Disorders of Upper Gastrointestinal Tract Part 2 (Stomach) PDF
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IMU University
2024
Dr Shanthi Dhandapani
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This document provides an overview of disorders of the upper gastrointestinal tract, focusing on the stomach. It details normal anatomy and physiology, explores various pathologies, and discusses clinical manifestations and treatment options, including gastric surgeries. Intended for internal university use at IMU University in Malaysia, this document serves as an educational resource.
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Disorders of Upper Gastrointestinal Tract Part 2 (Stomach) Module: NDT2359 Pathophysiology for Dietetics 2...
Disorders of Upper Gastrointestinal Tract Part 2 (Stomach) Module: NDT2359 Pathophysiology for Dietetics 2 Lecturer : Dr Shanthi Dhandapani Contact details: [email protected] Copyright (C) 2024. School of Health Sciences. IMU Inspire Empower Elevate For internal circulation in the IMU University ONLY Lesson Outcomes At this end of this lesson, you will be able to: Describe the normal anatomy and physiology of the upper gastrointestinal tract: oral cavity, esophagus and stomach Explain the aetiology, pathophysiology and clinical manifestations of oral infections and impaired taste, dysphagia, gastroesophageal reflux disease, gastritis, peptic ulcer disease and gastric surgery Undestanding the terminologies Chyme – The semifluid mass of partly digested food expelled by the stomach into duodenum. Strictures- A narrowing or constriction of a section of intestine, called a stricture, which may lead to an intestinal blockage Hyperosmolar- Blood has higher concentration of sodium,glucose and other substances Intramural Fluid- Fluid within bowel Achlorhydria- A condition stomach does not produce HCL Fluid Sequestration – Difference between the amount of the fluids administered and losses from the urine. Intrinsic Factor - Glycoprotein produced by parietal cells Prostaglandins –Nitric oxide helps to produce Prostaglandins ,a group of lipids with harmones like actions that the body makes primarily at the site of damage Stomach– Anatomy & Physiology (1) Stomach – Anatomy & Physiology (2) The stomach stores food and performs preliminary steps of digestion. Food is mixed at lower part of stomach by peristaltic waves that also propel the acid- chyme mixture against the pyloric sphincter. Increased contractions of the stomach push food through the sphincter and into small intestine as the stomach empties over a 1 to 2- hour period. Stomach – Anatomy & Physiology (3) Epithelial cells line at inner surface of stomach secrete gastric juices. Gastric juice (2-3liter/d) Secretions are controlled by nervous (smells, thoughts, and caffeine) and endocrine signals. Intrinsic Water HCl Pepsinogen factor (>98%) Activates pepsinogen Initiates protein Required for digestion vitamin Aids iron absorption B12 absorption Kills ingested bacteria Dyspepsia – Definition, Aetiology & Clinical Manifestations Persistent upper abdominal discomfort/pain related to GERD, gastritis/peptic ulcer disease, gallbladder disease, etc Symptoms: Vague abdominal discomfort Belching Bloating Functional dyspepsia Early satiety Unexplained Nausea persistent upper GI discomfort Gastritis - Aetiology & Clinical Manifestations Result from infectious, chemical or neural abnormalities disrupt mucosal integrity of stomach Most common cause Helicobacter pylori infection → achloryhdria, loss of IF & gastric cancer Can cause duodenitis if it colonizes gastric tissue that may be present in the duodenum Treatment → 2 to 3 antibiotics & acid suppressing medications for 1 to 2 weeks Gastritis (Non H Pylori) - Aetiology Chronic use of aspirin or other NSAIDs (inhibit prostaglandin synthesis), steroids, alcohol, erosive substances, tobacco, or any combination of these factors may compromise mucosal integrity and increase the chance for acquiring acute or chronic gastritis. Eosinophilic gastroenteritis (EGE) also may contribute to some cases of gastritis. the following mechanisms are responsible for the development of peptic ulcer disease (PUD)? I Helicobacter pylori Infection Peptic Ulcer Disease II. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) III Chronic autoimmune response (Definition) IV Increased gastric acid secretion ULCERS – erosion of the surface of the alimentary canal generally associated with some kind of irritants The following mechanisms are responsible for the development of peptic ulcer disease Helicobacter pylori Infection Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Increased gastric acid secretion Peptic Ulcer Disease - Pathophysiology Normal gastric & duodenal mucosa is protected by ❖ Secretion of mucus, Mucus layers ❖ Nitric oxide - Prostaglandins, ❖ Production of bicarbonate /Alkali ,pH Gradient ❖ Removal of excess acid by normal blood flow ❖ Rapid renewal & repair of epithelial cell injury- Epithelial Barrier Peptic ulcer - ulcer that occurs as a result of the breakdown of these normal defense & repair mechanism Stress Ulcers - Aetiology, Pathophysiology & Clinical Manifestations Occur as a complication of metabolic stress caused by trauma, burns, surgery, shock, renal failure, or radiation therapy, and potential for significant GI hemorrhage Significant cause of morbidity in the critically ill patient Gastric ischemia associated with GI hypoperfusion, oxidative injury, reflux of bile salts and pancreatic enzymes, microbial colonization, and mucosal barrier changes Occurs in fundus and body of stomach, may develop in the antrum, duodenum, or distal esophagus Typically shallow and causing oozing of blood from superficial capillary beds, stress ulcer lesions also may occur deeper, eroding into the submucosa, causing massive hemorrhage or perforation. Gastric Surgery Types of Gastric Surgeries Bariatric surgery: Roux-en-Y, Gastric banding, Sleeve gastrectomy, Vertical banding, gastroplasty, Jejunoileal bypass Gastrectomy Billroth I (gastroduodenostomy) (For Weight management/ Billroth II (gastrojejunostomy) Gastric cancer) Truncal vagotomy Vagotomy Parietal cell vagotomy Gastric Surgery Total gastrectomy Roux-en-Y Billroth I Billroth II (gastroduodenostomy) (gastrojejunostomy) involves removal of the jejunum is pulled up and involves removal of the involves removal of the entire stomach, anastomosed to the pylorus and/or antrum, stomach antrum and an is accompanied by a esophagus. and an anastomosis of anastomosis of the reconstructive procedure. The duodenum is then the proximal end of the remnant stomach to the A total gastrectomy is connected to the small duodenum to the side of the jejunum, performed for bowel so that bile and distal end of the remnant which creates a blind malignancies that affect pancreatic secretions can stomach. duodenal loop the middle or upper flow into the intestine. stomach. Roux-en-Y reconstruction is performed to maintain GI tract continuity Subtotal gastrectomy is when a portion of the stomach is removed Total gastrectomy Gastric Surgery Vagotomy – removing one of the branches of vagus nerve that communicates with stomach Parietal cell vagotomy (partial/selective) Affects only proximal stomach where gastric acid secretion occurs Antrum & pylorus remain innervated by vagus nerve Gastric nerve & gastric emptying can proceed more normally Pyloroplasty Enlarging pyloric sphincter Dumping Syndrome – Aetiology & Pathophysiology Occurs as a result of Total/partial gastrectomy Manipulation of pylorus After fundoplication After some bypass procedures for obesity Increased osmolar load enters small intestine too quickly from stomach Dumping Syndrome - Clinical Manifestations Characteristics ▪ 10-20 mins after eating Early dumping ▪ Distention of the small bowel from foods & liquids syndrome ▪ Fluid loss from vascular space into mesenteric bed & GI tract ▪ Fluid changes in vascular component result in dizziness, weakness & tachycardia ▪ 20-30 mins after eating Intermediate ▪ Food enters colon, fermentation & action of microflora cause production of gas, dumping abdominal pain, cramping and diarrhea syndrome ▪ Malabsorption of carbohydrates & other foodstuffs ▪ Subsequent fermentation of the substrates entering the colon ▪ 1-3hrs after eating, common after eating simple carbohydrates ▪ Rapid absorption in small intestine stimulates release of insulin Late dumping ▪ After quick absorption, no substrate for insulin to act upon syndrome ▪ Rapid change in blood glucose & the secretion of gut peptides, glucose, insulinotropic polypeptide, and GLP-1 ▪ Hypoglycaemia : shakiness, sweating, anxious, hungry, confusion & weakness POP QUIZ https://forms.office.com/r/ dN5MSfMGPq If you encounter issue to scan the code or click the link, please go to Elearn portal and access under Quiz KNOWLEDGE CHECK # 2 Copyright reserved 2020, IMU. All rights References 19 1. Marieb, E. N. and Hoehn, K. (2018) Human Anatomy and Physiology, 11th edition, Hoboken, New Jersey: Pearson Education, Inc. 2 Nelms, M. N., Sucher, K. and Lacey, K. (2020) Nutrition Therapy and Pathophysiology, 4th edition, Boston, MA, USA: Cengage Learning. ISBN: 9780357041710,2018965075 3.Krause and Mahan Nutrition care process , 2023 Janice Raymond Kelly Morrow 978-0- 323-81025-8 16th Edition ,Elsevier, Inc.. 4. Nieman DC (2019). Nutritional Assessment. 7th Edition. McGraw Hill, New York Acknowledgements: AP Dr Snigdha ,Yang wai Yew Misra and Dr Megan Chong for sharing their previous slides 4/8/2021 Lesson Outcomes At this end of this lesson, you will be able to: Describe the normal anatomy and physiology of the upper gastrointestinal tract: oral cavity, esophagus and stomach Explain the aetiology, pathophysiology and clinical manifestations of oral infections and impaired taste, dysphagia, gastroesophageal reflux disease, gastritis, peptic ulcer disease and gastric surgery THANK YOU