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• Overview
  • Classification of peptic ulcers
• Gastric Physiology
• Gastric Mucosa-Acid Secretion
  • oxidative phosphorylation
  • Regulation of Gastric Acid Secretion
    • Gastrin-stimulatory
    • Vagal effects-stimulatory
    • Role of Histamine
    • Parietal Cell Membrane Receptors
• Physiological Stumulants of Gastric Acid Secretion
  • Food
    • Cephalic
    • Gastric
    • Intestinal

• Physiological Inhibition of Gastric Acid Secretion
  • Factors
  • Somatostatin Effects
• Role of Pepsin in Peptic Ulcer Disease
• Pathogenic Factors
  • Helicobacter Pylorii
  • H. Pylorii Management: Clinical Efficacy
  • Other Pathogenic Factors

Drug Treatment

• Helicobacter pylorii
• Bismuth
• Triple Therapy
  • Drawbacks of Triple Therapy
• Antacids
• H₂ Receptor Antagonists
• Anticholinergic Drugs
• Coating Agents
  • Sucralfate
  • Colloidal Bismuth
• Prostaglandins
• Proton Pump Inhibitors

Other GI Drugs 

• Gastrokinetic Agents
• Antacids (used as preoperative medication)
• Antiemetic Drugs

Overview

• Peptic ulcer: stomach or duodenal mucosal lesion -- acid and pepsin: major pathogenic roles
• Classification of peptic ulcer:
  • Duodenal (DU)
  • Gastric (GU)
• Major causative factor:bacterium Helicobacter pylori
•  Helicobacter pylori: risk factor for:
  • gastric cancer
  • certain types of gastric lymphoma
•  Zollinger-Ellison syndrome {causative agent-gastrin-secreting islet cell tumor (gastrinoma)} -- considered a form of peptic ulcer
•  Ulcer Development:
  • cause by an imbalance between aggressive factors (mainly gastric acid and pepsin) and protective factors (mucosal defenses)

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Gastric Physiology

• Gastric mucosa: acid secretion
  • Oxidative phosphorylation dependent secretion by parietal cells.
    • Parietal cells: found in mucosal glands
    • of the body and fundus of the stomach.

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  • Regulation of gastric acid secretion-- many factors (chemical, neural, hormonal)
    • Stimulation:
      1. Gastrin-most potent stimulant
      2.  Activation of postganglionic vagal fibers (muscarinic cholinergic parietal cells receptor activation)
      3. Role of histamine:
         • Gastric mucosa contains large amounts of histamine in:
           1. mast cell cytoplasmic granules
           2. enterochromaffin-like cells (ECL)
         • H₂ receptor antagonists competitively inhibit histamine action on H₂ receptors, located on:
           1. gastric parietal cells
           2. cardiac atrial cells
           3. uterine smooth muscle cells
         • H₂ receptor antagonists (cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid)) inhibit:
           1. basal acid secretion
           2. secretion in response to feeding, gastrin, histamine, hypoglycemia, or vagal stimulation
         • Histamine is the most important gastric acid secretion stimulant and is released from enterochromaffin-like cells by gastric and cholinergic activity
      4. Basolateral parietal cells membranes contain receptors for:
         • histamine-- stimulation gastric acid secretion
         • gastrin-- stimulation gastric acid secretion
         • acetylcholine-- stimulation gastric acid secretion
         • prostaglandins --inhibition of gastric acid secretion
         • somatostatin -- inhibition of gastric acid secretion

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H₂ Histamine receptor blockers

• cimetidine (Tagamet)

• ranitidine (Zantac)

• famotidine (Pepcid)

•  nizatidine (Axid)

Antimuscarinic drugs

• Atropine

• Propantheline

• Pirenzepine

Proton pump inhibitor

• omeprazole (Prilosec)

• lansoprazole (Prevacid)

Mucosal protective agents

• sucralfate (Carafate)

• misoprostol (Cytotec)

Antidiarrheal drugs

• Diphenoxylate

• Kaopectate

• Bismuth Subsalicylate

• Loperamide

• Paragoric

Laxative Drugs

• Bisacodyl

• Magnesium Hydroxide

• Mineral Oil

• Docusate

• Lactulose

• Methyl Cellulose

• Psyllium

Antacids

• Magnesium hydroxide
• Aluminum hydroxide
• Calcium carbonate

Drugs that dissolve gallstones

• Chenodiol

• Monoctanoin

Drugs acting on G.I. motility

• Bethanechol

• Metoclopramide