Stomach Anatomy and Function Lecture PDF

Stomach anatomy and function Lecture Number 4.1 Status Done Type Lecture 4.1 Stomach anatomy and function Overview This lecture focuses on the anatomy and control of stomach functions, including hormonal and neural regulation of motility and secretion. It covers...

Stomach anatomy and function Lecture Number 4.1 Status Done Type Lecture 4.1 Stomach anatomy and function Overview This lecture focuses on the anatomy and control of stomach functions, including hormonal and neural regulation of motility and secretion. It covers the role of various cells such as enteroendocrine cells in modulating gastric function and explains how distension influences gastric acid secretion. The lecture also discusses key gastrointestinal hormones such as gastrin, somatostatin, and secretin, while emphasizing the basic functions of the stomach, including food storage, digestion, and protection against self-digestion. Blood supply, lymphatic drainage, and conditions that affect gastric function are also introduced. Learning Objectives Objective 1: Understand the hormonal, paracrine, and neural regulation of stomach motility and secretion. Objective 2: Describe the role of gastric acid in digestion, the motility functions of the stomach, and its protective mechanisms. Objective 3: Recognize the importance of enteroendocrine cells, such as G cells and D cells, in regulating digestive processes and maintaining stomach health. Objective 4: Identify conditions that affect stomach function, such as gastritis, ulcers, and Zollinger-Ellison syndrome. Objective 5: Understand the clinical relevance of stomach blood and lymphatic supply, and the role of the stomach in vitamin B12 absorption and iron metabolism. Key Concepts and Definitions Enteroendocrine cells: Specialized cells within the stomach lining that release hormones regulating stomach functions. These include G cells (gastrin), D cells (somatostatin), and S cells (secretin). G cells: Found in the antrum of the stomach, they secrete gastrin, which increases gastric acid secretion and enhances stomach motility. D cells: Located primarily in the antrum, they secrete somatostatin, which inhibits gastrin release and downregulates acid production. Parietal cells: Found in the fundus and body of the stomach, these cells secrete hydrochloric acid (HCl) and intrinsic factor (essential for vitamin B12 absorption). Chief cells: Located in the body and fundus of the stomach, they secrete pepsinogen, the inactive precursor of pepsin, which is critical for protein digestion. Gastrin : A hormone that stimulates gastric acid secretion, primarily in response to food intake and stomach distension. Somatostatin : Inhibits the release of gastrin and gastric acid, especially when the stomach pH drops too low. Secretin : Released from S cells in the duodenum in response to acidity, it stimulates bicarbonate secretion from the pancreas and inhibits gastric acid secretion. Oblique Muscle Layer: The stomach has an extra oblique layer in addition to the circular and longitudinal layers, facilitating grinding and mixing of food. Clinical Applications Case Study: A patient presents with recurrent peptic ulcers and excessive gastric acid production, diagnosed as Zollinger- Ellison syndrome. This condition is caused by gastrin-secreting tumours (gastrinomas), which lead to hypergastrinemia. Diagnosis involves fasting gastrin levels and imaging studies such as endoscopy and CT scans.  Diagnostic Approach: For suspected peptic ulcers or gastritis, endoscopy is used to assess mucosal integrity, and blood tests may check for elevated gastrin or somatostatin levels. Helicobacter pylori infection, a common cause of gastritis, can be detected through a urea breath test, stool antigen test, or biopsy. Treatment Options: Proton pump inhibitors (PPIs) reduce gastric acid production and promote healing of ulcers. In cases of Zollinger-Ellison syndrome, surgical resection of gastrinomas may be necessary alongside medical management. Pathophysiology Acid Secretion Pathway: Gastric acid (HCl) is secreted by parietal cells in response to stimulation by gastrin (from G cells), histamine (from enterochromaffin-like cells), and acetylcholine (from the vagus nerve). Gastrin is stimulated by stomach distension and the presence of food, particularly proteins. Regulation : Somatostatin from D cells inhibits acid production by downregulating gastrin secretion when the pH drops too low. This feedback loop is essential for preventing excessive acid buildup. Motility: The stomach's three muscle layers (longitudinal, circular, and oblique) allow for powerful mixing and grinding movements, turning ingested food into chyme, which is then gradually released into the duodenum. Protective Mechanisms: The stomach is protected from self-digestion by a thick layer of mucus and bicarbonate, which neutralizes acid near the epithelial surface. Prostaglandins also help maintain mucosal integrity and blood flow. Pharmacology Proton Pump Inhibitors (PPIs): These inhibit the H+/K+ ATPase (proton pump) in parietal cells, blocking the final step of acid production, and are commonly used to treat GERD, peptic ulcers, and Zollinger-Ellison syndrome. H2 Receptor Antagonists: Block histamine H2 receptors on parietal cells, reducing acid secretion. Used for conditions like GERD and mild peptic ulcers. Antacids: These over-the-counter agents neutralize stomach acid and provide rapid relief from symptoms like heartburn or indigestion. Differential Diagnosis Peptic Ulcer Disease (PUD): Characterized by epigastric pain, which may improve or worsen with food intake. Common causes include H. pylori infection and NSAID use. Diagnosis is confirmed through endoscopy, and treatment involves acid suppression and eradication of H. pylori if present. Gastritis: Inflammation of the stomach lining, typically due to H. pylori infection, chronic alcohol use, or NSAIDs. Symptoms include nausea, bloating, and epigastric pain. Hiatal Hernia: A condition where a part of the stomach pushes up into the chest cavity through the diaphragm. It can contribute to GERD and cause symptoms such as acid reflux and heartburn. Barrett’s Oesophagus: A complication of chronic GERD where the oesophageal lining changes, increasing the risk for oesophageal cancer. Investigations Endoscopy: Gold standard for diagnosing peptic ulcers, gastritis, and malignancies. It allows direct visualization of the gastric mucosa and biopsy of suspicious lesions. Gastrin Level Test: A high fasting gastrin level is indicative of conditions like Zollinger-Ellison syndrome, where excessive gastrin production leads to ulcer formation. H. pylori Testing: Detection of H. pylori through breath tests, stool antigen, or biopsy is essential for diagnosing gastritis and PUD. pH Monitoring: For patients with GERD, ambulatory pH monitoring helps quantify acid exposure in the oesophagus and confirm the diagnosis. Key Diagrams and Visuals Summary and Key Takeaways Takeaway 1: The stomach’s functions are regulated by a complex interaction of neural, hormonal, and paracrine signals, ensuring that acid secretion and motility are adjusted based on food intake and digestion needs. Takeaway 2: The protective mucus-bicarbonate barrier and prostaglandins are critical in maintaining the stomach’s defences against self-digestion, especially in preventing conditions like gastritis and ulcers. Takeaway 3: The stomach plays a crucial role in the absorption of vitamin B12 through the production of intrinsic factor and in iron metabolism by converting ferric to ferrous iron. Takeaway 4: Disruptions in these regulatory mechanisms, such as overproduction of gastrin (Zollinger-Ellison syndrome) or weakened mucosal defences (NSAID use), can lead to significant clinical conditions like ulcers and gastritis. Further Reading/References Resource 1: "Netter’s Gastroenterology" by Martin H. Floch, for comprehensive visuals and explanations of stomach anatomy and function. Resource 2: "Pathophysiology of Disease: An Introduction to Clinical Medicine" for detailed explanations of gastric disorders and their clinical presentations. Resource 3: "Robbins & Cotran Pathologic Basis of Disease" for insights into the pathological processes underlying gastritis, ulcers, and gastric cancer. Questions/Clarifications Question 1: How does chronic use of NSAIDs affect prostaglandin synthesis and increase the risk of peptic ulcers? Question 2: What are the clinical implications of hypochlorhydria (low stomach acid) in elderly patients?