Stomach Conditions Lecture Notes PDF

Stomach conditions Lecture Number 4.2 Status Done Type Lecture 4.2 Stomach conditions Overview This lecture focuses on common stomach conditions, including gastroesophageal reflux disease (GERD), gastritis, and peptic ulcer disease. It covers their clinical pr...

Stomach conditions Lecture Number 4.2 Status Done Type Lecture 4.2 Stomach conditions Overview This lecture focuses on common stomach conditions, including gastroesophageal reflux disease (GERD), gastritis, and peptic ulcer disease. It covers their clinical presentations, investigations, complications, and pharmacological treatments, with particular emphasis on the reduction of gastric acid secretion. The lecture also discusses the role of Helicobacter pylori in chronic gastritis and its effect on gastric physiology. Learning Objectives Objective 1: Describe the presentation, investigation, and complications of GERD, gastritis, and peptic ulcer disease. Objective 2: Outline the pharmacological interventions for reducing gastric acid secretion. Objective 3: Explain the role of Helicobacter pylori in chronic gastritis and its effects on gastric physiology. Key Concepts and Definitions GORD (Gastroesophageal Reflux Disease): A condition where gastric contents reflux into the oesophagus, causing symptoms such as chest pain, regurgitation, and cough. Gastritis: Inflammation of the stomach lining, which can be acute (due to factors like NSAID use or alcohol) or chronic (due to bacterial infection like H. pylori or autoimmune causes). Peptic Ulcer Disease (PUD): A defect in the gastric or duodenal mucosa, often caused by H. pylori or NSAID use, and involving full-thickness erosion through the muscularis mucosa. Clinical Applications Case Study: A 45-year-old male with chest pain, a burning sensation worsened by alcohol and coffee, and relief with Gaviscon. He has a history of smoking and blood pressure medications. Diagnostic Approach: In GORD, diagnosis is clinical, but endoscopy or oesophageal manometry may be used for patients with alarm symptoms or resistant cases. Treatment Options: Lifestyle modifications, pharmacological agents such as H2 antagonists (e.g., ranitidine) or PPIs (e.g., omeprazole), and in rare cases, surgical interventions like Nissen fundoplication. Pathophysiology GORD: Lower oesophageal sphincter (LES) incompetence leads to reflux of gastric contents into the oesophagus. LES dysfunction may be due to transient relaxations, hypotension, or anatomical changes such as a hiatal hernia. Gastritis: Acute gastritis results from direct mucosal damage by irritants (NSAIDs, alcohol). Chronic gastritis involves prolonged inflammation from H. pylori or autoimmune mechanisms. Peptic Ulcer Disease: Ulcers form due to an imbalance between aggressive factors (acid, pepsin) and defensive mechanisms (mucus, bicarbonate). Chronic ulcers may erode into the muscularis propria, leading to complications like perforation or haemorrhage. Pharmacology H2 Antagonists: Drugs like ranitidine and cimetidine reduce acid secretion by blocking H2 receptors on gastric parietal cells.  Proton Pump Inhibitors (PPIs): Drugs like omeprazole inhibit the H+/K+ ATPase on parietal cells, the final step in acid secretion, effectively reducing gastric acidity. Differential Diagnosis GERD: Distinguish from conditions like cardiac chest pain (angina), oesophageal motility disorders, and functional dyspepsia. Gastritis: Rule out peptic ulcer disease and gastroenteritis. Peptic Ulcer Disease: Consider other causes of upper abdominal pain, such as pancreatitis or biliary colic. Investigations Investigation 1: OGD (esophagogastroduodenoscopy) to visualize the oesophagus, stomach, and duodenum, often used for patients with alarm symptoms or persistent GORD. Investigation 2: Urea breath test or stool antigen test for diagnosing H. pylori infection. Key Diagrams and Visuals Summary and Key Takeaways Takeaway 1: GERD, gastritis, and peptic ulcer disease are common and have significant overlapping symptoms, but distinct aetiologies. Takeaway 2: H. pylori plays a critical role in chronic gastritis and peptic ulcer disease, and its eradication is key to management. Takeaway 3: Lifestyle modifications and pharmacological treatment (H2 antagonists and PPIs) are first-line therapies for reducing gastric acid and treating these conditions. Further Reading/References  Resource 1: NICE Guidelines on Dyspepsia and GERD (link) Resource 2: BMJ Best Practice, GORD Overview (link) Questions/Clarifications Question 1: What is the role of lifestyle modifications in the long-term management of GERD? Question 2: How does the long-term use of PPIs affect electrolyte balance, particularly magnesium levels?