peptikulser

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1.Introduction of ulcer Etiology General consideration: No Acid No Ulcer Main Destroy Factors: HCl, Pepsin, Hp Protective Barrier: Mucus-HCO3 - Physiology HCl: P-cell, H2, M1, G-R, H + -pump 2. Peptic Ulcer The term “peptic ulcer” refers to an ulcer in the lower Oesophagus, stomach, duodenum (commonly), jujenum and ileum (rarely) Gastric and duodenal ulcers may be acute or chronic Acute ulcer shows no evidence of fibrosis Both penetrate the muscularis mucosae Erosions do not penetrate the muscularis mucosae 3. Production of Gastric acid Secretion of gastric acid, mucus and bicarbonate. The control of the gastrointestinal tract is through nervous and humoral mechanisms. Acid is secreted from gastric parietal cells by a proton pump (K + /H + ATPase). The three endogenous secretagogues for acid are histamine, acetylcholine and gastrin. Prostaglandins E 2 and I 2 inhibit acid, stimulate mucus and bicarbonate secretion, and dilate mucosal blood vessels. The genesis of peptic ulcers involves: infection of the gastric mucosa with Helicobacter pylori.

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peptikulser

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PENGARUH PEMBERIAN OBAT-OBAT SARAF OTONOM: EPINEFRIN, PROPRANOLOL, PILOKARPIN, DAN ATROPIN TERHADAP SISTEM SARAF SIMPATIS DAN PARASIMPATIS PADA MENCIT (Mus musculus)

1.Introduction of ulcer Etiology General consideration: No Acid No Ulcer Main Destroy Factors: HCl, Pepsin, Hp Protective Barrier: Mucus-HCO3- Physiology HCl: P-cell, H2, M1, G-R, H+-pump 2. Peptic Ulcer The term peptic ulcer refers to an ulcer in the lower Oesophagus, stomach, duodenum (commonly), jujenum and ileum (rarely) Gastric and duodenal ulcers may be acute or chronic Acute ulcer shows no evidence of fibrosis Both penetrate the muscularis mucosae Erosions do not penetrate the muscularis mucosae

3. Production of Gastric acid Secretion of gastric acid, mucus and bicarbonate. The control of the gastrointestinal tract is through nervous and humoral mechanisms. Acid is secreted from gastric parietal cells by a proton pump (K+/H+ ATPase). The three endogenous secretagogues for acid are histamine, acetylcholine and gastrin. Prostaglandins E2 and I2 inhibit acid, stimulate mucus and bicarbonate secretion, and dilate mucosal blood vessels. The genesis of peptic ulcers involves: infection of the gastric mucosa with Helicobacter pylori. an imbalance between the mucosal-damaging (acid, pepsin) and the mucosal-protecting agents (mucus, bicarbonate, prostaglandins E2 and I2

4. H-2 Reseptor Antagonist Pharmacotherapeutics: Used therapeutically to: Promote healing of duodenal and gastric ulcers. Provide long-term treatment of pathological GI hypersecretory conditions. Reduce gastric acid production and prevent stress ulcers.Unwanted effects are rare

5. Proton Pump Inhibitors Pharmacotherapeutics: Indicated for: Short term treatment of gastric ulcers Active duodenal ulcers and peptic ulcers (H. pylori) Erosive esophagitis GERD Hypersecretory states Unwanted effects of this class of drugs are uncommon. They may include headache, diarrhoea (both sometimes severe) and rashes. Dizziness, somnolence, mental confusion, impotence, gynaecomastia, and pain in muscles and joints have been reported. Proton pump inhibitors should be used with caution in patients with liver disease, or in women who are pregnant or breast feeding. The use of these drugs may 'mask' the symptoms of gastric cancer.

6. Antimuscarinics Drugs M1 receptors antagonists : Pirenzepine, telenzepine (a more potent analog), reduce gastric acid secretion with fewer adverse effects than atropine and others. Contraindicated in some gastric ulcers as they may slow gastric emptying and prolong the exposure of the ulcer bed to acid.

7. Antacids Pharmacotherapeutics: Prescribed to relieve pain and promote healing in peptic ulcer disease. Also used to relieve symptoms of acid indigestion, heart-burn, dyspepsia, or GERD. Also used to prevent stress ulcers, GI bleeding, and hyperphosphatemia in kidney failure.

8. Mucosal Protective Agents Sucralfate is a complex of aluminium hydroxide and sulfated sucrose, which releases aluminium in the presence of acid. The residual complex carries a strong negative charge and binds to cationic groups in proteins, glycoproteins, etc. It can form complex gels with mucus, an action that is thought to decrease the degradation of mucus by pepsin and to limit the diffusion of H+. Sucralfate can also inhibit the action of pepsin and stimulate secretion of mucus, bicarbonate and prostaglandins from the gastric mucosa. All these actions contribute to its mucosa-protecting action. Unwanted effects are few, the most common being constipation, which occurs in up to 15% of patients treated. Less common effects include dry mouth, nausea, vomiting, headache and rashes. It should be used with caution in pregnancy, when breast feeding, or in patients for whom enteral feeding is in progress

9. Prostaglandins Analogue Prostaglandins of the E and I series have a generally protective action in the gastrointestinal tract, and a deficiency in endogenous prostaglandin production (after ingestion of a NSAID, for example) may contribute to ulcer formation. Misoprostol is a stable analogue of prostaglandin E1. It is given orally and is used to promote the healing of ulcers or to prevent the gastric damage that can occur with chronic use of NSAIDs. Unwanted effects include diarrhoea and abdominal cramps; uterine contractions can also occur, so the drug should not be given during pregnancy (unless deliberately to induce a therapeutic abortion

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Obat antiemetic

Caused by Nerveous or humoral mechanismCaused by H. Pilory