Peptic ulcer disease

PEPTIC ULCER DISEASE --Dr. Mansi

What is PEPTIC ULCER????? Breaks in mucosal surface >5mm in size Depth till submucosa In any part of GI tract exposed to aggressive action of acid pepsin juices. Can be acute or chronic Both can penetrate muscularis mucosae..

SITES Gastric and duodenal – 98 % Ratio of 1:4 Duodenum:1 st part >95% :ant & post walls Gastric :junctn b/w antrum &acid secr. mucosa :lesser curvature

Pathomorphology Round Punched out craters 2 to 4 cm diameter Margins – Perpendicular - No Elevatn or Beading Mild oedema of immediate adj. mucosa Surrounding Mucosal folds Radiate like Wheel Spokes Base Remarkably Clean

Duodenal ulcer Gastric ulcer Patho physiology Major causes Gastric acid Gastric emptying increasd decreased rapid delayed Bicarbonate secretion remarkably decreased H.pylori & NSAID H.pylori & NSAID Abnormal resting & stimulated Pyloric sphincter pressure

ETIOLOGY Predisposing factors Age :young in DU and peak inc. at 6 th decade in GU. Sex :GU commoner in males Causes H.Pylori NSAID Infection: CMV,herpes simplex,etc.. Other drug/toxin: bisphosphonates, chemo, clopidogrel , glucocorticoids Misc.:crohn,neoplasm,ashemia,infiltrating diseases,duodenal obstruction,etc..

Smoking Genetic : increased freq of blood group O and non secretor status Stress Diet : alcohol and caffeine Associations Systemic mastocytosis CRF, nephrolithiasis Hyperparathyroidism Cirrhosis Alpha antitrypsin deficiency CAD, pancreatitis, polycythaemia vera Pathogenetic factors not related to h.pylori & NSAID

Gram –ve S-shaped , flagellate Lies b/w mucous layer & gastric epithelium 1 st antrum then proximal segments. Dormant state – coccoid form Genome—1500 proteins Transmission:oral-oral/faeco-oral H.pylori

Cytokines-IL 1 α / β , IL6,IL2, IL8(recruits act. neutrophils) TNF- α ,IFN- γ HOST FACTORS Duration Location Apoptosis Cag PAI Mucosal nd systemic humoral response cagA into host cells BACTERIAL FACTORS 1st : Outer membrane proteins 2 nd :gastric residence-- Urease 3 rd :Mucosal damage vacA cagA Pathogenecity island cag Catalase, lipase, adhesins, platelet activating factors Proteases nd phospholipases Breaks glycoprotein lipid complex of mucous gel Damage surface epi. cells inflammatn Chronic gastritis Peptic ulcer Gastric MALT lymphoma Gastric adenocarcinoma V I R U L E N C E Pathophysiology of H.pylori ulcer

Gastric metaplasia Increased acid production Decreased duodenal mucosal bicarbonate production Then how does it cause Ulcers in duodenum?????

Endothelial defects Stasis--ischemia Direct toxicity by Ion trapping Epithelial effects Due to PG depletion HCL mucin bicarbonate Epi. cell proliferation ULCER erosions Healing (spontaneous Or therapeutic) NSAID induced PUD Pathophysiology Epithelial effects Due to PG depletion

Clinical features Abdominal pain * Epigastric Burning or gnawing discomfort* 90 min to 3 h after meal Frequently relieved by antacids or food in DU.* Awakes the pt from sleep b/w midnight & 3 am. Nausea Weight loss Dyspepsia if not relieved by food antacids , radiates to back—penetrating ulcer

Perforation: Gastric outlet obstruction Bleeding Symptom : sudden continuous generalized abd pain Examn : severly tender board like abdomen Common in elderly and with NSAID Penetration Complications Symptoms : Pain worsening with meals, nausea and vomiting of undigested food Examn : succusion splash Symptoms : Tarry stools or coffee ground emesis Acute hematemesis Anemia Examn : tachycardia and orthostasis suggesting dehydration

NUD : non ulcerative dyspepsia D/D OF ULCER LIKE SYMPTOMS Proximal GI tumors Gastro esophageal reflux Vascular disease Pancreaticobiliary disease Crohn’s disease Differential diagnosis

D/D OF EPIGASTRIC PAIN Gastric Duodenal Gall bladder Pancreas Colon Superficial / radicular pain Nervous dyspepsia

Barium studies of proximal GI Endoscopy Tests for detection of H.Pylori Occasionally serum gastrin level gastric acid analysis screen for NSAIDs Non invasive: serology Urea breath test Stool antigen Invasive : rapid urease histology culture Duodenal ulcer Gastric ulcer

Cimetidine 400mg bid Ranitidine 300mg hs Famotidine 40mg hs Nizatidine 300mg hs : Magnesium Hydroxide ,Aluminum Hydroxide , Sodium Bicarbonate , Calcium Carbonate :100 – 150 meq/l 1 & 3 hrs after the meal & hs Acid Suppressing Drugs Antacids H2 Receptor antagonists Proton Pump Inhibitors (PPIs) Omeprazole 20mg/day Lansoprazole 30mg/day Rabiprazole 20mg/day Pantoprazole 40mg/day Esomeprazole 20mg/day

Mucosal Protective Agents Sucralfate Prostaglandin Analogue Bismuth Containing Compounds -Sucralfate – 1gm qid -Misoprostol - 200 μ g qid

Regimens for Eradication Of H.Pylori Triple Therapy Bismuth Subsalicylate + -2 tablets qid Metronidazole + -250mg qid Tetracycline -500mg qid 2 . Ranitidine Bismuth Citrate + -400mg bid Tetracycline + -500mg bid Clarithromycin / Metronidazole -500mg bid

Regimens for Eradication Of H.Pylori 3. Omeprazole + - 20mg bid Claithromycin + -250/500mg bid Metronidazole / -500mg bid Amoxicillin - 1gm bid

Quadruple therapy Treatment of complications Therapy for NSAID injury Surgical Therapy

Surgical Therapy Duodenal Ulcer Vagotomy & Drainage (By Pyroloplasty , Gastrodudenostomy , Gastrojejunostomy) Highly Selective Vagotomy (does not require drainage procedure) Vagotomy with Antrectomy

Surgical Therapy Gastric Ulcer Antral Ulcer – Antrectomy with Billroth I anastomosis Ulcer Excision with Vagotomy & Drainage 3.High GU – Csende’s Procedure Subtotal Gastrectomy with a Roux-en-Y Oesophagogastrojejunostomy Kelling Madlener Procedure antrectomy + intraop. ulcer biopsy + vagotomy

Surgical complications Recurrent ulceration Afferent loop syndromes Dumping syndromes Post vagotomy diarrhea Bile reflux gastropathy Maldigestion & malabsorption Gastric adenocarcinoma

Peptic ulcer disease

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