anticoagulants and Anti-platelet agents Produced by prostaglandins Mucosal barrier Defensive factors: 1% - 2% of NSAID users develops ulcer with in 1 year Misprostol (PGE inhibitor) +/or Celecoxide (selective COX-2 inhibitor) So NSAID will have less bicarbonate – Idiopathic (non-H.pylori, nonNSAID) Etiology and Pathophysiology Oral bisphosphonates – Hypersecretion of gastric acid SSRIs (Selective Serotonin Reuptake Inhibitors) Uncommon causes of PUD – Viral infections gastric acid hypersecretion – Radiation therapy recurrent peptic ulcers – Chemotherapy ZES is characterized by: that result from a gastrinproducing tumor 3-4 cm most common (2 cm) Zollinger-Ellison Syndrome (ZES) Chronic and recurrent disease More than 50% of gastrinomas are malignant Deep and sharply demarcated Ulcer risk is proportional to the number of cigarettes per day > 95% in the duodenal bulb Duodenal Ulcer 6-15% of western populations Cigarette smoking: Impairs ulcer healing and increases the risk of recurrence Spontaneous healing and recurrence PUD tend to be more adversely affected by stress smoking the use of NSAIDs, alter inflammatory response Natural history Stress may induce behavioral risks that increases Other Potential Factors in the Development of PUD Occurrence: resistance to HP infection – Foods: Coffee, tea, carbonated beverages, beer, milk, spices) may cause dyspepsia but do not increase the risk of developing PUD Gastric Ulcer Dietary factors: visualizing the ulcer crater by upper GI endoscopy Imaging and Endoscopy: – Rapid urease testing – good in active bleeding cases Invasive testing: endoscopy with biopsy – at least 5 samples (from stomach) at or near the right-hand region of the stomach and most frequently on the posterior wall. Appears as an eroded or "punched out" area of mucosa surrounded by inflamed and swollen tissue. 3 - 8% / 5% that are radiographically benign are malignant. Stimulated by Diagnosis Gastric mucus gel layer: Expensive Not tell you eradication Intercellular tight junctions Gastric mucosal barrier: Luminal surface Tests for Helicobacter pylori: – Serological antibody detection test bile acids, Pathogenesis of PUD: Defensive Almost impermeable to H ion back diffusion • Interrupted by When does antibodies develop? salicylates, alcohol, weak organic acids Expensive Rapid cholinergic stimulation Increased by prostaglandin Cheap After 3 weeks of infection mechanical & chemical irritation Slows down ionic diffusion (Hemostatic local application of -> Epinephrine ) not accurate (Most last part) / pylorus sphincter Malignant- lesser curve (antrum area), larger ulcers – Histology – Culture Recurrence may be asymptomatic 60% of GU are located within 6 cm of the pylorus, Psychological stress: Show size , location + everything (e.g. Zollinger Ellison syndrome) – Urea breath test: 14C isotopes Noninvasive testing: Aspirin + NSAIDs Accurate Ionic-Trap: – Fecal antigen test – useful in children If he is taking (Sucralfate) So need a test before 4 weeks Penetration layers in gastric So more absorption of acidic drugs Cause ulcer Symptoms depends on location, etiology, and age. HP Sensitivity: Wash up period before + PPI need 3 weeks Elderly, have few or even no symptoms Pain in the epigastrium is the most common (subastrium) symptom Signs and Symptoms Described as burning, cramping, or hunger The severity of pain more often in the spring or fall. fourthsemester Pain episodes occur in clusters - lasts a few weeks. Heartburn, Along with pain also: belching, bloating. Gastric acid is continuous & produce abnormally !