Gastric Disease 2025 PDF | Lecture Slides | Gastroenterology

Gastrointestinal System Session 5 Gastric Disease Prof. Dr. Hadeel a. karbel Learning outcomes 1. Describe the prevalence and incidence of common disorders affecting the stomach 2. Describe the presentation, investigation and outline the management of common Gastric disorder...

Gastrointestinal System Session 5 Gastric Disease Prof. Dr. Hadeel a. karbel Learning outcomes 1. Describe the prevalence and incidence of common disorders affecting the stomach 2. Describe the presentation, investigation and outline the management of common Gastric disorders 3. Describe the clinical features and natural history of ulcer disease 4. Explain the importance of Helicobacter Pylori in causing chronic gastritis 5. Outline the principles of modern ulcer treatment 6. Outline the ways in which gastric acid secretion may be reduced by drugs References Gastrointestinal system – crash course. 4th Edition, Mosby 1. Describe the prevalence and incidence of common disorders affecting the stomach Gastrointestinal (GI) symptoms are widespread and carry heavy economic and social consequences. It is estimated that in the United States 11% of the population suffer from a chronic digestive disease, with a prevalence rate as high as 35% for those 65 years and over. Functional gastrointestinal disorders (FGIDs), represented by functional dyspepsia (FD) and irritable bowel syndrome (IBS), include variable combinations of chronic or acute gastrointestinal symptoms not explained by structural or biochemical abnormalities. Worldwide the prevalence rates in the general population of dyspepsia/FD and IBS according to Rome III diagnostic criteria are 5.3–20.4% and 1.1–29.2%, respectively. 2. Describe the presentation, investigation and outline the management of common Gastric disorders Gastro-oesophageal reflux disease (GERD): A condition in which reflux causes troublesome symptoms (typically including heartburn or regurgitation) and/or esophageal injury/complications. The most common endoscopic finding associated with esophageal mucosal injury is reflux esophagitis The most common endoscopic finding associated with esophageal mucosal injury is reflux esophagitis NERD (non-erosive reflux disease): characteristic symptoms of gastroesophageal reflux disease in the absence of esophageal injury, such as reflux esophagitis, on endoscopy (50–70% of GERD patients). ERD (erosive reflux disease): gastroesophageal reflux with evidence of esophageal injury, such as reflux esophagitis, on endoscopy (30–50% of GERD patients)  anti-reflux mechanisms: Lower oesophageal sphincter – which is usually closed and transiently relaxes as part of physiology of swallowing to allow bolus to move into stomach Oesophagus enters stomach in abdominal cavity Pressure in abdominal cavity is higher than that of thoracic Right crus of diaphragm acts as sling around the lower oesophagus Clinical features of GORD occur when antireflux mechanisms fail and there is prolonged contact of gastric juices with lower oesophageal mucosa. Clinical features Dyspepsia (heartburn) is the medical term for indigestion, a symptom which includes epigastric pain, heartburn, distension, nausea or ‘an acid feeling’ occurring after eating or drinking. CAUSES functional dyspepsia reflux disease ulcer disease gastric cancer biliary tract disease chronic pancreatitis, pancreatic cancers hepatic Diabetes mellitus. Antibiotics, iron and other medications. NSAIDs Investigations and diagnosis Usually, clinical diagnosis made without investigation on symptoms alone, no need to investigate unless alarming symptoms (such as dysphagia) or hiatus hernia is suspected (which would be investigated by endoscopy) Management Lifestyle Lose weight. stop smoking. reduce alcohol consumption. reduce consumption of food groups known to aggravate the symptoms(e.g. chocolate, fatty foods, coffee). eating smaller meals Medications Simple antacids – e.g. calcium carbonate (neutralises acid) Raft antacids– e.g. Gaviscon liquid, taken after eating which creates protective raft that sits on top of stomach contents to prevent reflux PPIs – e.g. omeprazole – reduction in acid secretion by parietal cells H2 antagonists – e.g. ranitidine – blocks H2 receptors which reduced acid secretion Complications Continual contact of gastric juices with oesophageal mucosa can lead to metaplastic change à Barrett’s oesophagus Additional complications Reflux esophagitis Erosive esophagitis Iron deficiency anemia. Esophageal stricture Complications due to aspiration of gastric contents Reflux laryngitis: 3. Describe the clinical features and natural history of ulcer disease Peptic ulcer disease (PUD): Peptic ulcer is break in superficial epithelial cells penetrating down into Muscularis mucosa of either stomach (GU) or duodenum (DU). Most DUs are found in duodenal cap and GU are most commonly seen in lesser curvature of stomach. Ulcer disease has become a disease predominantly affecting the older population, with the peak incidence occurring between 55 and 65 years of age. pathogenesis Gastric hyperacidity is fundamental to the pathogenesis of PUD. The acidity that drives PUD may be caused by : 1. H. pylori infection. 2. parietal cell hyperplasia. 3. excessive secretory responses, or impaired inhibition of stimulatory mechanisms such as gastrin release. For example, Zollinger-Ellison syndrome, characterized by multiple peptic ulcerations in the stomach, duodenum, and even jejunum.  Cofactors in peptic ulcerogenesis include chronic NSAID use. cigarette smoking, which impairs mucosal blood flow and healing. high-dose corticosteroids, which suppress prostaglandin synthesis and impair healing. Peptic ulcers are more frequent in persons with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism ، In the latter two conditions, hypercalcemia stimulates gastrin production and therefore increases acid secretion. Finally, psychologic stress may increase gastric acid production and exacerbate PUD. Injury to gastric and duodenal mucosa develops when deleterious effects of gastric acid overwhelm the defensive properties of the mucosa. Inhibition of endogenous prostaglandin synthesis leads to a decrease in epithelial mucus, bicarbonate secretion, mucosal blood flow, epithelial proliferation, and mucosal resistance to injury. Lower mucosal resistance increases the incidence of injury by endogenous factors such as acid, pepsin, and bile salts as well as exogenous factors such as NSAIDs, ethanol and other noxious agents Epidemiology Duodenal Ulcers found in ~10% adult population and are 2-3 times more common than GUs. In developed countries increased prevalence of NSAID-associated GUs and decreasing prevalence of H pylori associated ulceration  Clinical features Recurrent, burning epigastric pain (pain is often worse at night and when hungry with Duodenal Ulcers and relieved when eating). Persistent, severe pain suggest penetration of ulcer into other organs Back pain suggest penetrating posterior ulcer. nausea, vomiting. With GUs can get weight loss and anorexia May be asymptomatic and present for first time with hematemesis when ulcer has perforated blood vessel(s) Investigations Investigate H pylori infection In older patients (over 55y/o) or with other alarming symptoms à endoscopy to exclude cancer Management The goal of therapy for peptic ulcer disease is to relieve symptoms, heal craters, prevent recurrences, and prevent complications. Medical therapy should include treatment with drugs, and attempt to accomplish the following: 1) reduce gastric acidity by mechanisms that inhibit or neutralize acid secretion. 2) coat ulcer craters to prevent acid and pepsin from penetrating to the ulcer base. 3) provide a prostaglandin analog. 4) remove environmental factors such as NSAIDs and smoking, and 5) reduce emotional stress (in a subset of patients). Management cont. If due to H pylori infection à Triple Therapy Proton Pump Inhibitor – Omeprazole Antibiotics – Clarithromycin / Amoxicillin H2 Antagonist – Cimetidine If taking NSAIDs – stop or review – use alternatives (NSAIDs with lower risk of causing PUD), or use prophylactic PPI as well as NSAID Surgical therapy  Complications of PUD Haemorrhage of blood vessel which ulcer has eroded à presents with hematemesis and melena Perforation of the ulcer – more common in DUs than GUs – usually perforate into peritoneal cavity Gastric outlet obstruction à can be pre-pyloric, pyloric or duodenal. Occurs either because of active ulcer with oedema or due to healing of an ulcer with associated fibrosis (scarring). Gastric outlet obstruction normally presents as vomiting without pain. Malignant transformation GU High malignant potential (progression to cancer in 5–10% of cases), Malignancy should be ruled out with biopsy. DU Usually benign Routine biopsy is not required. 4. Explain the importance of Helicobacter Pylori in causing chronic gastritis Helicobacter pylori infection : H pylori is a gram negative, aerobic, helical, urease producing bacterium that resides in the stomach of infected individuals. Production of urease produces ammonia, which neutralises acidic environment, which allows bacterium to survive.  Gastric ulcers: H. pylori secretes urease → conversion of urea to NH3 → alkalinization of acidic environment → survival of bacteria in gastric lumen Bacterial colonization and attachment to epithelial cells → release of cytotoxins (e.g., cagA toxin) → disruption of the mucosal barrier and damage to underlying cells Duodenal ulcers: H. pylori inhibits somatostatin secretion → ↑ gastrin secretion → ↑ H+ secretion → excess H+ delivery to the duodenum Direct spread of H. pylori to the duodenum → inhibition of duodenal HCO3- secretion→ acidification and insufficient neutralization of duodenal contents Diagnosis IgG detected in serum (relatively good sensitivity and specificity) 13C-urea breath test (13C-urea ingested – if H pylori present the urease produced will break down 13C-urea to NH3 and CO2 – CO2 (where the carbon is 13C) will be exhaled on breath and detected). Can also take gastric sample by endoscopy and detect by histology and culture. And Rapid urease test. Treatment Triple therapy. Proton Pump Inhibitor – Omeprazole Two Antibiotics – Clarithromycin / Amoxicillin H2 Antagonist (if severe) 7-14 day treatment – 14 days more effective but side-effects of treatment may put patients off finishing two week course H pylori causing gastric disease: Gastritis Usual effect of infection, which is usually asymptomatic. Duodenal ulcers (DUs) à prevalence of DU due to H pylori is falling due to decreased prevalence of H pylori infection. If ulcers due to H pylori infection, eradication of infection relieves symptoms and decreases chances of recurrence. Gastric ulcers (Gus) Ulceration thought to occur due to reduction in gastric mucosal resistance due to cytokine production as a result of infection Gastric cancer 5.Outline the principles of modern ulcer treatment If due to H pylori infection à Triple Therapy Proton Pump Inhibitor – Omeprazole Two Antibiotics – Clarithromycin / Amoxicillin H2 Antagonist (if severe) If taking NSAIDs – stop or review – use alternatives (NSAIDs with lower risk of causing PUD), or use prophylactic PPI as well as NSAID PPI – e.g. omeprazole  6. Outline the ways in which gastric acid secretion may be reduced by drugs Acid secretion may be reduced by inhibition of: Histamine at H2 Receptors antagonists reduce gastric acid production by blocking the H2 receptor on the parietal cell E.g. Cimetidine, ranitidine, famotidine and nizatidine. Removes the amplification of Gastrin/Ach signal Proton Pump Inhibitors (PPIs) E.g. Omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole inactivates the parietal cell hydrogen-potassium ATPase located on the lumenal surface. ATPase acts as a proton pump and constitutes the final common pathway in the secretion of hydrogen ions. This class of medicines is now considered the gold standard in medical therapy of peptic ulcer disease