ACID PEPTIC DISORDERS -Gastritis, GERD and Ulcers

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1. ACID PEPTIC DISORDERS 1

2. INTRODUCTION The acid peptic disorders are a collection of diseases involving acid production in the stomach and nearby parts of the gastrointestinal tract. It includes G astroesophageal reflex disease G astric ulcer, duodenal ulcer, oesophageal ulcer Zollinger -Ellison syndrome. Acid peptic disorders are the result of distinctive, but overlapping pathogenic mechanisms leading to either excessive acid secretion or diminished mucosal defence. 2

3. GASTRITIS The term gastritis should be reserved for histologically documented inflammation of the gastric mucosa. Gastritis is not the mucosal erythema seen during endoscopy and is not interchangeable with “dyspepsia.” The etiologic factors leading to gastritis are broad and heterogeneous. Gastritis has been classified based on time course (acute vs chronic), histologic features, and anatomic distribution or proposed pathogenic mechanism. The correlation between the histologic findings of gastritis, the clinical picture of abdominal pain or dyspepsia, and endoscopic findings noted on gross inspection of the gastric mucosa is poor. Therefore, there is no typical clinical manifestation of gastritis. 3

4. Acute Gastritis The most common causes of acute gastritis are infectious. Acute infection with H. pylori induces gastritis. Other Causes – Aspirin, NSAIDs, Alcohol, Severe physiological Stress like Multiorgan failure, burns, CNS trauma, bile reflux, viral, syphilitic, parasitic, fungal infection. It is reported as presenting with sudden onset of epigastric pain, nausea, and vomiting, and limited mucosal histologic studies demonstrate a marked infiltrate of neutrophils with edema and hyperemia. If not treated, this picture will evolve into one of chronic gastritis. 4

5. Chronic gastritis Chronic gastritis is identified histologically by an inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells, with very scant neutrophil involvement. Distribution of the inflammation may be patchy, initially involving superficial and glandular portions of the gastric mucosa. This picture may progress to more severe glandular destruction, with atrophy and metaplasia. CLINICAL PRESENTATIONS: manifestations are vague Anorexia Feeling of fullness, Dyspepsia, Belching, Vague epigastric pain Nausea or Vomiting Intolerance to spicy and fatty foods 5

6. TYPES/CLASSIFICATION The early phase of chronic gastritis is superficial gastritis. The inflammatory changes are limited to the lamina propria of the surface mucosa, with edema and cellular infiltrates separating intact gastric glands. The next stage is atrophic gastritis. The inflammatory infiltrate extends deeper into the mucosa, with progressive distortion and destruction of the glands. The final stage of chronic gastritis is gastric atrophy. Glandular structures are lost, and there is a paucity of inflammatory infiltrates. Endoscopically, the mucosa may be substantially thin, permitting clear visualization of the underlying blood vessels Chronic gastritis is also classified according to the predominant site of involvement. Type A refers to the body-predominant form (autoimmune), and type B is the antral-predominant form (H. pylori–related). 6

7. MANAGEMENT OF ACID PEPTIC DISORDERS S.No DRUG CLASS DRUGS USES 1. PROTON PUMP INHIBITORS Omeprazole, esomeprazole, lansoprazole, rabeprazole and pantoprazole Lansoprazole - dual delayed systemic release – GERD lansoprazole – naproxen – in NSAID induced GI injury 2. H2 RECEPTOR ANTAGONISTS Cimetidine, Ranitidine, Famotidine and Nizatidine Acid peptic ulcers in combination with antibiotics. It may lead to patient developing tolerance to H2 blockers 3. ANTACID Aluminium hydroxide and manganese hydroxide Calcium carbonate and sodium bicarbonate Rarely used 1) ACID NEUTRALIZING/ INHIBITORY DRUGS 7

8. MUCOSAL PROTECTIVE AGENTS S.No DRUG CLASS DRUGS USES 1. PROTECTANTS Sucralfate Promoting a trophic action by binding growth factors such as EGF, enhances prostaglandin synthesis, stimulates mucus and bicarbonate secretion and enhances the mucosal defence and repair. 2. PROSTAGLANDIN ANALOGUES Latanoprost and Travoprost Enhances the mucosal defence and repair 3. BISMUTH – CONTAINING PREPARATIONS Colloidal bismuth subcrite (SBS) and bismuth subsalicylate ( BSS, Pepto - Bismol ) H. pylori eradication. 8

9. H. pylori eradication therapy Indication Definite indication – Peptic ulcer, MALToma , H. pylori positive dyspepsia. Not indicated in – Gastro- oesophageal reflux disease, Asymptomatic. Uncertain - Family history of gastric ulcer, non-ulcer dyspepsia, long – term NSAID users. In peptic ulcer Independent of time of presentation, severity of the symptoms, presence of risk factors therapy can be administered. In remmision ulcers With history of peptic ulcer disease with positive H. pylori. Patient using NSAIDs for long term with prior history of peptic ulcer disease. All these conditions are indicated for the administration of H. pylori eradication therapy. Side effects of eradication therapy - Diarrhoea Flushing and vomiting when taken with alcohol Nausea and vomiting Abdominal cramp Headache rashes 9

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12. THANK YOU 12