Gastroenterology E-Book

Satish Keshav

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: Clinical Cases
• Sprache: Englisch

Seitenzahl: 442

Veröffentlichungsjahr: 2011

Beschreibung

Gastroenterology is a critically important specialty in medicine, encompassing the GI tract and two vital organs - the pancreas and the liver. Gastroenterology: Clinical Cases Uncovered includes reference to the new JCHMT curriculum for acute and internal medicine concerning gastroenterology and hepatology and presents real-life patient cases and outcomes as seen on the wards and in exams leading students through a practical approach to recognize, understand, investigate and manage gastroenterological and hepatological disorders and conditions.

Following a question-answer approach, with self-assessment MCQs, EMQs and SAQs, and a 'refresher' section on basic science, Gastroenterology: Clinical Cases Uncovered features investigations and the treatment options available for patients with upper and lower GI disorders, liver disease, biliary and pancreatic disease, and problems of nutrition.

Gastroenterology: Clinical Cases Uncovered is ideal for medical students, junior doctors on the Foundation Programme, GP trainees, specialist nurses and nurse practitioners and gastroenterology trainees on the specialty training programme.

Leseprobe

Contents

Preface

How to use this book

List of abbreviations

Part 1 Basics

Basic science

Approach to the patient

Part 2 Cases

Upper gastrointestinal

Case 1 A 61-year-old woman with progressive dysphagia

Case 2 A 52-year-old man with atypical chest pain

Case 3 A 57-year-old woman with upper abdominal discomfort

Case 4 A 36-year-old man with upper abdominal discomfort and heartburn

Case 5 A 27-year-old woman with nausea and vomiting

Case 6 A 73-year-old man with haematemesis and melaena

Case 7 A 68-year-old woman with fatigue, weight loss and altered bowel habit

Lower gastrointestinal

Case 8 A 23-year-old woman with constipation

Case 9 A 24-year-old woman with chronic diarrhoea

Case 10 A 51-year-old woman with acute nausea, vomiting and diarrhoea

Case 11 A 79-year-old woman with altered bowel habit and weight loss

Case 12 A 54-year-old man with rectal bleeding

Case 13 A 66-year-old woman with anaemia

Liver disease

Case 14 A 64-year-old man with abnormal liver function tests

Case 15 A 45-year-old man with acute jaundice

Case 16 A 53-year-old woman with jaundice and abnormal liver tests

Case 17 A 53-year-old man with abdominal swelling

Case 18 A 36-year-old man who drinks alcohol

Biliary and pancreatic disease

Case 19 A 79-year-old man with right upper quadrant colicky abdominal discomfort

Case 20 A 19-year-old man with acute abdominal pain

Nutrition

Case 21 A 35-year-old woman with anorexia

Case 22 A 48-year-old man with an increased body mass index

Functional disorders

Case 23 A 21-year-old student with chronic abdominal pain

Part 3 Self-assessment

MCQs

EMQs

SAQs

Answers

Further reading

Index of cases by diagnosis

Index

This edition first published 2011 © 2011 by Satish Keshav and Emma Culver

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Library of Congress Cataloging-in-Publication Data

Keshav, Satish.

Gastroenterology / Satish Keshav, Emma Culver.

p.; cm. – (Clinical cases uncovered)

Includes bibliographical references and indexes.

ISBN 978-1-4051-6975-2 (pbk. : alk. paper)

1. Gastroenterology–Case studies. 2. Digestive organs–Diseases–Case studies. I. Culver, Emma. II. Title. III. Series: Clinical cases uncovered.

[DNLM: 1. Digestive System Diseases–diagnosis–Case Reports. 2. Digestive System Diseases– diagnosis–Problems and Exercises. WI 18.2]

RC808.K47 2011

616.3′3–dc22

2010039153

Preface

Clinical gastroenterology is both simple and complex. The simplicity comes from the finite number of diagnoses that are commonly encountered, and the relatively limited number of symptoms that typically indicate disease of the gastrointestinal system. However, there are hidden depths to the practice of the speciality. Gastroenterologists deal with disease affecting many separate organs that all form part of the same system – the liver, pancreas, stomach, etc. The clinical consequences of some diseases can be dramatic and complex, particularly, for instance, dysfunction of the liver. Symptoms such as abdominal pain, altered bowel function and changes in weight can be combined in myriad ways to pose true clinical puzzles. This book aims to guide the reader through this complexity by offering real case studies and showing how, in practice, clinicians can achieve some degree of clarity, and offer to patients a reasonable diagnostic and therapeutic plan.

In the first section, the book offers a basic and brief overview of anatomical, physiological and pharmacological facts that inform our thinking about gastroenterological problems, and suggests how best to approach the patient in the second chapter. Thereafter, in the second section, each chapter deals with presenting symptoms and signs and the subsequent chapters are arranged in six sections to cover disease processes affecting the upper gastrointestinal tract, lower gastrointestinal tract, liver, pancreas and biliary tract, nutrition, and so-called functional bowel disorders. These are important and often overlooked because there is a profound lack of understanding about their pathogenesis. However, there are many patients with irritable bowel syndrome and the like, and a robust and reliable clinical approach to treating them is essential.

In each of the symptom- or sign-based chapters, the emphasis is on clinical reasoning and strategy, and the reader will have an opportunity to examine how the many possible paths are in practice negotiated to reach a diagnosis and formulate a plan for managing the situation. Exact doses and tests are de-emphasised, while strategies, categories and context are highlighted, all within the framework of dealing with the particular human patient whose predicament is being examined.

Boxes and lists are strategically placed to aid memory and recall, and to emphasise key facts. The last section, which comprises a set of questions to test understanding, is based on the contents of each chapter, and the emphasis in these is on core knowledge rather than the esoteric or arcane.

Writing this book has proved to be an education as well being hugely enjoyable, and our hope is that the reader too will gain knowledge and understanding of the complexity of gastroenterological medicine, whilst acquiring some practical understanding of how to approach the patient with gastrointestinal problems, and some sense of satisfaction and fun. The typical reader might be a medical or nursing student in their clinical years, or a doctor in training, either in their foundation years or in early speciality training. The book will be useful as preparatory reading before joining the gastroenterology firm in a clinical rotation, or as an aid to revision before written and clinical examinations.

Satish Keshav

Emma Culver

How to use this book

Clinical Cases Uncovered (CCU) books are carefully designed to help supplement your clinical experience and assist with refreshing your memory when revising. Each book is divided into three sections: Part 1, Basics; Part 2, Cases; and Part 3, Self-assessment.

Part 1 gives you a quick reminder of the basic science, history and examination, and key diagnoses in the area. Part 2 contains many of the clinical presentations you would expect to see on the wards or to crop up in exams, with questions and answers leading you through each case. New information, such as test results, is revealed as events unfold and each case concludes with a handy case summary explaining the key points. Part 3 allows you to test your learning with several question styles (MCQs, EMQs and SAQs), each with a strong clinical focus.

Whether reading individually or working as part of a group, we hope you will enjoy using your CCU book. If you have any recommendations on how we could improve the series, please do let us know by contacting us at: [email protected].

Disclaimer

CCU patients are designed to reflect real life, with their own reports of symptoms and concerns. Please note that all names used are entirely fictitious and any similarity to patients, alive or dead, is coincidental.

List of abbreviations

ACEangiotensin-converting enzymeADHantidiuretic hormoneAFPα-fetoproteinAIDSacquired immune deficiency syndromeAIHautoimmune hepatitisALPalkaline phosphataseALTalanine aminotransferaseAMAantimitochondrial antibodyANAsantinuclear antibodiesanti-SMAsanti-smooth muscle antibodiesARDS acuterespiratory distress syndrome5-ASA5-aminosalicylatesASCAanti-Saccharomyces cerevisiae antibodyASTaspartate aminotransferaseβ-HCGbeta-human chorionic gonadotrophinBCG bacilleCalmette-Guérin (vaccine)BMIbody mass indexBSGBritish Society of GastroenterologyCBDcommon bile ductCMVcytomegalovirusCOPDchronic obstructive airways diseaseCRPC-reactive proteinCTcomputed tomographyCXRchest X-rayDEXAdual energy X-ray absorptiometric scanDICdisseminated intravascular coagulationDREdigital rectal examEBVEpstein–Barr virusECGelectrocardiogramERCPendoscopic retrograde cholangiopancreatographyEUSendoscopic ultrasoundFDAFood and Drug Agency of the USAFDGfluorodeoxyglucoseFOBfaecal occult bloodγ-GTgamma glutamyl transferaseGAHSGlasgow alcoholic hepatitis scoreGIgastrointestinalGORDgastro-oesophageal reflux diseaseG6PDglucose-6 phosphate dehydrogenaseGTNglyceral trinitrateHBcAbhepatitis B core antibodyHBeAbhepatitis B ‘ e ’ antibodyHBeAghepatitis B ‘e’ antigenHBsAbhepatitis B surface antibodyHBsAghepatitis B surface antigenHBVhepatitis B virusHCChepatocellular carcinomaHCVhepatitis C virusHCVAbhepatitis C antibodyHHChereditary haemochromatosisHIVhuman immunodeficiency virusHLAhuman leukocyte antigenH2RAH2-receptor antagonistHUShaemolytic uraemic syndromeIBDinflammatory bowel diseaseIBSirritable bowel syndromeIgAimmunoglobulin AINRinternational normalised ratioJVPjugular venous pressureLDHlactate dehydrogenaseLDLlow density lipoproteinLFTsliver function testsLKMAsliver–kidney microsomal antibodiesMALTmucosal-associated lymphoid tissueMCVmean corpuscular volumemDFMaddrey’s discriminant functionMDTmultidisciplinary teamMHCmajor histocompatibility complexMRCPmagnetic resonance cholangiopancreatographyMRImagnetic resonance imagingNAFLDnon-alcoholic fatty liver diseaseNASHnon-alcoholic steatohepatitisNSAIDsnon-steroidal anti-inflammatory drugsPBCprimary biliary cirrhosisPCRpolymerase chain reactionPDHpyruvate dehydrogenasePETpositron emission tomographyPPIprotein pump inhibitorPTprothrombin timeSA-AGserum ascites?albumin gradientSIRSsystemic inflammatory response syndromeT3tri-iodothyronineT4thyroxineTIBCtotal iron-binding capacityTIPSStransjugular intrahepatic portal-systemic shuntTNF-αtumour necrosis factor αTSHthyroid-stimulating hormonetTGtissue transglutaminaseTTPthrombotic thrombocytopenic purpuraVIPvasoactive intestinal peptidevWFvon Willebrand factorWBCwhite blood cell count

Part 1 Basics

Basic science

Introduction

The intestinal tract is essential for maintaining nutrition by appropriate intake of macronutrients, micronutrients, fluid and electrolytes. Intestinal failure can lead to nutritional catastrophe and imbalances in fluid and electrolytes.

The pancreas is the main producer of digestive enzymes that facilitate the extraction of nutrients from food. Pancreatic dysfunction can cause malabsorption of food.

The liver has an essential and central role in metabolism, critical functions in detoxifying and excreting endogenous and exogenous molecules in bile, and in synthesising essential serum proteins such as albumin and clotting factors. Liver failure is rapidly fatal.

Embryology

The entire intestinal tract is derived embryologically from the endoderm, and can be conceptualized as a hollow tube stretching from the mouth to the anus, with the liver and pancreas as gland-like specialised appendages, connected to the main tract by ducts.

Structure

The main intestinal tract has a basic structure that is preserved throughout:

The innermost layer, facing the hollow lumen, is lined by a specialised layer of epithelial cells that vary from region to region.The epithelium is supported by a layer of connective tissue, the lamina propria.The lamina propria is surrounded by a layer of smooth muscle, the muscularis mucosae.The muscularis is surrounded by the submucosal connective tissue.Outside of this are strong layers of muscle, the muscularis propria. This is generally organised in an inner circular layer with fibres running at right angles to the long axis of the tube, and an outer longitudinal layer with fibres running along the long axis.The outermost layer of much of the intestinal tract is the visceral peritoneum, which is an epithelial layer.

Most lengths of the small and large intestine are attached to the posterior wall of the abdominal cavity by a length of mesentery, which is comprised of connective tissue covered by a continuation of the visceral peritoneal layer, and through which blood and lymphatic vessels and nerves run.

Blood supply

The arterial blood supply to the intra-abdominal intestinal organs, from stomach to rectum, and including the liver and pancreas, is derived from the coeliac, superior mesenteric and inferior mesenteric arteries, which are direct branches of the abdominal aorta.

The venous drainage of most of the intra-abdominal organs is via the hepatic portal vein, which enters the liver, and provides 75% of the hepatic blood supply. This hepatic portal flow system means that absorbed nutrients first enter the liver, before reaching the systemic circulation.

Nerve supply

Most of the gastrointestinal tract is innervated by the autonomic nervous system with parasympathetic and sympathetic branches. The intestine also contains an intrinsic nervous system organised into interconnected plexuses in the submucosa and the muscularis propria, which is termed the enteric nervous system. This provides isolated segments of intestine with the ability to coordinate secretion and motility without external innervation.

Immune system

The intestinal tract encounters food particles, antigens and potentially harmful microorganisms constantly. Arguably, it must contend with the greatest challenge in defending the organism against infection and other danger, as unlike other areas exposed to the external world, such as the skin and lungs, it also has to make fine distinctions between substances that could be either essential food or lethal foe – ‘salmon or Salmonella?’.

As a consequence, the immune system of the gastrointestinal tract is highly developed and specialised, and contains approximately 70% of all the immune cells in the body.

Anatomy and function

The intestinal tract

Mouth, pharynx and oesophagus

The mouth with teeth, tongue and salivary glands is essential for ingestion of food and nutrition. The senses of taste and smell serve to identify healthy food, and coordinated activity of the muscles of mastication, the tongue and pharynx allow food to be processed and swallowed safely.

The mouth, pharynx and oesophagus are all lined by a stratified squamous epithelium. The muscle layers of the

Fig A Overview of gastrointestinal function.

Fig B Organisation of the hollow organs.

upper oesophagus are striated skeletal-type muscle, while the muscle layers of the distal oesophagus, like the rest of the intestinal tract, comprise smooth, non-striated fibres.

Stomach

The stomach is J-shaped, wider at the proximal, upper end, known as the body, and narrowing distally to form the antrum, from which the pylorus leads to the duodenum. This shape means that the stomach can act as a reservoir for food after a meal. Strong churning movements of the stomach convert solid food boluses from the oesophagus into slurry called chyme, which passes easily into the duodenum.

The gastric epithelial lining is comprised of a single layer of columnar cells, which is also the case for the rest of the intestinal tract distal to the stomach. In the stomach this epithelial layer is specialised to produce hydrochloric acid from parietal cells, via a specialized K+/H+ transporter, popularly known as the proton pump. This initiates the process of digestion by activating the enzyme pepsinogen, produced by oxyntic cells in the gastric epithelim.

Duodenum

Anatomy

The epithelium of the duodenum is specialised for absorption, comprising a single layer of columnar cells that are lined with microscopic microvilli to increase the surface area for absorption. Furthermore, specialised molecules on the cell surface, including transporters and enzymes, are critically important for this digestive and absorptive function.

The lining of the duodenum, like the rest of the small intestine, is arranged into finger-like projections into the lumen, called villi, which serve to increase the surface area, and indentations into the wall of the intestine, called crypts. The stem cells, from which the entire epithelial lining is renewed, approximately every 7 days, are located in the crypts. The stem cells provide, by division and differentiation, all the major cells of the intestinal lining; these include:

Absorptive enterocytes.Goblet cells, which produce mucus.Paneth cells, which have a role in antibacterial defence.Neuroendocrine cells, which produce a variety of enteric hormones such as somatostatin, cholecystokinin, gastrin, vasoactive intestinal peptide (VIP) and glucacon-like peptides.

Function

Bile from the gallbladder, and pancreatic secretions enter the duodenum through the ampulla of Vater, providing bicarbonate-rich alkaline secretions, bile salts to emulsify fats, and carbohydrate, protein and fat-digesting enzymes, which neutralise acid chyme from the stomach, and begin the major work of digestion. Thus the duodenum is a crucial region for digestion and absorption.

Jejunum and ileum

Anatomy

The basic structure of the distal small intestine is identical to the duodenum, with villi, crypts, submucosa and circular and longitudinal muscle layers.

Blood and lymphatic supply

The blood supply is from the superior mesenteric artery. The venous drainage is via the superior mesenteric vein, joining the splenic vein to form the hepatic portal vein, which enters the liver carrying nutrients from the small intestine.

The lymphatic drainage of the small intestine, which carries fat-rich particles absorbed from food, enters the thoracic duct, emptying into the systemic venous circulation. The smallest lymph channels, called lacteals, are found in the central core of each villus, strategically placed to absorb triglyceride-rich chylomicrons.

Function

These segments of the small intestine are essential for absorbing food. The minimum length of small intestine necessary to sustain life is approximately 100 cm, and the function of this minimum length is enhanced if the ile-ocaecal valve is intact.

There is some regional specialisation – the jejunum is the main site of absorption of folic acid, and the ileum is essential for the absorption of vitamin B12 and of bile salts, which are recycled via an enterohepatic circulation.

Box A Specialisation in the small bowel

Ileum: absorption of vitamin B 12 and bile saltsJejunum: absorption of folic acid

Constant peristaltic activity of the small intestine, including a daily migrating motor complex wave that clears the intestine, together with many antibacterial substances secreted into the intestine, keep the number of bacteria in the small intestine relatively low, certainly compared to the large intestine. This may be important for optimum absorption of nutrients, and, in certain pathological conditions, bacterial overgrowth in the small intestine can cause diarrhoea and malabsorption.

The large intestine

Anatomy

The basic structure of the large intestine is similar to the small intestine. The differences are:

The external longitudinal layer of smooth muscle in the large intestine is collected into bands called taenia.There are no villi in the large intestine.

The ileum enters the caecum, which is the most proximal part of the large intestine, via the ileocaecal valve, which partially prevents the reflux of bacteria into the small intestine. Distal to the caecum is the ascending colon, situated along the right flank, the transverse colon extending from just below the liver to just below the spleen, the descending colon situated along the left flank, the sigmoid colon curving over the pelvic brim, and the rectum which is situated in front of the sacrum and ends at the junction of rectum and anus.

The anus is the muscular sphincter that maintains the continence of faeces and flatus in the rectum, and is comprised of an inner layer of smooth muscle, the internal sphincter, and an outer layer of voluntary muscle, the external sphincter. The lining of the anus is a stratified squamous epithelium that blends into the skin at the anal verge.

Box B Structural components of the large intestine (proximal to distal)

Ileocaecal valveCaecumAscending colonHepatic flexureTransverse colonSplenic flexureDescending colonSigmoid colonRectumAnus

Blood supply

The vascular supply of the colon is derived from the superior and inferior mesenteric arteries, and the venous drainage is via the superior and inferior mesenteric veins. The venous return from the rectum is into the systemic circulation so that portosystemic shunts can form in this region, as they can in the distal oesophagus.

Nerve supply

Defecation is controlled by both autonomic and somatic nerves, and the nerve supply of the rectum is from the sacral plexus.

Function

The main function of the large intestine is to reabsorb water from the small intestinal effluent. When patients undergo a colectomy and are left with an ileostomy, fluid losses from the stoma can be of the order of litres per day; this is in contrast to the normal volume of faecal output, which is approximately 200 mL.

Specialised cells

The main epithelial cells, colonocytes, are specialised for the absorption of electrolytes and water, and there are many goblet cells and few or no Paneth cells in the crypts of the colon.

Hepatobiliary system and pancreas

Liver

Anatomy

The liver is the largest single organ in the body at approximately 1.5 kg in weight. It is located in the right upper quadrant of the abdomen, directly under the right hemi-diaphragm. The arterial supply is via the hepatic branch of the celiac artery, and the portal vein. The venous drainage via the hepatic veins is into the inferior vena cava.

The secretory product of the liver, bile, is excreted via biliary canaliculi that coalesce to form bile ducts. The bile ducts in turn form the main intrahepatic bile ducts, which form the hepatic duct. This is joined by the cystic duct from the gallbladder, which has the capacity to store and concentrate bile, to form the common bile duct. This exits the liver, and is joined by the main pancreatic duct before entering the duodenum at the ampulla of Vater.

Box C Functions of the liver

Amino acid synthesisCarbohydrate metabolism (gluconeogenesis, glycogenosis, glycogenesis)Protein metabolism, synthesis and degradationLipid metabolism, cholesterol synthesis and lipogenesisCoagulation factor production (fibrinogen, prothrombin) and protein C, protein S and antithrombinAlbumin productionAngiotensinogen synthesis (hormone raising blood pressure if activated by renin)Bile production and excretionImmunological effects via the reticuloendothelial systemStorage of glucose (as glycogen) and vitaminsDetoxification, converting ammonia to ureaBreakdown of toxic substancesBreakdown of haemoglobin, insulin and other hormonesExcretion of waste products

Function

The liver is the main organ of metabolic control, maintaining circulating levels of glucose and fats, and providing essential circulating proteins such as albumin, carrier proteins and a number of clotting factors and complement components. The liver also receives almost the entire venous drainage of the intestinal tract, performing an essential regulatory and detoxifying role. When this circulation is disrupted, patients suffer consequences such as severe neurological dysfunction, which can lead to coma and death, known as hepatic encephalopathy. In addition, the liver metabolises and is essential for the excretion of endogenous and exogenous waste products such as bilirubin derived from the breakdown of haem, and of ammonia from the breakdown of amino acids, which is excreted in the form of urea.

Without the liver, life cannot be sustained for more than a few hours, and there is as yet no adequate artificial liver substitute.

Specialised cells

The liver is composed of a huge number of hepatocytes, which are arranged in columns and sheets with intervening channels through which blood courses, known as sinusoids; between adjacent hepatocytes are the microscopic biliary canaliculi into which bile is secreted. The sinusoids are lined by an endothelial cell layer that, unlike vascular endothelia in other organs, is relatively loosely organised, with many gaps in the lining.

Between the vascular endothelium and the hepatocytes is the space of Disse in which specialised stellate cells of the liver are located. These cells store retinoic acid and have a critical function in repairing liver injury and forming scar tissue that can lead to hepatic cirrhosis. Immune cells including lymphocytes and resident hepatic macrophages known as Kupffer cells reside in the sinusoidal and peri-sinusoidal spaces.

Hepatocytes are specialised to process, store and export sugars, fats and proteins, and to metabolise and detoxify endogenous and exogenous organic compounds. Typical ultrastructural features of hepatocytes include numerous mitochondria, extensive rough and smooth endoplasmic reticulum, Golgi apparatus, fat-filled vacuoles and glycogen-storage granules.

Pancreas

Anatomy

The pancreas is a large exocrine secretory organ located in the epigastrium, inferior to the stomach and to the left of the duodenum. The pancreas also contains endocrine islets that produce the essential hormones insulin and glucagon, which maintain glucose homeostasis.

The exocrine pancreas comprises secretory epithelial cells organised into acini, with the secretions draining into ducts. These ducts coalesce to form the main pancreatic duct; this drains into the duodenum at the ampulla of Vater.

Function

Pancreatic secretions provide the great bulk of digestive enzymes, including proteases, lipases and amylases. The pancreas also produces to neutralise stomach acid and create the optimal pH for digestive action.

Pancreatic enzymes have the capacity to cause autodigestion of the gland itself, and of intestinal tissues. Enzymes are therefore produced as larger proteins, known as pro-enzymes that are inactive; they are activated by cleavage after they have been secreted into ducts and the intestine.

Damage to the pancreas, which may release enzymes into the gland itself, can cause severe damage and a life threatening condition – acute pancreatitis. Diseases that damage the pancreatic capacity to produce enzymes, such as chronic pancreatitis, reduce the digestive capacity and cause malabsorption of fats, carbohydrates and proteins.

Digestion and absorption

The intestine is essential for processing and obtaining nutrition from food, regulating metabolism, and maintaining aspects of fluid and electrolyte balance. This is mediated by integrated action of all parts of the gastrointestinal tract, including the luminal organs from oesophagus to colon, and the pancreas and liver.

Digestion

Mechanical dissolution of food after chewing and swallowing is continued by the stomach, producing slurry known as chyme. The smaller the particles of food, the greater the surface area to volume ratio, providing a more tractable target for digestive enzymes including those produced by the pancreas and secreted into the duodenum. Fat is poorly soluble in the aqueous chyme, and bile salts secreted in bile help to disseminate fat from the diet into micelles, allowing greater access for fat-digesting enzymes. Thus obstruction to bile flow compromises the digestion and absorption of fats and fat-soluble vitamins such as D and K.

Digestion is the process of enzyme-mediated hydrolysis of macromolecules such as starch, triglycerides and proteins in food. The products of digestion are the constitutive components of these macromolecules – monosaccharides, free fatty acids, amino acids and short peptides – which are absorbed through the intestinal epithelium into the vascular and lymphatic circulation via specific transporter proteins. These transporters typically have exquisite specificity, for example for glucose coupled with Na + ions, or fructose, or acidic, basic and neutral amino acids.

Fatty acids absorbed from the diet are reconstituted in the epithelial cells into triglycerides and are secreted into lacteals as chylomicrons, for transport into the circulation. Other transport systems are responsible for the transport of micronutrients, that is, mineral

Fig C Hepatobiliary and pancreatic function.

elements and vitamins. These systems are regionally distributed, so that, for example, most absorption of iron occurs in the duodenum, while absorption of vitamin B12 occurs in the terminal ileum. Damage to the intestinal epithelium in different regions may therefore produce distinct patterns of malabsorption and deficiency.

Reabsorption

Digestive enzymes are secreted in large quantities of fluid and electrolytes, and if all of the secreted electrolytes and fluids were not reabsorbed the body would be depleted. Some reabsorption takes place in the distal small intestine; however the greatest capacity is in the colon, and the ileal effluent of over 1 L of fluid per day is reduced to

Fig D Digestion and absorption.

approximately 200 mL. Reabsorption of water is accompanied by the reabsorption of salts, particularly Na+, Cl− and .

Diarrhoeal illness

In diarrhoeal illnesses, the overall volume of stool is increased. It is possible to distinguish if this is due to one of the following processes:

Hypersecretion, for example caused by cholera toxin, which activates secretion from intestinal epithelial cells.Inf ammation, where secretion may be stimulated and the reabsorptive capacity of the intestine is compromised.Osmotic diarrhoea, whereby osmotically active substances in the intestinal content prevent reabsorption of water by creating a steep osmotic pressure gradient.Hypermotility, where increased peristalsis results in a rapid transit of intestinal contents through the intestine, exceeding the rate at which fluid can be reabsorbed.

Because absorption of water from the intestine follows electrolytes and osmotically active molecules such as sugars, diarrhoeal losses can be counteracted by providing luminal salt and sugar in the correct proportions. This is the basis of oral rehydration solutions to combat diarrhoea, which typically provide Na+ and glucose to exploit the Na+ /glucose transporter. Hypotonic fluids such as plain water dilute the luminal Na+ and reduce the capacity for absorption of water.

Gastrointestinal pathology

Infection

Gastrointestinal infection accounts for a major part of morbidity and mortality worldwide. Simple enteric infections, food poisoning and gastroenteritis, and specific infections such as cholera, which occur in outbreaks following the ingestion of contaminated food and water, can cause severe illness and death, particularly in the very young and the elderly and frail. Lack of sanitation and

Fig E Infections of the gastrointestinal tract.

reliable, safe drinking water, coupled with inadequate basic health care in poor regions of the world mean that gastroenteritis and diarrhoeal illness causes over 1 million excess deaths in childhood worldwide.

Gastroenteritis

Gastroenteritis is usually self-limiting. However, gastroenteritis can lead to dehydration that may cause death; and malnutrition and enfeeblement, where social circumstances and health care are inadequate, predispose to illnesses such as pneumonia. Agents that cause gastroenteritis include the following:

Viruses such as rotavirus, adenovirus and norovirus.Bacteria such as Escherichia coli, Campylobacter, Shigella and Vibrio cholerae.Parasites such as amoeba can cause dysentery, while others such as round worms, tapeworms and hookworms infest the intestine and cause chronic intestinal disease,

Fig F Drugs and toxins in the gastrointestinal tract.

malnutrition and iron deficiency by chronic low-volume bleeding.

Helicobacter pylori infection

Helicobacter pylori is a bacteria that is specialised for colonising the gastric mucosa, where it secretes a urease enzyme that locally neutralises gastric hydrochloric acid by hydrolysing urea to CO2 and NH4. Approximately 80% of the world ’s population is chronically infected with H. pylori , although the proportion is lower in rich countries with high standards of hygiene. Infection with H. pylori predisposes individuals to gastritis, peptic ulceration and stomach cancer – links that were discovered by Drs Warren and Marshall, leading to their winning the Nobel Prize for Medicine in 2005.

H. pylori infection can now be detected and is readily eradicated by a combination of acid suppression and antibiotics.

Viral infections

Viral infections, particularly by the hepatitis viruses A, B, C and E, are a major cause of liver disease. Hepatitis A and E cause acute hepatitis that is usually self-limiting, although patients may be quite ill with malaise and jaundice. Hepatitis viruses C and B cause chronic hepatitis that can progress to cirrhosis and liver cancer. Both forms of chronic viral hepatitis can now be treated with antiviral drugs.

Toxic damage

Alcohol

Alcohol is a major cause of liver disease as well as other illness. Chronic excessive use of alcohol causes chronic liver damage; the healing process, which includes regeneration of liver cells in the form of nodules rather than well-ordered plates and sheets, and fibrotic scarring, can lead to cirrhosis.

Fig G (a) Intestinal immunity and (b) autoimmunity.

Medications

The liver is also readily damaged by a whole range of medical drugs, many of which have a tendency to cause a typical pattern of injury:

Cholestasis may be due to flucloxacillin, co-amoxiclav and chlorpromazine, which damage the biliary epithelium.Acute liver damage may be due to antituberculosis drugs and anticonvulsants, which can mimic viral hepatitis.Massive necrosis of the liver may be caused by an overdose of the widely used analgesic paracetamol (acetaminophen). This can lead to acute liver failure, and is a medical emergency.

Autoimmune damage

Immune-mediated damage to the gastrointestinal system is a major cause of luminal disease, liver disease and in some cases pancreatic disease. The aetiology of the major immune-mediated diseases of the intestine remain unknown, although recent advances, particularly in genetic and immunological research, suggest a critical role for the innate immune system and the relation of the host to microorganisms that reside in the intestinal lumen.

Coeliac disease

One of the major immune-mediated diseases of the intestine is coeliac disease, which is caused by an inherited predisposition to react adversely to peptides derived from the digestion of gluten in cereals such as wheat, barley and rye. This affects as many as 1:100 people in parts of Europe and is associated with inheritance of the HLA-DQ2 allele in the MHC (major histocompatibility complex) class II locus.

In people with coeliac disease, gliadin peptides interact with the MHC to stimulate the aberrant proliferation of T lymphocytes, which causes damage to the intestinal mucosa, particularly in the duodenum. This can lead to malabsorption and weight loss, and because iron is mainly absorbed in the duodenum, to anaemia. The only successful treatment for coeliac disease is to avoid gluten in the diet.

Infammatory bowel disease

Other major immune-mediated disease of the intestine includes inflammatory bowel disease (IBD), which is mainly subdivided into Crohn ’ s disease and ulcerative colitis. Both can cause diarrhoea, abdominal pain, rectal bleeding from the inflamed and ulcerated colonic mucosa, and weight loss. Inflammation is localized to the colonic mucosa in ulcerative colitis, and may affect almost any part of the intestine, extending into the sub-mucosa and deeper layers in Crohn ’ s disease. The treatment remains empirical, and involves immunosuppression in many cases.

Primary biliary cirrhosis

Primary biliary cirrhosis (PBC) is a major cause of chronic liver disease, and is considered an autoimmune disease with damage limited to the biliary epithelium. It tends to affect women more than men, and progresses insidiously.

A simple diagnostic test for PBC is the presence of a circulating autoantibody to the mitochondrial enzyme pyruvate dehydrogenase (PDH). It is unknown why the presence of this autoantibody, which is the basis of the antimitochondrial antibody (AMA) test should be so strongly and specifically associated with PBC. AMA has no pathogenic effect, and the antigen is found in all cells that contain mitochondria.

There is no proven treatment for PBC, and in cases that have progressed to cirrhosis and liver failure, liver transplantation is the only therapeutic option.

Neoplasia

Cancer in the gastrointestinal system is a major cause of disease and death worldwide. For example, colon cancer is now the leading cause of death from cancer in the Western world, after lung and breast cancer in men and women, respectively. All parts of the intestinal tract can develop malignant tumours, although the colon, pancreas, oesophagus, stomach and liver are most frequently affected.

Genetic and environmental factors

Cancer typically develops as a stepwise process in which previously normal cells develop mutations in genes that alter their function and gradually release them from the normal restraints on growth and differentiation. Genetic and environmental factors play a strong role in the pathogenesis of cancer.

There is marked geographic variation in the incidence of various forms of cancer:

Liver cancer associated with chronic infection with hepatitis B virus is highly prevalent in the Far East.Colon cancer is especially prevalent in the West and is associated with a diet rich in red meat.Gastric cancer is rare in the West and frequent in Japan.

Fig H Neoplasia of the gastrointestinal tract.

Oesophageal squamous carcinoma is highly prevalent in parts of sub-Saharan Africa.Oesophageal adenocarcinoma is increasingly in incidence in the West.

Familial syndromes may increase the risk of certain types of cancer, for example colorectal cancer. It is also known that chronic inflammation, caused for example by H. pylori in the stomach, or hepatitis B virus in the liver, predisposes to the development of cancer.

Box D Colorectal cancer hereditary syndromes

Hereditary non-polyposis colorectal cancer (HNPCC)Familial adenomatous polyposis (FAP)MUTYH-associated polyposis (MUTYH is a human gene encoding a DNA glycosylase)Peutz-Jeghers syndrome (PJS)Juvenille polyposis

Colon cancer

In colon cancer, for example, this progressive change can be detected in pre-malignant lesions that are dysplastic rather than neoplastic. Typically dysplastic colonic epithelial cells form protuberances into the lumen of the colon called polyps which can be removed and examined in the laboratory. The removal of dysplastic polyps also arrests the development of cancer in that particular site.

Partly as a consequence of this reproducible adenoma to carcinoma sequence of development, the sequential genetic changes that lead to cancer are particularly well elucidated in colon cancer. We know, for example, that the earliest genetic change that occurs is a mutation in the APC tumour suppressor gene, and that one of the final changes that occurs before an adenoma becomes malignant is a mutation in the p53 gene.

Prevention

Strategies to prevent cancer in the gastrointestinal tract include measures to arrest chronic inflammation. These include:

Eradication of H. pylori infection.Treating oesophagitis caused by the reflux of gastric acid.Treating and preventing hepatitis B virus infection.Colonoscopy to detect and remove adenomatous polyps before they become malignant also prevents colon cancer. It is increasingly advocated in those regions where there is a high prevalence of this disease, such the USA and UK.

Approach to the patient

Gastrointestinal diagnosis relies heavily on a careful and thorough history. A detailed description of the symptoms and ancillary data, such as exposure to contaminated food or water, previous episodes of illness, consumption of potentially toxic drugs, heritable illness, etc., is critically important.

KEY POINT

Always introduce yourself and obtain verbal consent from the patient before proceeding with a detailed history and examination.

Presenting complaint

History taking should always start with an open question; asking the patient to ‘describe in their own words what the trouble is’ is helpful. If the answer is vague or non specific, more structured questions can then be asked. This is important for two reasons:

1 First, some symptoms, such as heartburn or dysphagia are so characteristically associated with certain conditions that the symptom naturally leads to the appropriate diagnostic hypothesis.

2 Second, where there may be a constellation of symptoms that need to be managed, knowing the patient ’ s priorities guides the appropriate treatment strategy.

Gastrointestinal symptoms are often non-specific. For example, abdominal pain may indicate life-threatening acute pancreatitis or may be a feature of irritable bowel syndrome, which usually runs a benign course. Many serious diseases are asymptomatic until the late stages, and may only manifest with mild, vague symptoms such as malaise and fatigue. Be vigilant for changes-for example a change in bowel habit, change in food tolerance, change in energy levels, etc.

Where patients use terms that are subject to interpretation, clarify the meaning. Words like diarrhoea, constipation, nausea, heartburn, etc., mean different things to different people. People are also frequently embarrassed about bodily functions such as defecation, and will use euphemisms that are even more idiosyncratic.

Use the interview to show that as a professional you are knowledgeable, interested and non-judgemental, and give the patient the opportunity to talk freely, possibly for the first time, about their symptoms.

KEY POINT

Always clarify the meaning of symptoms, as certain terms are subject to interpretation.

Gastrointestinal s ymptoms

Disorders of the gastrointestinal system may present with a wide range of symptoms. When enquiring about gastrointestinal illness it is worth asking specifically about certain symptoms, even if only to have a confirmed negative. The following list could guide the consultation:

Dry mouth (xerostomia) or painful mouth.Excess salivation (waterbrash).Altered taste sensation (dysgeusia) or smell.Bad breath (halitosis).Lump in the throat (globus).Difficulty with swallowing (dysphagia).Pain on swallowing (odynophagia).Nausea and vomiting.Heartburn and reflux: epigastric or retrosternal burning or acid indigestion.Abdominal pain or discomfort.Dyspepsia: epigastric discomfort particularly related to eating.Bloating or abdominal distension.Hiccups.Excessive belching or flatulence.Diarrhoea: increased frequency or volume of stool, or looser motions.Urgency of defecation.Incontinence of faeces or flatus.Constipation: reduced frequency or volume of stool, difficulty passing stool.Incomplete evacuation (tenesmus).Defecation difficulty.Any altered bowel habit.Any altered stool character.Rectal bleeding: fresh or altered blood or melaena stool.Loss of weight.Change in appetite: loss of appetite, increased appetite.Jaundice.Itch (pruritis).

Painful mouth

Causes of a painful mouth include infections, trauma, vitamin deficiency, medications, systemic disorders and dermatological conditions. Gastrointestinal disorders causing painful mouth ulceration include coeliac disease and inflammatory bowel disease. Idiopathic apthous ulcers may run in families and be exacerbated by menstruation.

Box E Causes of a painful mouth

Infection: candidiasis, herpes simplex, ulcerative gingivitis, infectious mononucleosisTrauma: dentures or teethMedication: cytotoxic drugs, sulphonamidesVitamin deficiency: vitamin B12, folate, ironUlceration from systemic disease: inflammatory bowel disease, coeliac disease, Behçet ’ s diseaseDermatological condition: lichen planus, erythema multiforme, pemphigoid and pemphigusMalignant: leukoplakia, carcinomaIdiopathic: apthous mouth ulcers

Dysphagia and odynophagia

Key factors to define are:

1Level of swallowing difficulty : oropharangeal dysphagia causes difficulty in initiating a swallow, problems within a second of initiating a swallow or repeated attempts at swallowing. Oesophageal dysphagia causes difficulty in swallowing seconds after initiating a swallow.

2Type of swallowing difficulty : this may be for solids, liquids or both. Swallowing solids with ‘ sticking ’ and impact pain suggests a mechanical cause such as a stricture. Difficulty with liquids with spluttering and repeated swallows may represent a high pharyngeal cause. Nasal regurgitation, spluttering and aspiration may be due to achalasia or a pharyngeal pouch. A pouch may also cause bulging of the neck, gurgling or a nocturnal cough. The inability to swallow both solids and liquids may be a feature of oesophageal dysmotility or a more worrisome oesophageal carcinoma; the order of symptoms, speed of onset and associated alarm features are important to differentiate this.

3Duration and pattern of swallowing difficulty : the duration and progression of dysphagia will determine if this is a benign or malignant process. A short progressive history is more suggestive of malignancy. A longer history intermittently over years suggests a more benign cause such as oesophageal dysmotility or an oesophageal web.

4Pain on swallowing (odynophagia) : retrosternal chest pain on swallowing is characteristic of inflammatory disorders of the oesophagus. This may be the result of oesophageal candidaisis, herpes simplex oesophagitis, severe ulcerated reflux oesophagitis, oesophageal spasm or achalasia.

5Previous history of reflux disease or swallowing disorder.

!RED FLAG

The following symptoms should act as an alarm:

Unintentional weight loss.Short history of progressive dysphagia.

Predisposing f actors for d ysphagia

Foreign body (fibrous or dry foods, tablets, solid objects).Corrosive material.Prolonged acid reflux and heartburn.Medication: bisphosphonates, non-steroidal antiinflammatory drugs (NSAIDs), steroid inhalers.Smoking.Alcohol consumption.Previous history of Barrett’s or peptic stricture.Neck surgery or radiotherapy.Connective tissue disease such as scleroderma.Neurological disorder with a bulbar palsy.Family history of gastrointestinal malignancy or familial tylosis.

Complications of dysphagia

Aspiration of oesophageal contents into the bronchial tree.Oesophageal rupture or tear.

Nausea and vomiting

Nausea and vomiting may be caused by gastrointestinal disorders or conditions affecting other organ systems. In most cases, vomiting is preceded by nausea, but in the case of intracranial tumour or hyperemesis of pregnancy, there may be no warning. Vomiting may also be self-induced in cases of bulimia or to relieve symptomatic pain or satiety. A careful description of what is meant by each of these terms is required.

Features of history

Duration of symptoms.Timing and frequency of vomiting, such as early morning.Contents of vomit, taste, colour, quantity and smell. Bile is yellow-green and bitter and from the distal duodenum. Faeculant vomit is brown and malodorous suggesting small bowel of colonic obstruction or a fistula.Presence of blood: fresh red blood may arise from an oesophageal lesion, dark blood with clots suggests profuse bleeding from a peptic ulcer or varicies, coffee ground vomit is altered blood due to gastric acid exposure. Also ask if there was intense retching prior to this, suggesting a Mallory-Weiss tear.Exacerbating factors, such as certain foods or smells.Relieving factors.

Associated gastrointestinal symptoms that may give a clue about aetiology

Swallowing difficulties: perhaps a pouch or stricture is present.Abdominal pain or discomfort, such as in peptic ulceration, pancreatitis and gallstones.Refux of acid or heartburn in ulcer disease.Loss of appetite or weight: think malignancy and malabsorption.Jaundice with or without pruritis in hepatobiliary disease.Fever or rigorsChange in colour of the stools or urine.Change in bowel habit.

Associated non-gastrointestinal symptoms that may give aclue about aetiology

Menstrual disturbance: could patient be pregnant?Neurological symptoms: headaches, visual disturbance, neck stiffness, weakness or paraethesia, vertigo.Disorder of hearing or balance in labyrnthitis or Meniére’s disease.Excessive thirst or urination, indicating diabetes.Rash (hyperpigmentation) of Addison’s disease.

Predisposing factors

Medical conditions: neurological disorder, diabetes, thyroid disease, cardiovascular disease, arrhythmia.Psychiatric history, asking specifically about bulimia.Medications, such as chemotherapy agents, analgesics, antiarrthymics, diuretics, hormonal drugs, antibiotics and antivirals, anticonvulsants, anti-parkinsonian drugs.Infection exposure.Travel history.Smoking and amount.Alcohol consumption.Recreational drug use.

Box F Causes of nausea and vomiting

Gastrointestinal

AchalasiaPyloric stenosisIntestinal stricturesGastroparesisPeptic ulcer diseaseNon-ulcer dyspepsiaPseudo-obstructionGastrointestinal infections and food poisoningPancreatitisCholecystitis and cholangitisAcute hepatitisMesenteric ischaemiaGastric cancer

Other causes

PregnancyIntracranial pathology: raised ICP, meningitis, migraine, seizures, tumoursEar problems: labyrnthitis, Menière ’ s diseaseEndocrine disorders: diabetic ketoacidosis, Addison ’s disease, hyper-and hypoparathyroidismMetabolic disorders: uraemia, hypercalcaemia, hyponatremiaMedications: chemotherapy agents, analgesics, antiarrthymics, diuretics, hormonal drugs, antibiotics and antivirals, anticonvulsants, anti-parkinsonian drugsAlcoholNicotinePsychological and psychiatric disorders: bulimia, depression, voluntary emesis, strong emotions such as disgust

Heartburn and reflux

Heartburn or acid indigestion is highly suggestive of gast ro-oesophageal reflux. Most individuals have experienced this in their lifetime. It is typically aggravated by large meals, stooping over, lying down, straining on exercise and during pregnancy. It may be relieved by antacids. There may be an altered taste sensation or increased salivation (waterbrash). There may be associated swallowing difficulties due to oesophagitis. It must be differentiated from cardiac, respiratory and musculoskeletal causes of chest pain.

!RED FLAG

Alarm symptoms to exclude in patients with heartburn:

Progressive unintentional weight loss.Progressive dysphagia.Persistent nausea and vomiting.Symptomatic gastrointestinal blood loss: haematemesis or melaena.

Predisposing factors

Medications causing inflammation such as bisphosphonates or slow-release potassium.Medications causing motility problems such as theophylline-based tablets.Smoking.

Abdominal pain

Abdominal pain and discomfort is the most common gastrointestinal symptom. It needs to be defined further.

Features of history

There are ten characteristics that should be sought in any abdominal pain history:

Character: dull ache, colicky spasms, deep or superficial. Colicky pain, occurring in waves, suggests coincidence with peristaltic waves in an obstructed hollow organ. Dull, constant and gnawing pain occurs in peptic ulcer disease, penetrating into the retroperitoneal tissue.Location: epigastric pain is said to be frequently due to disease of foregut structures such as the stomach or duodenum. Peri-umbilical pain is said to be due to midgut structures such as the small intestine or appendix. Lower abdominal pain may be the result of disease in hindgut structures such as the colon and rectum. The site of pain may not indicate the site of the problem.Radiation: radiation to back, loins, groin, chest, shoulder tip or other area of the abdomen. Disease of the liver or gallbladder is typically felt in the right upper quadrant, and may affect the lower chest or even the tip of the shoulder by irritating the diaphragm. Disease of the pancreas causes epigastric pain that may radiate into the back.Onset: sudden or gradual. Sudden onset severe pain may occur in pancreatic inflammation, obstruction of a bile duct by a gallstone or ischaemia of the intestine.Progression: is it becoming more severe and intense or constant?Intensity: estimate on a grading scale from 1 to 10, with 10 the worst pain imaginable.Frequency: this can be number of times in a day/week/ month/year.Duration: when was it first noticed (this may be a prior episode)? The chronicity of pain is important; for example, the internationally agreed criterion for irritable bowel syndrome (IBS) is that abdominal pain should have been present for the majority of time for at least 6 months. Colicky pain from gallstone disease may occur intermittently in recurrent bouts over months before being diagnosed.Aggravating and relieving factors: posture, eating meals; worsened by movement, inspiration or coughing, better on lying still. Pain from peptic ulcers may be made worse by eating, or by fasting, causing so-called hunger pangs. Fatty meals, which stimulate contraction of the gallbladder, aggravate pain due to gallstones. Colonic disease may cause pain that precedes defecation and urges defecation. Typically in IBS, defecation relieves abdominal pain temporarily.Associated symptoms: a change in the pattern of symptoms should alert you to a change in pathology; consider the development of a new pathology, a complication of the original pathology or an incorrect initial diagnosis.

Box G Common causes of abdominal pain

Gastrointestinal causes

Peptic ulcerPancreatitisBiliary colicRenal colicMesenteric ischaemia or arterial occlusionVolvulusStrangulated herniaObstructionPerforation of stomach (peptic ulcer) or colon (carcinoma, diverticular)AppendicitisDiverticulitis

Non-gastrointestinal causes

Myocardial infarction and arrhythmiasDissecting aortic aneurysmPleurisyVertebral prolapse or collapseCord compressionDiabetic ketoacidosisEctopic pregnancyTestes or ovarian torsionHerpes zoster infection

Bloating or abdominal distension

Abdominal distension is caused by one of the ‘ five Fs’:

Fat: adipose deposition due to excess food consumed or alcohol.Fluid: consider ascites, bladder distension and ovarian cyst.Faeces: constipated stool and obstruction or Hirschsprung ’ s disease.Flatus: obstruction and pseudo-obstruction.Fetus: could she be pregnant?

Fluctuating abdominal swelling with diurnal variation is common in women and rarely caused by organic disease. It is a feature of irritable bowel syndrome.

Belching and flatulence

Repeated belching is of no major significance, indicating the swallowing of air, usually unintentionally. It may be associated with acid reflux or anxiety symptoms. Excessive flatus or rectal flatulence, which may be malodorous is troublesome, and may represent intestinal malabsorption or lactase deficiency. A full diet history should be taken and any intolerance documented. The absence of flatus is concerning and indicates intestinal obstruction.

Altered bowel habit

The normal bowel habit is different for every individual and should be defined. The normal bowel habit varies from three or so evacuations per day to one every 3 days. Changes in bowel habit may be an early sign of serious disease.

Features of history

How does the current bowel habit differ from normal?Duration of symptoms: acute or chronic.Intermittent or persistent or alternating bowel habit change.Frequency day and/or night.UrgencyNature of the stool: consistency, colour, odour, presence of mucus.Blood present: mixed in or separate.