rabeprazole 20 medical ppt
TRANSCRIPT
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Rabeprazole Narveer Shekhawat
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Rabe. 20 We will discussGI systemAcid secretion processAcid related disordersTreatment options & limitationsRabeprazole
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Human Gastro-Intestinal System(Digestive System)
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The Stomach
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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
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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.
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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.
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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
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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.
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Acid SecretionThere are 3 phases of acid secretion1. 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.
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Acid Secretion3. 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.
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Formation of HCL
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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.
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Altered acid physiology & consequencesA 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
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Gastric Acid PathogenesisGastric 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
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Reflux EsophagistisReflux 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.
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Symptoms
Bad taste in the mouthLoss of tooth enamelChronic sore throat HoarsenessChoking Cough or wheezing
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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.
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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.
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Gastro Esophageal Reflux DiseaseGastro 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
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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
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Factors causing reflux and contribute to GERD
Increased Gastric Pressure1. Delayed gastric emptying2. Obesity3. Pregnancy Others1. Certain medications2. Smoking
Sometimes if pylorus is impaired, bile and other duodenal contents reflux from duodenum to stomach and to esophagus adding aggravation GERD.
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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
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Non-erosive reflux diseaseNERD is defined as the presence of classic
GERD symptoms in the absence of esophageal mucosal injury.
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Symptomspersistent heartburnacid regurgitationNauseaHoarseness in the morning or trouble swallowingMay feel like food is stuck in the throatBad breathPersistent dry cough but they do not have visible esophageal
injury.
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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.
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SymptomsNon-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.
HeartburnFluid regurgitationBitter or sour taste
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Functional DyspepsiaFunctional Dyspepsia defined as discomfort
or pain in the upper part of the abdomen.
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Symptomspostprandial fullness and bloatingEpigastric painEarly satietyNauseaBelching
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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.
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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.
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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.
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Complications of PU
Bleeding ulcersPerforation into the peritoneal cavityPenetration into adjacent organsGastric/intestinal passage obstruction
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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.
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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 hypergastrinemiaassociated with hyperhistaminemiaunknown etiology
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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)
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SymptomsBurning pain in the abdomenNauseaDiarrheaVomitingBleeding from the stomachWeaknessFatigue
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Pharmacotherapy for Acid Suppression
Different medications are available to inhibit the acids.
ANTACIDS
Histamine H2-Receptor Antagonists
Proton Pump Inhibitors
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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
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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).
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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.
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P.P.I. -
1. OMEPRAZOLE……1988
2. LANSOPRAZOLE…1991
3. PANTOPRAZOLE …1994
4. RABEPRAZOLE…..1999
Are all PPI’s the same..????
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Comparison of all PPIAll 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
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Comparison of all PPIPharmacokinetic Profiles
Pharmacodynamic Parameter
Lansoprazole Omeprazole Rabeprazole
At a pH of 1.2 2 2.8 1.3At 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
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Comparison of all PPIFood 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
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Rabe.. 20
Indications:
Reflux Esophagistis
Non-erosive reflux disease
Non-cardiac chest pain
NSAID Induced gastritis
Peptic Ulcers
Functional Dyspepsia
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Rabe… 20
Dosage and Administration20 OD for 4 to 8 weeksAnd in complicated ARD up to 40 mg for 4 to 8 weeks
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Rabe…20USPs
The latest and potent PPIMaximum speed of onset of actionMaximum acid controlMaximum gastroprotectionGreater and faster symptom reliefSafe and convenient