Perforated Peptic Ulcer in Khartoum State

Total Page:16

File Type:pdf, Size:1020Kb

Perforated Peptic Ulcer in Khartoum State ﺑﺴﻢ ﺍﷲ ﺍﻟﺮﲪﻦ ﺍﻟﺮﺣﻴﻢ UNIVERSITY OF KHARTOUM Faculty of Medicine Postgraduate Medical Studies Board Perforated peptic ulcer in Khartoum state By Dr. Al Fatih Mohamed Ahmed Alnajib M.B.B.S (University of Gezira) A thesis Submitted in partial fulfillment for the requirements of the Degree of Clinical MD in Surgery, October, 2002 Supervisor Prof. Mohamed El Makki Ahmed MS, FRCSI, Professor of Surgery ﺑﺴﻢ ﺍﷲ ﺍﻟﺮﲪﻦ ﺍﻟﺮﺣﻴﻢ ﻗﺎﻝ ﺍﷲ ﺗﻌﺎﻟﻰ : } ﻗﺎﻟﻮﺍ ﺳﺒﺤﺎﻧﻚ ﻻ ﻋﻠﻢ ﻟﻨﺎ ﺇﻻ ﻣﺎ ﻋﻠﻤﺘﻨﺎ ﺇﻧﻚ .{ ﺃﻧﺖ ﺍﻟﻌﻠﻴﻢ ﺍﻟﺤﻜﻴﻢ ﺻﺪﻕ ﺍﷲ ﺍﻟﻌﻈﻴﻢ CONTENTS Page Dedication I Acknowledgements II List of abbreviations III English abstract IV V Arabic abstract VI List of tables VIII List of figures CHAPTER ONE 1 Introduction and Literature review Objectives 25 CHAPTER TWO Patients & Methods 26 CHAPTER THREE Results 28 CHAPTER FOUR Discussion 58 Conclusion 65 Recommendations 67 References 68 APPENDIX Questionnaire 69 APACHE II Score 73 Dedications To my parents, teachers, Sisters & brothers ACKNOWLEDGEMENT I will always feel indebted to my supervisor Prof. Mohamed El Makki Ahmed, Professor of surgery, Faculty of Medicine, University of Khartoum, for his kind and meticulous supervision, encouragement, and guidance in this work with great patience from it’s beginning to the final touches. I would also like to express my sincere thanks and gratitude to my colleagues the registrars of surgery and the house officers who help a lot in data collection, their indefatigable efforts and cheerful co-operation are without parallel. Special thanks for all those helped or participated in this work to come to the light, not forgetting to thank Miss. Widad for help in typing and Mr. Hassan for the data analysis. ABBREVIATIONS APACHE Acute physiology and chronic health evaluation CXR Chest X-ray COX Cyctooxygenase DU Duodenal ulcer GU Gastric ulcer H2 receptors Histamine 2 receptors H. pylori Helicobacter pylori PPI Proton pump inhibitor PPU Perforated peptic ulcer ZES Zollingar Ellesions Syndrome PUD Peptic ulcer disease ABSTRACT Background: Although perforated peptic ulcer (PPU) is evaluated in different parts of the World, no study was held to evaluate the disease in Sudan. This study aimed to evaluate the incidence, clinical presentation, management and outcome of perforated peptic ulcer. Methods: Data from 58 consecutive patients with PPU was collected and analysed in the period between November 1999 and April 2002. Fifty-two (89.6%) were male patients and six (10.4%) females. Results: Twenty-five (43.1%) of the studied group were below 30 years of age, only 10(17.2%) were known cases of peptic ulcer disease. Twenty-two (40%) of perforations occurred during the month of Ramadan and most of the patients were fasting 20(34.4%). Forty-two (72.4%), of the total number of patients, presented during the winter season. Fifty- three (91.3%) were perforated duodenal ulcers and three (5.2%) were perforated gastric ulcers. Fifty-five (94.8%) had surgical treatment, 53(91.3%) patients had simple closure with omental patch. Postoperative complications occurred in 18 (31%) patients and there were seven (12%) deaths. The most significant factors for both morbidity and mortality were old age group, late presentation, concomitant medical illness, size of perforation more than two cm and shock on presentation. Conclusion: PUP predominantly occurred in young age group as compared to International data and most of the patients were not known to suffer from peptic ulcer disease. The incidence increased in winter season and during fasting. ﻤﻠﺨﺹ ﺍﻷﻁﺭﻭﺤﺔ ﺗﻘﺪﱘ: ﱂ ﻳﺘﻢ ﺗﻘﻴﻴﻢ ﺍﻧﻔﺠﺎﺭ ﺍﻟﻘﺮﺣﺔ ﺍﳍﻀﻤﻴﺔ ﻣﻦ ﻗﺒﻞ ﰱ ﺍﻟﺴﻮﺩﺍﻥ، ﺃﺟﺮﻳﺖ ﻫﺬﻩ ﺍﻟﺪﺭﺍﺳﺔ ﻟﺘﺴﻠﻴﻂ ﺍﻟﻀﺆ ﻋﻠﻰ ﺍﳊﺪﻭﺙ ﻭﺍﺠﻤﻟﻰﺀ ﺍﻟﺴﺮﻳﺮﻱ، ﺍﳌﻌﺎﳉﺔ ﻭﺍﻟﻨﺎﺗﺞ. ﺍﻟﻔﻜﺭﺓ: ﺘﻡ ﺘﺠﻤﻴﻊ ﺍﻟﻤﻌﻠﻭﻤﺎﺕ ﻋﻥ ﺜﻤ ﺎﻨﻴﺔ ﻭﺨﻤﺴﻴﻥ ﻤ ﺭ ﻴ ﻀ ﺎﹰ ﻋﻠﻰ ﺍﻟﺘﺘﺎﻟﻲ ﻤﺼـﺎﺒﻴﻥ ﺒﺎﻟﻘﺭﺤـﺔ ﺍﻟﻬﻀﻤﻴﺔ ﺍﻟﻤﻨﻔﺠﺭﺓ ﻭﻤﻥ ﺜﻡ ﺘﻡ ﺘﺤﻠﻴﻠﻬﺎ. ﺍﻟﻨﺘﺎﺌﺞ: ﻤﻥ ﺸﻬﺭ ﻨﻭﻓﻤﺒﺭ ﻋﺎﻡ 1999ﻡ ﻭﺤﺘﻰ ﻤﺎﺭﺱ 2002ﻡ، ﺤﻀﺭ 52 ﺫﻜﺭ ﻭﺴﺕ ﺇﻨﺎﺙ ﻤﺼﺎﺒﻭﻥ ﺒﺈﻨﻔﺠﺎﺭ ﺍﻟﻘﺭﺤﺔ ﺍﻟﻬﻀﻤﻴﺔ. ﺃﻜﺜﺭ ﺍﻷﻋﻤﺎﺭ ﺘ ﺄ ﺜ ﺭ ﺍﹰ ﻫﻡ ﻤﺎ ﺩﻭﻥ ﺍﻟﺜﻼﺜﻴﻥ ﺴﻨﺔ . ﻋﺸﺭﺓ ﻤﺭﻀﻰ ﻓﻘﻁ ﻜﺎﻨﻭﺍ ﻤﻌﺭﻭﻓﻴﻥ ﺍﻹﺼﺎﺒﺔ ﺒﻤﺭﺽ ﺍﻟﻘﺭﺤﺔ ﺍﻟﻬﻀﻤﻴﺔ ﻗﺒل ﺤﺩﻭﺙ ﺍﻹﻨﺜﻘﺎﺏ، 40% ﺘﻘﺭﻴﺒﹰﺎ ﻤﻥ ﺠﻤﻠﺔ ﺤﺎﻻﺕ ﺍﻹﻨﺜﻘﺎﺏ ﺤـﺩﺜﺕ ﺨـﻼل ﺸﻬﺭ ﺭﻤﻀﺎﻥ "ﻋﺩﺩ 22 ﻤﺭﻴﺽ ". ﻜﺎﻥ ﻤﻌﻅﻡ ﺍﻟﻤﺭﻀﻰ ﺼﺎﺌﻤﻴﻥ "ﻋﺩﺩ 20 ﻤﺭﻴﺽ "، 42(24.7%) ﻤﻥ ﺤﺎﻻﺕ ﺇﻨﻔﺠﺎﺭ ﺍﻟﻘﺭﺤﺔ ﺤﺩﺜﺕ ﺨﻼل ﺍﻟﺸﺘﺎﺀ . 53(96.4%) ﻤﻥ ﺍﻟﺤﺎﻻﺕ ﻜﺎﻨﺕ ﻗﺭﺤـﺔ ﺍﻷﺜﻨـﻲ ﻋﺸـﺭ، ﻭﺜﻼﺙ ﻤﻥ ﺍﻟﺤﺎﻻﺕ ﻜﺎﻨﺕ ﻗﺭﺤﺔ ﺍﻟﻤﻌﺩﺓ . ﻜل ﺍﻟﻤﺭﻀﻰ ﺘﻘﺭﻴﺒﹰﺎ "ﻋﺩﺩ 55" ﺘﻤﺕ ﻤﻌﺎﻟﺠﺘﻬﻡ ﺠ ﺭ ﺍ ﺤ ﻴ ﺎﹰ ﺒﻭﺍﺴﻁﺔ ﺍﻟﻘﻔل ﺍﻟﺒﺴﻴﻁ ﻤﻊ ﺭﻗﻌﺔ ﺍﻟﺜﺭﺏ . ﻤﻀﺎﻋﻔﺎﺕ ﺒﻌﺩ ﺍﻟﻌﻤﻠﻴﺔ ﺤﺩﺜﺕ ﻓﻰ 17 (31.8%) ﻜﻤﺎ ﺃﻥ ﻫﻨﺎﻟﻙ ﺴـﺒﻌﺔ ﺤﺎﻻﺕ ﻭﻓﺎﺓ. ﺍﻟﻌﻭﺍﻤل ﺍﻷﻜﺜﺭ ﺇﻋﺘﺒﺎﺭﻴﺔ ﻤﻥ ﺤﻴﺙ ﺍﻟﻤﺭﺍﻀﺔ ﻭﺍﻟﻭﻓﺎﺓ ﻜﺎﻨﺕ، ﻜﺒﺭ ﺍﻟﺴﻥ، ﻋﻨﺼـﺭ ﺍﻟﻨﺴـﺎﺀ ، ﺍﻟﺤﻀﻭﺭ ﺍﻟﻤﺘﺄﺨﺭ، ﻭﺠﻭﺩ ﻤﺭﺽ ﻤﻌﺎﺼﺭ، ﺤﺠﻡ ﺍﻟﺜﻘﺏ ﺍﻜﺜﺭ ﻤﻥ 2 ﺴﻡ، ﺍﻟﺼﺩﻤﺔ ﺍﻟﺩﻭﺭﺍﻨﻴﺔ ﻋﻨﺩ ﺍﻟﺤﻀﻭﺭ ﺒﺎﻹﻀﺎﻓﺔ ﺇﻟﻰ ﻨﻘﺹ ﺍﻟﺼﻭﺩﻴﻭﻡ ﻭﺍﻟﺒﻭﺘﺎﺴﻴﻭﻡ. ﺍﻟﺨﻼﺼﺔ: ﻴﺒﺩﻭ ﺃﻥ ﺍﻨﻔﺠﺎﺭ ﺍﻟﻘﺭﺤﺔ ﺍﻟﻬﻀﻤﻴﺔ ﻤﺭﺽ ﻴﺼﻴﺏ ﺍﻟﺸﺒﺎﺏ ﻏ ﺎ ﻟ ﺒ ﺎﹰ ﻟﻴﺴـﻭﺍ ﻤﺭﻀـﻰ ﻤﻌﺭﻭﻓﻴﻥ ﺒﺎﻟﻘﺭﺤﺔ ﺍﻟﻬﻀﻤﻴﺔ ﻭﺘﺯﻴﺩ ﺤﺎﻻﺕ ﺍﻟﺤﺩﻭﺙ ﻓﻰ ﻓﺼل ﺍﻟﺸﺘﺎﺀ ﻜﻤﺎ ﻭﺃﻥ ﺍﻟﺼـﻴﺎﻡ ﻴﺒـﺩﻭ ﻜﻤﺤﻔـﺯ ﻟﺤﺩﻭﺙ ﺍﻻﻨﻔﺠﺎﺭ. INTRODUCTION Peptic ulcer perforation (PUP) occurs in about 10% of patients with peptic ulcer disease. (1) It is the commonest perforation of the upper gastrointestinal tract. Being a life threatening complication of Peptic ulcer disease (PUD) it needs prompt resuscitation and appropriate surgical management, if mortality and morbidity are to be avoided. It is the deep penetrating ulcers in the anterior surface of the duodenum and stomach that usually perforate in the peritoneal cavity. (2) Posterior surface lesions usually penetrate into the pancreas and present as bleeding rather than free perforation. A revolution in both diagnosis and management of PU disease occurred in the last few decades namely the H. pylori relations to the disease together with H2 receptor antagonists and PPI remedies and improvement in endoscopic facilities. In spite of all these, the incidence of PUP seems to be unaffected,(3) the thing which could be attributed to NSAIDs ingestion. ¾ Anatomy: The stomach lies in the left upper quadrant crossing the midline at the pylorus. The most proximal part is the cardia, small area, just distal to the GOJ. Populated by mucus gland cells. The corpus is the largest portion, lies between the cardia and antrum. It contains mucus, parietal and chief cells, the last two secrete acid and pepsin respectively. The antrum separated from the corpus by the incisura in the lesser curvature and the point where the left gastroepiploic artery enter the stomach along the greater curvature. Its populated by G- cells which secret gastrin which important in regulation of gastric acid secretion. The pylorus has strong muscles; it pumps the gastric contents into the duodenum. Blood supply: The left gastric artery is the largest artery supplying the stomach. It arises from the celiac trunk and runs a long the lesser curvature. The right gastric artery, from the common hepatic. The right gastroepiploic artery from the gastroduodenal artery, courses a long the greater curvature from right to left. The left gastroepiploic artery, a branch from the splenic artery, supplies the greater curvature of the fundus. The duodenum is supplied in it is superior part by the superior pancreaticoduodenal artery, a branch of gastroduodenal artery. The inferior part is supplied by the inferior pancreato-duodenal artery, a branch of the superior mesenteric artery. The stomach and duodenum have extensive submucosal channels that ensure a rich blood supply to the mucosa. This ensures adequate blood supply to the stomach even if only one of the four major vessels is intact. Venous drainage is through coronary, gastroepiploic and splenic vein to the portal vein.(4) Nerve supply: The stomach is supplied by the two major vagal trunks. The largest is the posterior, which is closely adherent to intra-abdominal oesophagus and slightly to the left of the midline. It’s large and easily identified during surgery. The anterior vagus resides slightly to the right of the intraabdominal oesophagus, it’s much smaller than the anterior and more difficult to localize. The nerve of Grassi is a branch of the posterior vagus that innervates the fundus. Failure to ligate this branch may result in ulcer recurrence following vagotomy. The nerves of Laterjet (Crow’s foot) are a tangle of nerves, Branches from the main trunks at the incisura. They innervate the antrum (5) and must be spared in highly selected vagotomy. ¾ Physiology: Acid secretion: Acid secretion occurs in the gastric corpus and fundus by the parietal cells. These cells secrete acid against very high concentration gradients. The maximum luminal acid concentration is 0.15N so acid concentration is more than ten million times the concentration of hydrogen in the blood. Acid in this concentration is highly corrosive and would disintegrate any tissue coming into contact. The stomach has several protective mechanisms against acid digestions; The tight intercellular junctions prevent luminal acid from penetrating the gastric epithelium; The luminal bicarbonate secretion, for each acid molecule generated a molecule of bicarbonate ion is secreted. Although most of it is carried away by gastric blood flow, some is secreted into the thick mucus gel. It also has a thick alkaline mucus gel lies immediately adjacent to the gastric epithelium, protecting it from injury. There is also a net outward fluid flux into the lumen which must exist with both acid and bicarbonate, this flux of water has a greater ability to maintain the gradient than any amount of mucus or bicarbonate. Because of the constant exposure to very high concentration of acid, gastric ulceration is unrelated to acid production. The primary responsible mechanism is the loss of gastric epithelial protective mechanism.(2,5) Signals of gastric acid secretion: Vagal activation: Stimulates secretion by several mechanisms; the release acetylcholine in the immediate vicinity of parietal cell. This cholinergic stimulation results in increase intracellular calcium of the parietal cells which leads to acid secretion. Stimulation of antral interneurons to release gastrin releasing peptide "GRP", which stimulates antral G.
Recommended publications
  • 4. Pathology Esophagus and Stomach
    Pathology of esophagus and stomach. Pathology of esophagus and stomach. I. Microspecimens: № 176. Acute gastric ulcer. (H.E. stain). Indications: 1. The superficial layer of the ulcer, consisting of leukocytes and erythrocytes. 2. Necrotic masses and tissue debris in the area of the ulcer. 3. Foci of necrosis in the muscular layer of the gastric wall. 4. Leukocyte infiltration in the edges and bottom of the ulcer. A lesion in the gastric wall is observed, which involves the mucosa, the muscularis mucosa and the submucosa; the bottom of the ulcer is presented by necrotic masses with diffuse leukocyte infiltration, which extends into the muscular layer of the gastric wall; blood vessels are dilated, hyperemic; there is no granulation tissue or mature fibrocollagenous tissue. Acute gastric ulcers are located more frequently on the lesser curvature, in the antral and pyloric region, they can also be on the greater curvature. They are usually multiple, more often round in shape, diameter up to 1.0-1.5 cm, the bottom is dark brown due to the accumulation of the hemoglobinogen pigment, hydrochloric hematin. The edges and bottom have a flaccid consistency, they are not hardened, the arrangement of the folds of the adjacent mucosa is not changed. In some cases, the acute ulcer can progress with involvement of the muscular layer of the gastric wall and even the serosa, which can lead to perforation and peritonitis. Deep acute ulcers often look like a funnel, with the base facing the gastric mucosa and the tip facing the serous membrane. Another complication is gastric bleeding.
    [Show full text]
  • Role of Yoga in Acid Peptic Disease: a Review
    wjpmr, 2021,7(9), 133 – 136. SJIF Impact Factor: 5.922 WORLD JOURNAL OF PHARMACEUTICAL Review Article Navedita et al. World Journal of Pharmaceutical and Medical Research AND MEDICAL RESEARCH ISSN 2455-3301 www.wjpmr.com Wjpmr ROLE OF YOGA IN ACID PEPTIC DISEASE: A REVIEW *1Dr. Navedita Kumari and 2Dr. Anupam Pathak 1PG Scholar, Dept of Swasthavritta & Yoga, SriGanganagar College of Ayurvedic Science and Hospital, Tanta University, SriGanganagar. 2HOD, Dept of Swasthavritta & Yoga, SriGanganagar College of Ayurvedic Science and Hospital, Tanta University, SriGanganagar. *Corresponding Author: Dr. Navedita Kumari PG Scholar, Dept of Swasthavritta & Yoga, SriGanganagar College of Ayurvedic Science and Hospital, Tanta University, SriGanganagar. Article Received on 15/06/2021 Article Revised on 05/07/2021 Article Accepted on 25/07/2021 ABSTRACT The acid peptic diseases, also known as acid peptic disorders are a collection of diseases involving acid production in the stomach and nearby parts of the gastrointestinal tract. It includes gastroesophageal reflux disease, gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer, Zollinger–Ellison syndrome and Meckel's [1] diverticulum ulcer. Acid peptic disorders are the result of distinctive, but overlapping pathogenic mechanisms [1] leading to either excessive acid secretion or diminished mucosal defense. Acid peptic disease – commonly called APD – includes a number of conditions. All these conditions are the result of damage from acid and peptic activity in gastric secretions. APD occurs when the acid starts irritating the inner cells (mucosal layer) of the stomach. Acid [2] peptic diseases mostly affect the oesophagus, stomach, and duodenum. “Acid peptic disease” is a collective term used to include many conditions such as gastro-esophageal reflux disease (GERD), gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer, Zollinger Ellison Syndrome (ZES) and Meckel‟s diverticular ulcer.
    [Show full text]
  • Peptic Ulcer Disease
    \ Lecture Two Peptic ulcer disease 432 Pathology Team Done By: Zaina Alsawah Reviewed By: Mohammed Adel GIT Block Color Index: female notes are in purple. Male notes are in Blue. Red is important. Orange is explanation. 432PathologyTeam LECTURE TWO: Peptic Ulcer Peptic Ulcer Disease Mind Map: Peptic Ulcer Disease Acute Chronic Pathophysiology Morphology Prognosis Locations Pathophysiology Imbalance Acute severe Extreme Gastric Duodenal gastritis stress hyperacidity between agrresive and defensive Musocal Due to factors increased Defenses Morphology acidity + H. Pylori infection Mucus Surface bicarbonate epithelium barrier P a g e | 1 432PathologyTeam LECTURE TWO: Peptic Ulcer Peptic Ulcer Definitions: Ulcer is breach in the mucosa of the alimentary tract extending through muscularis mucosa into submucosa or deeper. erosi on ulcer Chronic ulcers heal by Fibrosis. Erosion is a breach in the epithelium of the mucosa only. They heal by regeneration of mucosal epithelium unless erosion was very deep then it will heal by fibrosis. Types of Ulcer: 1- Acute Peptic Ulcers ( Stress ulcers ): Acutely developing gastric mucosal defects that may appear after severe stress. Pathophysiology: All new terms mentioned in the diagram are explained next page Pathophysiology of acute peptic ulcer Complication of a As a reult of Due to acute severe stress extreme gastritis response hyperacidity Mucosal e.g. Zollinger- inflammation as a Curling's ulcer Stress ulcer Cushing ulcer Ellison response to an syndrome irritant e.g. NSAID or alcohol P a g e | 2 432PathologyTeam
    [Show full text]
  • The Gastrointestinal Tract Frank A
    91731_ch13 12/8/06 8:55 PM Page 549 13 The Gastrointestinal Tract Frank A. Mitros Emanuel Rubin THE ESOPHAGUS Bezoars Anatomy THE SMALL INTESTINE Congenital Disorders Anatomy Tracheoesophageal Fistula Congenital Disorders Rings and Webs Atresia and Stenosis Esophageal Diverticula Duplications (Enteric Cysts) Motor Disorders Meckel Diverticulum Achalasia Malrotation Scleroderma Meconium Ileus Hiatal Hernia Infections of the Small Intestine Esophagitis Bacterial Diarrhea Reflux Esophagitis Viral Gastroenteritis Barrett Esophagus Intestinal Tuberculosis Eosinophilic Esophagitis Intestinal Fungi Infective Esophagitis Parasites Chemical Esophagitis Vascular Diseases of the Small Intestine Esophagitis of Systemic Illness Acute Intestinal Ischemia Iatrogenic Cancer of Esophagitis Chronic Intestinal Ischemia Esophageal Varices Malabsorption Lacerations and Perforations Luminal-Phase Malabsorption Neoplasms of the Esophagus Intestinal-Phase Malabsorption Benign tumors Laboratory Evaluation Carcinoma Lactase Deficiency Adenocarcinoma Celiac Disease THE STOMACH Whipple Disease Anatomy AbetalipoproteinemiaHypogammaglobulinemia Congenital Disorders Congenital Lymphangiectasia Pyloric Stenosis Tropical Sprue Diaphragmatic Hernia Radiation Enteritis Rare Abnormalities Mechanical Obstruction Gastritis Neoplasms Acute Hemorrhagic Gastritis Benign Tumors Chronic Gastritis Malignant Tumors MénétrierDisease Pneumatosis Cystoides Intestinalis Peptic Ulcer Disease THE LARGE INTESTINE Benign Neoplasms Anatomy Stromal Tumors Congenital Disorders Epithelial Polyps
    [Show full text]
  • Path GI – Liver – Gallbladder Paragraph Style
    Path GI – Liver – Gallbladder Paragraph Style Esophagus Congenital Hemorrhage Esophagitis Tumors Fistula Mallory‐Weiss GERD Sqaumous Cell Carcinoma Webs Esophageal Varices Barrett’s Adenocarcinoma Achalasia Chemical CONGENITAL Fistula. Fistulas often occur together with atresias. Atresias are where a tube (in this case the esophagus) ends in a blind pouch. A Fistula is where a tube connects to another tube. A Tracheoesophageal fistula is a connection between the trachea and the esophagus. Over 80% of these lesions occur with atresia of the proximal esophagus, and a fistula of the distal esophagus to the trachea. This means that when the baby swallows, the food goes into the trachea! This is pretty clear early on, presenting with dysphagia (spitting up, not vomiting, food), and Coughing + Cyanosis during feeding. Air in stomach may be seen as well. This must be surgically corrected, which is easy to do. Webs. Esophageal webs are simply extensions of mucosal epithelium into the lumen of the esophagus. They act as nets which can catch food trying to be swallowed. This presents with dysphagia and foul breath as the food that gets stuck putrefies in the esophagus. Webs are associated with Plummer‐ Vinson Syndrome from the Heme block, presenting with iron deficiency anemia and an increased risk for sqaumous cell carcinoma. These will persist into adulthood Achalasia. This is a failure of the LES to relax. When food is swallowed, it cannot pass into the stomach, causing distension of the esophagus (megaesophagus) and dysphagia. Over time, the food is pushed through the tight sphincter. It is caused by death of ganglionic cells in the LES.
    [Show full text]
  • Gastroesophageal Reflux Disease & Peptic Ulcer
    Case scenario L1&2: Gastroesophageal Reflux Disease & Peptic Ulcer objectives ● Describe the definition, pathogenesis, clinical features, pathology (gross and microscopic features) and complications of reflux esophagitis. ● Describe the definition, main cause, pathology (gross and microscopic features) and complications (dysplasia and adenocarcinoma) of Barrett esophagus. ● Define ulcer and erosion. ● Describe the pathogenesis, pathology and clinical features of acute gastric ulcers. ● Describe the pathogenesis (H pylori, NSAID, Z-E syndrome), clinical features, pathology (gross and microscopic features) and complications (bleeding, perforation, obstruction) of chronic peptic ulcers. Black: original content Orange: Doctor notes Red: Important Grey: Extra/Robbins Green: only found in males slides Purple: Only found in females slides Editing File Lecture Content Physiological GERD reflux Esophagitis (pathological) Severe stress Acute gastritis Hyperacidity response Acute Ulcers Chronic Gastric Duodenal NSAIDs Bile Reflux H. pylori Infection Hyperacidity Esophagitis Reflux esophagitis ● Symptoms or mucosal damage produced by the abnormal reflux of gastric content into the esophagus, often chronic and relapsing. ● Esophagitis is rarely caused by anything other than reflux. ● May see complications of GERD in patients who lack typical symptoms. ● Some other causes include: ○ Infective ■ Fungal infection (common): candida albicans. ■ Viral infection: Herpes simplex and cytomegalovirus in AIDS patients. ■ Bacterial infection is very rare. ○ Physical Agent
    [Show full text]
  • Internal Biliary Fistula Secondary to Cushing's Ulcer in a Child
    A CASE REPORT A CASE REPORT Internal Biliary Fistula Secondary to Cushing’s Ulcer in a Child by Allison Ta, Suchitra Hourigan, Otto Louis-Jacques INTRODUCTION nternal biliary fistulas are abnormal communications On HD 11, she became acutely hypotensive and her between the extrahepatic biliary tree and another hemoglobin dropped from 10 to 5.1g/dL. Nasogastric Iorgan. These fistulas are rare disorders, typically (NG) tube lavage revealed brown colored fluid. She affecting elderly patients as complications of biliary was resuscitated with packed red blood cells and disease or, less commonly, peptic ulcer disease or fluids. Urgent esophagogastroduodenoscopy (EGD) cancer requiring surgical intervention. We present the discovered a large, non-bleeding duodenal ulcer. An case of a cholecystoduodenal fistula (CDF) secondary orifice was seen medially within the ulcer bed (Figure to a perforated duodenal ulcer in a pediatric patient 1). Biopsies taken at the time of EGD confirmed with posterior fossa tumor. We discuss the success ulceration and ruled out Helicobacter infection. An of medically treating this patient with proton pump abdominal computed tomography (CT) scan revealed inhibitors and subsequent resolution of the fistula. air and contrast in a normal-appearing gallbladder, with a small communication between gallbladder and duodenum, consistent with a cholecystoduodenal Case Report fistula (Figure 2). Pediatric surgery was consulted and A 10 year-old female presented to the hospital with recommended medical management. complaints of headache, vomiting, abnormal gait and The patient was started on intravenous pantoprazole upper extremity weakness for approximately eight at 120 mg daily (roughly 1.6mg/kg/day), total parenteral months. She utilized ibuprofen or acetaminophen nutrition and a NG tube was placed for gastric several times a week for her symptoms.
    [Show full text]
  • Peptic Ulcer Disease
    19 September 2018 Surgery of the stomach and duodenum: Peptic ulcer disease *- Congenital hypertrophic pyloric Nature stenosis Sites of peptic ulcer disease Etiology *- Acute gastric dilatation Types: *- Peptic ulcer disease (acute erosions – *- Gastric erosions (erosive gastritis) chronic peptic ulcer) *- Stress ulcers e.g. ICU patients, trauma patients, intra- *- Gastric volvulus cranial trauma or operations (Cushing ulcer), burned patients (Curling ulcer) *- Bezoars Clinical presentations *- Gastric neoplasms Diagnosis *- Gastrectomy, and its complications Treatment: Medical treatment *- Gastrostomy Endosc. treatment ( injections , Laser, or thermal ttt ) *- Gastric role in bariatric surgery Surgical treatment Gastrectomy ?? 1 Prof. Alaa Ahmad Redwan, 2017 19 September 2018 *- Chronic peptic ulcer Etiology: Increased gastric acidity is the main association, multifactorial by * Genetic predisposition (large parietal cell mass) * Increased vagal tone mainly by night may be by worry or stress * Abnormality in gastrin release and inhibition * Helicobacter pylori causing gastritis, duodenal ulcer and sometimes MALT lymphoma. * Hypergastrinaemia by pancreatic gastrinoma (Zollinger Ellison syndrome) * Spicy meals, drinks, smoking, alcohol , drugs, 2 Prof. Alaa Ahmad Redwan, 2017 19 September 2018 Clinical presentation: Incidence: *- Pain (post prandial , localized , deep, severe, Decreasing incidence of ulcer disease with 50-60% increased by codiments, wores by night) increased GE reflux and gastritis More common in males (5:1), age is around middle *- Nausea and vomiting age (??) *- Periodicity (periods of activity followed by DU : GU = 25 : 1 period of quiescence),loss of periodicity signats 15-20% 15-20% complications , penetration, or spastic pyloric Pathology: stenosis Site gastric , duodenal (Kissing ulcers) Size Single or multiple *- Complications as bleeding (hematemesis, or Shape Edge Floor Base melena, hematochasia?? ), penetration (pancreatitis), perforation (peritonitis), or ?10% pyloric obstruction.
    [Show full text]
  • Peptic Ulcers and Their Complications
    OESOPHAGUS AND STOMACH non-steroidal anti-inflammatory drugs (NSAIDS) and infection Peptic ulcers and their with Helicobacter pylori play by far the biggest roles. The reporting of the Campylobacter-like organism H. pylori, complications by Warren and Marshall in 19843 marked a giant leap in medical understanding of peptic ulceration. This Gram-negative, helical, Duncan J Stewart microaerophilic, flagellated bacterium has since been recognized Roger Ackroyd to be responsible for up to 95% of duodenal and 70% of gastric ulcers.4 Furthermore, it is present in up to 10% of patients with dyspepsia without ulceration. Infection with H. pylori is wide- spread and probably acquired in childhood via the faecaleoral Abstract route, although this is yet to be confirmed. In addition, socio- The incidence and management of peptic ulcer disease have changed economic status appears to be inversely related to the prevalence considerably since the first surgical interventions, carried out less than of infection.5 H. pylori colonizes only gastric mucosa, predomi- a century ago. Operative techniques refined during the early second nantly in the antrum and pyloric canal. It possesses a urease half of the 20th century have become almost obsolete in today’s practice enzyme which converts urea to ammonia and carbon dioxide, for two principal reasons. Firstly, understanding of the aetiology of the buffering gastric acid in its vicinity facilitating its survival in the disease process has taken a dramatic step forward with the discovery acidic gastric environment. of Helicobacter pylori now known to be associated with 95% of cases There are a number of mechanisms by which H.
    [Show full text]
  • Boerhaave's Syndrome
    Boerhaave's Syndrome: The Importance of Early Diagnosis and Treatment JOSEPH J. CURCI, M.D.,* MARC J. HORMAN, M.D.t Boerhaave's syndrome, spontaneous esophageal rupture, is asso- From the Department of Surgery and the Pulmonary Section, ciated with a 70% survival with surgical intervention. Mortality Abington Memorial Hospital, Abington, Pennsylvania and morbidity are increased in direct proportion to the time be- tween diagnosis and appropriate surgical intervention. Sepsis, hypovolemia and shock are the predominant causes of morbidity and mortality in Boerhaave's syndrome. Two cases of Boerhaave's Two recent cases ofspontaneous rupture ofthe esopha- syndrome are presented which were diagnosed rapidly, and gus successfully treated at Abington Memorial Hospital were managed surgically, resulting in survival of the patients. in Abington, Pennsylvania, will be presented along with A review of the literature is also presented with emphasis on a the clinical and roentgenologic methods of diagnosis of spon- review of the recent literature. taneous esophageal rupture. Particular attention is given to the fact that early diagnosis and treatment will unquestionably Case Reports reduce the morbidity of this syndrome. Case 1: H.F., a 49-year-old Caucasian man, was seen in the Emer- gency Room of Abington Memorial Hospital at 5:00 pm after two epi- B AROGENIC rupture of the esophagus, the so-called sodes of vomiting approximately one hour prior to admission. The "Boerhaave Syndrome," is the most serious and second episode was followed by severe epigastric pain radiating to the rapidly lethal perforation of the gastro-intestinal tract.33 midback area and associated with diaphoresis.
    [Show full text]
  • [ ​Color Index​ | ​ Important​ | ​Notes​ ​ | ​Extra​ ]
    Objectives: ● The surgical anatomy of stomach and duodenum, their blood supply, nerve supply & lymphatics. ● The surgical physiology of gastric motility and secretions. ● Special forms of peptic ulceration. ● Management of uncomplicated peptic ulcer disease. ● Complications of peptic ulceration requiring operative intervention including: ○ Perforation ( perforated ulcers). ○ Acute hemorrhage. ○ Pyloric stenosis. ● Benign Gastric neoplasms. Resources: ● Davidson’s. ● Slides ● Surgical recall. ● Raslan’s notes. ● Current diagnosis and treatment (colored in blue) ● Team 434 Done by: ​Lama​ ​AlZamil & Aljohara Almazroua Sub-leader: ​Abdullah Alghizzi Leaders:​ ​Monerah Alsalouli & Abdulrahman Alsayyari Reviewed by:​ ​Ahmad Alyahya [ Color index | Important | Notes | Extra ] ​ ​ ​ ​ ​ ​ ​ ​ ​ [ Editing file | Feedback | Share your notes | Shared notes ] ​ ​ ​ ​ ​ ​ ​ ​ ​ Basic review(anatomy): Doctor said:Stomach & Duodenum anatomy (including its blood supply & their origins) and physiology are included in the examination and you need to cover it(check the MCQ’s in the last page) ​ Stomach subdivided into 5 parts (each part has secretory and nonsecretory function) Part Notes Cardia Site for Barrett's disease Fundus Secretory: parietal cell and Neurogenic: hunger feeling Body Secretory: parietal cell Antrum Site for surgical ulcer treatment: by cutdown the acid secretion (site for gastrin) Even if the ulcer in the duodenum. Pylorus Site for Dumping Syndrome (food goes immediately to SI) Duodenum parts : 25 cm long and subdivided into 4 parts Part Name Level Common site for First Upper 1st LV Ulcer Second Vertical 2nd LV Diverticulum Third Horizontal 3rd LV Superior Mesenteric Artery Syndrome Fourth Ascending 3rd LV - The 1st part of Duodenum: (Relations) - Anteriorly:The quadrate lobe of the liver and the gallbladder . - Posteriorly: The lesser sac (first inch only), the gastroduodenal artery ( that’s why Posterior ulcer bleed), the bile duct and portal vein, and the inferior vena.
    [Show full text]
  • Pathophysiology of GIT I
    GIT • 1- oesophagus Pathophysiology of • 2- organs of peritoneal cavity GIT I • 3- stomach (1.5l) • 4- gastroesophageal junction Oral cavity and salivary glands • 5- pylorus • 6- small intestine (4.5 – Oesophagus 6m) Stomach and duodenum • 7- duodenum • 8- jejunum Small and large intestine • 9- ileum • 10- ileocaecal valve • 11- large intestine • ascendant • horizontal • descendant • rectum + anus 1 2 Pathophysiology of oral cavity Pathophysiology of oral cavity • salivary glands - salivation (1 - 1.5l/day) • continual production by small salivary glands • large glands secerns only upon stimulus • centrum in medulla oblongata → sal. glands (via n. facialis) • afferentation from upper centres (cortex, hypothalamus) upon stimuli (taste, smell, chewing, …) • enzymes and ions of saliva • α-amylase (polysaccharides), lipase • lysozyme (bactericide) + + - - • K , Na , Cl , HCO3 • disease of oral cavity • abnormal secretion of saliva • ↑ - inflammation (e.g. tonsillitis), mechanical irritation • ↓ (xerostomy) - dehydration, Sjögren syndrome, drugs • abnormal chewing • painful mandibular joint • injury of tongue • painful teeth • mucosal inflammation • infections • herpetic (HSV-1), bacterial, candidiasis (in immune compromised patients) • diseases of temporomandibular joint • pain • dislocation (habitual) • precanceroses and tumors of oral cavity • leucoplakia • carcinoma – smokers, alcoholics • signs of systemic diseases in oral cavity • anaemia • vitamin and iron carrncy • malnutrition • cyanosis • Crohn’s disease 3 4 Reflexive salivation
    [Show full text]