Rabeprazole 20 medical ppt


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Rabeprazole 20 medical ppt

  1. 1. Rabe. 20 We will discuss  GI system  Acid secretion process  Acid related disorders  Treatment options & limitations  Rabeprazole
  2. 2. The Stomach
  3. 3. The Stomach Stomach consists of 3 parts viz. Fundus, Body and Antrum. Stomach is the part of the GIT, which produces Hydrochloric acid. Functions of HCl are 1.Destroying the bacteria present in the food 2.Chemical breakdown of food 3.Activation of digestive enzyme pepsin
  4. 4. The Stomach FUNDUS: Food enters the upper section of the stomach, called the FUNDUS. Contains rugae folds to help with expansion when food enters stomach, which the main function of the fundus. BODY: It is the middle part of the stomach, which follows after fundus. Food remains here for some time, mixes with gastric juices and then forwarded to the antrum. The body of the stomach consists of majority of secreting cells.
  5. 5. The Stomach ANTRUM: The lower region of the stomach is called as ANTRUM. Grinds up swallowed food and regurgitates the hydrochloric acid that is produced by the fundic and body parietal cells.
  6. 6. Anatomy of Stomach Stomach contain 5 types of Cells Name of the Cell Function Parietal Cell To Secrets HCL G Cell To Secrets Gastrin Chief Cell To Secrets Pepsin Mast Cell To Secrets Histamine Mucus cell To Secrets Mucin
  7. 7. Acid Secretion Acid secretion in the stomach is a continuous process. Acid secretion is increased at the sight or smell of food, at the meal times and during stress.
  8. 8. Acid Secretion There are 3 phases of acid secretion 1. Basal acid secretion: This secretion is devoid of any stimulation and is governed by circadian system of the body 2. Gastrin stimulated acid secretion: In this phase, secretion is initiated by the presence of food in stomach, sight, smell or even thought of food.
  9. 9. Acid Secretion 3. Histamine stimulated acid secretion: Mast cells secrete histamine. Stress and tensions influence secretion of histamine. This secretion is controlled by vagal stimulation.  Vagal stimulation also releases acetylcholine. These in turn stimulate histamine (H2) and muscarinic receptors respectively present on the parietal cells leading to increased gastric acid secretion.
  10. 10. Formation of HCL
  11. 11. Role of HCL  Strongly acidic fluid - Kills many microbes in food  Stimulates the secretion of hormones that promote the flow of bile and pancreatic juice.  It is required for digestion of Proteins.  Chemical breakdown of food.  Create an environment for absorption of Nutrients, Vitamin B12 and calcium.
  12. 12. Altered acid physiology & consequences A mismatch between aggressive forces (mainly acid and pepsin) and defensive forces (mucosal integrity) is responsible for various acid related disorders. This mismatch can occur because of  Increased acid secretion, and/or  Decreased mucosal defenses like- 1. Mucus 2. Mucosal blood flow 3. Bicarbonate 4. Cell renewal 5. Endogenous prostaglandins
  13. 13. Gastric Acid Pathogenesis  Gastric acid plays a pivotal role in the pathogenesis of various acid related disorders or acid-peptic disorders, including  Reflux Esophagistis  Non-erosive reflux disease  Gastro Esophageal Reflux Disease  Non-cardiac chest pain  NSAID Induced gastritis  Peptic Ulcers  Functional Dyspepsia  pathologic gastrointestinal hypersecretory conditions
  14. 14. Reflux Esophagistis  Reflux esophagitis is better known as “heartburn.”  It is often felt behind the breastbone as a burning chest discomfort, feeling of food coming back into the mouth as an acid or bitter taste.  It mostly happens after meals and last a couple of minutes to a couple of hours. It may not be relieved by rest nor be caused by exercise, and may become worse if you lie flat or bend over.
  15. 15. Symptoms  Bad taste in the mouth  Loss of tooth enamel  Chronic sore throat  Hoarseness  Choking  Cough or wheezing
  16. 16. Complications of Reflux Esophagistis  If RE is not treated, the inflamed area may bleed slowly. Too much blood loss may cause low blood count.  Damage to the lower esophagus may also cause scars to form. Too much scarring causes the lower end of the esophagus to narrow, making it harder and harder to swallow.  Some patients with severe scarring may have trouble swallowing.
  17. 17. Complications of Reflux Esophagistis  Barrett esophagus: sometimes called Barrett syndrome or columnar epithelium lined lower oesophagus (CELLO), refers to an abnormal change in the cells of the lower portion of esophagus.  When the normal squamous epithelium lining of the esophagus is replaced by goblet cells (cells usually found lower in the gastrointestinal tract), Barrett's esophagus is diagnosed.  A small number of people with Barrett’s esophagus develop a rare but often deadly type of cancer of the esophagus.
  18. 18. Gastro Esophageal Reflux Disease  Gastro Esophageal Reflux Disease is the result of the reflux of gastric contents into the esophagus such an extent that it overcomes the mucosal defense and causes injury to the esophageal mucosa
  19. 19. Factors causing reflux and contribution to GERD  LES Related Disorder 1. A mechanical defect in LES 2. Inappropriate transient relaxation of LES 3. Hiatal hernia (also provides a reservoir for acid)  Type of food 1. Fatty and/or spicy food eating habit 2. Coffee, citrus or tomato juices
  20. 20. Factors causing reflux and contribute to GERD  Increased Gastric Pressure 1. Delayed gastric emptying 2. Obesity 3. Pregnancy  Others 1. Certain medications 2. Smoking Sometimes if pylorus is impaired, bile and other duodenal contents reflux from duodenum to stomach and to esophagus adding aggravation GERD.
  21. 21. GERD Symptoms Intermittent substernal burning of pain (heartburn) is characteristic of GERD. Other symptoms include 1. Angina-like chest pain 2. Laryngitis 3. Hoarseness 4. Chronic cough 5. Bronchitis 6. Aspiration pneumonia
  22. 22. Non-erosive reflux disease  NERD is defined as the presence of classic GERD symptoms in the absence of esophageal mucosal injury.
  23. 23. Symptoms  persistent heartburn  acid regurgitation  Nausea  Hoarseness in the morning or trouble swallowing  May feel like food is stuck in the throat  Bad breath  Persistent dry cough but they do not have visible esophageal injury.
  24. 24. Non-cardiac chest pain  When acid from the stomach flows up into the esophagus, it can cause a burning sensation in the chest that's often mistaken for angina or a heart attack  Because the pain is similar to heart pain (called angina), patients present to emergency rooms concerned about a heart attack and commonly undergo cardiac tests). After these cardiac tests fail to show evidence of heart disease, the patients receive the diagnosis of NCCP.
  25. 25. Symptoms  Non-cardiac chest pain typically is felt behind the breast bone (sternum) and is described as oppressive, squeezing or pressure-like. It may radiate to the neck, left arm or the back (the spine). It may be precipitated by food intake.  Heartburn  Fluid regurgitation  Bitter or sour taste
  26. 26. Functional Dyspepsia  Functional Dyspepsia defined as discomfort or pain in the upper part of the abdomen.
  27. 27. Symptoms  postprandial fullness and bloating  Epigastric pain  Early satiety  Nausea  Belching
  28. 28. Peptic Ulcer  The two major risk factors known to impair mucosal defenses and lead to peptic ulcers are bacterium Helicobacter pylori (H. pylori) and the frequent use of NSAIDs.  Gastric acid, further, contributes to formation of ulcers once mucosal defenses are impaired. But acid usually does not cause ulcers independently.
  29. 29. Helicobacter pylori  The risk of PUD is up to seven times higher in patients with H. pylori infection than in general population.  More than 70% of patients with gastric ulcers and more than 90% of patients with duodenal ulcers are infected with H. pylori.  H. pylori is thought to damage the gastric mucosa.
  30. 30. Symptoms of PU  Main symptom is dull aching or gnawing epigastric pain or burning 1 to 3 hours after eating as per the location of ulcer.  It is often relieved by eating or by antacids. Pain may worsen in night because of increased acid secretion and lack of food material in stomach to dilute the acid.  The nighttime paid normally interferes with sleep. Nausea, vomiting and bloating are the other symptoms.
  31. 31. Complications of PU  Bleeding ulcers  Perforation into the peritoneal cavity  Penetration into adjacent organs  Gastric/intestinal passage obstruction
  32. 32. NSAIDs Induced gastritis Non Steroidal Anti-inflammatory Drugs NSAIDs damage the GI mucosa by dual mechanism. 1. They cause direct irritation to GI mucosa. 2. They inhibit prostaglandin synthesis leading to reduced mucosal integrity & mucosal defense. The acid then contributes to formation of ulcers. Use of NSAIDs increases the risk of PUD upto 20 fold.
  33. 33. pathologic gastrointestinal hypersecretory conditions  Gastric acid secretion is largely control by cholinergic, histaminergic and peptidinergic(especially gastrin) pathways. Disorders in a number of these pathways can lead to gastric acid hypersecretion. Classification of gastric acid hypersecretory state  associated with hypergastrinemia  associated with hyperhistaminemia  unknown etiology
  34. 34. Zollinger-Ellison Syndrome  ZES is a clinical syndrome characterized primarily by refractory peptic ulcer disease which is due to ectopic release of gastrin by gastrinoma resulting in gastric acid hypersecretion.  Complications of Zollinger-Ellison Syndrome  A person who has Zollinger-Ellison syndrome may have only one gastrinoma or may have several  In some ZES patient gastrinomas may be malignant (cancerous)
  35. 35. Symptoms  Burning pain in the abdomen  Nausea  Diarrhea  Vomiting  Bleeding from the stomach  Weakness  Fatigue
  36. 36. Pharmacotherapy for Acid Suppression Different medications are available to inhibit the acids.  ANTACIDS  Histamine H2-Receptor Antagonists  Proton Pump Inhibitors
  37. 37. Limitation of Antacids  Antacids relieve the symptoms but cannot healing in recommended dosage  Have short duration of action (about 2 hours) and need frequent dosing  Antacids are ineffective for eradication H. pylori  Rebound acid secretion phenomenon may be problematic  Adverse effects (constipation with aluminum salts and diarrhea with magnesium salts)  Drug interactions  Hampered absorption of other drugs because of change in pH
  38. 38. Limitations of H2-Receptor Antagonists  Controls mainly histamine related acid secretions and has very low efficacy in gastrin related secretions  Recurrence rate is high in patients with H. pylori infection  Healing is delayed in smokers and recurrence rate is high  May interact with other medications  Though generally well tolerated, H2-Receptor Antagonists can cause headache and other side4 effects like confusion, diarrhea & gynecomastia (with cimetidine).
  39. 39. Proton Pump Inhibitors  Proton Pump inhibitors were introduced in late 1980s.  Proton Pump inhibitors bind to the Proton Pump on parietal cell and inhibit the acid secretion regardless of whether it is stimulated by histamine, acetylcholine or gastrin.  Proton Pump Inhibitors also have in vitro antimicrobial activity against H. pylori though they cannot eradicate H. pylori when used alone.
  40. 40. P.P.I. - 1. OMEPRAZOLE……1988 2. LANSOPRAZOLE…1991 3. PANTOPRAZOLE …1994 4. RABEPRAZOLE…..1999 Are all PPI’s the same..????
  41. 41. Comparison of all PPI  All PPIs are effective in healing and maintenance of ARD but they differ in their ability to control symptoms rapidly and consistently  Rabeprazole is different from other PPI because of more rapid rate of activation, Rabeprazole results in a faster onset of action and faster symptoms control than other PPIs
  42. 42. Comparison of all PPI Pharmacokinetic Profiles Pharmacodynamic Parameter Lansoprazole Omeprazole Rabeprazole At a pH of 1.2 2 2.8 1.3 At a pH of 5.1 90 84 7.2 At 10min 66% 47% 100% At 45 Min 100% 83% 100% Activation Time(min) % Inhibition of the H+/K+-ATPase
  43. 43. Comparison of all PPI  Food does not affect degree of absorption  Rabeprazole, involving both cytochrome P450 mediated reaction in the liver and nonenzymatic reactions, appears to confer an advantage over other PPIs
  44. 44. Rabe.. 20 Indications:  Reflux Esophagistis  Non-erosive reflux disease  Non-cardiac chest pain  NSAID Induced gastritis  Peptic Ulcers  Functional Dyspepsia
  45. 45. Rabe… 20 Dosage and Administration  20 OD for 4 to 8 weeks  And in complicated ARD up to 40 mg for 4 to 8 weeks
  46. 46. Rabe…20 USPs  The latest and potent PPI  Maximum speed of onset of action  Maximum acid control  Maximum gastroprotection  Greater and faster symptom relief  Safe and convenient