Upper GIT Pathologies 1 Slide PP PDF

Upper Gastrointestinal Tract Conditions Conditions of the Upper Gastrointestinal Tract Dr Nicola Eastaff-Leung We acknowledge the Kaurna people, the original custodians of the Adelaide Plains and the land on which the University of Adelaide's campuses at North Terrace, Waite, and Roseworthy are...

Upper Gastrointestinal Tract Conditions Conditions of the Upper Gastrointestinal Tract Dr Nicola Eastaff-Leung We acknowledge the Kaurna people, the original custodians of the Adelaide Plains and the land on which the University of Adelaide's campuses at North Terrace, Waite, and Roseworthy are built. Upper Gastrointestinal Tract Revision: Food passes into the mouth and through the oral cavity to the pharynx and oesophagus It then enters the stomach and is mechanically broken down before passing into the small intestine for nutrient absorption and then to the large intestine for compaction of waste Lecture Outline 1. Oesophageal Disease: Oesophageal varices Gastroesophogeal reflux disease Barrett’s oesophagus Oesophageal cancer 2. Peptic Ulcer Disease 3. Coeliac Disease Learning Objectives for Conditions of the Upper GIT Understand the common causes of these conditions Identify the most common symptoms of these conditions Describe the pathogenesis of each condition Identify the complications associated with these conditions Summarise the management and treatment options available Oesophageal Varices Oesophagus Revision Muscular tube Approx 25cm long From pharynx to stomach Transports food from the pharynx to the stomach Upper and lower oesophageal sphincters control the movement of food Muscular layer contribute to peristalsis Lower oesophageal sphincter keeps stomach contents in the stomach Oesophageal varices – Definition and prevalence What are oesophageal varices? Enlarged veins in the oesophagus These can be diagnosed via endoscopy Life threatening complication of portal hypertension Prevalence seen in up to 50% of patients with liver disease such as liver cirrhosis 25-40% of sufferers will experience bleeding. 15% of these will die from blood loss Oesophageal varices – Symptoms and signs There are no symptoms of oesophageal varices until they rupture Signs of bleeding can include vomiting of blood, dark or tarry stools Signs of blood loss – light headedness, confusion, loss of consciousness Oesophageal varices – Pathogenesis Pathogenesis: Caused by obstructed blood flow through the portal vein. Cirrhosis of the liver can result in portal hypertension, where blood flow is backed up Increased pressure causes veins of the esophagus to become dilated and swollen Oesophageal varices – Management Treatment: Lifestyle modifications – weight loss, stopping all alcohol Medication to lower blood pressure – beta blockers Surgery – variceal band ligation  Gastro-oesophageal Reflux Disease (GORD) GORD – Definition and Prevalence Definition: Gastro-oesophageal reflux disease (GORD/GERD) Where stomach acid or bile is not contained within the stomach and repeatedly flows back into the oesophagus Prevalence: 10-20% of the population in Western countries Common in people aged 40+ GORD – Symptoms and Signs Symptoms: Heartburn – burning chest pain that can mimic angina pectoris Pain is often worse after eating, when lying down and with emotional stress Regurgitation of sour-tasting gastric content Nausea, burping Dry cough and sore throat GORD - Pathogenesis Three factors can cause GORD: 1. Poor oesophageal clearance efficient peristalsis and saliva production limits the exposure of the oesophagus to the acid and bile in the stomach 2. Dysfunctional lower oesophageal sphincter (LOS) The LOS relaxes to allow the passage of food into the stomach and closes to protect the oesophagus from the acid in the stomach Alcohol and smoking, obesity, pregnancy, smoking 3. Delayed gastric emptying causing the stomach to overfill An increase in gastric pressure can put pressure on the LOS GORD - Management Management: Avoiding specific foods and drinks, losing weight, stopping smoking Medication - Proton pump inhibitors (reduces stomach acid production) Surgery Complications: A chronic complication of GORD is Barrett’s oesophagus Barrett’s Oesophagus Barrett’s Oesophagus – Prevalence and Symptoms Epidemiology: Occurs in up to 10% of people with GORD, and 2% of the general population Most common in caucasian men aged between 40-60 years Symptoms: Same symptoms as GORD such as heartburn, a sour burning sensation in the back of the throat Can also include a chronic cough and laryngitis Barrett’s Oesophagus - Pathogenesis Pathogenesis: Normal oesophageal epithelium is replaced with metastatic columnar cells The cells lining the esophagus have adapted to prolonged exposure to stomach acid The normal stratified squamous epithelium is replaced with simple columnar epithelium Stratified squamous epithelium Simple Complications: columnar epithelium There is an increased risk of progression to adenocarcinoma Red flag symptoms of malignancy includes dysphagia, weight loss, malaise, loss of appetite Barrett’s Oesophagus - Management Management: Lifestyle modifications Proton pump inhibitors – high doses twice a day Avoidance of medications that can damage the stomach protective barrier such as NSAIDs Regular endoscopies to monitor any potential progression to adenocarcinoma Oesophageal Cancer Oesophageal Cancer - Prevalence Ninth most common cancer in Australia It is three times more common in men than women Most common in men aged between 45- 65 years There is an increased rate of oesophageal cancer in Indigenous than non-Indigenous Australians, and an increased rate in low socioeconomic areas. Oesophageal Cancer – Risk Factors Squamous Cell carcinoma occurs anywhere in the oesophagus where there is squamous cells Most common in middle and upper esophagus Risk factors - cellular injury and chronic inflammation: Smoking, Alcohol, Diet. Adenocarcinoma: Occurs in the lower oesophagus only Risk factors – Acid damage: Barrett’s oesophagus, hiatus hernia, obesity Oesophageal Cancer – Treatment Surgery will depend on staging Neoadjuvant treatments such as chemotherapy and radiation therapy Radiation therapy can cause scarring of the oesophagus however stents can be used to hold the oesophagus open Peptic Ulcer Disease (PUD) Peptic Ulcer Disease – Definition and Prevalence Definition: The presence of chronic mucosal ulceration in the lining of the stomach or the duodenum Prevalence: Peptic ulcer disease affects 0.1- 0.2% of the worlds population Peptic Ulcer Disease - Symptoms Abdominal pain that is often worse after meals indigestion weight loss nausea Blood in vomit or bowel motions complications of bleeding ulcers can result in iron deficiency anaemia Severe bleeding can cause death Peptic Ulcer Disease – Pathology Perforated ulcer - fatal Healed Ulcer – non-fatal Peptic Ulcer Disease - Pathophysiology Two main causes of PUD: 1. Helicobacter Pylori Infection 2. Non-steroidal anti-inflammatory use: NSAIDS like ibuprofen are non-specific COX inhibitors They work by decreasing prostaglandins that serve as messengers that promote pain. COX-2 is involved in inflammation Prostaglandins are also important in protecting the stomach lining from stomach acid and maintaining a healthy stomach lining These protective prostaglandins require the enzyme COX-1 for their production COX-1 is essential for the normal functioning of the gastrointestinal tract Peptic Ulcer Disease - Pathophysiology H.Pylori was first Identified as causing PUD in 1982 by Dr Barry Marshall and Dr Robin Warren and earned them a Noble prize No one believed bacteria could survive in the acidic environment of the stomach Dr Robyn Warren ingested H. Pylori and gave himself a peptic ulcer Peptic Ulcer Disease – H. Pylori Helicobacter pylori: A rod-shaped, gram negative bacterium with flagellated tail Transmitted by contaminated food and water Infections are very common is Asia with as many of 70% of the population affected. In Western Countries, infections occur in approximately 10% of people aged between 18-30, and 50% of people aged over 60 Infection of H.pylori does not guarantee PUD and many infections are asymptomatic H.pylori infection can increase the risk of gastric cancer Peptic Ulcer Disease – H. Pylori Flagella allows the H. pylori to propel itself rapidly through the gastric acid and burrow under the mucus layer of the stomach Peptic Ulcer Disease – H. Pylori H. pylori is also capable of producing urease which neutralises the gastric acid and provides a protective ammonium bubble while being surrounded by stomach acid. The H.Pylori then burrows into the gastric epithelium and colonises. Peptic Ulcer Disease – H. Pylori Ammonia and proteases produced by H. pylori is damaging to the mucosal epithelial cells Mucosal damage occurs Peptic Ulcer Disease Complications: Bleeding, penetration into solid organs (eg pancreas) H.Pylori infection is the strongest known risk for gastric cancer, which is the second leading cause of cancer related deaths world wide Peptic Ulcer Disease Management Eradication of H. pylori – non invasive testing: Urea breath test Antibiotics if positive for H. pylori Discontinue NSAIDs Cessation of smoking, reduction of alcohol https://www.ureabreathtests.com/ consumption Medication – proton pump inhibitor Surveillance – endoscopy if symptoms persist despite medication https://www.researchgate.net/ Coeliac Disease Coeliac Disease – Definition and Prevalence Coeliac Disease: An autoimmune disease where the ingestion of gluten results in the damage of the mucosa of the small intestine Prevalence: Affects approximately 1% of the worlds population, although rates of up to 5% are seen in Africa and 2.5% in Finland Diagnosis can occur between 10-40 years Coeliac Disease - History The earliest accounts of coeliac disease was 8000 years ago in Ancient Greece The cause of this “failure to thrive” wasn’t discovered until during WW2 where there were massive bread shortages Children in hospices suddenly recovered when their diet was potato based Coeliac Disease – Symptoms and Signs Symptoms: abdominal pain and bloating chronic diarrhea or constipation iron deficiency, chronic fatigue headache Osteoporosis Symptoms of Vitamin and mineral malabsorption Coeliac Disease - Pathophysiology Genetic (HLA genes) and environmental risk factors (Breast feeding, caesarian birth, microbiome) Coeliac disease is the result of an immune reaction to the components of gluten In healthy individuals wheat is broken down to gluten, and then this is incompletely digested and results in a large gliadin peptides. People with coeliac disease are reactive to the gliadin in gluten Coeliac Disease - Pathophysiology The large gliadin peptides are normally absorbed by enterocytes and do not cause any problems However in coeliac disease the gliadin peptides enters the lamina propria of the small intestine and initiates an immune response There is a T cell mediated autoimmune inflammatory reaction which results in marked atrophy or total loss of villi Coeliac Disease – Pathophysiology/Histology Coeliac Disease – Endoscopy Normal Duodenum Normal Duodenal endoscopy Duodenal folds are regular Villi are visible as finger-like projections www.endoscopy-campus.com Coeliac Disease – Endoscopy Coeliac Duodenum Coeliac endoscopy: Granular appearance of duodenal folds Loss of villi www.endoscopy-campus.com Coeliac Disease – Complications Severe symptoms can cause other conditions such as anaemia due to severe malabsorption. Malabsorption can also result major vitamin deficiencies that can cause neurological conditions, osteopenia and severe metabolic disturbances Untreated coeliac disease increases the risk for T cell lymphoma Coeliac Disease - Treatment Usually the gastroenterologist will refer newly diagnosed coeliac patients to a dietician. Gluten needs to be totally removed from the diet. Even trace amounts can cause changes to the gastrointestinal mucosa. Increased risk of T cell lymphoma with non-compliance Foods that most people don’t realise contain gluten: beer, stock cubes, chewing gum, some lollies, icecream, processed meats, tomato sauce and other condiments, hot chips etc Lecture Review Oesophageal varices Definition of disease Gastroesophogeal reflux disease Prevalence of disease Barrett’s oesophagus Clinical symptoms and signs Oesophageal cancer Pathophysiology Peptic Ulcer Disease Complications Coeliac Disease Treatment and Management