GI Pharmacology. Dr. Alia Shatanawi 5/4/2018

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1 GI Pharmacology Dr. Alia Shatanawi 5/4/2018

2 Drugs Used in Gastrointestinal Diseases Drugs used in Peptic Ulcer Diseases. Drugs Stimulating Gastrointestinal Motility &Laxatives. Antidiarrheal Agents. Drugs used in Irritable Bowel Syndrome. Antiemetic Agents. Drugs used in Inflammatory Bowel Disease. Pancreatic Enzyme Supplements. Bile Acid Therapy for Gall stones. Drugs used in Variceal Hemorrhage.

3 Upper GI Drugs Peptic ulcer is a defect in the lining of the stomach or the duodenum

4 Causes of Peptic Ulcer The most common cause is infection of the stomach by bacteria called Helicobacter pylori (H.pylori). Ulcers can also be caused or worsened by drugs such as aspirin, ibuprofen, and other NSAIDs Other factors: Smoking, Stress, Spices (diet) and alcohol. Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors

5 Treatment Approach Peptic ulcer 1. Reduce acid secretion from parietal cells 2. Neutralize acid in the lumen 3. Protect the mucosa from acid destruction 4. Antibiotics to eradicate Helicobacter pylori

6 Physiology of gastric secretion HCl Gastrin Histamine Pepsin

7 Three pathways control parietal cell acid secretion

8 Acetylcholine receptor pathway Sight, smell, taste of food cause stimulation of vagal nerve to release acetylcholine. Ach binds to M3 receptor and Ca i rises activating phosphokinases H + K + ATPase translocates to the secretory canaliculus. K + in extracellular space exchanged for H +. Cl - diffuse across cell membrane to form HCl in canaliculus. Ach increases gastrin and histamine release.

9 Gastrin receptor pathway Digested food in stomach stimulates release of gastrin from G cells in antrum of stomach; distention releases Ach increasing gastrin levels. Gastrin binds to CCK-B receptor and Ca i rises activating phosphokinases. H + K + ATPase translocates to the secretory canaliculus. K + in extracellular space exchanged for H +. Cl - diffuse across cell membrane to form HCl in canaliculus. Gastrin increases histamine release.

10 Histamine receptor pathway Ach and gastrin release stimulates ECL cells to release histamine. Histamine binds to H 2 receptor and Ca i and camp rises activating phosphokinases. H + K + ATPase translocates to the secretory canaliculus. K + in extracellular space exchanged for H +. Cl - diffuse across cell membrane to form HCl in canaliculus.

11 Antacids Were used long time ago, and were mainstay of treatment. Nonprescription remedies. Are weak bases that react with gastric HCl to form salt and water. Also stimulate mucosal prostaglandin production, therefore may promote mucosal defense mechanisms.

12 Antacids Given after a meal, can neutralize acidity for up to 2 hours. Efficacy varies according to rate of dissolution, water solubility, rate of reaction with acid and the rate of gastric emptying. May affect the absorption of other medications by binding to drugs or by changing ph, therefore, dissolution.

13 Antacids Sodium Bicarbonate (Baking Soda): Reacts rapidly with acid to produce NaCl and CO2. CO2 leads to gastric distension and belching. NaCl may exacerbate fluid retention. Systemic absorption leads to metabolic alkalosis.

14 Antacids Magnesium Hydroxide. Aluminum Hydroxide. React slowly and without gas formation. Metabolic alkalosis is also uncommon. Mg salts cause diarrhea. Aluminum salts cause constipation. Usually given in combination. Contraindicated in renal insufficiency.

15 Neutrolization of acid Antacids Aluminum antacids absorb or chelate many drugs; most common used. Magnesium antacids have laxative action; diarrhea. Calcium antacids stimulates acid rebound by promoting gastrin release. Sodium antacids should be avoided; aggravate CHF and counteracts diuretic therapy for HBP, short duration of action, followed by acid rebound, highly absorbed.

16 H 2- Receptor Antagonists(1970s-1990s) Cimetidine, prototype, many problems. Ranitidine. Famotidine. Nizatidine. Were the most commonly prescribed drugs in the world.

17 H 2- Receptor Antagonists(1970s-1990s) Selective competitive inhibitors of the parietal cell H 2 receptors and suppress basal and meal-stimulated acid secretion in a dosedependent manner. Also decrease volume of secretion and pepsin concentration. Decrease secretion stimulated by: Histamine. Gastrin. Acetylcholine.

18 H 2- Receptor Antagonists(1970s-1990s) Duration of action: 12 hours. Inhibit 60-70% of total 24-h acid secretion. 90% of nocturnal acid. 60% of day-time and meal- stimulated acid..

19 H 2 Receptor Antagonists Competitively inhibit the interaction of histamine with H 2 receptors. Selective for H 2 over H 1 receptors; appear to only interfere with H 2 physiological functions on gastric acid secretion. Well-absorbed orally and reach peak serum concentration in 1-3 hours. Found in cerebrospinal fluid, cross placental barrier, and excreted in breast milk.

20 H 2 Receptor Antagonists Developed in 1970 s. Inhibit basal (fasting) and nocturnal acid secretion. Decreases volume of gastric juice and [H + ]. Decreases acid secretion stimulation by food, distention, and pharmacological agents. Used for Zollinger-Ellison syndrome, ulcers, GERD. OTC preparations advertised for heartburn. Histamine Cimetidine (many side-effects) Ranitidine Famotidine (Most potent) Nizatidine

21 Cimetidine (Tagamet) Inhibits cytochrome P450 activity; will slow down metabolism of other drugs. Anti-androgen activity; loss of libido, impotence Increases plasma estradiol in men; increases secretion of prolactin. CNS effects in elderly with systemic illnesses; confusion, agitation, lethargy.

22 H 2- Receptor Antagonists Duration of action: 12 hours. Inhibit 60-70% of total 24-h acid secretion. 90% of nocturnal acid. 60% of day-time and meal- stimulated acid.

23

24 H 2- Receptor Antagonists Clinical Uses: Gastroesophageal Reflux: Prophylactically, before meals. Afford healing for erosive esophgitis in less than 50% of patients. Proton pump inhibitors are preferred. Non Ulcer Dyspepsia. Stress- Related Gastritis: Can prevent bleeding, usually given IV.

25 H 2- Receptor Antagonists Peptic Ulcer Disease: Replaced by PPI. Healing rate greater than 80-90% after 6-8 weeks. Not effective in the presence of H. pylori infection. Not effective if NSAID is continued.

26 Adverse Effects: H 2- Receptor Antagonists Extremely safe drugs, but can (in 3% of patients) cause diarrhea, headache, fatigue, myalgia and constipation. CNS: Confusion, hallucinations and agitation occur only with IV cimetidine to elderly patients in ICU.

27 Adverse Effects: H 2- Receptor Antagonists Endocrine Effects: Again only with cimetidine, can inhibit DHT binding to its receptor, estradiole metabolism, and can increase prolactin serum levels. Pregnancy and Nursing Mothers: Can cross placental barrier and appear in breast milk. Other Effects: Rarely can cause blood dyscrasias, bradycardia and hypotension.

28 H 2- Receptor Antagonists Drug Interactions: Cimetidine can inhibit cytochrome P450 enzymes(cyp1a2, CYP2C9, CYP2D6, and CYP3A4), so can increase half life of many drugs. Ranitidine binds 4-10 times less. Nizatidine and famotidine binding is negligible.

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